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DEPRESSION ON CAMPUS: Record numbers of college students are seeking treatment for depression and anxiety. Schools can't keep up  LMC SOURCE 3

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DEPRESSION ON CAMPUS: Record numbers of college students are seeking treatment for depression and anxiety. Schools can't keep up  LMC SOURCE 3

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What is Reaction Formation Psychology?

Reaction formation is a term used in psychology to describe a defense mechanism people may use to reject how, unconsciously, they or their 'ego' really feel. Instead, someone behaves in a way that is exactly the opposite - and often at the extreme in an amplified or exaggerated way.
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Defense mechanisms in themselves are not necessarily a bad thing. Many people use defense mechanisms unconsciously as coping strategies from time to time, particularly as a means of addressing anxiety or if they feel threatened. Defense mechanisms are often an unconscious way to protect and buy time to deal with a situation in a healthy way - but they can affect a person's wellbeing, and other people around them, particularly if left unchecked.

Reaction Formation Definition

The concept of reaction formation was originally developed by Sigmund Freud in the early 1900s with regard to sexuality. Other social scientists have further expanded on the theory since then within different contexts. In definitions, the Freudian concept of 'ego' is often referenced as the part of the self that that constructs the defense. The American Heritage Science Dictionary defines reaction formation as " A defense mechanism by which an objectionable impulse is expressed in an opposite or contrasting attitude or behavior." ( Retrieved April 5, 2018).

What this means is the person not only acts in the direct opposite way to their feelings, impulses, or desires, but they may overcompensate in order to convince themselves, and others, that they are not who, or what, they feel compelled to reject. It is more than a 'fake it until you make it' internal drive. The original impulse or feeling of the ego isn't replaced but is instead only covered over by engaging in the opposite attitudes and behavior.

Social and cultural influences can play a large part in the use of reaction formation as a coping mechanism. An individual who may not have the same shared values expected of their immediate or wider family, community or society may unconsciously reject their own feelings in order to continue to feel like they belong or risk rejection. Equally, if an individual's true feelings are morally or legally unacceptable within society the person's drive to deny these and overcorrection may occur.
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Reaction formation is often characterized by polarized thinking or pairs of opposites. Something is either this or that, whether it is good or bad, black or white, love or hate, right or wrong - finding middle ground or a happy medium is not part of the equation. It is usually behavior or attitudes seen or perceived as "bad" that is reacted to. The result is overboard behavior and attitudes that are perceived as "good" so the person feels protected any risk of seeming to be outside the norm.

This type of behavior is usually compulsive - it is difficult for a person to control. The intrinsic need of the ego to protect itself and prevent others from seeing and experiencing what they are really feeling comes from a place of self-preservation rather than one of dishonesty. The reaction formation behavior can become obsessive, with the individual becoming argumentative and defensive if challenged or questioned.

Reaction formation as a defense mechanism is an unconscious reaction as opposed to a conscious response. An impulsive reaction can be hard to control as compared to a measured and considered response at the best of times. There are many factors at play - a person's identity or their sense of self, their feelings of acceptance within their community and their overall self-esteem.

Reaction Formation Examples

Some examples of situations where reaction formation may manifest as an ego-defense mechanism include the following:

Sexuality: A person who has been socialized to believe that intimate same-sex relationships are wrong or sinful, but is attracted to members of their same sex. They may be overtly public or promiscuous with heterosexuality or marry someone of the opposite sex to 'prove' they are not gay. They may be very vocal about being anti-gay or homophobic in order to fit in as one of the 'boys', or not be seen to go against the spiritual belief system they have been raised in.

Family/Parenting: An absent parent or a parent who does not feel they have bonded or have any affection for a child or other family members, including in-laws, may overcompensate with gifts and gestures. On the other hand, a parent not wishing to "spoil" their children may be an overly critical parent. The idealization of what constitutes a "perfect" family can result in reaction formation if an individual is not able to come to terms with the reality.

Addictions: A person with an addiction, whether alcohol or other drugs may be a proponent abstinence, harsh reforms or penalties for substance abuse, but not be able to see or acknowledge their own dependence and addiction.

Culture/Ethnicity: A person with beliefs that people of other ethnicities, cultures or races are inferior to their own may go out of their way to support and publically advocate for "minority" groups. Alternatively, someone who feels shame for their own culture may seek acceptance from another culture by adopting their beliefs and values.

Conflict: Rather than confront any actual or potential conflict with another individual or address any feelings of dislike a person may go out their way to be overly kind and nice to people they do not naturally gel with.

Other Defense Mechanisms
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There are many types of types of ego-defenses people commonly use to distance themselves from perceived harm and keep safe. Some of these are:

Denial: If something is just too much to cope with or too big to handle, a person may refuse to accept what has happened, or is happening in their lives. They may simply refuse to believe it is true and act as if nothing has happened. For example, an alcoholic who denies the effect their drinking has on themselves and those around them. Or someone who only smokes on social occasions may not consider themselves a smoker.

Projection: If a person doesn't have insight or awareness of their own behavior and attitudes, they may attribute and project what they are unable to acknowledge about themselves, and lay blame on others for their own actions. For example, a person that does not like their boss may convince themselves that their boss does not like them even though there are no indicators that say they do.

Displacement: Displacement is when somebody redirects their feelings about someone or something onto another person or object. In other words, they act out on impulse when they have not felt like they have managed a situation well, or got their own way but focus elsewhere. For example, lashing out physically or verbally at family members instead of working through conflict with work colleagues.

Sublimation: Sublimation is also redirecting feelings to another source, but this time in a more positive or constructive way. For example, using music or art as a medium to relieve stress and express emotions that are not socially acceptable to display, or playing an aggressive sport.

Repression: With repression, a person unconsciously blocks a painful event, situation, thought or condition completely. The memory is buried by the ego, but not gone forever. If asked, they will say they have no recollection of the disturbing memory. People may also experience a form of repression when they forget to go to an appointment or a meeting they were previously dreading.

Regression: When a person uses regression as a defense mechanism, they revert back to behavior or an attitude from a previous developmental stage as a means of. For example, an older child starting to re-wet their bed, a newly independent teenager becoming overly dependent and childlike again, or an adult throwing a toddler-like tantrum.

Disassociation: Dissociation involves a person detaching themselves emotionally and mentally from a person or situation. At one end of the scale, daydreaming is a form of disassociation as a way of coping with boredom. At the other end, disassociation can be a reaction to abuse and trauma. A person may fantasize about how the problem can be solved but unable to take steps to remedy it. Or a person may disengage with their surroundings and people in their lives.

All ego-defense mechanisms can play a role in protecting a person from what they may feel is overwhelming. However, they may not be effective and can become habitual ways of managing stress that may not be the most beneficial in the long term.

Closing Thoughts on Reaction Formation
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Reaction formation is one of the more complex defense mechanisms. A clinician or mental health professional will take into consideration whether a person's attitudes and behavior are blatant, overly exaggerated, inflexible, compulsive and hard for them to control. Whether a person tends to view life in strictly delineated or binary way can also be a factor in whether they are masking their true feelings. Reaction formation is a defensive mechanism to cope with feelings, impulses, and desires - the key may be to find a way to understand self-acceptance and/or how to meet in the middle.

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Reaction Formation: 8 Signs You Use This Defense Mechanism | Depression Alliance

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Reaction Formation: A Comprehensive Guide4.5 (90.2%) 49 votes Table of Contents What is Reaction Formation Psychology?Reaction Formation DefinitionReaction Formation ExamplesOther Defense MechanismsClosing Thoughts on Reaction Formation What is Reaction Formation Psychology? Reaction formation is a term used in psychology to describe a defense mechanism people may use to reject how, unconsciously, they or their 'ego' ...

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Diathesis stress or differential susceptibility? testing longitudinal assoc...: Discovery Service for Los Medanos College

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Psychology Perspectives | Simply Psychology

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(1) Beck's Negative Triad: Beck believed that depressed people think as they do because their thinking is biased towards negative interpretations of the world and they lack a perceived sense of control.

Negative Schema: Depressed people have acquired a negative schema during childhood - a tendency to adopt a negative view of the world. This may be caused by a variety of factors, including parental and/or peer rejection and criticisms by teachers. These negative schemas (e.g. expecting to fail) are activated when an individual encounters a new situation (e.g. an exam) that resembles the original condition of when the schemas were learned. Negative schemas lead to systematic cognitive biases in thinking. For example, individuals over-generalise, drawing a sweeping conclusion regarding self-worth on the basis of one small negative piece of feedback.

One of the clearest examples of the cognitive approach to psychopathology is Beck's model of depression, known as the negative triad (sometimes also referred to as the cognitive triad). Beck uses the term negative triad to refer to the three main forms of negative thinking - negative views of:

The self ('I am worthless', I am, plain, undesirable, is there to like about me? I'm unattractive and seem to bore everyone)

The world - life experiences, ('Everything is against me, I can understand why p eople don't like me. They would all prefer someone else's company. Even my boyfriend left me')

The future (Nothing will ever change, I am always going to be one my own, there is nothing that is going to change this').

(2) Ellis' ABC Model:
Ellis proposed that many problems are caused by irrational and self-defeating beliefs that put unreasonable demands on the individual. Ellis particularly focuses on how self-defeating attitudes cause problems when something unpleasant happens (such as in the example given over the page - failing a driving test - or an A level exam!)

Ellis believes that activating events (A) in an individual's life have consequences (C) such as feelings and actions. However, these consequences are affected by beliefs (B)
about these events.
Mustabatory Thinking:
The source of irrational beliefs lies in mustabatory thinking - thinking that certain ideas or assumptions must be true in order for an individual to be happy. Ellis identified the three most important irrational beliefs.

I must be approved of or accepted by people I find important.

I must do well or very well, or I am worthless.

The world must give me happiness or I will die.

Other irrational assumptions include; 'others must treat me fairly and give me what I need' and 'people must live up to my expectations or it is terrible'.

An individual who holds such expectations is bound to be disappointed and is at risk of becoming depressed. An individual who fails an exam becomes depressed not because they have failed the exam but because they hold an irrational belief regarding that failure (e.g.' I must do well so failing the exam means I'm stupid.') In order to treat depression which arises out of negative thinking, such irrational thoughts need to be challenged and turned into more positive beliefs.
Evaluation, AO3 of Cognitive Explanations of Depression:
(1) POINT: A strength of the Cognitive explanation of depression is that there is evidence to support the role of irrational thinking. EXAMPLE: Bates et al (1999) found that depressed participants who were given negative automatic thoughts statements become more and more depressed. EVALUATION: This is a strength because the research supports the view that negative thinking leads to depression.

(1) POINT: The cognitive explanations of depression can be criticised for being reductionist: EVIDENCE: For example, the cognitive explanation states that if an individual thinks in a negative way/has negative automatic thoughts they are likely to develop disorders such as depression. EVALUATION: This is a weakness because this theory of depression ignores the fact that biological research has indicated that depression can be down to low levels of the neurotransmitter serotonin and therefore, the cognitive approach can be seen to be too simplistic.

(2) POINT: A weakness of the cognitive approach to depression is that it blames the patient. EVIDENCE: For example, the cognitive approach suggests disorders are simply in the patient's mind (e.g. an individual is depressed because they think in a negative automatic way/operate under the negative triad) this could lead to situational factors (e.g. family) being overlooked. EVALUATION: This is a problem because it may be unhelpful to place a large burden of blame on a person prone to negative thoughts and depression, as a result, if individuals feel responsible for their own abnormality this could lead to delays in treatment (the individual may not have the motivation to treat a disorder that they feel ultimately responsible for).

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The Cognitive Approach to Explaining Depression (Beck's Negative Triad and Ellis' ABC Model)

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The Cognitive Approach to Explaining Depression (Beck's Negative Triad and Ellis' ABC Model) Description, AO1: (1) Beck's Negative Triad: Beck believed that depressed people think as they do because their thinking is biased towards negative interpretations of the world and they lack a perceived sense of control.

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Language: English | French

Abstract

Developmental delay is common in children deprived of normal sensory stimulation - for example, in premature neonates and some institutionalized children. Touch has emerged as an important modality for the facilitation of growth and development; positive effects of supplemental mechanosensory stimulation have been demonstrated in a wide range of organisms, from worm larvae to rat pups to human infants. Animal models are being used to elucidate the cellular and molecular mechanisms underlying these effects. In rats, the amount of maternal licking received as a pup has a profound impact on the behaviour and physiology of the adult; in the microscopic roundworm Caenorhabditis elegans, physical interactions with other worms promote growth and increase adult responsiveness to mechanosensory stimuli. By understanding the underlying mechanisms, as well as the timing and degree of stimulation required to fully reverse the effects of early childhood deprivation, strategies can be developed to best help those in need.

Keywords: Caenorhabditis elegans, Kangaroo mother care, Maternal patterns of care, Preterm birth, Rats, Sense of touch

Résumé

Le retard de développement est courant chez les enfants privés de stimulation sensorielle normale, par exemple, chez les nouveau-nés prématurés et certains enfants institutionnalisés. Le toucher a émergé comme une modalité importante pour favoriser la croissance et le développement. Les effets positifs d'une stimulation mécanosensorielle supplémentaire sont démontrés chez toute une série d'organismes, des larves de vers aux nourrissons humains en passant par les ratons. On utilise des modèles animaux pour élucider les mécanismes cellulaires et moléculaires à l'origine de ces effets. Chez les rats, la quantité de léchage que reçoit le raton de sa mère a d'importantes répercussions sur son comportement et sa physiologie à l'âge adulte. Chez les nématodes Caenorhabditis elegans microscopiques, les interactions physiques avec d'autres vers favorisent la croissance et augmentent la réceptivité de l'adulte aux stimuli mécanosensoriels. Si on comprend les mécanismes sous-jacents, le moment et le degré de stimulation nécessaires pour supprimer entièrement les effets d'une privation pendant la première enfance, on pourra élaborer des stratégies pour aider les enfants dans le besoin.

Developmental delay is often seen in children receiving inadequate or inappropriate sensory stimulation. For example, orphaned infants exposed to the bleakest of conditions in eastern European institutions exhibited impaired growth and cognitive development, as well as an elevated incidence of serious infections and attachment disorders ( 1). Much evidence now points to the importance of touch in child development and suggests the possibility that these orphaned infants are not suffering from maternal deprivation, per se, but from sensory deprivation, and more specifically a deprivation of mechanosensory stimulation. In early studies on human infants, Hopper and Pinneau ( 2) found that 10 min of additional handling per day resulted in a significant reduction in regurgitation. In addition, Casler ( 3) reported that institutionalized infants receiving an additional 20 min of tactile stimulation per day for 10 weeks had higher scores on developmental assessments. Since then, several studies have documented mechanosensory stimulation facilitating growth and development in children deprived of normal sensory stimulation, such as premature neonates.

Premature infants are often isolated in incubators and deprived of much of the mechanosensory stimulation they would otherwise receive. Field et al ( 4) and Scafidi et al ( 5) investigated the effects of tactile and kinesthetic stimulation on the development of premature/low birth weight neonates. In the studies, 20 preterm neonates, recently transferred from the neonatal intensive care unit to the transitional care unit, were given 15 min of mechanosensory stimulation three times per day for 10 days. The procedure was tightly controlled: infants received body stroking for the first and final 5 min of stimulation, and their limbs were gently flexed upward during the intervening 5 min. Several clinical and behavioural variables were monitored, and the stimulated infants were compared with unstimulated controls equivalent in their gestational age (approximately 31 weeks), birth weight (approximately 1.27 kg) and duration of intensive care (approximately 20 days). The data showed that extra mechanosensory stimulation led to superior growth and developmental performance. Although caloric consumption did not differ between the two groups, infants receiving mechanosensory stimulation averaged 47% greater weight gain per day than the unstimulated controls and were discharged an average of six days earlier. The stimulated infants also spent more time awake and active, and exhibited more mature habituation, orientation, motor and range-of-state behaviours on the Brazelton Neonatal Behavioral Assessment Scale. The positive effects appear to be persistent; when retested eight and 12 months after treatment, the stimulated infants were in a higher weight percentile group, scored better on the Bayley mental and motor assessment tests, and had a reduced incidence of neurological soft signs (minor neurological abnormalities indicating nonspecific cerebral dysfunction).

Research on the benefits of touch for premature infants has already led to procedural changes at many hospitals, with the implementation of 'kangaroo care' as a standard care option for both premature and full-term infants. In kangaroo care, the infant only wears a diaper and is held upright against the bare chest of the carrier. Feldman et al ( 6) studied the long-term effects of this technique and found that premature infants who had received at least 1 h of kangaroo care daily for at least two weeks, beginning between 31 and 34 weeks postconception, scored higher on both the mental and motor domains of the Bayley assessment tests at six months. The importance of mechanosensory stimulation in development is a highly conserved phenomenon, and current work on animal models is beginning to elucidate the underlying cellular and molecular mechanisms.

THE IMPORTANCE OF TOUCH FOR RAT PUPS: BEHAVIOURAL STUDIES

In 1922, in one of the earliest studies on the benefits of touch, Hammett ( 7) reported that rats that were infrequently handled were more timid, apprehensive and high strung than rats that had been 'petted and gentled'. They were also six times less likely to survive thyroidectomy. For the developing rat pup, mothers and littermates are the major sources of sensory input. A useful approach to evaluating the importance of this input is to remove it completely and observe what happens. Gonzalez et al ( 8) compared the adult behaviour of maternally reared rats with those isolated in plastic cups, from postnatal days 4 to 20. Despite receiving comparable nutritional input, the pups raised in cups weighed less at weaning. Although this difference did not persist into adulthood, early deprivation did affect adult maternal and emotional behaviour. Compared with maternally reared controls, isolate-reared rats were less attentive to their own offspring, performing fewer pup retrievals and spending less time licking and crouching over pups and spending more time digging, biting the cage, hanging from the top of the cage, eating and tail chasing. In an attempt to reverse the effects of isolation on adult behaviour, the pups in cups were stroked with a warm wet paintbrush to simulate maternal licking. The minimally stimulated pups received 45 s of anogenital stroking twice a day to promote urination and defecation. The maximally stimulated pups received 2 min of full-body stroking five times per day. When the pups were studied as adults and the way they mothered their own offsprings was examined, it was found that full-body stroking partially rescued the behavioural deficits of isolation, with the maximally stimulated pups exhibiting maternal behaviours of durations intermediate to those of the maternally reared and minimally stimulated pups. Thus, tactile stimulation can ameliorate some of the deficits resulting from isolate rearing in rats.

Based on the behavioural profile of rats reared in cups, it was hypothesized that early isolation impaired their attentional processing. Lovic and Fleming ( 9) assessed the performance of isolate-reared rats on two attentional tasks: prepulse inhibition of the startle response and attentional set shifting. Isolate-reared rats showed decreased prepulse inhibition and more trials to criterion in several stages of the attentional set-shifting task. These results suggest that sensory deprivation as a pup leads to attentional deficits later in life; however, Lovic and Fleming ( 9) demonstrated that these deficits could be reversed by tactile stimulation with a paintbrush: isolated pups who received paintbrush stroking for 2 min eight times per day performed as well as maternally reared controls on these tasks. In summary, isolate-reared rats were hyperactive, easily distracted and less attentive to their own pups - behaviours which could be rescued by introducing licking-like stimulation with a paintbrush.

Licking is clearly an important component of maternal care in rats. A number of studies ( 10- 13) have monitored natural variation in maternal licking/grooming (LG) of rat pups. Mothers whose frequency scores for LG were more than 1 SD above the mean were considered to be high lickers/groomers, while those whose frequency scores for LG were more than 1 SD below the mean were considered to be low lickers/groomers. Francis et al ( 10) compared adult offspring of low and high LG mothers, and found that LG behaviour was transmitted across generations, because female offspring of high LG mothers licked/groomed their own pups more than those of low LG mothers. Furthermore, cross-fostering experiments demonstrated that the mechanism of inheritance was nongenomic: biological female offspring of low LG mothers fostered into the litter of high LG mothers displayed increased LG levels comparable with unfostered offspring of high LG mothers and vice versa. What then are the long-term effects of being licked more or less? Compared with offspring of high LG mothers, those reared by low LG mothers displayed impaired learning and memory in the Morris water maze and in object recognition ( 11, 12), and showed substantially more fearful behaviour, as measured by a longer latency to eat food in a novel environment and decreased open-field exploration ( 13, 10). These behavioural studies demonstrate that mechanosensory stimulation can alter the developing rat brain. The next series of studies highlights some of the cellular and molecular mechanisms underlying the behavioural changes that have been described.

THE IMPORTANCE OF TOUCH FOR RAT PUPS: CELLULAR AND MOLECULAR MECHANISMS

A study by Liu et al ( 14) showed that maternal licking altered the pup's hypothalamic-pituitary-adrenal (HPA) stress reactivity through changes in gene expression in areas of the brain that regulate the behavioural and endocrine response to stress. Adult offspring of low LG mothers had higher HPA responses to restraint stress than those of high LG mothers. An elevated HPA stress response highlights the importance of early intervention programs for children; elevated exposure to stress hormones has been implicated in the development of many conditions, including visceral obesity, hypertension, diabetes, depression, anxiety, drug addiction and multiple forms of coronary artery disease. Before policies are drafted for practical applications in humans, a better understanding of the cellular and molecular mechanisms underlying mechanosensory-mediated developmental plasticity is needed.

Briefly, in response to stressors, the periventricular nucleus of the hypothalamus secretes corticotrophin-releasing hormone (CRH). In the pituitary, CRH stimulates the synthesis and release of adrenocorticotropic hormone, which in turn induces the release of glucocorticoids from the adrenal gland. A negative feedback loop for this stress response is initiated by the binding of glucocorticoids to glucocorticoid receptors (GR) in the hippocampus. Liu et al ( 14) showed that as adults, the offspring of low LG mothers had decreased GR expression in the hippocampus, resulting in diminished glucocorticoid feedback sensitivity and increased CRH synthesis and release of plasma adrenocorticotropic hormone. Weaver et al ( 15) demonstrated that maternal care programs GR gene expression levels in the hippocampus for the lifespan of the animal via epigenetic modification of the GR gene. Beyond GR levels, maternal LG has widespread effects on gene expression in the brain, basically increasing the expression of genes that provide metabolic support, mediate experience-dependent neuronal activation, and support the growth and survival of synapses ( 16). Thus, licking-like stimulation has also been studied in the context of brain injury.

Stroking has been shown to facilitate functional recovery and synaptic organization following brain lesions in rat pups. In one study ( 17), rats were given medial prefrontal cortex (mPFC) or posterior parietal cortex lesions on post-natal day 3. It was found that administering 15 min of tactile stimulation with a small brush three times per day resulted in increased dendritic spine density in animals with mPFC lesions and increased dendritic length in animals with posterior parietal lesions. The mechanism of action appears to be the release of fibroblast growth factor-2 (FGF-2), because both FGF-2 and its receptor were upregulated in the skin and brain of stimulated rats ( 17). FGF-2 is produced in the skin, but can pass the blood-brain barrier, where it is hypothesized to stimulate synaptic changes. In support of this hypothesis, animals receiving FGF-2 showed better recovery following mPFC or posterior parietal lesions than vehicle-treated animals ( 17). Remarkably, stroking a pregnant mother rat also ameliorated the effects of future cortical lesions in her pups, as did prenatal pretreatment with FGF-2 ( 17). These findings hold great promise for medicine, but translational research requires continued work on the fundamental biology in model systems.

THE IMPORTANCE OF TOUCH FOR A WORM

The benefits of touch have become a recurring theme in human, monkey and rat development, but the importance of physical contact is not limited to mammals. Rose et al ( 18) showed that a microscopic nematode, known as Caenorhabditis elegans, is also sensitive to touch deprivation. Approximately 40 years ago, Sydney Brenner chose C elegans as the ideal model system for studies in developmental biology and neuro-science. Now, the worm is one of the best understood organisms on the planet. It is morphologically very simple, which has allowed researchers to create a complete neural wiring diagram and cell lineage: the adult hermaphrodite has only 959 cells, 302 of which are neurons forming approximately 5000 chemical synapses, 600 gap junctions and 2000 neuro-muscular junctions ( 19). Furthermore, its small size (approximately 1 mm), short life cycle (less than three days) and ability to survive being frozen for long-term storage make it highly amenable to laboratory research.

Similar to the studies in rats and humans described above, Rose et al ( 18) found that worms reared in isolation had a smaller body size ( Figures 1A and ​and1B) 1B ) and a delayed onset of egg laying compared with colony worms reared in groups of 30 to 40. C elegans develops from egg to the adult stage in three days, going through four larval stages - L1, L2, L3 and L4 - and then a young adult stage. Rai and Rankin ( 20) found that the body size of isolated worms could be rescued if they were transferred into colonies before the end of stage L3. This suggests that exposure to other worms alters adult body size and that there is a critical period (stages L1 to L3) for this exposure to have its effect.

Growing up alone on a smooth agar surface in an insulated incubator, isolated worms, similar to premature neonates, were deprived of mechanosensory stimulation. As a result, they showed significantly smaller withdrawal responses (backward swimming) to a tap delivered to the side of their petri plate ( Figure 1C ). In an attempt to rescue the effects of isolation on withdrawal behaviour, isolated worms were given supplemental mechanosensory stimulation during development. This was done with 30 taps at a 10 s inter-stimulus interval (5 min of stimulation). Administering this nonlocalized mechanosensory stimulation at any point during development, rescued responses to tap in the isolated adult worms, although their body size remained smaller than worms reared in colonies ( 20). This suggests that development of the neural circuitry underlying the tap withdrawal response is activity dependent. Looking at pre- and postsynaptic markers within the mechanosensory circuit, Rose et al ( 18) found that worms reared in isolation had weaker synapses than colony-reared worms, but 30 taps administered early in development were sufficient to strengthen them. As the worm aged, progressively greater amounts of stimulation were required to fully reverse the effects of isolation - 400 taps at stage L2 or L3 and 800 taps at stage L4 or the young adult stage ( 20). Thus, in attempting to reverse the effects of early deprivation, it is important to remember that different aspects of development require different amounts and timing of supplemental stimulation. A major advantage of using C elegans is the ability to relate animal behaviour to changes in identified neurons.

CONCLUSION

Organisms need sensory stimulation for normal development. Mechanosensory stimulation has proven to be exceptionally important - a fact demonstrated in organisms across phylogeny. In rats and worms, researchers are able to examine the effects of sensory deprivation from the behavioural to the molecular level. These studies have shown that sensory stimulation can alter many aspects of development by a number of different mechanisms. Reversing the effects of early deprivation is not simple, but the importance of touch is undeniable. Finally, you need not be a worm larvae, rat pup or even human child to reap the rewards of touch. For example, employees receiving chair massages showed a significant reduction in blood pressure ( 21), anxiety ( 22) and job stress, and had increased speed and accuracy on math problems ( 23). Furthermore, patients with ailments ranging from burns ( 24) to eating disorders ( 25) have been shown to benefit from massage therapy, with reductions in stress hormone levels, anxiety and clinical symptoms; HIV-positive men receiving daily massages had an increased number of immune cells to combat the virus ( 26). To paraphrase, a kiss may just be a kiss, a sigh may just be a sigh, but a touch can change your life (or at least your nervous system)!

Footnotes

DISCLOSURE: All authors have reviewed and agreed with the content of the article. There are no potential, actual or perceived conflicts of interest to disclose.

REFERENCES

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22. Shulman KR, Jones GE. The effectiveness of massage therapy intervention on reducing anxiety in the work place. J Appl Behav Sci. 1996;32:160-73. [ Google Scholar]

Articles from Paediatrics & Child Health are provided here courtesy of Oxford University Press

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Developmental delay is common in children deprived of normal sensory stimulation - for example, in premature neonates and some institutionalized children. Touch has emerged as an important modality for the facilitation of growth and development; ...

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Abstract

Risky decision-making is characteristic of depression and of addictive disorders, including pathological gambling. However it is not clear whether a propensity to risky choices predisposes to depressive symptoms or whether the converse is the case. Here we tested the hypothesis that rats showing risky decision-making in a rat gambling task (rGT) would be more prone to depressive-like behaviour in the learned helplessness (LH) model. Results showed that baseline rGT choice behaviour did not predict escape deficits in the LH protocol. In contrast, exposure to the LH protocol resulted in a significant increase in risky rGT choices on retest. Unexpectedly, control rats subjected only to escapable stress in the LH protocol showed a subsequent decrease in riskier rGT choices. Further analyses indicated that the LH protocol affected primarily rats with high baseline levels of risky choices and that among these it had opposite effects in rats exposed to LH-inducing stress compared to rats exposed only to the escape trials. Together these findings suggest that while baseline risky decision making may not predict LH behaviour it interacts strongly with LH conditions in modulating subsequent decision-making behaviour. The suggested possibility that stress controllability may be a key factor should be further investigated.

Introduction

Risky decision-making is a characteristic of depression and of addictive disorders, including problem gambling1,2,3,4,5,6,7,8,9. However it is not clear whether predisposition towards risky choices increases the likelihood of depressive disorders, whether the converse is the case, or whether the two traits are independently associated to a third factor. One common factor in both addictive and depressive disorders is significant sensitivity to stress; exposure to stress in both humans and animals has been associated with increases in drug seeking and risky decision-making. Stress is also strongly implicated in depressive illness, and it is noteworthy that virtually all animal models of depression are stress-based13. An increased sensitivity to the depressive impact of stress could potentially increase vulnerability to engage in risky choices, gambling, and other types of addictions. Conversely, traits predisposing to risky or disadvantageous decision-making could conceivably increase vulnerability to depression-inducing effects of stress. The latter possibility has received less experimental attention than the former.

Preclinical models could add valuable insight into the relationships between depressive-type behaviour and risky decision-making, particularly since the direction of such relationships is typically difficult to determine in human populations. Among the better established models of depression is learned helpleness (LH), as a general protocol where exposure to inescapable stress subsequently affects escape responding or ability to cope, presumably by inducing a state of "helplessness". In the last few years behavioural paradigms have also been successfully developed to model gambling and decision-making behaviour in rodents. Here, we investigated the effects of learned helplessness on risky decision-making as assessed in the rat Gambling Task (rGT)18, a paradigm based on the human Iowa Gambling Task where amount of reward and probability of reward are inversely related. In the rGT behavioural choices associated with high reward/low probability ("high risk, high reward") are commonly regarded as indices of risky or "impulsive" decision-making, as recently supported by a meta analysis20. To address potential bidirectional effects between rGT and LH, our overall experimental approach was to use the rGT to establish a baseline of decision-making behaviour, then expose the animals to a learned helplessness protocol, and then reassess behaviour in the rGT. We were particularly interested in testing the hypothesis that exposure to the LH protocol would increase risky decision-making in the rGT.

Methods

Subjects

Male Fischer-344 rats ( n = 45) (Charles River, Quebec), initially weighing 250-275 g, were individually housed in a temperature-controlled colony room on a 12 h light-dark cycle (lights on at 8:00 A.M.; temperature 21 ± 1 °C). After one week of acclimation with free access to food and water, rats began a food restriction protocol (20-22 g per day) to stay at approximately 85% of their initial free feeding body weight. Water was available ad libitum throughout the study. Experimental protocols were approved by the Animal Care Committee at the Centre for Addiction and Mental Health and complied with Canadian Council on Animal Care and NIH standards and guidelines.

Rat Gambling Task (rGT)

rGT training began one week following the start of food restriction. Animals were tested between 8:00 AM and 3:00 PM five days per week. The rGT experimental protocol has been previously described18,21. Testing was carried out in commercial chambers (30.5 × 24 × 21 cm; Med Associates Inc., St. Albans, VT, USA) in sound-attenuated cabinets. Each chamber had four active response holes on one wall and a food dispenser on the opposite wall. Each response hole (termed P1, P2, P3, and P4) was associated with the delivery of a specific number of sucrose pellets (1, 2, 3 or 4, respectively) each with a defined probability (0.9, 0.8, 0.5 and 0.4, respectively). Rewards consisted of 45-mg sucrose pellets (Formula P, BioServ, New Jersey). 'Punishment' in this paradigm consists of corresponding time-out periods for the non-rewarded trials (5, 10, 30, or 40 sec, respectively), with probabilities of 0.1, 0.2, 0.5 or 0.6, respectively, for each of the 4 choices18. A fixed intertrial interval (ITI) of 5 sec was used. Since each session had a fixed duration of 30 min, the choice that maximized the number of possible pellets to be earned in a session was P2, followed by P1, P3 and P4. For each session the choice score for each of the four rGT options was calculated as a percent (number of choices of a particular option/number of total choices made in the session). Also recorded were the number of omissions (failures to make a choice within a trial), premature responses (making a choice before the 5-sec ITI ended), and perseverative responses per session. In the rGT trained rats typically show a very high preference for the optimal P2 choice, usually around 80% of the choices made, with the riskier P3 and P4 choices occurring only 7-10% of the time.

Daily rGT sessions proceeded until rats showed a stable responding over three consecutive sessions, which in this study was achieved after 15 sessions. Since there was a particular interest in risky, disadvantageous decision-making behaviour, we focused on the option associated with maximal possible gain with the lowest probability of occurrence (P4). Mean percent P4 responding across all sessions was therefore used to define three levels of "impulsivity": High impulsivity (HI) rats were defined as those with a mean P4 response level in the upper 33% of the P4 distribution; rats with mean P4 levels in the middle 33% of the distribution were classified as Medium Impulsivity (MI); and those in the lower 33% of the P4 distribution were classified as Low Impulsivity (LI) animals.

Learned helplessness protocol and rGT retest

Once stable rGT responding was achieved, a 12-day rest period was given and then rats were subjected to the stress protocol. Forty-five rats were exposed to the LH protocol. Following well established procedures, the target LH group (N = 27) was exposed to one session of inescapable stress (0.8 mA scrambled footshocks) delivered on in operant boxes (35 × 30 × 21.5 cm; Med Associates, St Albans, VT). One hundred shocks of variable duration (1.5-60 sec) were given at variable intervals (1-30 sec) resulting in a total 25 min of shock over the entire session. Twenty-four hours later this group was subjected to an active avoidance session consisting of 15 trials where footshock could be terminated by a single bar press. The maximal duration of each trial was 60 sec and a fixed intertrial interval of 15 sec was used. For each trial latency to escape footshocks was recorded. Impaired escape learning in this group is commonly described as "learned helplessness"15,22. Impaired escape behaviour in LH protocols is defined by comparison to a separate group that undertakes the active avoidance test without prior exposure to inescapable stress (e.g. refs 23, 24, 25, 26). This group is referred to as the Learning Control (LC) group, as it serves to verify that rats not previously stressed can in fact learn the avoidance task (N = 10). A third group (N = 8) was not exposed to avoidance trials and remained in their home cages (Cage Control groups, CC). The pre-stress baseline distribution of rGT choices was the same for the three groups (LH, LC and CC) in the LH protocol (Supplymentary Fig. 1). The target LH group included 10 LI, 10 HI and 5 MI rats. An attempt was made to distribute the remaining LI, MI and HI rats equally among CC and LC groups ( Table 1).

Table 1: Group sizes for experimental conditionsa.

Once the LH protocol was completed all rats were given a 10-day rest period and were then reassessed in the rGT protocol (7 sessions), as described above.

Statistical analyses

Statistical analyses were conducted with SPSS (version 21, Chicago, IL, USA). Pre- vs. post LH protocol changes were analyzed with MANOVA or repeated measures ANOVA using test time (pre- vs. post-LH protocol) as a within-subjects factor and LH group (LH, LC or CC) and/or Impulsivity (HI, MI or LI) as between-subject factors. Post-hoc tests used Bonferroni-adjusted comparisons, with p  < 0.05 as a criterion for statistical significance.

Results

Baseline rGT performance

Choice distribution over the sessions is shown in Fig. 1a. As summarized in Fig. 1B, rats on average significantly favoured the optimal P2 option (71.4% ± 0.078 of all choices made per session), followed by P1 (17.9% ± 0.05), P4 (7.2% ± 0.01) and P3 (3.5% ± 0.02). This choice pattern was established relatively early and appeared quite stable over time. When animals were divided into High-, Medium- or Low-impulsivity subgroups on the basis of their mean P4% scores ( Fig. 2), one-way ANOVAS confirmed that the three groups differed significantly in P2 and P4 choices (F 2,42  = 8.04, p  < 0.001 and F 2,42 =  p < 0.0001, respectively), as intended. Bonferroni-adjusted post-hoc tests confirmed that HI rats significantly favoured P4 significantly more often that LI and MI rats ( p < 0.05) while showing a corresponding decrease in preference for P2 ( p < 0.05). The three Impulsivity groups did not differ among themselves in P1 or P3 choices, nor in number of omissions or premature responses (all p values >0.05).

Figure 1: Baseline rGT choice behaviour.

( A) Distribution of choice behaviour for all rats (N = 45), expressed as mean percent of total choices per session in the course of 15 sessions. Error bars are omitted for clarity. ( B) Mean and SEM values for each choice averaged over the 15 sessions. On average rats showed a strong preference for P2 option, followed by P1, P4 and P1.

Figure 2: Baseline rGT choice distribution of Low, Medium and High Impulsivity rats.

Pre-stress levels of rGT for the three Impulsivity groups, defined as the lower, medium and higher 33% of the P4 distribution. Accordingly, N = 15 for each group. As intended, High-impulsivity rats had higher P4 values and lower P2 values than the other groups. * p < 0.05; ** p  < 0.01, Bonferroni-adjusted comparisons.

Active avoidance in the LH protocol

Figure 3 shows latencies to escape for LH and LC groups over the 15 trials of the active avoidance session. While latencies in the LC group declined sharply over the 15 trials, latencies in the LH group seemed to decline at a slower rate if at all ( Fig. 3). Although a repeated measures ANOVA did not indicate a significant Trials X LH group interaction (F 4,124 = 0.95, p = 0.44), statistical comparison of the two linear slopes indicated a significant difference between the two groups (t ₈  = 2.44, p < 0.04).

Figure 3: Escape latencies across 15 active avoidance trials.

LH rats (N = 27) had one prior session of inescapable stress, whereas LC (N = 10) only experienced the escapable stress session. Although the LH group X Trials ANOVA interaction was not statistically significant, the slopes of the two regression lines were significantly different * p  < 0.05. Values are mean latencies to escape footshock (and SEM) in blocks of 3 trials.

Effects of baseline "impulsivity" on LH behaviour

To examine potential relationships between baseline impulsivity and escape deficits in the LH paradigm a continuous "impulsivity score" was created by computing a ratio of the two riskiest rGT choices (P4 and P3) against the two safest choices (P2 and P1). This impulsivity score was then used to assess Pearson's correlations between impulsivity and latency to escape ( Table 2), first for all tested rats, and then for LH and LC groups separately. As shown in Table 2, no significant correlations were found, suggesting that baseline impulsivity does not predict escape deficits in the LH paradigm. Nor were any significant correlations observed when latencies were broken down into categories (e.g. less than 5 sec; between 5 and 20 sec; and over 20 sec) ( Table 2). Similar correlation analyses performed for premature responding in the rGT likewise failed to indicate any association between premature responding at baseline and subsequent escape response in the LHs protocol ( Table 2).

Table 2: Correlations between baseline rGT measures and avoidance latencies.

rGT choice behaviour after the LH protocol

The pre-LH baseline distribution of rGT choice behaviour was the same for each of the three groups in the LH protocol (Supplymentary Fig. 1). In order to assess the effects of the LH protocol on rGT retest behaviour repeated measures ANOVAs were performed for each rGT choice, using LH protocol group as a between-subject factor with three levels (LH, LC and CC) and Time (pre- and post-LH) as a within-subject factor. Results indicated a significant main effect of Time for P1 ( F 1,42 = 10.16, p = 0.003), P2 ( F 1,42 = 12.77, p < 0.001) and P3 choices ( F 1,42 = 18.53, p = 0.0001). No significant main effects of the LH protocol were observed. A significant interaction between Time × LH was only seen for the P4 choice ( F 2,42 = 4.43, p = 0.018). This suggested that the three conditions in the LH phase of the study differentially affected subsequent P4 selection in the rGT. Bonferroni-adjusted pairwise comparisons revealed that rats in the LH group significantly increased subsequent P4 selection compared to rats in the LC group ( p < 0.005). Figure 4 depicts this result using pre- vs. post-LH differences.

Figure 4: Pre-post LH protocol changes in rGT choices in the 3 LH conditions.

After the LH protocol, a general tendency was observed for CC (N = 8) and LC (N = 10) rats to decrease P1, P3 and P4 responding and to increase P2 responding. In contrast rats in the LH stress group (N = 27) showed a significant increase in P4 choices relative to their own pre-stress baseline (*** p  < 0.0001, paired t test). Values are mean difference (SEM) scores; the dotted line indicates the 0% change value.

Pre- vs. post-LH choices in the rGT were then analyzed for each group in the LH protocol, using a multivariate ANOVA (MANOVA) that considered the four rGT choices simultaneously. In the CC group ( Fig. 5A) significant pre- vs. post-LH protocol differences were seen for P1 ( F 1,7 = 8.470, p = 0.023), P2 ( F 1,7 = 5.18, p = 0.023) and P3 ( F 1,7 = 106.15, p = 0.0001). The slight increase in P2 in this group thus may have been due primarily to a decrease in P1 and P3 ( Fig. 5A), consistent with possible effects of additional rGT trials in the absence of other manipulations. In the LC group ( Fig. 5B), a significant pre- vs. post-LH difference was seen for P2 ( F 1,9 = 6.31, p = 0.033) and P4 ( F 1,9 = 6.80, p = 0.028). Figure 5B suggests that the decrease in P4 derived from an increase in P2. In the target LH group ( Fig. 5C), significant pre- vs. post-LH effects were seen in P1 ( F 1,26 = 7.39, p = 0.012), P3 ( F 1,26 = 22.14, p = 0.0001) and P4 ( F 1,26 = 5.54, p = 0.026). In this group increases in P4 may have been due to decreases in P1 and P3. In all cases the data in Fig. 5 indicate that the optimal P2 responses remained the overwhelming choice in all groups.

Figure 5: rGT choice changes in Cage Control, Learning Control and LH groups.

( A) CC rats (N = 8) showed a significant increase in P2 ( p < 0.01) and a significant decrease in P1 ( p < 0.02) on rGT retest. ( B) LC rats (N = 10) subjected to a single active avoidance session showed a significant increase in P2 ( p < 0.05) and a significant decrease in P4 ( p < 0.05) on rGT retest. ( C) LH rats (N = 27) showed a significant increase in P4 responding ( p < 0.025) and significant decreases in P1 ( p < 0.05) and P3 (p < 0.01) on rGT retest. Values are means and SEMS. * p  < 0.05, **p < 0.025, ***p < 0.01 pre- vs. post-stress comparisons.

Effects of the LH protocol on P4 selection in High- vs. Low-Impulsivity rats

The data in Fig. 5B and C suggested that the LH protocol could be having opposite effects on P4 responding in rats in the LH group as compared to LC rats. To further explore this possibility the two extreme Impulsivity groups (High and Low) and the two groups subjected to avoidance sessions (LH and LC) were subjected to further analyses focusing on the target "high risk, high reward" P4 response. ANOVA revealed a significant 3-way interaction between Time × LH group ×  Impulsivity ( F 1,28 = 7.48, p = 0.011), a significant interaction of LH group × Impulsivity ( F 1,28 = 11.97 p = 0.002), and significant main effects of Impulsivity ( F 1,28 = 20.63, p < 0.0001) and LH group ( F 1,28 = 11.00, p = 0.003) on P4 choice. As can be seen in Fig. 6, following the LH protocol Low-impulsivity rats did not show much change in P4 selection compared to their own pre-LH levels, and this was true for both LH and LC rats ( Fig. 6). In contrast, High-impulsivity rats in the LH group showed a significant increase in P4 choices as compared both to their own pre-LH levels (paired t 6 = 3.97, p = 0.007) and to the LC group (independent t 8 = 2.78, p = 0.024). While high-impulsivity rats in the LC condition decreased their P4 responding by approximately 30% after the stress protocol, High-impulsivity animals in the LH group showed a 56% increase in P4 responding following exposure to stress ( Fig. 6).

Figure 6: Effects of the LH protocol on Low vs. High Impulsivity rats.

Rats defined as a low impulsivity at baseline (N = 15) did not show significant pre-post LH differences. In contrast, rats showing high impulsivity at baseline (N = 15) reacted in opposite ways when exposed to LH vs. Learning Control conditions. Values are means and SEMS. ###p  < 0.01 compared to their own pre-stress values; **p < 0.025 compared to the post-stress Learning Control group.

Effects of the LH protocol on subsequent omissions, premature responding and perseverative responses in the rGT

Following the same analysis strategy as used for rGT choice options, omissions were found to be unaffected by the LH protocol (Supplymentary Fig. 2). A significant reduction in the number of premature responses was observed in CC rats (−35%, p < 0.05) but not in LC or LH rats. When perseverative responding was considered, significant and uniform reductions were seen in all three groups in the LH protocol (39-40%, all p values <0.01; Supplymentary Fig. 2).

Discussion

Three main findings emerge from this study. First, baseline impulsivity, as defined by risky choices in the rGT, did not predict escape deficits in the LH protocol. In turn, exposure to the LH protocol had significant effects on subsequent impulsive choice in the rGT. Second, these effects were opposite in the target LH group as compared to Learning controls. Finally, effects induced by the LH protocol were different in rats with high baseline impulsivity levels compared to those with low baseline impulsivity levels.

Baseline impulsivity levels did not correlate with subsequent escape deficits induced by the LH protocol. To the extent that such escape deficits are commonly regarded as an index of depressive-like failure to cope or 'helplessness' behaviour, these observations suggest that stable impulsivity traits may not in themselves be predictors or risk factors for depressive-type behaviour.

In contrast to the apparent lack of effect of basal impulsivity on LH-induced escape deficits, the effects of the LH protocol on subsequent impulsive choices in the rGT were pronounced. Rats in the target 'helplessness' group showed a small but significant increase in P4 responses compared to their own pre-LH levels, with correspondingly less responding for P3 and P1 options. In contrast, LC rats showed a significant increase in optimal P2 responding and a corresponding decrease in P4 responding, suggesting a clear improvement in decision-making behaviour in this group. Cage control rats showed an overall improvement in P2 responding at the expense of P1 and P3 responding while P4 responding was not altered, suggesting that this control group may have simply benefitted from additional trials.

The fact that opposite changes in P4 responding were observed in LH vs. LC rats ( Fig. 5B and C) was unexpected and merits further consideration. One readily apparent difference between these groups is that LH rats were exposed to two stress sessions (one inescapable and one escapable) whereas the LC group was exposed to only one (escapable) stress session. It could thus be argued that the different effects of the LH protocol on subsequent rGT responding could have simply resulted from the additional stress experienced by the LH group compared to the LC group. This however seems unlikely for it would imply that behavioural effects on rGT responding in the LC group should be accentuated in the LH group as a result of additional stress. Instead, what was observed was a decrease in P4 responding in LC rats and an increase in P4 responding in LH rats.

An alternative and possibly more likely explanation would focus on the fact that the LH group had an experience of inescapable stress that subsequently compromised responses to escapable stress, whereas the LC group only experienced escapable stress. It is conceivable that the experience of escapable, and hence "controllable", stress could account for the beneficial effects seen in the LC group. As noted below, if this suggestion is correct it would fall in line with other evidence suggesting that controllable stress may serve as "behavioural training" thereby exerting positive effects on behaviour27.

Further analysis revealed that baseline impulsivity in rGT, while not a predictor of depressive-type behaviour, interacted strongly with the LH protocol in affecting subsequent decision-making behaviour ( Fig. 6). Thus, following exposure to the LH protocol choice of the riskier P4 option was significantly increased in High-impulsivity but not in Low-impulsivity rats. However this increase in P4 responding in High-impulsivity rats only occurred in rats in the LH group. Strikingly, High-impulsivity rats in the LC group actually decreased P4 responding on retest. These results appear to have uncovered an interesting role for baseline impulsivity interacting with stress to affect subsequent decision making behaviour.

Stress effects on decision making

Learned helplessness involves exposure to inescapable stress. Previous animal studies have addressed general effects of stress on decision-making. Exposure to chronic unpredictable stress in adolescence was found to negatively impact aspects of decision-making28 and risk-assessment29, and to increase impulsive choice in adulthood. Rats receiving chronic corticosterone during adolescence (mimicking the effects of chronic stress) showed increased impulsive choice marked by an increased preference for small-immediate rewards rather than larger-delayed ones in a delayed-discounting task30. Effects of acute stress on decision-making have been less clear. Shafiei and co-workers reported that one hour of restraint stress did not alter preference between small/immediate vs. larger/delayed rewards in a delay-discounting task31. Koot et al.11 used a different adaptation of the Iowa Gambling Task for rats (rIGT) to assess the effects of corticosterone given 30 or 180 min prior to testing. Control rats improved performance on the rIGT over blocks of trials by decreasing the number of visits to the high-risk/disadvantageous arm of the apparatus, shifting choice preference toward the long-term advantageous arm. This however was not observed in rats given corticosterone 30 min prior to testing; in fact, the latter group consistently preferred the disadvantageous arm.

The present results are similar to those of Koot et al.11 using a different stressor and a different paradigm to assess decision-making. It thus seems possible to suggest that in our study the LH condition induced an apparent risk-proneness profile and impaired optimal use of choice strategy. This would be in line with a growing body of clinical evidence finding impulsive decision-making and increased risk-taking following stress exposure. Clinical studies have reported impulsive decision-making in healthy subjects submitted to acute stress12,32, in pathological gamblers, and in depressed individuals36,37. It is unclear exactly how stress impacts subsequent decision-making. It is known, however, that key brain regions implicated in decision-making overlap to some extent with those that are involved in stress reactions and are therefore sensitive to stress-induced changes.

Chronic stress in rodents has been reported to disrupt decision-making by impairing the ability to select appropriate actions on the basis of previously-learned outcomes and the ability to shift to goal-directed behaviour. In particular, animals exposed to chronic stress show an impaired ability to perform based on the consequences of their previous choices38. It is also possible that stress effects on reward-related processing may play a role in the observed decision-making changes. Stress enhances sensitivity to appetitive behaviours such as drug or food intake and gambling42. Corticosteroids released during stressful situations have been linked to altered dopamine activity in the nucleus accumbens and prefrontal cortex, both of which are regions implicated in incentive reward processing and motivated behaviours46,47. For example, acute footshock increases dopamine release in these brain areas48 and increased in dopaminergic signalling in the striatum in response to acute stress has been linked to increased reward-seeking in rodents15,49,50,51,52. It is thus conceivable that stress-induced modulation of these brain regions may increase sensitivity to reward, promote risk-taking, and increase preference for impulsive options associated with immediate potential gains, regardless of negative long-term consequences.

Could stress controllability be a factor?

Irrespective of specific mechanism(s) involved, a striking finding in the current study was the unexpected improvement in rGT decision-making in Learning control rats. It has been previously demonstrated that exposure to inescapable footshocks disrupts subsequent behavioural functions including avoidance learning, whereas exposure to identical but escapable shocks blunts such deficits15,51,52,53. Similar effects have been observed when animals are allowed some degree of control over stressful events54,55. Conceivably, prior exposure to escapable stress may help organisms develop more effective strategies to cope with future challenges such as decision-making by increasing vigilance or sensitivity to losses56. It seems therefore possible to suggest that the experience of stress controllability may at least in part account for the beneficial effects observed in the LC group, particularly in high-impulsivity rats. This suggestion could be tested using yoked control paradigms. If this hypothesis is confirmed it could provide a basis for potentially using behavioural training strategies in problem gambling in humans. Our results would further suggest that this might be particularly helpful in individuals with high baseline impulsivity levels.

In summary, while baseline impulsivity did not predict escape deficits in the LH paradigm, exposure to the LH protocol resulted in a subsequent increase in risky decision-making in the GT. This however occurred only in rats in the target LH group, for subsequent choice performance was actually improved in learning control rats. Further, these effects were primarily restricted to subjects with high baseline impulsivity levels in the rGT. The exact mechanism underlying these interactions between stress in the LH protocol and decision-making remains to be determined but the data are consistent with the possibility of opposite effects of controllable vs. uncontrollable stress on decision-making processes, a possibility that would be of translational interest and should thus be addressed in future work.

Additional Information

How to cite this article: Nobrega, J. N. et al. Strong interactions between learned helplessness and risky decision-making in a rat gambling model. Sci. Rep. 6, 37304; doi: 10.1038/srep37304 (2016).

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References

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Acknowledgements

Supported by internal CAMH funds.

Author information

These authors contributed equally to this work.

Affiliations

1. Department of Psychiatry, University of Toronto, Toronto, ON, Canada

2. Departments of Psychology and Pharmacology & Toxicology, University of Toronto, Toronto, ON, Canada

3. Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, ON, Canada

4. Institute of Medical Science, University of Toronto, Toronto, ON, Canada

Authors

1. Search for José N. Nobrega in:

2. Search for Parisa S. Hedayatmofidi in:

3. Search for Daniela S. Lobo in:

Contributions

J.N. and D.L. conceived the study, performed data analyses and prepared the final version of the manuscript. P.H. conducted the experimental work, conducted initial analyses and prepared the first draft of the manuscript.

Competing interests

The authors declare no competing financial interests.

Corresponding author

Correspondence to José N. Nobrega.

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Strong interactions between learned helplessness and risky decision-making in a rat gambling model

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Risky decision-making is characteristic of depression and of addictive disorders, including pathological gambling. However it is not clear whether a propensity to risky choices predisposes to depressive symptoms or whether the converse is the case. Here we tested the hypothesis that rats showing risky decision-making in a rat gambling task (rGT) would be more prone to depressive-like behaviour in the learned helplessness (LH) model.

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Theory of Mind in Major Depressive Disorder.: Discovery Service for Los Medanos College

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Center for Effective Living, serving West Side Cleveland, Ohio

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Wil Wheaton shared this cartoon on Twitter today with this preface: "I have depression and anxiety, and I'm not ashamed. I got help and meds. You can too." If you, or someone you love, is also struggling with depression, anxiety or any mental health issues, take a note from this celebrity alum of Star Trek: The Next Generation, and don't be ashamed. Seek help the same way you would for anything else that ailed you. You are not alone.

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Wil Wheaton shared this cartoon on Twitter today with this preface: "I have depression and anxiety, and I'm not ashamed. I got help and meds. You can too." If you, or someone you love, is also struggling with depression, anxiety or any mental health issues, take a note from this celebrity alum of Star Trek: The Next Generation, and don't be ashamed.

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Abstract

As advances in neuroscience and genetics reveal complex associations between brain structures, functions and symptoms of mental disorders, there have been calls for psychiatric classifications to be reconfigured, to conceptualize mental disorders as disorders of the brain. In this paper, I argue that this view is mistaken, and that the level at which we identify mental disorders is, and should be, the person, not the brain. This is not to deny physicalism or argue that the mental realm is somehow distinct from the physical, but rather to suggest the things that are going 'wrong' in mental disorder are picked out at the person-level: they are characterized by breaches in epistemic, rational, evaluative, emotional, social and moral norms. However, as our scientific understanding of the brain becomes advanced, what makes an identified neurobiological difference in brain structure or functioning indicative of pathology is its association with these behaviours at the person-level. Instead of collapsing psychiatry into biomedicine, biomedicine may benefit from drawing closer to the expertise of psychiatry, as it is able to accommodate social, psychological and biological explanations while focusing on the person, within their environment.

Keywords: Jaspers, mental disorder, psychiatric classification, psychiatry, psychological realism, stigma

Introduction

The relation between the mental and the physical, and between mental and physical disorders, has a long, complex and contentious history, both in the philosophy of mind and science and in conceptualizing the nature and role of medicine. In this paper, I want to skip over some of the more profound philosophical questions about the nefariously tricky relation between mind and body, mental causation and the nature of mental content.

Instead, I focus on a conceptual question with clear practical consequences: are mental disorders, disorders of the brain? To do this, I first consider why this distinction matters, and highlight some areas of difference between mental and physical disorders. I will put forward an argument that mental disorders ought not to be thought of as disorders of the brain, and consider some implications that follow if they are conceptualized as brain disorders. I am largely in agreement with White's diagnosis of the problem , which is, in brief, that psychiatric classifications reflect an anachronistic division between mind and brain fail to keep up with current scientific understanding of mental disorders and are highly stigmatizing. However, I disagree that the prescription for the cure is to conceptualize mental disorders as disorders of the brain.

Mind or brain: why does the distinction matter?

The classification of mental disorders is a contentious area, and it is important to understand that debates over the validity, vocabulary and conceptualizations of mental disorder are not merely the academic and theoretical concerns of philosophers and nosologists. Although primarily an epidemiological and research tool, coding in the major systems of classification determines how a psychiatric problem is clinically approached, the treatments available to patients and, in insurance-based health care systems such as that in the USA, determine what treatments can be paid for. Classifications are intended to divide up the landscape of mental disorders in empirically valid and clinically reliable way. Perhaps more so than with any other type of illness, how their condition is defined can be an extremely important issue for patients with a mental disorder diagnosis: in no other domain of medicine is there a vociferous and substantial survivor and service-user movement critical of the way their disorders are classified, and patients treated. One of the most prominent issues of recent times is the extent to which mental disorders can and ought to be classified as medical conditions, as opposed to, for example, problems in living . The question of whether mental disorders are disorders of the brain represents one aspect of this conceptual issue for classification, which has long, deep political and social implications.

Such questions in psychiatry are not new. The year 2013 is the centenary of the publication of Karl Jaspers' General Psychopathology and psychiatry is now finding itself a subject to similar debates and controversies as those which dogged the field 100 years ago . Jaspers wrote that text in response to what he considered to be an unhelpful biological reductionism that accompanied rapid advances in medical understanding of the brain in the late 19th and early 20th centuries. Around that time, the eminent neurologist and psychiatrist Wilhelm Griesinger had insisted that 'all mental illnesses are cerebral illnesses' and this position has recently been gaining currency within the profession once more. However, Jaspers argued that 'there has been no fulfilment of the hope that clinical observation of psychic phenomena, of the life-history and of the outcome might yield characteristic groupings which would subsequently be confirmed in the cerebral findings ' (, p.568). It is this theme I wish to pick up on in this paper; to consider the relation between disorders, we identify through their physical pathology, and those which, I will argue, we do not and indeed should not, whatever advances in neuroscience may reveal about the complex workings of the brain.

Psychiatry is fundamentally different from medical disciplines such as cardiology or oncology, and we can perfectly and consistently hold this view without falling prey to accusations of Cartesian dualism or claims that mental illness is 'all in the mind'. One can legitimately hold both that ultimately, the mind is made up of brain stuff, and that mental disorders are not reducible to brain disorders. To understand this, let us consider how physical and mental disorders are identified.

Physical and mental disorders

In the case of physical conditions, what picks out a condition as being a disorder is that there is presumed or found to be some dysfunction (howsoever construed, whether biostatistically (e.g. Boorse ) or evolutionarily (e.g. Wakefield ) as deviation from a norm of functioning in the body. More recent models have advanced an actuarial, risk-based model of disease but on both kinds of account, the problem is thought to lie in the internal workings of the biological body. Across the straightforwardly physical realm, there are three main divisions in the classification of how this internal failing or dysfunction is characterized. Some disorders are grouped according to known aetiology, for example cancers or genetic conditions. Others are grouped pragmatically, by the medical specialization most appropriately suited to treating them. Conditions treated in obstetrics and geriatrics are two such examples. Thirdly, some disorders are classified by the organ system affected, for example respiratory disorders or those of the gastrointestinal tract. Neurology falls under this heading, treating disorders of the central nervous system.

By contrast, in the mental case, what is picked out as disordered or problematic is that there is a disturbance of some kind in the person's thoughts, feelings or behaviours. Classificatory systems such as the DSM-IV and ICD-10 identify mental disorders as patterns of behavioural and psychological states associated with distress, disability, risk of suffering or a significant loss of freedom (along with other criteria). The predominant neo-Kraeplinian classification systems categorize mental disorders as clusters of self-reported and behavioural signs and symptoms, with no implication in terms of underlying aetiology or physical process: this provides a basis from which to initiate subsequent physical investigation . Criteria for classification are thus observational and not themselves indices of biological or cognitive functioning. However, arguments, such as White et al. 's have recently been put forward that our understanding of the scientific basis of mental disorders is advancing enough for classification to undergo a radical shift to categorize according to the dysfunction or deviation occurring in the known organ affected: the brain. I suggest that this is a mistake, for two reasons. Firstly, despite significant technological progress, it should not be assumed that specific brain pathologies or deviations in functioning will be found that inform our understanding and classification of mental disorders. Secondly, and more importantly, classifying according to signs and symptoms such as patterns of thought, expression and behaviour retains the use of person-level concepts and thus better reflects the nature of the disorders themselves. I will address these reasons in turn.

Pathologies in the brain?

There have been many astonishing advances in our understanding of neuroscience, of genetics and epigenetics, and of neurodevelopment, but there is not a single identifiable biomarker for any mental disorder . Robust evidence suggests strong genetic components to many disorders that do not necessarily correspond with current classifications . Further developments in the science of the brain are highly likely to reveal heretofore unknown and surprising links between brain circuits, genetics, thought patterns and behaviour. A Nature editorial in 2010 deemed this current decade the decade for psychiatric disorders, and argued that our understanding of such disorders will be revolutionized by progress in genetics and neuroscience. For my present purposes, the interest in the increasing prevalence of natural science-based explanations is the implication that psychiatric disorders are identifiable as disorders of the brain, explained in terms of neurobiological pathology. The question I wish to press is this: should these technological and neuroscientific advances make a difference to how mental disorders are classified, identified, diagnosed and treated?

A prominent interpretation of the goals and methods of psychiatry suggests they should. The 'strong' interpretation of the medical model leads either to eliminitavism about psychiatric categories (the belief that they will eventually be superseded by neurobiological categories) or essentialism (the view that psychiatry will and should be reduced to neurology through the matching of psychiatric categories to an underlying biological 'essence'). On both of these views, disease and disorder should be understood in terms of morbid anatomy and physiology; eventually, it will be possible to generate causal hypotheses about psychiatric disorders in terms of neuropathology or dysregulation. Whether the key theoretical concepts come from cognitive neuroscience, molecular biology or some other basic brain science, the strong interpretation of the medical model assumes that explanations for mental disorders can be sought that cite pathogenic processes in brain systems, and that furthermore, future classifications should reflect this knowledge. Many different causal processes may operate, including social and psychological ones, but the strong interpretation relies on neurobiology and cognitive processes being fundamental, and for explanations of these varied causal processes to be reducible to the vocabulary of the brain sciences. If we are to be eliminativists or essentialists about mental disorder, this would have a significant and rapid impact on our classificatory systems: labels such as schizophrenia or bipolar disorder would be replaced, superseded perhaps, by classifications based on the presence or absence of a particular copy number variant, or a statistical variation in the structure or activity of a particular region of the brain.

It is worth taking a moment to consider whether this is a plausible view. Might there be a molecular or neurobiological reduction of the kind of symptoms and problems implicated in mental disorders? The notions of shame and guilt are central to depression ; childhood abuse or neglect and socio-economic factors such as unemployment are powerful predictors of mental illness. Undoubtedly, these factors have effects in the brain, perhaps altering certain neural pathways from how they otherwise would have developed. However, this does not entail that there are identifiable pathologies of the brain associated with such complex sociocultural and psychological factors: ' They have brain effects, but the brain effects vary across classes of individuals in ways that depend on other environmental and genetic contexts' . There is huge variation in the clinical presentations of every psychiatric disorder, and the ongoing challenge for psychiatry is to provide some method of grouping and classifying this diversity in a way that is useful both for diagnosis and treatment in the clinic, and for research. Even with a complete map of brain functioning and connectivity, there may be no underlying unified account of what's 'wrong' across different brains of people exhibiting similar symptoms, nor whether particular treatments are likely to affect brains (and people: an important distinction to acknowledge) in similar ways.

Psychological realism

This brings us to the second reason for rejecting the conceptualization of mental disorders as brain disorders: what it is that identifies a person as suffering from a mental disorder in the first place? In some loose sense, in psychiatric disorders the person's self is affected, and the functional norms that he or she breaches are primarily epistemic (believing strange things), rational (thinking irrational thoughts, making incoherent connections), emotional (experiencing extremes of emotion that seems inappropriate or disproportionate to the situation), moral (doing or wanting things that contravene a societal moral code) or social (identified by others as being bizarre or objectionable) and those of self-knowledge (for example, experiencing problems with memory and intention). Thus the primary locus of disorder is among mental relationships, within a person's own psychological life, and in interpersonal relationships . In other words, the correct level of analysis for picking out that something is wrong, is the person, the self. The manifestation of the illness occurs at the level of observable behaviour and felt experience. Indeed, in no other medical discipline is the subjective experience of the patient quite so crucial to diagnosis and the aims of treatment.

Whatever the aetiology of the condition or its causal pathways in the brain - whether it is genetic, the product of gene-environment interactions, psychological, social or spiritual causes - the attribution of 'disorder' applies to the thoughts, feelings and behaviours of the person. Mental disorders are not mental disorders because of an assumed mental cause, but rather because they identify problems in the person's mental life and relationships. In this regard, I suggest that if we want to align psychiatry with one of the three main forms of categorization for physical disorders outlined above, we can think of current psychiatric nosology as based not on aetiology, nor on clinical pragmatism, but on the idea that the 'organ' affected is the person, within their environment. It would be a fallacy to suggest that the brain is the locus of disorder.

Many of the key features of psychiatric disorders can only be characterized and understood using the language of the mental realm. Establishing whether a given behaviour, thought pattern or emotional response is indicative of a disorder invokes precisely those concepts that reductionist accounts of psychiatry seek to eliminate or reinterpret in neurobiological terms: the psychological. This is not to deny that there is very likely to be a neurobiological basis to the behaviour, thought pattern or emotional response, and that the cause of these manifestations of pathology is biological. It is, rather, to argue that the level at which disorder can be identified is that of the person, who has both a brain, and a relevant social and environmental context. This view is called psychological realism, and it insists that whatever the technological and scientific advances we make in understanding the brain, its development and degeneration, we require psychological predicates in order to pick out instances of disorder .

It is of course true that many psychiatric disorders have clear physical symptoms: tiredness, pain, insomnia, changes in appetite. At the same time, physical disorders often have a strong psychological or emotional components or consequences: depression is commonly associated with Parkinson's; stress is strongly implicated in hypertension. None of this should give us undue cause for concern regarding our ontological commitments, or require us to defend a philosophically robust account of mental causation. At the level of ontology, of what exists in the world, one can be a physicalist but also hold that the 'person' level of analysis is conceptually irreducible to the stuff of the brain. It is important to remember that we are talking here about identifying the level at which disorder or dysfunction can be identified.

The problems of locating mental disorders in the brain

Much research on the social determinants of health is revealing that environment has a causal impact on the functioning of the brain and body, but it also leads us to question where we should attempt to locate disorders themselves. Take, for example, a person who is a single parent on a run-down council estate, with a low-paid service job that provides little opportunity for meaningful interaction, control or fulfilment. He goes to his general practitioner (GP) complaining of fatigue, a sense of helplessness and hopelessness, loss of appetite and losing the enjoyment he used to feel when playing with his children. A diagnosis of depression would not be surprising under these circumstances, and a likely outcome from the GP appointment is a prescription for antidepressants and possibly an offer of a course of psychological therapy. Here, we can argue that the patient has a depleted level of serotonin in his brain, and a course of selective serotonin reuptake inhibitors may well help him to lift the black and bleak feelings that have descended upon him. But is this where we think the locus of disorder is? Is his brain malfunctioning in some respect?

I suggest that in focusing the attribution of disorder on the goings on in the brain, we are missing the essence of what is going 'wrong' for the individual attempting to get on with his or her life. This is not to say that biological explanations ignore or sideline social and psychological causes; quite the opposite, many attempts to develop biological explanations explicitly seek to account for the causative influences of social and psychological environment, through finding demonstrable impacts on brain function . Rather, it is to suggest that in championing the brain as the locus of disorder at the expense of the person-level, we are making a powerful, and in my view, mistaken, judgement about how the disorder is conceptualized and what kinds of approaches should be taken towards treatment. A recent controversial article in the New York Times sums up this problem well. Dr. Michael Anderson, a child psychiatrist in Georgia, frequently prescribes medication such as Ritalin and Adderall to children from poor socio-economic backgrounds who are struggling academically in inadequate, underfunded schools. He argues 'we've decided as a society that it's too expensive to modify the kid's environment. So we have to modify the kid' . His results in terms of improvements to academic grades are impressive and satisfactory for the parents of his patients, but there is an understandable feeling of unease associated with the idea that fixing the 'problem' via medication is a clinically or ethically justified solution.

Yet if mental disorders are conceptualized as brain disorders, with many and varied associated social and psychological causes, the conceptual primacy of the neurobiological would be deemed explanatorily satisfactory, and all causal pathways explained through their effect on the brain. The sheer complexity of the brain is one barrier to these kinds of explanations. But even if we did find strong evidence that there are specific, consistent, reliable neurobiological differences between those suffering from psychiatric disorders and those that do not, it is not clear that any such differences could be conceived as pathological without begging the question about what constitutes the disorder in the first place. What I mean by this is that neurobiological differences in themselves are not what ought to characterize disorder. There is much talk in the empirical literature about brain 'abnormalities', 'deficits' and 'alterations' associated with mental disorder symptoms. But conceptually, what marks these differences as indicative of disorder or dysfunction? It is the association they bear with deviations from epistemic, evaluative, emotional, moral and social norms of functioning, in other words, the person-level constructs I have been advocating as the locus at which mental disorders are and should be identified and classified. If we lose sight of these, and focus solely on differences at the neural level between people, we are left unable to say which differences matter for attributions of disorder. It is only by paying attention to what is going wrong at the person-level that it is possible to argue that an associated neural structure or function is indicative of pathology or problematic abnormality.

Bringing psychiatry in from the cold

One of the major arguments in support of reconceptualizing mental disorders as brain disorders is the potential to make psychiatry seem more like other branches of medicine and reduce the stigma associated with having a 'mental' illness. Mental disorder does not necessarily mean 'mental', or in some sense 'non-physical', cause. Yet there remains a damaging hang up about having a mental disorder, which is perhaps a relic from the Cartesian distinction between mind and body. Patients with psychiatric diagnoses often feel poorly understood by clinicians, and fear that they are being judged as making up their symptoms, or that their pain, impairments and suffering are 'all in the mind'. This phrase captures one of the key problems with the notion that there may be a psychological (rather than clear 'physical') basis for a person's symptoms: that because they are 'mental', they either do not really exist, or they should be able to be controlled or ameliorated by the person if they only tried hard enough. Symptoms can be perceived as moral failings and weakness of the will or of character, and also carry implications of malingering. The phrase 'it's all in your mind' continues to exert a strong moral judgement, despite the fact that we acknowledge the mind is indeed a very powerful thing. It is socially acceptable to cite stress as a cause of fatigue or hypertension, and psychological trauma is known to cause striking physiological responses. The placebo effect, a psychological phenomenon, can be extremely strong. The efficacy of cognitive behavioural therapy and other psychological interventions indicate the power of the mind to generate physical effects and alleviate distressing states ranging from anxiety, to the positive symptoms of schizophrenia. Yet the idea that one's symptoms may in some sense be psychological continues to generate stigma.

It is not clear, however, that classifying mental disorders as brain disorders, drawing psychiatry closer to other branches of medicine, and generating explanations of symptoms in terms of neuropathology or problems in brain functioning indicates the right direction of travel for classification, or indeed the means by which to reduce stigma. The further the scientific understanding of the brain advances, the more we are able to appreciate how complex the interrelations can be between genetics, development, brain structure and function, life events, interpersonal relationships and the social, cultural and economic environment. This suggests that the conceptual direction of travel for understanding mental disorders will need to be against the tide of conceptualization in biological, subperson-level terms. Rather than reducing mind to the functions and dysfunctions of the brain, it would be more astute to recognize the importance of person-level constructs in conceptualizing mental disorder, and use these as the anchor for psychiatric nosology, taking into account factors ranging from the broadly social to the narrowly genetic. As for stigma, perhaps increasing recognition that social and psychological factors are implicated in many physical health conditions may help mitigate against continued perceptions of a mind/body divide, and thus reduce the negative connotations of having a mental (as opposed to physical) disorder? It is beyond the scope of this paper to flesh out this consideration, but I raise it only to emphasize that reduction of mind to brain is not the only way to potentially positively affect social perceptions of mental disorder.

There are powerful and compelling sociological and institutional reasons to bring the fields of psychiatry and neurology closer together. After all, psychiatrists are first and foremost medically trained doctors, able to prescribe pharmaceuticals and investigate the pathology of the body. But this does not mean psychiatry, and the classification of mental disorders, ought to be collapsed into neurology and the study of brain diseases. If anything, the close relation between the mind and the body, the mental and the physical, and the psychiatrist's expertise in dealing with complex psychological and social issues, suggests neurology and other medical disciplines ought to draw closer to psychiatry.

As a multi-level science, psychiatry is actually ahead of the game in incorporating different levels of explanation, and different potential treatments targeting the brain, the person and their psychosocial environment. It has the scope to act as an intermediary between biomedicine, psychology and social work, and to remain agnostic about the relevant causal pathways that lead to disorder. Social determinants of health reveal these extrinsic factors are crucial to health although disciplinary specialities artificially separate them: every condition is both a physical and a mental disorder.

Jaspers argued that in order to understand psychopathology, we must not lose sight of attending to the patient's experience, not only for the purposes of treatment but also for keeping track of precisely what the phenomena are that we are interested in. A century later, amidst a flurry of exciting and revelatory discoveries about the workings of the brain, Jaspers' tenet is a timely reminder. Conceptualizing mental disorders as brain disorders, even while giving due to their biopsychosocial context, would mistake what picks out a condition as a mental illness in the first place, that is, that something is going wrong at the person-level. The field of psychiatry may well be in the best position to accommodate the notion of multiple, multi-level causal pathways for disorders, and translate this understanding into good care and treatment for patients, if it does not make the conceptual error of assuming its subject matter necessarily needs to be characterized as pathologies of the brain.

Footnotes

¹ Editor's note: for a discussion of these broader questions and their relevance to practice, see the Conference Report section of this issue, which provides an overview of the workshop at which this paper was initially presented.

² The social model of disability (e.g. Oliver & Sapey ) rejects this view, which nonetheless predominates in medicine.

References

2. Szasz T. The Myth of Mental Illness: Foundations of A Theory of Personal Conduct. New York: Harper Collins; 1961.

3. Jaspers K. Allgemeine Psychopathologie. Berlin: Springer, 1913. English Translation of the 7th Edition: General Psychopathology. Baltimore, MD: Johns Hopkins University Press; 1997.

4. Maj M. 'Mental disorders as "brain diseases" and Jaspers' legacy. World Psychiatry. 2013;12(1):1-3. [ PMC free article] [ PubMed]

5. Griesinger W. Die Pathologie Und Therapie Der Psychischen Krankheiten. Stuttgart: Krabbe; 1845.

6. Boorse C. A rebuttal on health. In: Humber JM, Almeder RF, editors. What Is Disease? Totowa, NJ: Humana Press; 1997. pp. 1-134.

8. Greene J. Prescribing by Numbers. Baltimore, MD: Johns Hopkins University Press; 2007.

9. Oliver M, Sapey R. Social Work with Disabled People. 3rd edn. Hampshire: Palgrave Macmillan; 2006.

11. Stein DJ, Phillips KA, Bolton D, Fulford KWM, Sadler JZ, Kendler KS. What is a mental/psychiatric disorder? From DSM-IV to DSM-V. Psychological Medicine. 2010;40(11):1759-1765. [ PMC free article] [ PubMed]

14. Murphy D. Psychiatry in the Scientific Image. Cambridge, MA: MIT Press; 2006.

17. Bortolotti L, Broome MR. Mental illness as mental: in defence of psychological realism. Humana Mente. 2009;11:25-43.

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Mental disorders are not brain disorders

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As advances in neuroscience and genetics reveal complex associations between brain structures, functions and symptoms of mental disorders, there have been calls for psychiatric classifications to be reconfigured, to conceptualize mental disorders as disorders of the brain.

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The latest confusion about mental illness is this meme that demonstrates the absurdity that would ensue if we reacted to physical illness the way we do to mental illness-telling someone with a gunshot wound that they're just not trying hard enough, for example. The implication is that we should treat, say, depression the way we do a gunshot wound, something like, "Of course you didn't do the dishes, you poor dear; you have depression."

The first confusion is the way we lump primarily biological illnesses in with primarily behavioral problems. Almost all schizophrenias, an unknown but probably high percentage of bipolar disorders, and about 10% of depressions and maybe a similar percentage of anxiety disorders are biologically based to the point where they might be called illnesses. Schizophrenia used to be different, closer to 90-10, but new definitions of the term have all but eliminated the behavioral ones. Of course, all psychopathology or disadvantageous behavior has a biological base, since it is all expressed by a body, but there is a difference between a behavioral response to a peculiar learning history and a behavioral response to a broken biological system.

These biological disorders often resemble in public the condition of being partially deaf. A woman who is deaf in one ear is repeatedly treated as if she is rude, because she doesn't respond to what people say to her. It's fine to ask the public to treat every non-responsive person as if they are deaf, but you might as well ask the public to become Buddha or Jesus. Instead, the person with an invisible disability is likely to find more peace by making her disability visible. It's simple to say, I can't hear out of that ear; it's more complicated to know what to say about schizophrenia or autism. Maybe, "My brain is wired so that I don't always react emotionally." And that would be fine for under-reacting, but nothing is going to make people welcome histrionics, prolixity, or violence. Even a gunshot victim can be annoying if he screams long enough.

But most so-called mental illnesses are not of this type. Personality disorders and most depressions and anxieties are learned. The normally operative reinforcers are ineffective, and the person behaves accordingly, seeking (instead of affection, approval, intimacy, and achievement) admiration, chaos, clarity, destruction, or sexual validation (among others) at other people's expense. Or the person has given up on reinforcement after a history of failure. Or the person doesn't know what to do and over-reacts to mistakes. Calling these behavioral repertoires "mental illness" allows for payment by insurers, which would be a good thing except that it also allows for them to be treated chemically, and insurers prefer the cheaper chemicals (even though psychotherapy may be cheaper in the long run).

These varieties of psychopathology are best described as disadvantageous behavior, and since our social world is so important, that means that the kinds of things commonly called mental illness are actually behavioral repertoires that other people find annoying. With personality disorders, the fundamental annoyance is the recognition that you are just not that important to the person, that you are a stage prop or a minor character in the other person's drama. Virtually the only hope of motivating the person to change is for the person to get a dose of your annoyance. If we treated such people the way we treat people with the flu, we'd spend all our efforts hiding from them, because we avoid annoyances we cannot express annoyance about. Are we really supposed to say, "She takes up all the space in every room she's in, but that's because she has a personality disorder, so let's let her keep doing it"? The term, "mental illness," when used with such people, is nothing other than an effort to insulate them from the natural social consequences of their behavior. If you don't like the way the world reacts to your behavior, behave differently (again, thinking for the moment of those who can).

I think it was Talcott Parsons who re-interpreted Freud's ideas about toilet training and control. The idea was that there is a natural interaction between the child and the social environment in which the child's soiling is treated as excusable and normal until the parents get sick of it. This leads to the questions of control and autonomy, not anything about anal needs. Similarly, someone said that people grieve until their community gets tired of their grieving, at which point they get messages that it's time to start behaving differently. Most people won't sacrifice their normal reinforcers for grief, and then we say that they are making peace with their loss (for extreme losses) or getting over it (for minor losses), but what we really mean is that the affection and approval that was unbroken during their grief is starting to depend on a little more effort.

Similarly, other people are sympathetic to anxiety and depression up to a point. You don't insist on going to a party when your spouse is feeling blue, and you learn to shrug about your spouse's excessive worrying when you drive in the snow. But when your spouse demands that you call her when you get there or spends weeks sulking in a darkened room, you put your foot down in a way you never would if your spouse were gravely ill. Otherwise, you'd be enabling, not empathic.

Besides discouraging those who can change from doing so, the analogy to physical illness misses the point that for many serious mental illnesses and personality disorders, the issue is that they don't "get" other people. Making allowances for that is asking us to treat ourselves as much like objects as the person in question does. Such allowances also defeat recovery, since they treat the illness as causing the annoying behavior rather than treating the behavior as something that the person is doing to themselves and others.

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We Shouldn't Treat Mental Illness Like Physical Illness

# data[].attributes.attachment_link.description
The latest confusion about mental illness is this meme that demonstrates the absurdity that would ensue if we reacted to physical illness the way we do to mental illness-telling someone with a gunshot wound that they're just not trying hard enough, for example.

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Pashak TJ*

Department of Psychology, Saginaw Valley State University, USA

*Corresponding Author:

Travis J Pashak, Ph.D
Assistant Professor of Psychology
Saginaw Valley State University, USA
Tel: 989-964-2696
E-mail: [email protected]

Received date: July 02, 2017; Accepted date: July 26, 2017; Published date: August 02, 2017

Citation: Pashak TJ (2017) Mental Disorders are Not Real: Using Skepticism and Critical Thinking to Challenge Key Myths in the Science of Mental Health. J Ment Disord Treat 3: 140. doi:10.4172/2471-271X.1000140

Copyright: © 2017 Pashak TJ. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Abstract

This review aims to identify and correct several prevalent misunderstandings about mental health and mental disorders which are potentially damaging to society. Organized into themes around four myths about mental disorders, this discussion provides readers with helpful information and references to other useful readings to support their skepticism and critical thinking about psychopathology. The four myths identified here are that mental disorders are unimportant, are solely biomedical entities, are only treatable with medication or CBT, and are real. In each case, the author makes a reasoned argument to the contrary, culminating in a discussion about how mental disorders are actually not real, but are nevertheless very important considerations. Throughout the discussion several logical fallacies are introduced (e.g., confusing correlation with causation, the nominal fallacy, the reification fallacy), as well as brief historical notes on the field of psychology (e.g., varying treatment modalities, schools of thought around treatment impactfulness, and problems with language progression in research).

Keywords

Mental disorders; Myth; Diagnosis; Psychotherapy; Effectiveness

Mental Disorders are Not Real: Using Skepticism and Critical Thinking to Challenge Key Myths in the Science of Mental Health

In this brief manuscript, I aim to identify several critical misunderstandings about mental health and provide readers with information to correct these common errors. My hope is that this review may serve as a useful reading resource for undergraduate students enrolled in courses such as Abnormal Psychology or Introduction to Clinical Psychology, as a prompt for critical thinking discussion for graduate students in clinical/counseling psychology or social work, as a quick teaching tool for psychiatry training, or even as a helpful reminder for those already engaged in the helping professions. By no means are the myths listed here a comprehensive or empirically-derived list of all significant problems in the science of psychopathology; however, they are a set of important and damaging assumptions I find myself addressing repeatedly with my own students and clients. Thus, I felt the need to compile these issues into an easily shared open-access format. Read on for a short list of key myths about mental disorders and ways to challenge those faulty beliefs.

Myth #1: Mental Disorders are Unimportant

This is absolutely false. While most people taking the time to read this article would probably not endorse this belief, there nevertheless exists a prevalent viewpoint which devalues the science of psychopathology and individuals' mental health experiences, and is dismissive of psychology in general. Themes commonly bundled into this belief include the notions of blame (e.g., "he's not depressed, he's just lazy"), disinterest (e.g., "why would I care about someone's touchy-feely issues?"), distrust (e.g., "I think those labels are just excuses"), prejudice (e.g., "I won't associate with crazies like her"), minimization (e.g., "it's a waste of time and energy to consider those things"), illegitimacy (e.g., "psychology isn't a real science like chemistry or physics"), disbelief (e.g., "they just act that way for attention"), antipathy/apathy (e.g., "they need to pull it together, they've got it no harder than everyone else") and possibly even fear (e.g., "that neighbor seems disturbed, maybe he's dangerous"). For many laypeople, these and other similar themes drive a general sense of unimportance regarding mental health and mental disorder.

Why do many outside the field disregard mental disorders despite their conceptual value as meaningful and important tools for understanding others? Numerous explanations can contribute, including Lilienfeld's themes of seeing psychology as common sense, perceiving a lack of scientific rigor, denying generalizations due to individual uniqueness, claiming the results are non-replicable, seeing findings as imprecise, and being unable to see the utility of the field [ 1]. Specific to the public devaluing of mental disorders as helpful constructs, I would propose two additional explanations: anecdotal thinking and difficulties with empathy. Regarding the former, I would argue that many who experience mental health throughout much of life simply have no lived experience from which to understand the mental unhealth of others, and therefore determine that something about the idea of disorders must be dishonest or otherwise amiss. In other words, they engage in the hasty generalization fallacy (e.g., "Since I've never had those thoughts/behaviors/experiences, I don't see why anyone else would), extrapolating from their lived experience of n=1 to build a general rule by which they perceive all others in the world. Regarding the latter, I would argue that empathy (for those mentally unhealthy) is simply difficult for many to muster. Without first-hand experience, relevant observations of close friends or family members, or extensive training, people likely find great challenge in trying to understand the thoughts/feelings/behaviors of those struggling with mental health problems. Indeed, research has shown that deep and accurate empathy on other topics (e.g., experiences of racism) is hard work and only results from active perspective-taking and exposure [ 2].

While there may be numerous reasons for public denial of mental disorders, the evidence is clear that mental health problems are in fact common, important considerations, and are related to a plethora of human difficulties. For instance, epidemiological data show that approximately one quarter of American adults experience a mental disorder in a given year, nearly half will experience a mental disorder some time in life, and that suicide is a leading cause of death worldwide [ 3, 4]. Further, the World Health Organization estimates that mental disorders fall in the top 20 causes for disability, and are also a significant source of lost years of life, particularly for women and racial minorities [ 5]. Lastly, the worldwide cost of mental illness has been estimated at a staggering 2.5 trillion US$ as of 2010 [ 6]. Certainly, mental health and mental disorders are important considerations in making sense of the human condition.

Myth #2: Mental Disorders are Biomedical Problems

This is false; or at least mostly false. Although the psychiatric approach, the traditional "medical model" of diagnostics, television advertisements for prescription psychoactive medications, and many other sources might lead to the belief that disordered mental health is entirely a biomedical issue (i.e., of the body and rooted solely in biological/genetic factors), this is simply not the case. While the general public and certain training contexts may have a truncated perspective, the majority of contemporary clinicians and researchers in psychopathology value what is called the biopsychosocial model [ 7]. This model is a collective set of findings from biological approaches (e.g., biochemistry, genetics, nutrition, neurology), psychological approaches (e.g., cognition, behaviorism, development, personality, psychoanalysis), and social approaches (e.g., sociology, cultural anthropology, politics, history), which all contribute to the understanding of mental health and mental disorder. To view mental disorders as strictly somatic/ bodily constructs is to completely disregard two-thirds of this widely accepted model. Further, some researchers have actually found evidence that it is damaging to view mental disorders this way. Specifically, one study showed that those who held biogenetic explanations of mental disorders were more fearful of and pessimistic for those struggling with mental health problems, which could serve to exacerbate stigma [ 8].

Some readers may be frustrated at this point, having believed for years that depression, for instance, is caused by a "chemical imbalance." This and other similar attributions for mental disorders fail to utilize the entirety of the biopsychosocial model, and may engage in confusion of correlation versus causation. While it is true that, since the 1960's and 1970's, the monoamine theory of depression (e.g., serotonergic malfunctioning and norepinephrine depletion) gained significant attention as a possible explanation for mood problems [ 9], contemporary psychiatric research concludes that "simple biochemical theories that link low levels of serotonin with depressed mood are no longer tenable" [ 10]. This is in part because the logic is seriously flawed. Finding that a neurochemical pattern is related to a behavioral pattern (i.e., correlation) does not imply that the neurochemical pattern precedes, explains, and directly influences the behavioral pattern (i.e., causation). Rather, the evidence appears to show that, sometimes, those two features co-occur. Further, even in causal laboratory studies of induced serotonin depletion resulting in depressive symptoms, the findings do not show that all depressive episodes are caused by faulty neurotransmitter patterns- just that this phenomenon may be a part of the explanatory puzzle. Extremely compelling evidence for the etiology (i.e., cause) of depression comes from other approaches within the biopsychosocial model; consider for instance that approximately 66% of those meeting criteria for Major Depressive Disorder in the firstwave National Comorbidity Survey were dealing with bereavement or some other recent major loss [ 11]. If someone experiences the death of their child, divorce from their spouse, or loss of their job, then it seems quite illogical to blame their subsequent depressive mood on faulty serotonergic functioning.

Major Depressive Disorder is hardly the only mental disorder to defect from the solely biomedical conceptualization. For instance, Schizophrenia, largely considered the "poster child" of psychiatric biomedically-oriented mental health problems, is still only approximately 40-50% genetically heritable, leaving much of the etiology to other psychosocial influences or other non-genetic factors (e.g., advanced paternal age, urban birth, migrant status, and prenatal infection) [ 12]. None of this is to say, of course, that biomedical variables are irrelevant- just that they are not the only factors involved. In other words, psychology (and therefore psychopathology) must be approached with an appreciation for both its natural science and social science components [ 13]. As an example, consider the widely utilized diathesis-stress model [ 14], which combines nature and nurture in its attempt to explain the causes of mental disorders. Originally formulated to address the etiology of Schizophrenia, but later applied to most other disorders, the diathesis-stress model postulates that a combination of diatheses and stressors can be used to statistically predict the likelihood of a mental disorder occurring. In this model, diathesis refers to one's personal vulnerabilities, disposition/personality/character traits, early formative experiences, and genetically inherited probability of a disorder. Thus, one's diathesis is their cumulative risk level for a certain disorder, given early/lifelong factors. Then, stress refers to current or recent difficulties, negative life events, challenging situations, injury/ change to the central nervous system, emotional strain, and even trauma. Thus, one's stress is the cumulative level of difficulty currently being faced. So together, the diathesis-stress model argues that diatheses (such as genetic vulnerability) are not the sole explanation for mental disorders, rather, they interact with individuals' current stress levels to influence the possibility of distress and impaired functioning. Some use the analogy of a "loaded gun" to help explain this model, such that some individuals are more "loaded" for a disorder than others (i.e., they possess a stronger level of diathesis) but nevertheless the environment is necessary to "trigger" the disorder onset (i.e., push the stress level high enough for disordered problems to manifest). In any case, this empirically supported approach to etiology certainly relies on both biomedical and psychosocial influences.

Additionally, there is in fact an inherent indication in the term "mental disorders" which differentiates them from solely biomedical entities. That differentiator is the term disorder as opposed to the term disease [ 15]. This subtle distinction may be lost on many outside the field, but it is an important acknowledgment of the nature of the problems themselves. The term disease is used to refer to problems in human functioning which have a known/identifiable pathophysiological process- thus diseases have an objectively observable set of bodily indicators (e.g., breast cancer involves observable malignant cell growth in breast tissue; pneumonia involves observable lung tissue inflammation and accompanying consolidation of fluid in air sacs). A disorder, on the other hand, refers to a problem in human functioning which lacks a clear pathophysiological process- in other words, the working of that problem is either not grounded exclusively in observable bodily processes, or, current research is in conflict as to why the problem occurs. With this comparison in mind, the fact that most mental health problems are named disorders (e.g., Major Depressive Disorder, Generalized Anxiety Disorder, Posttraumatic Stress Disorder, Borderline Personality Disorder) or are given other similarly-defined terms such as syndrome (e.g., Munchausen Syndrome by Proxy (i.e., Factitious Disorder - Imposed on Another) and Restless Legs Syndrome), dysphoria/dysmorphia (e.g., Gender Dysphoria and Muscle Dysmorphia), and nervosa (e.g., Anorexia Nervosa and Bulimia Nervosa), seems to support the notion that these constructs are indeed not solely biomedical, as they lack any clear pathophysiologic process [ 16]. Mental disorders are certainly not to be solely understood as biomedical entities, but rather, are best explained utilizing all levels of the biopsychosocial model.

Myth #3: Mental Disorders Must be Treated with Medication or CBT

Again, this is a commonly held notion which is mostly false. Psychoactive medications and/or cognitive behavioral therapy (CBT) can both be appropriate forms of treatment for certain mental health problems, but the issue here is that many assume those are the only legitimate options, and this is simply incorrect.

If the logic is sound against framing mental disorders as solely biomedical entities and instead utilizing the biopsychosocial model, as argued in the prior section, then one would be wise to approach treatment with similar thinking. Unfortunately, many in the general public and within the field have a woefully narrow view of which mental health treatments are appropriate. The overarching treatment message many receive from television/radio media, online advertisements, and other contemporary information sources (often including their primary care physicians) consists of a glowing recommendation for psychotropic substances such as Paxil (Paroxetine), Xanax (Alprazolam), Prozac (Fluoxetine), or Celexa (Citalopram)- with no mention of counseling, psychotherapy, support groups, or other routes to improvement. This misinformation is a serious detriment to society, as psychological treatments have much to offer.

Evidence abounds that psychotherapy is effective in the treatment of mental health problems. Since the first major meta-analysis in 1980 and onward, researchers have consistently found positive data supporting the notion that psychological treatments have a significant impact [ 17]. Recent meta-analytic studies have been similarly optimistic for psychological interventions. For instance, in the treatment of depression, average effect sizes for psychotherapy appear to fall around 0.73 [ 18], while effect sizes for antidepressant medications appear to fall around 0.31 [ 19], indicating that while both approaches can be impactful, there may be reason to prefer psychological treatments. Further, another recent meta-analysis of numerous studies occurring since the 1990's shows that psychological treatments are similar, and at times more effective (either immediately or a later follow-up) than psychoactive medications in the treatment of issues including stress, depression, panic attacks, and insomnia [ 20]. Importantly, my aim here is not to argue against the responsible use of psychotropic medication, when necessary (and many clinicians would agree that pharmacological treatment is needed for more severe/disabling forms of mental disorders, such as those in the psychotic or bipolar categories), but rather to showcase evidence that psychological treatments such as individual psychotherapy do deserve serious consideration as effective forms of intervention.

Within those willing to accept the evidence that psychological treatments are effective, many appear to hold attitudes falling into the second part of this myth: that only cognitive-behavioral therapy (CBT) is an appropriate form of treatment modality. This too is patently false. Territory wars over the statuses of effective or efficacious have raged in the field of psychotherapy for decades, with various models of treatment each experiencing their heyday. Psychoanalysis, psychodynamic psychotherapy, humanistic psychotherapy, interpersonal psychotherapy, existential psychotherapy, behavioral treatments and behavior modification, cognitive psychotherapy, CBT, feminist therapy, multicultural counseling, eclectic or integrative approaches, and a whole host of more recent additions to the counseling tradition (e.g., mindfulness-based psychotherapy, dialectical-behavior therapy, etc.) have all clamored for an ever-elusive standing as the unanimously agreed-upon "best practice." By all accounts, CBT is currently experiencing a period of popularity in the field's history, and with changes being made to the structures of health insurance and treatment provision in many countries, now is an important time to disseminate accurate information about these therapies.

Probably most importantly, I will point out that longstanding research has shown most/all psychotherapies to be effective, and to be not significantly different from one another in their level of effect (sometimes dubbed the "dodo bird verdict") [ 21, 22]. Although the theorists behind each modality of psychotherapy/counseling have extensively researched and prolifically written about all the nuances of their respective treatment's "bells and whistles," the practice is nevertheless primarily comprised of a set of common factors (i.e., shared among nearly all modalities) which appear to statistically account for a greater degree of variance than the unique factors. In other words, sitting down to talk with a professional who patiently listens, deeply cares, accurately empathizes, non-judgmentally explores, authentically validates, and gently challenges a client with mental health concerns (when, of course, the clinician is adequately trained in ethics, cultural competence, etc.)- this is meaningful and effective. Whether the clinician tends to focus most on thoughts, behaviors, relationships, interactions, memories, impulses, desires, fears, etc., these details may steer the content the of treatment but many not greatly alter the ultimate level of impact.

Despite the fact that many practicing clinicians are intimately aware of the dodo bird verdict and treat their clients accordingly, utilizing skills from the modalities best suiting their personalities and their clients' needs, there continues to exist a widespread push toward empirical "proof " of superiority for one model or another. Primarily led by academic researchers (who typically conduct psychological treatments far less frequently, if at all, compared to their peers in applied settings), this search for a gold standard has led to some rifts in the fields of psychopathology and clinical/counseling psychology. Of note is the contention around evidence of impact, and the forms of evidence which are acceptable. One "camp" approves of the Empirically- Supported Treatments (EST) model, whereas the other camp approves of the Evidence-Based Practices (EBP) model. There is much literature on this divide [ 23, 24], but briefly, the EST model tends to focus on the evaluation of a treatment's efficacy (i.e., ability to alleviate a specific symptom or symptom cluster) through tightly controlled internally valid laboratory studies such as randomized clinical trials, whereas the EBP model tends to focus on the evaluation of a treatment's effectiveness (i.e., overall impact upon general improvement) through studies which more closely mirror real-life clinical work with external validity. Broadly, the EST model tends to value empirical data such as experiments and meta-analyses, whereas the EBP model would value that data plus other sources of clinical knowledge (e.g., clinical expertise, case studies, supervision, correlational data, etc.). So, the EST model tends to be narrower in how it delineates which treatments are valid. When CBT's heyday is combined with the current trend of hiring primarily CBT-oriented researchers to tenure-track positions in psychology, as well as other historical factors in the field, the consequence is that CBT treatments tend to receive privilege and priority over other modalities in terms of trainee exposure, frequency of publications, and available evidence.

At the crux of the EST/EBP rift is a debate over how to view clinical work, and how to view psychology in general. Academic researchers in psychology and exclusively-CBT practitioners (particularly those adhering to manualized therapies) typically orient themselves around a positivistic view of the world, where only tightly internally valid data can contribute to the discussion- all else would detract from psychology's stance as a science. This status preservation, keeping psychology aligned with the STEM fields, is so precious to some that it may significantly bias their views toward the field and its constituents' activities. For instance, even in a recent article in The Clinical Psychologist with a balanced-sounding title of "Epistemic Humility," the tone still centered around positivistic empiricism-only attitudes and the near exclusion (or even disregard) of humanistic/hermeneutic clinical work [ 25]. Many clinicians, however, appreciate and understand the scientific underpinnings of the field while also valuing the inherent art involved in the counseling relationship- a subjective, phenomenological, and experiential endeavor which may lose generalizability if placed under a microscope. With this in mind, it is no surprise that proponents of CBT (or generally EST) are likelier to engage in scientific research, publish articles, and promote the idea that CBT is superior- because proponents of psychodynamic, existential, or feminist therapies for example (and generally EBP) may be likelier to spend their time in the provision of psychological services, supervision of trainees, or writing theory-building articles rather than contributing to the growing EST literature. In other words, a lack of empirical evidence supporting a certain modality does not necessarily equate to support against that modality. And researchers outside the CBT tradition are indeed beginning to make an empirical impact. For instance, consider that a recent series of studies and meta-analyses on psychodynamic psychotherapy are highlighting evidence that the treatment modality is frequently equally impactful to CBT, more impactful than medications, and often yields long-term continued growth of functioning/insight at follow-up which other treatments may not offer, across a variety of types of concerns/disorders [ 26, 27, 28]. Certainly, non-CBT modalities have much to offer, as do non-individual modalities (e.g., couples' psychotherapy/counseling, family interventions, and group therapy). These alternatives to the now-popular individual-CBT approach should all be taken seriously as legitimate options for treating mental disorders.

Finally, I would also like to point out that a plethora of meaningful "treatments" exist outside of the realm of formalized psychiatric and psychological care, which can possibly contribute to mental health. For instance, many individuals can find growth through: improvement of their physical fitness (e.g., exercise classes, running, massage therapy, chiropractic, diet/nutrition management); exploration of their religiosity/spirituality (e.g., worship groups, scripture readings, yoga, pastoral counseling, prayer); enhanced social connection (e.g., activity clubs, anonymous substance-use meetings, grief support groups, online forums); and self-help (e.g., books, online materials, audio recordings). Mental disorders need not be treated exclusively with psychotropic medications or cognitive-behavioral therapy; rather, many other forms of psychological treatment are valid and effective.

Myth #4: Mental Disorders are Real

Mental disorders are not, in fact, real. At least not in the concrete sense of the word "real." Before any readers become infuriated with me, remember that in the prior sections I argued that mental disorders are indeed important and that they can also be treated, so I am certainly not aiming to invalidate the mental health struggles of millions of people. Rather, the mythical belief I am addressing here is that many think of mental disorders as real things, pseudo-physical entities which are unique, classifiable, and can cause symptoms, and which therefore need to be cured. This line of thinking, while possibly comforting, is based largely on logical errors and fallacies.

Collections, Not Causes

First, consider how disorders are defined and described in the professional literature. The Diagnostic and Statistical Manual of Mental Disorders (DSM, currently in its fifth edition [ 16] gives a general definition focused on disturbance, clinical significance, and problems in thought, feeling, and/or behavior. Then, throughout the DSM, individual lists are provided which detail the symptoms of each of several hundred disorders. The leap in thought taken by many is that the disorders included in the DSM actually cause their respective symptom lists (as would be true for diseases which cause symptoms), but this is actually not the case. Rather, the list of symptoms is the disorder - causality in any direction is not presumed. A disorder is really a collection of problems which often seem to co-occur; the etiology of this cluster of symptoms is a much larger discussion (which, as addressed earlier, calls upon the biopsychosocial model and diathesis-stress model rather than solely biomedical findings). This misunderstanding is prevalent throughout the general public and often within the field as well. Hearing someone say "my social anxiety makes it hard for me to speak in large groups" likely doesn't sound shockingly illogical at face value - but the thought process does in fact engage in a form of circular logic called the nominal fallacy (i.e., the belief that because something has been named, it has also been explained). The key word in that example is "makes," which implies that the individual's Social Anxiety Disorder (a named collection of symptoms involving discomfort over fear of judgment) somehow caused a specific experience to occur (feeling anxious with large crowds). As astutely commented by Jonathan Shedler, this logic "...makes no more sense than saying 'anxiety is caused by anxiety.' The label is not the cause." [ 29].

Labels, Not Labeled

Even if they are collections of symptoms, why can't disorders be causes? A crucial reason is that they are socially-constructed labels, rather than tangibly existent entities which come to be labeled. Pardon the cliché, but consider Shakespeare's commentary on a rose: by any other name (i.e., label), it would still remain a rose, and thus smell just as sweet. The rose itself is a real thing which exists in nature, in a tangibly observable way, which would continue to exist unchanged even if described/named/labeled differently by society. Mental disorders, on the other hand, do not exist in the natural world in some tangibly observable way (because as discussed earlier, they are not solely biomedical entities like tumors; they are complex biopsychosocial constructs). So, if a new DSM were written (as happens every several years) and a current disorder were edited to include different symptoms, then the entire construct would be changed and would no longer remain in its prior form (e.g., consider some of the changes made to the definition of "trauma" within Posttraumatic Stress Disorder, or the fact that Asperger's Syndrome was completely removed in DSM-5) [ 16].

Categories, Not Classifications

Part of the reason people have come to view mental disorders as real things, I believe, is due to the medicalized "hard-science" language developed to describe them, which is somewhat misleading. In the natural sciences, many phenomena can be classified into an organizational structure via unique characteristics (e.g., the classification of animals into their kingdom, phylum, class, order, genus, and species; the classification of physical materials by their composite parts using the periodic table of the elements). This clean and tidy arrangement of information is an appealing epistemology to many in the social sciences as well, and has often been attempted - the taxonomy of disorders in the DSM being a prime example. However, the organization of disorders differs from the organizing principles in the natural sciences in a very important way: the DSM is based on clusters of symptoms via self-report from those experiencing the symptoms (i.e., it is phenomenological) rather than being based on objectively observable characteristics as a true nosology would. Thus, in having to rely on subjective factors rather than unique natural traits, the disorder taxonomy is inherently less stable, prone to change over time, likely to have cluster-overlap, is hedged in majority culture rather than representing all humanity, and can only provide estimations of categories rather than legitimate classifications. This is why many students in undergraduate Abnormal Psychology classes are stunned when they hear that two individuals both diagnosed with Major Depressive Disorder may not technically share a single symptom; that the difference between Bipolar I and Bipolar II rests on a loose clinical judgement of "severity" of the already severe manic episode; that Posttraumatic Stress Disorder and Acute Stress Disorder basically are only separated by an arbitrary cutoff of 1 month; and that those with at least one mental disorder are likelier to have two or more rather than being uniquely classified with solely one label (i.e., the problem of comorbidity) [ 16].

Constructs, Not Concrete

A final form of misunderstanding, with regard to mental disorders being "real," is that some people begin with a reasonable grasp on disorders as constructs, but inadvertently slip into viewing them as concrete as time passes and discussion continues. To be clear, a construct is a hypothetical explanation used to aid in understanding when no existent observable process is available. Mental disorders are indeed constructs, and this is why they are referred to as "socially-constructed" (i.e., society, via the DSM and other sources, has constructed these labels). Synonyms for construct in this sense could include concept, idea, and notion. Most of the time, when faced with the statement "disorders are not real, they are constructs" people can initially follow along. However, before long, many will subtly revert back to assigning disorders the properties which only existent concrete objects can have. As Eacker explains it, many people (even psychological researchers) have a bad habit of "mistaking as things entities which are not things." [ 30]. This happens in part through a grammatical shift in language, which is then believed to be accurate. One specific form of this problem is called the reification fallacy, or the logical error of treating a construct as though it were real in nature. For instance, consider introversion: early social science researchers found interest in studying those who were shy, less-outgoing, less-assertive, etc., and decided upon the name "introverted" as an adjective to describe them (e.g., "he is introverted"). Then, before long, people began to discuss the term as a noun instead of an adjective (i.e., "he has the trait of introversion"). Lastly, as a noun, people begin to apply existent and causal properties to the construct, which is ultimately illogical (e.g., "his introversion caused him to stay at home instead of going to the party"). This subtle shift of the reification fallacy has an insidious tendency to manifest with many social science phenomena, and the notions of mental disorders are probably one of the strongest examples with real-world consequences. This process leads people to believe that mental disorders are real, existent, tangible, physical entities which can be possessed by individuals and which have causal powers - but this is all false. Just like an individual cannot possess love, but they can be in love; and love does not cause them to feel a certain way, rather, it is the label for how they feel, so too with psychopathology constructs: he does not have depression, he is depressed; his anxiety is not causing his symptoms, it is his symptoms. And while these distinctions may appear to be pedantic grammatical minutia at first glance, they can indeed have negative consequences. As researchers and clinicians alike have already begun to notice [ 15, 31], the reification of mental disorders has done a major disservice to the public, misinformed millions of consumers of mental health treatments, tarnished the scientific credibility of the field, and stymied research progress in psychopathology for decades.

Conclusion

In this manuscript, I have attempted to compile and critique numerous major misunderstandings about mental disorders, synthesized under the headings of four commonly held myths: that mental disorders are unimportant, that mental disorders are biomedical entities, that mental disorders can only be treated with medication or CBT, and that mental disorders are real. Given that some of my statements may come across as controversial, please allow me to be clear in reiterating my intent with this piece: I do not aim to invalidate or minimize the mental health struggles experienced by anyone - your perspective matters, your pain is real, and as a clinician myself I hope to be as empathic as possible. What I do hope to address are the misunderstandings about mental health and the science of psychopathology floating about in society, which have the potential to be damaging and to worsen an already contentious field. Thus, I felt compelled to find a way to package this discussion briefly and accessibly to various audiences of readers.

Considering the available research literature and theoretical writings, extensive clinical supervision and consultation, and first-hand experiences with clients and students alike, I feel confident in making the following conclusions: Mental disorders are extremely important considerations, and mental health work is deserving of parity with other forms of human health and functioning. Mental disorders are best viewed through multi-systems thinking, for instance using the biopsychosocial model, and other platforms which value the enormous complexity of the human condition and its many layers of function and dysfunction. Mental disorders (and more importantly, the humans experiencing mental unhealth) can be successfully and effectively treated through a variety of means, including psychotherapy/counseling which spans a history of various schools of thought, each with their valuable kernels of wisdom and insight. Finally mental disorders are not real - but they are socially-constructed descriptive labels to be understood with nuance and empathy.

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Mental Disorders are Not Real: Using Skepticism and Critical Thinking to Challenge Key Myths in the Science of Mental Health

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Pashak TJ* Department of Psychology, Saginaw Valley State University, USA *Corresponding Author: Travis J Pashak, Ph.D Assistant Professor of Psychology Saginaw Valley State University, USA Tel: 989-964-2696 E-mail: [email protected] Received date: July 02, 2017; Accepted date: July 26, 2017; Published date: August 02, 2017 Citation: Pashak TJ (2017) Mental Disorders are Not Real: Using Skepticism and Critical Thinking to Challenge Key Myths in the Science of Mental Health.

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It is very common when I first encounter a client struggling with mental health issues that they report their problem is that they feel anxious or depressed. Here is a typical exchange:
Me: So, can you share with me what brings you in?
Client: Well, I have not been feeling good. I have these low moods that I can't shake off. I want to stop feeling depressed.
Me: What is it that gets you feeling depressed?
Client: I don't know. Nothing really. It just comes out of the blue. And I just wish I did not feel this way.

Then I begin to gather data about their lives, and almost always, the reason for depression (or anxiety) emerges. The most common narrative is something like the following (these elements would usually unfold over a half an hour to an hour of exploration-they are accelerated here for clarity and put in the context of a male college student):
Me: So, tell me a little bit about what is going on. What does your life look like here at college?
Client: I go to class, but I really am not that interested in what I am doing. But obviously I need a college degree if I am going to get a decent job. I have a few people who I hang out with, but they don't really know what is going on with me, and I don't feel like talking about it. Lately, since I feel bummed, I often just stay in my room.
Me: What about romantic relationships?
Client: I hooked up once last semester. But I don't have any romantic relationships.

Client: No.
Me: Tell me about your relationship with your parents.
Client: It is fine, I guess. I talk with them some.
Me: Do they know about your moods?
Client: No. They care about my grades, but I don't want to burden them with my moods.
Me: What was your relationship like them growing up?
Client: Fine, I guess. They divorced when I was 12. My mom left my dad and my brother and I moved in with her boyfriend, now my step-dad.
Me: How is your relationship with him?
Client: Not good. He is an asshole.
Me: Did that put a strain on your relationship with your mother?
Client: I don't know. We never talked about it.

One of the things that folks are most confused about when it comes to anxiety and depression is the relationship between the feelings and the root nature of the problem. Our society confuses these things and way too often labels the feelings as the problem. Consider it this way. If you break your arm and then go into the emergency room, you don't say, "I have pain-in-my-arm disorder". The pain is the signal that there is the problem. Or if you are outside for a long time in the cold with no jacket, upon feeling very cold, you don't say that you have "a coldness disorder". Or if you don't eat for a long time and you feel famished, you don't have a " hunger disorder". Feeling pain, cold, and hungry are signals that your basic needs for bodily integrity, warmth and food were not met. The feelings are not the problem, per se.

Negative feelings like depression and anxiety function the same way. Depression and anxiety are, for the large majority of cases, emotional signals that one's psychological health is not ideal and that one's psychosocial/relational needs are not being met. Indeed, the first place that I look when I see depression and anxiety is the need for relational value. As deeply relational beings, humans have needs for relational value in the following areas: 1) family; 2) peers/friendships; 3) romantic partners and 4) group/occupational/social identity. There is also the relationship they have with themselves and the extent to which they feel proud and accepting of themselves (or the reverse). In other words, it is crucial that we feel known and valued by our family, our friends and our lovers and that we have a way to be known and valued in terms of how we contribute to society. And it is crucial that we respect and have compassion for ourselves.

Now look back at the exchange above. One can see immediately that the client is low on all these domains. He feels alienated from his family; he lacks intimate friendships; he has had no romantic involvements; and he does not see a clear pathway that he can contribute to society in a way that feels valuable. And he has no idea about how to think about himself in a positive light.

Depression is a way the emotional system signals that things are not working and that one is not getting one's relational needs met. If you are low on relational value in the key domains of family, friends, lovers, group and self, feeling depressed in this context is EXACTLY like feeling pain from a broken arm, feeling cold being outside in the cold, and feeling hungry after going 24 hours without food.

It is worth noting that, given the current structure of society, depression often serves not to help reboot the system and enlist social support, but instead contributes to the further isolation of the individual, which creates a nasty, vicious spiral of shutting down, doing less, feeling more isolated, turning against the self, and thus getting even more depressed. As such, depressive symptoms often do contribute to the problem, and folks do suffer from Negative Affect Syndromes, where extreme negative moods are definitely part of the problem.

BUT, everyone should be clear, first and foremost, that anxiety and depression are symptoms of psychosocial needs and threats. They should NOT be, first and foremost, considered alien feelings that need to be eliminated or fixed, any more than we would treat pain from a broken arm, coldness and hunger primarily with pills that takes away the feelings, as opposed to fixing the arm, getting warmer or feeding the hungry individual.

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Anxiety and Depression Are Symptoms, Not Diseases

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It is very common when I first encounter a client struggling with mental health issues that they report their problem is that they feel anxious or depressed. Here is a typical exchange: Me: So, can you share with me what brings you in? Client: Well, I have not been feeling good.

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It's not unusual to have "the blues" or feel down occasionally-especially when you are in middle or high school. Bodies go through major chemical changes as you mature. The expectations of your teachers, family and friends-and the fear of not meeting them-can create stress and worry. When things go wrong at school or at home, you may feel unsure of yourself or wonder how you fit in. The idea of preparing for college or making decisions about your future can be overwhelming. On top of that, you face choices about friendships, sex, alcohol, and drugs. You may feel like you are getting mixed messages from parents, teachers, friends, and society.

Feeling down from time to time is different than having depression. When you have depression, it feels like there is a dark cloud over everyone and everything, and it is hard to feel good.

Signs of Depression

It is important to recognize depression so it can be treated. The earlier you get help, the sooner you can get back to feeling like yourself again. If you have some of the symptoms below, you might be dealing with depression.[3]

Having trouble with schoolwork

Not participating in activities you used to enjoy

Sadness and hopelessness

Lack of enthusiasm, energy or motivation

Anger and rage

Overreaction to criticism

Feelings of being unable to meet expectations

Poor self-esteem or guilt

Problems with making decisions, lack of concentration or forgetfulness

Restlessness and agitation

Changes in eating or sleeping patterns

Rebelling against parents, teachers, or other authority figures

Suicidal thoughts or actions

Don't Suffer in Silence

Depression can make people feel hopeless about their current circumstances or the future. Left untreated, depression can cause some young people to think about doing drastic or violent things.

If you see suspicious posts on social media or hear people say things that suggest they might be planning to hurt themselves or other people, tell an adult right away. If you feel this way, don't suffer in silence! It is important to remember that there is help and there is hope.

If you or someone you know is experiencing suicidal thoughts, seek immediate help by calling 911 or going to the closest emergency room. Trust your instincts, and if necessary, break a confidence in order to save a life.

If you just don't feel right or notice that someone else is struggling, it's important to get help sooner rather than later. Reach out to a friend or trusted adult and tell them how you feel or that you are worried about someone. If you need help starting a conversation, visit http://www.mentalhealthamerica.net/timetotalk for tips on how to get started.
Sources
[1] Substance Abuse and Mental Health Services Administration. (2017). Key substance use and mental health indicators in the United States: Results from the 2016 National Survey on Drug Use and Health (HHS Publication No. SMA 17-5044, NSDUH Series H-52). Rockville, MD: Center for Behavioral Health Statistics and Quality, Substance Abuse and Mental Health Services Administration.
[2] Proprietary data from mhascreening.org.
[3] American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing.

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It's not unusual to have "the blues" or feel down occasionally-especially when you are in middle or high school. Bodies go through major chemical changes as you mature. The expectations of your teachers, family and friends-and the fear of not meeting them-can create stress and worry.

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Information about Mental Illness and the Brain

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We can all be "sad" or "blue" at times in our lives. We have all seen movies about the madman and his crime spree, with the underlying cause of mental illness. We sometimes even make jokes about people being crazy or nuts, even though we know that we shouldn't.

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The nature of mental illness has been the subject of passionate discussion throughout history. In ancient Greece Plato,1,2 promoting a mentalist definition of mental illness, was the first to coin the term "mental health," which was conceived as reason aided by temper and ruling over passion. At around the same time, Hippocrates,3 taking a more physicalist approach, defined different mental conditions as a variety of imbalances between different kinds of "humours." Griesinger4,5 almost 2 centuries ago was the first to state that "mental illness is brain illness," an expression that has provided a strong impetus to the more recent medical conception of mental illness. The substantial progress accomplished in genomics and brain imaging in the last few decades made biological psychiatry stronger than ever and contributed to the reification of mental disorders as illnesses of the brain. The almost exclusively biogenetic conceptual framework for understanding mental illness has acquired a hegemony that has influenced mental health practitioners while also influencing campaigns designed to improve public attitudes toward the mentally ill. As a result, the statement "mental illness is like any other illness" has become almost axiomatic and, therefore, by definition it embodies an accepted truth not in need of a proof.

This view of mental illness is presented for better acceptance of the mentally ill by the public and of treatment by those experiencing mental illness and is indeed based on accumulated, albeit limited, knowledge in the neurobiology of mental disorders. However, anything that reaches axiomatic proportions needs a serious examination. In this editorial we examine the reasons underlying this perspective, its consequences and the evidence to support or refute its continued justification. We then present a position that we believe best fits the current state of knowledge and is closest to clinical realities and public perceptions of mental illnesses.

What does the statement actually imply?

The statement that "mental illness is like any other medical illness" implies that mental illness has a biological basis just like other medical illnesses and should be treated in the public's eye in a similar manner. The purpose of this article is not to present a philosophical or ideological argument in favour of or against a biological basis explaining mental illness, but rather to examine the clinical and public utility of presenting a dominant neurobiological model of mental illness to patients, their families and the public at large.

Illness, pathophysiology and the "self''

To understand the justification of equating mental and medical disorders, a comparison often made between type 2 diabetes and mental disorders, especially schizophrenia, other psychoses and depression, is worth examining in some detail. Diabetes, although very complex, is understood as the result of dysfunctional glucose metabolism related to absolute or relative insufficiency of insulin signalling. This dysfunctional metabolism is the consequence of endogenous predispositions, such as hereditary diathesis, and environmental factors, including personal choices, such as poor diet and sedentary life style. Therefore, by improving glucose metabolism, either through medication, insulin replacement or changes in lifestyle, positive health outcomes can be expected. Diabetes is diagnosed by confirming high levels of fasting glucose and other related biochemical markers of glucose metabolism. Further, the cascade of its effects on other systems (e.g., cardiovascular, central nervous system) are, or could be, well explained on the basis of physiologic mechanisms. They can also be prevented/treated by better and early control of diabetes. All through this, however, the patient is aware of the nature of his or her problems, including personal choices, and diabetes generally does not affect his or her day-today thinking, behaviour or perception. Except for mental health complications due to neurologic illnesses (e.g., delirium in the context of severe metabolic complications, depression as a consequence of awareness of the life and death implication of the disorder, abnormal perceptions in the case of some neurologic conditions), it can be stated that somatic illnesses, such as diabetes do not usually alter the core self of a person substantially. More importantly, the model of attribution presented to the patient is congruent with the scientific "facts," thereby making it easier for the person as well as society to accept the condition.

Mental disorders, on the other hand, affect the very core of one's being through a range of experiences and phenomena of varying severity that alter the individual's thinking, perception and consciousness about the self, others and the world. This is seen to an extreme degree with more serious mental disorders, such as psychoses and bipolar disorders, but to a lesser albeit significant degree with anxiety, mood, eating and other psychiatric disorders. Emotion, perception, thought and action are the essence of human identity and the concept of "self," and these are the prime domains altered in mental disorders. The precise definition of what constitutes the self and whether the location of a state of self is a material reality in the brain, its form and the brain-related factors that influence it are deeply philosophical issues,6,7 but not the subject of this editorial. Suffice it to say that factors involved in increasing the risk for mental disorders are endogenous (genetics is recognized as a major contributor to most mental disorders) as well as environmental, much like most medical disorders. Psychological deprivation and trauma, social defeat and isolation, poverty and poor family environment are but some of the environmental factors that have been reported to increase the risk for mental disorders. In addition to changes at the physiologic level, common to somatic and mental disorders the latter encompass changes in one's definition of "self," and are not situated outside the "self." It can even be argued that in the absence of any substantiated biological marker for mental disorders (only 1 has been included in the recent DSM-5: orexin change in narcolepsy),8 the hallmark defining features of mental disorders, at least for now, remain the changes in how the patients feel, think and act and how these changes affect their relation to themselves and to others.

As a first corollary of this definition, contrary to medical conditions where restoring dysfunctional physiologic mechanisms is the main target of therapeutic interventions, this is only 1 part of the therapeutic interventions for mental disorders. The primary focus of therapeutic interventions in mental disorders is helping the patient to feel better and interact more adaptively with his or her social and physical environments. Although there is little doubt that all medical conditions require psychological attention, mental health interventions focus primarily on achieving a positive change in feeling, self-esteem, mood, perceptions, thoughts and action - all changes in the "self" that are not primarily targeted in the treatment of medical conditions. Different models of psychological and social interventions are the main ingredients for these desired changes in the self.

A second corollary of this definition is the fact that mental health is very laden with values, not because scientific factors are lacking, but because values become of the utmost importance - more so than for medical disorders - when we deal with the self and its restoration. While somatic illnesses such as diabetes are primarily defined and shaped by biologically discernible facts, values do play a certain role but do not define the disorder. Societal and personal values are important in the treatment of most medical disorders, but acquire paramount importance in the case of mental disorders. Societal and cultural values even define variations in diagnoses over time and across geographic locations. Compulsory treatments, a particularity in the mental health field, are a strong testimony of how mental health can interfere with the self and how the personal values of the patient can clash with the societal values, thus necessitating legal, value-laden mitigation.

Neurobiology and experience of mental illness

Advances in neurosciences have surely given us much better biological mechanistic explanations of many of the uniquely human cognitive, emotional and conative functions, such as memory, thinking, perception, mood and action. This knowledge has informed us that many mental illnesses derive their vulnerability from underlying biological variations. However, we are far from being able to explain in neurobiological terms many of the behaviours and experiences that constitute the core presentations of mental disorders. Even if neurobiology one day were to provide better explanations of the workings of the brain, more elaborately explain the role of genes in increasing the risk for mental illness and the mechanisms behind complex human behaviour, one would still need to understand the experiences of patients with different forms of mental illness in psychological terms, as recently described by Kendler9 so eloquently. By equating mental illness with any medical illness and, therefore, situating it in an organ within the human biology and not recognizing its unique nature in the way it affects the "self" cannot be justified on the basis of current state of knowledge nor may it serve our patients and society well, as we explain in the rest of this editorial.

Mental illness and the utility of explanatory models

Indeed, it is envisaged that putting mental illness on the same footing as medical illness, society will understand it better and not react negatively toward those with mental illnesses. It is hoped that as a result those with mental illness may face less social stigma - a major obstacle to people seeking and/or receiving help - and reducing stigma may help individuals regain eventual acceptance by society as productive members. Interestingly, the public's explanatory models of mental illness do not follow this narrative and, on the contrary, the public have multiple models of explaining mental illness varying across cultures and times.

One needs to ask the pragmatic question of whether the strategy of using a biogenetic model of mental illness and equating it with medical illness has actually helped. There are 2 areas worthy of examination in this regard.

Explanatory models, stigma and society

The first is to examine the effect of the statement, "mental illness is like any other medical illness," on social stigma toward people with mental illness. As indicated previously, implicit in the axiomatic statement is a primarily biological origin of the behaviour and suffering that characterize mental illness. Let us examine the evidence in this regard. In the last decade or 2, biogenetic attribution of all mental disorders, having acquired a hegemoneous status10 has been used primarily to inform campaigns for reducing stigma and promoting better acceptance of mental illness and the people with mental illnesses by society.11,12 Several well-conducted studies have concluded, almost uniformly, that this strategy has not only not worked, but also may have worsened public attitudes and behaviour toward those with mental illnesses. Investigations of stigma have shown that those who consider mental disorders as primarily attributable to biological forces, just like other medical disorders, while absolving the mentally ill person of responsibility for their behaviour and actions, tend to feel less optimistic about their ability to get better and function well, are less accepting of them and feel less positively toward them.13⁻16 In a review of the literature related to the concept of mental illness being like any other illness, Read and colleagues17 reported that biogenetic causal theories and diagnostic labelling as illness are both positively related to perceptions of dangerousness and unpredictability and to fear of and desire for social distance. The attitudes investigated in these studies are reflected in individuals' responses to whether they would live next door to, socialize or make friends with or have a close relative get married to a person described as being mentally ill. There is also evidence to suggest that biogenetic explanatory models may have negative consequences for those with mental illness in terms of their implicit self concept and explicit attitudes, such as fear.18 Further, campaigns to reduce stigma that encourage people to think about mental illness as simply another form of medical illness have produced results that show effects to the contrary. For example, a recent study showed that over a 10-year period of deliberate use of the biogenetic explanatory model for campaigning to reduce stigma has resulted in worsening of most, if not all, aspects of public attitudes toward individuals with mental illnesses.19,20 The strength of these perhaps counterintuitive findings comes from the fact that these studies were adequately designed, well powered and, most importantly, replicated in several countries (e.g., United States, Britain, Germany) with very similar results. It is acknowledged that these relatively negative attitudes may be particularly stronger in relation to certain forms of mental illness (e.g., psychosis, manic depressive illness) and addictions.

Explanatory models of mental illness and the mentally ill person

Another domain - perhaps the most important - of examination is the individual with mental illness. In clinical practice, telling patients that their presenting mental illness is like any other medical illness may initially reassure some and assist them in accepting to take medication, especially during the distressing acute phases of a serious mental disorder. They or their families may welcome a simple explanation for encouraging them to accept treatment, which in many cases includes medication. While this strategy can achieve something very important in acute crisis-like situations, it may become problematic, if persistent over time, in getting individuals to accept other highly effective psychological and social treatments. These latter interventions are highly effective and considerably less noxious than often less effective medications for some forms of mental illness, such as mild to moderate depression, anxiety and eating disorders, and emotional dysregulation associated with several long-standing mental illnesses. Even in the most serious mental disorders, such as psychotic, bipolar and severe major depressive disorders, where medications are invariably an essential part of treatment, psychological and social therapeutic interventions are the essential bridge between pharmacological interventions during the acute crises and the need for their sustained use in the long term while at the same time achieving the essential goals of relief of internal distress, restoration of self and a return to productive social and working lives.

Furthermore, presenting mental illness as any other medical illness often implies a medical treatment (medication in most cases) as the dominant treatment strategy. Patients' rejection of the treating clinician's medical illness model is generally described as lack of insight and starts the cycle of nonadherence to medication, which then translates into nonadherence to treatment. In reality, if patients and families are allowed to articulate their attributional models, given credit for their "experiential knowledge" and encouraged to enter into a dialogue with the treating clinician, it is more likely there will be some consensus on acceptance of recommended treatment. This may prevent the cycle of disengagement and decline in the course that follows.

What needs to be done?

In clinical practice, if we are to take seriously the multidimensional goals of providing mental health services, as articulated by those seeking and receiving help for mental illness, clinicians have to work within an attributional model that makes sense to the person receiving service, that can be supported by sound argument and evidence and that provides a framework within which those receiving service and those providing it can share a common language. Such a framework will need to include the biogenetic model of attribution of mental illness as 1 of several parallel and equally authentic social, psychological, environmental and cultural models offered by service providers and researchers (acquired knowledge) as well as those who experience mental illness (experiential knowledge). There is a need to create a common language in order to come to an understanding of the person's experience and to promote such an understanding among the public at large. Denying the special nature of mental illness is unlikely to achieve these important goals.

Some recent developments, such as the promotion of a recovery model21⁻23 and the early intervention movement,24,25 may hold more promise in improving both the quality of care and possibly involvement of and improvement in public attitudes. The former has emerged from experiential knowledge and advocacy from service users, supported later by sound qualitative research, whereas the latter has emerged from a combination of a shift in philosophy of delivery of care on the part of service providers, parallel generation of evidence of its effectiveness26,27 and greater acceptance by service users and their families, who have now joined the movement as advocates. A third emerging movement, the concept of positive mental health,28,29 may prove to be effective in combating the negative image of mental illness. This movement promotes and is based on human resilience and positive aspects of the experience of mental illness. There is a burgeoning literature emerging in this field, which may balance the rather deterministic, deficit oriented and largely pessimistic miasma created by using an exclusively biogenetic model to explain mental disorders.

Conclusion and recommendations

Simply seeking an axiom of "mental illness is like any other medical illness" is at best simplifying a complex human problem and at worst doing a major disservice to patients, their families and the mental health field. Our dialogue should incorporate the general complexity of human thinking, behaviour, memories and the idea of self and consciousness, including knowledge emerging from sophisticated biogenetic and social science research while attending to the specific complexities that each of us as human beings carry as part of our life stories. That is true for those receiving and those providing services.

We therefore argue that we should continue to have a social and a professional conversation where we find a proper place for neurobiology, social, cultural and environmental forces, personal histories and the uniqueness of each individual when trying to understand, explain and treat mental disorders while avoiding a simplistic reductionism that may be perceived at best as patronizing but ultimately harmful, even though the intentions may be noble. We propose that future antistigma campaigns should give up the axiom of "mental illness is like any other medical illness" and instead present the complex and multifaceted explanations of mental illness as unique along with the positive aspects as discussed here. These campaigns need to be informed not only by the acquired knowledge of service providers and scientists but equally by the experiential knowledge from service users and their families, taking into consideration new knowledge emerging from fields of recovery, early intervention and positive mental health. For clinicians, it would be equally important to embrace explanatory models of mental illness that are based on evidence in science and to include biogenetic, social and cultural models as well as those told to them by the very people they are trying to serve.

Footnotes

Editors' note: The ideas expressed in this editorial are not necessarily those of the journal. Importantly, JPN continues to focus on publishing "papers at the intersection of psychiatry and neuroscience that advance our understanding of the neural mechanisms involved in the etiology and treatment of psychiatric disorders."

Competing interests: See jpn.ca for R. Joober. None declared by A. Malla or A. Garcia.

References

2. Kenny A. The anatomy of the soul: historical essays in the philosophy of mind. Blackwell; 1973. [ Google Scholar]

3. Lloyd GER, Chadwick J, Mann WN. Hippocratic writings. Vol. 451. Penguin UK; 1983. [ Google Scholar]

4. Griesinger W. Die pathologie und therapie der psychischen krankheiten: für aerzte und studirende. A. Krabbe; 1861. [ Google Scholar]

7. Fulford B, Thornton T, Graham G. Oxford textbook of philosophy and psychiatry. Oxford University Press; 2006. Philosophical outputs in mental health practice and research; pp. 111-138. [ Google Scholar]

11. US Department of Health Human Services. Achieving the promise: transforming mental health care in america: the president 's new freedom commission on mental health report. Bethesda, MD: 2003. [ Google Scholar]

Articles from Journal of Psychiatry & Neuroscience : JPN are provided here courtesy of Canadian Medical Association

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"Mental illness is like any other medical illness": a critical examination of the statement and its impact on patient care and society

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The nature of mental illness has been the subject of passionate discussion throughout history. In ancient Greece Plato,1 , 2 promoting a mentalist definition of mental illness, was the first to coin the term "mental health," which was conceived as reason aided by temper and ruling over passion.

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The brain has not always been esteemed as the locus of that highly complex and contradictory entity, the human mind. In ancient Egypt, the soul and all mental functioning were thought to be located in the heart, although some scholars assigned this role to the liver. Hippocrates, in fourth-century (B.C.)

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The term psychological disorders is sometimes used to refer to what are more frequently known as mental disorders or psychiatric disorders.

Mental disorders are patterns of behavioral or psychological symptoms that impact multiple areas of life. These disorders create distress for the person experiencing the symptoms.

The DSM-5-TR lists hundreds of distinct conditions. Anxiety and depression are among the most common types of mental health conditions that people experience. While the DSM provides diagnostic information about such conditions, including the age at which they typically appear, it does not provide guidelines for treatment or predictions related to the course of illness.

While not a comprehensive list of every mental disorder, the following list includes some of the major categories of disorders described in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and the fifth edition, text revision (DSM-5-TR). The DSM is one of the most widely used systems for classifying mental disorders and provides standardized diagnostic criteria.

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Neurodevelopmental Disorders

Neurodevelopmental disorders are those that are typically diagnosed during infancy, childhood, or adolescence. These psychological disorders include:

Intellectual Development Disorder

Sometimes called intellectual disability, this type of developmental disorder originates prior to the age of 18 and is characterized by limitations in both intellectual functioning and adaptive behaviors.

Limitations to intellectual functioning are often identified through the use of IQ tests, with an IQ score under 70 often indicating the presence of a limitation. Adaptive behaviors are those that involve practical, everyday skills such as self-care, social interaction, and living skills.

Global Developmental Delay

This diagnosis is for developmental disabilities in children who are under the age of five. Such delays relate to cognition, social functioning, speech, language, and motor skills.

It is generally seen as a temporary diagnosis applying to kids who are still too young to take standardized IQ tests. Once children reach the age where they are able to take a standardized intelligence test, they may be diagnosed with an intellectual development disorder.

Communication Disorders

These disorders are those that impact the ability to use, understand, or detect language and speech. The DSM-5 identifies four different subtypes of communication disorders: language disorder, speech sound disorder, childhood-onset fluency disorder (stuttering), and social (pragmatic) communication disorder.

Autism Spectrum Disorder

Autism is characterized by persistent deficits in social interaction and communication in multiple life areas as well as restricted and repetitive patterns of behaviors.

The DSM specifies that symptoms of autism spectrum disorder must be present during the early developmental period and that these symptoms must cause significant impairment in important areas of life including social and occupational functioning.

Attention-Deficit Hyperactivity Disorder (ADHD)

ADHD is characterized by a persistent pattern of hyperactivity and impulsivity and/or inattention that interferes with functioning and presents itself in two or more settings such as at home, work, school, and social situations.

The DSM-5 specifies that several of the symptoms must have been present prior to the age of 12 and that these symptoms must have a negative impact on social, occupational, or academic functioning.

Bipolar and Related Disorders

Bipolar disorder is characterized by shifts in mood as well as changes in activity and energy levels. The disorder often involves experiencing shifts between elevated moods and periods of depression. Such elevated moods can be pronounced and are referred to either as mania or hypomania.

Mania is characterized by a distinct period of elevated, expansive, or irritable mood accompanied by increased activity and energy. Periods of mania are sometimes marked by feelings of distraction, irritability, and excessive confidence.

When mania progresses, there is also the possibility of psychotic symptoms such as grandiose delusions and hallucinations. While mania occurs with bipolar I disorder, hypomania is a marker of bipolar II.

Hypomanic episodes are characterized by elevated, expansive, or irritable moods like manic episodes. However, hypomania is less severe and generally shorter in duration than mania.

Depressive Episodes

These episodes are characterized by feelings of a depressed or sad mood along with a lack of interest in activities. They may also involve feelings of guilt, fatigue, and irritability. During a depressive period, people with bipolar disorder may lose interest in activities that they previously enjoyed, experience sleeping difficulties, and even have thoughts of suicide.

Both manic and depressive episodes can be frightening for both the person experiencing these symptoms as well as family, friends, and other loved ones who observe these behaviors and mood shifts. Fortunately, appropriate and effective treatments, which often include both medications and psychotherapy, can help people with bipolar disorder successfully manage their symptoms.

Anxiety Disorders

Anxiety disorders are characterized by excessive and persistent fear, worry, anxiety and related behavioral disturbances. Fear involves an emotional response to a threat, whether that threat is real or perceived. Anxiety involves the anticipation that a future threat may arise. Types of anxiety disorders include:

Generalized Anxiety Disorder (GAD)

This disorderis marked by excessive worry about everyday events. While some stress and worry are a common part of life, GAD involves worry that is so excessive that it interferes with a person's well-being and functioning.

Social Anxiety Disorder

Social anxiety disorder is a fairly common psychological disorder that involves an irrational fear of being watched, judged, humiliated, and/or embarrassed. The anxiety caused by this disorder can have a major impact on an individual's life and make it difficult to function at school, work, and other social settings.

Specific Phobias

These phobias involve an extreme fear of a specific object or situation in the environment. Some examples of common specific phobias include fear of spiders, fear of heights, or fear of snakes.

The four main types of specific phobias involve natural events (thunder, lightning, tornadoes), medical (medical procedures, dental procedures, medical equipment), animals (dogs, snakes, bugs), and situational (small spaces, leaving home, driving).

Panic Disorder

This psychiatric disorder is characterized by panic attacks that may seem to strike out of the blue and for no reason at all. Because of this, people with panic disorder often experience anxiety and preoccupation over the possibility of having another panic attack.

People may begin to avoid situations and settings where attacks have occurred in the past or where they might occur in the future. This can create significant impairments in many areas of everyday life and make it difficult to carry out everyday routines.

Separation Anxiety Disorder

This condition is a type of anxiety disorder involving an excessive amount of fear or anxiety related to being separated from attachment figures. People are often familiar with the idea of separation anxiety as it relates to young children's fear of being apart from their parents, but older children and adults can experience it as well.

The person experiencing these symptoms may avoid moving away from home, going to school, or getting married in order to remain in close proximity to the attachment figure.

Trauma- and Stressor-Related Disorders

Trauma- and stressor-related disorders involve exposure to a stressful or traumatic event. These were previously grouped with anxiety disorders but are now considered a distinct category of disorders. Disorders included in this category include:

Acute Stress Disorder

Acute stress disorder is characterized by the emergence of severe anxiety for up to one month after exposure to a traumatic event. Some examples of traumatic events include natural disasters, war, accidents, and witnessing a death.

As a result, the individual may experience dissociative symptoms such as a sense of altered reality, an inability to remember important aspects of the event, and vivid flashbacks as if the event were reoccurring. Other symptoms can include reduced emotional responsiveness, distressing memories of the trauma, and difficulty experiencing positive emotions.

Adjustment Disorders

Adjustment disorders can occur as a response to a sudden change such as divorce, job loss, end of a close relationship, a move, or some other loss or disappointment. This type of psychological disorder can affect both children and adults and is characterized by symptoms such as anxiety, irritability, depressed mood, worry, anger, hopelessness, and feelings of isolation.

Post-Traumatic Stress Disorder (PTSD)

PTSD can develop after an individual has experienced exposure to actual or threatened death, serious injury, or sexual violence. Symptoms of PTSD include episodes of reliving or re-experiencing the event, avoiding things that remind the individual about the event, feeling on edge, and having negative thoughts.

Reactive Attachment Disorder

Reactive attachment disorder can result when children do not form healthy relationships and attachments with adult caregivers during the first few years of childhood. Symptoms of the disorder include being withdrawn from adult caregivers and social and emotional disturbances that result from patterns of insufficient care and neglect.

Dissociative Disorders

Dissociative disorders are psychological disorders that involve a dissociation or interruption in aspects of consciousness, including identity and memory. Dissociative disorders include:

Dissociative Amnesia

This disorder involves a temporary loss of memory as a result of dissociation. In many cases, this memory loss, which may last for just a brief period or for many years, is a result of some type of psychological trauma.

Dissociative amnesia is much more than simple forgetfulness. Those who experience this disorder may remember some details about events but may have no recall of other details around a circumscribed period of time.

Dissociative Identity Disorder

Formerly known as multiple personality disorder, dissociative identity disorder involves the presence of two or more different identities or personalities in one person. Each of these personalities has its own way of perceiving and interacting with the environment.

People with this disorder experience changes in behavior, memory, perception, emotional response, and consciousness.

Depersonalization/Derealization Disorder

Depersonalization/derealization disorder is characterized by experiencing a sense of being outside of one's own body (depersonalization) and being disconnected from reality (derealization). People who have this disorder often feel a sense of unreality and an involuntary disconnect from their own memories, feelings, and consciousness.

Somatic Symptom Disorders

Formerly referred to as somatoform disorders, this category is now known as somatic symptom disorders. Somatic symptom disorders are a class of psychological disorders that involve prominent physical symptoms that may not have a diagnosable physical cause.

In contrast to previous ways of conceptualizing these disorders based on the absence of a medical explanation for the physical symptoms, the current diagnosis emphasizes the unusual thoughts, feelings, and behaviors that occur in response to these symptoms. Disorders included in this category are:

Somatic Symptom Disorder

Somatic symptom disorder involves a preoccupation with physical symptoms that make it difficult to function. This preoccupation with symptoms results in emotional distress and difficulty coping with daily life.

It is important to note that somatic symptoms do not indicate that individuals are faking their physical pain, fatigue, or other symptoms. In this situation, it is not so much the actual physical symptoms that are disrupting the individual's life as it is the extreme reaction and resulting behaviors.

Illness Anxiety Disorder

Illness anxiety disorder is characterized by excessive concern about having an undiagnosed medical condition. Those who experience this psychological disorder worry excessively about body functions and sensations are convinced that they have or will get a serious disease, and are not reassured, even when medical tests don't detect any illnesses.

Conversion Disorder

Conversion disorder involves experiencing motor or sensory symptoms that lack a compatible neurological or medical explanation. In many cases, a person develops the disorder after experiencing a real physical injury or stressful event, which then results in a psychological and emotional response.

Factitious Disorder

Factitious disorder used to have its own category, but it is now included under the somatic symptom and related disorders category of the DSM-5. A factitious disorder is when an individual intentionally creates, fakes, or exaggerates symptoms of illness. Munchausen syndrome, in which people feign an illness to attract attention, is one severe form of factitious disorder.

Feeding and Eating Disorders

Eating disorders are characterized by obsessive concerns with weight and disruptive eating patterns that negatively impact physical and mental health. Types of eating disorders include:

Anorexia Nervosa

Anorexia nervosais characterized by restricted food consumption that can lead to weight loss. Some people with anorexia are underweight, while others may be of average or above-average weight. Those who experience this disorder also have a preoccupation and fear of gaining weight as well as a distorted view of their own appearance and behavior.

Bulimia Nervosa

Bulimia nervosainvolves binge eating and then taking extreme steps to compensate for these binges. These compensatory behaviors might include self-induced vomiting, the abuse of laxatives or diuretics, or excessive exercise.

Rumination Disorder

Rumination disorder is marked by regurgitating previously chewed or swallowed food in order to either spit it out or re-swallow it. Rumination disorder can occur in infants, children, teens, and adults. It's also more common in people who have anxiety, depression, or another psychiatric disorder.

Pica involves craving and consuming non-food substances such as dirt, paint, or soap. Pica is more common among young children than adults, but it is also known to occur during pregnancy. A lack of nutrients may also trigger non-food cravings in some instances.

Binge Eating Disorder

Binge eating disorder involves episodes of binge eating where the individual consumes an unusually large amount of food during a short time period, such as a couple of hours.

People with binge-eating disorder often feel they have no control over their eating. Binge eating episodes are sometimes triggered by certain emotions such as feeling happy, anxious, or bored, or following stressful events.

Sleep-Wake Disorders

Sleep disorders involve an interruption in sleep patterns that leads to distress and affects daytime functioning. Examples of sleep disorders include:

Narcolepsy

Narcolepsy is a condition in which people experience an irrepressible need to sleep. People with narcolepsy may experience a sudden loss of muscle tone, also known as cataplexy.

They are also prone to hypnagogic hallucinations, which happen as someone falls asleep, and hypnopompic hallucinations, which happen as someone wakes up.

Insomnia Disorder

Insomnia disorder involves being unable to get enough sleep to feel rested. While all people experience sleeping difficulties and interruptions at some point, insomnia is considered a disorder when it is accompanied by significant distress or impairment over time.

Hypersomnolence

Hypersomnolence disorder is characterized by excessive sleepiness despite an adequate main sleep period. People with this condition may fall asleep during the day at inappropriate times such as at work and school.

Breathing-Related Sleep Disorders

Breathing-related sleep disorders are those that involve breathing anomalies-such as sleep apnea-that can occur during sleep. These breathing problems can result in brief interruptions in sleep that can lead to other problems including insomnia and daytime sleepiness.

Parasomnias

Parasomnia is a term that describes sleep disorders that feature unusual behaviors. Such disorders include sleepwalking, sleep terrors, sleep talking, and sleep eating.

Restless Legs Syndrome

Restless legs syndrome is a neurological condition that involves having uncomfortable sensations in the legs and an irresistible urge to move the legs in order to relieve the sensations. People with this condition may feel tugging, creeping, burning, and crawling sensations in their legs resulting in an excessive movement which then interferes with sleep.

Disruptive, Impulse Control and Conduct Disorders

Disruptive, impulse control and conduct disorders are those that involve an inability to control emotions and behaviors, resulting in harm to oneself or others.

These challenges with emotional and behavioral regulation are characterized by actions that violate the rights of others such as destroying property or physical aggression and/or those that conflict with societal norms, authority figures, and laws. These disorders include:

Kleptomania

Kleptomania involves an inability to control the impulse to steal. People who have kleptomania will often steal things that they do not really need or that have no real monetary value. Those with this condition experience escalating tension prior to committing a theft and feel relief and gratification afterwards.

Pyromania involves a fascination with fire that results in acts of fire-starting that endanger the self and others. People who struggle with pyromania purposefully and deliberately have set fires more than one time. They also experience tension and emotional arousal before setting a fire.

Intermittent Explosive Disorder

Intermittent explosive disorder is characterized by brief outbursts of anger and violence that are out of proportion to the situation. People with this disorder may erupt into angry outbursts or violent actions in response to everyday annoyances or disappointments.

Conduct Disorder

Conduct disorder is a condition diagnosed in children and adolescents under the age of 18 who regularly violate social norms and the rights of others. Children with this disorder display aggression toward people and animals, destroy property, steal and deceive, and violate other rules and laws. These behaviors result in significant problems in a child's academic or social functioning.

Oppositional Defiant Disorder

Oppositional defiant disorder begins prior to the age of 18 and is characterized by defiance, irritability, anger, aggression, and vindictiveness.

Depressive Disorders

The category of depressive disorders includes a number of conditions. They are all characterized by the presence of sad, empty, or irritable moods accompanied by physical and cognitive symptoms. They differ in terms of duration, timing, and causes. Some include:

Disruptive mood dysregulation disorder: A childhood condition characterized by extreme anger and irritability. Children display frequent and intense outbursts of temper.

Major depressive disorder: A condition characterized by loss of interest in activities and depressed mood which leads to significant impairments in how a person is able to function.

Persistent depressive disorder:This is a type of ongoing, chronic depression that is characterized by other symptoms of depression. While the symptoms are often less severe, they are longer lasting. Diagnosis requires experiencing a depressed mood on most days for a period of at least two years.

Other specified depressive disorder: This diagnosis is for cases when symptoms do not meet the criteria for the diagnosis of another depressive disorder, but they still create problems with an individual's life and functioning.

Premenstrual dysphoric disorder: This condition is a form of premenstrual syndrome (PMS) characterized by significant depression, irritability, and anxiety that begins a week or two before menstruation begins. Symptoms usually go away within a few days following bleeding.

Substance/medication-induced depressive disorder: This condition occurs when an individual experiences symptoms of a depressive disorder either while using alcohol or other substances or while going through withdrawal from a substance.

Depressive disorder due to another medical condition: This condition is diagnosed when a person's medical history suggests that their depressive symptoms may be the result of a medical condition. Medical conditions that may contribute to or cause depression include diabetes, stroke, Parkinson's disease, autoimmune conditions, chronic pain conditions, cancer, infections and HIV/AIDS.

Depressive disorders are all characterized by feelings of sadness and low mood that are persistent and severe enough to affect how a person functions.

The diagnostic criteria vary for each specific condition. For major depressive disorder, diagnosis requires an individual to experience five or more of the following symptoms over the same two-week period.

One of these symptoms must include either depressed mood or loss of interest or pleasure in previously enjoyed activities. Other symptoms can include:

Significant weight loss or gain

Decreased or increased appetite

Sleep disturbances (insomnia or hypersomnia)

Feelings of slowed physical activity or restlessness

Lack of energy or fatigue that lasts most or all of the day

Feelings of guilt or worthlessness

Difficulty thinking or concentrating

Preoccupation with death or thoughts of suicide

Treatments for depressive disorders often involve a combination of psychotherapy and medications.

Substance Use and Addictive Disorders

Substance-related disorders are those that involve the misuse of different substances such as cocaine, methamphetamine, opiates, and alcohol.

These disorders may include substance-induced conditions that can result in many associated diagnoses including intoxication, withdrawal, or the emergence of psychosis, anxiety, and delirium. Examples of substance-related disorders include:

Alcohol-related disorders: Theseinvolve the consumption of alcohol, one of the most widely used drugs in the United States.

Cannabis-related disorders: These disordersinclude symptoms such as using more marijuana than originally intended, feeling unable to stop it, and continuing to use it despite adverse effects in one's life.

Inhalant-use disorders: Theseinvolve inhaling fumes from things such as paints or solvents. As with other substance-related disorders, people with this condition experience cravings for the substance and find it difficult to control or stop engaging in the behavior.

Stimulant use disorder: Thisinvolves the use of stimulants such as meth, amphetamines, and cocaine.

Tobacco use disorder: This is characterized by symptoms such as consuming more tobacco than intended, difficulty cutting back or quitting, cravings, and experiencing adverse social consequences as a result of tobacco use.

Gambling Disorder

Neurocognitive Disorders

Neurocognitive disorders are characterized by acquired deficits in cognitive function. These disorders do not include those in which impaired cognition was present at birth or early in life. Types of cognitive disorders include:

Delirium is also known as acute confusional state. This disorder develops over a short period of time-usually a few hours or a few days-and is characterized by disturbances in attention and awareness.

Other Neurocognitive Disorders

Major and mild neurocognitive disorders have the primary feature of acquired cognitive decline in one or more areas including memory, attention, language, learning, and perception.

These cognitive disorders can be due to medical conditions including Alzheimer's disease, HIV infection, Parkinson's disease, substance/medication use, vascular disease, and others.

Schizophrenia Spectrum and Other Psychotic Disorders

Schizophrenia is a chronic psychiatric condition that affects a person's thinking, feeling, and behavior. It is a complex, long-term condition that affects less than 1% of people in the United States.

The DSM-5 diagnostic criteria specify that two or more symptoms of schizophrenia must be present for a period of at least one month.

One symptom must be one of the following:

Delusions: Beliefs that conflict with reality

Hallucinations: Seeing or hearing things that aren't really there

Disorganized speech: Words that do not follow the rules of language and may be difficult or impossible to understand

The second symptom may be one of the following:

Grossly disorganized or catatonic behavior: Confused thinking or bizarre behavior or movements

Negative symptoms: The inability to initiate plans, speak, express emotions, or feel pleasure

Diagnosis also requires significant impairments in social or occupational functioning for a period of at least six months. The onset of schizophrenia is usually in the late teens or early 20s, with men usually showing symptoms earlier than women. Earlier signs of the condition that may occur before diagnosis include poor motivation, difficult relationships, and poor school performance.

The National Institute of Mental Health suggests that multiple factors may play a role in the development of schizophrenia including genetics, brain chemistry, environmental factors, and substance use.

Obsessive-Compulsive and Related Disorders

Obsessive-compulsive and related disorders is a category of psychiatric conditions that include:

Each condition in this classification has its own set of diagnostic criteria.

Obsessive-Compulsive Disorder

The diagnostic criteria in the DSM-5 specify that in order to be diagnosed with obsessive-compulsive disorder, a person must experience obsessions, compulsions, or both.

Obsessions: Defined as recurrent, persistent thoughts, impulses, and urges that lead to distress or anxiety

Compulsions: Repetitive and excessive behaviors that the individual feels that they must perform to reduce anxiety or to prevent some dreaded outcome from occurring

Treatments for OCD usually focus on a combination of therapy and medications. Cognitive-behavioral therapy (CBT) or a form of CBT known as exposure and response prevention (ERP) are commonly used. Antidepressants such as Anafranil (clomipramine) or Prozac (fluoxetine) may also be prescribed to manage symptoms.

Personality Disorders

Personality disorders are characterized by an enduring pattern of maladaptive thoughts, feelings, and behaviors that can cause serious detriments to relationships and other life areas. Types of personality disorders include:

Antisocial Personality Disorder

Antisocial personality disorder is characterized by a long-standing disregard for rules, social norms, and the rights of others. People with this disorder typically begin displaying symptoms during childhood, have difficulty feeling empathy for others, and lack remorse for their destructive behaviors.

Avoidant Personality Disorder

Avoidant personality disorder involves severe social inhibition and sensitivity to rejection. Such feelings of insecurity lead to significant problems with the individual's daily life and functioning.

Borderline Personality Disorder

Borderline personality disorder is associated with symptoms including emotional instability, unstable and intense interpersonal relationships, unstable self-image, and impulsive behaviors.

Dependent Personality Disorder

Dependent personality disorder involves a chronic pattern of fearing separation and an excessive need to be taken care of. People with this disorder will often engage in behaviors that are designed to produce care-giving actions in others.

Histrionic Personality Disorder

Histrionic personality disorder is associated with patterns of extreme emotionality and attention-seeking behaviors. People with this condition feel uncomfortable in settings where they are not the center of attention, have rapidly changing emotions, and may engage in socially inappropriate behaviors designed to attract attention from others.

Narcissistic Personality Disorder

Narcissistic personality disorder is associated with a lasting pattern of exaggerated self-image, self-centeredness, and low empathy. People with this condition tend to be more interested in themselves than in others.

Obsessive-Compulsive Personality Disorder

Obsessive-compulsive personality disorder is a pervasive pattern of preoccupation with orderliness, perfectionism, inflexibility, and mental and interpersonal control. This is a different condition than obsessive compulsive disorder (OCD).

Paranoid Personality Disorder

Paranoid personality disorder is characterized by a distrust of others, even family, friends, and romantic partners. People with this disorder perceive others' intentions as malevolent, even without any evidence or justification.

Schizoid Personality Disorder

Schizoid personality disorder involves symptoms that include being detached from social relationships. People with this disorder are directed toward their inner lives and are often indifferent to relationships. They generally display a lack of emotional expression and can appear cold and aloof.

Schizotypal Personality Disorder

Schizotypal personality disorder features eccentricities in speech, behaviors, appearance, and thought. People with this condition may experience odd beliefs or magical thinking as well as difficulty forming relationships.

A Word From Verywell

Various factors influence a person's risk of developing a psychological disorder, including biological, social, environmental, cultural, and economic factors. Factors such as social support and coping skills can have protective effects.

Some conditions are short-term, while others may be lifelong. Conditions can also change over time.

Psychological disorders can cause disruptions in daily functioning, relationships, work, school, and other important domains. However, with appropriate diagnosis and treatment, people can find relief from their symptoms and discover ways to cope effectively.

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Explore a List of Psychological Disorders From the DSM-5

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Psychological disorders are grouped into different categories in the DSM-5. Explore this list of different types of mental disorders and how they are categorized.

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NAMI Awards Each year NAMI recognizes outstanding achievements and celebrates accomplishments made by individuals and organizations that advance NAMI's mission to improve the lives of people affected by mental illness and their loved ones. Learn More Work at NAMI Become part of a team that is committed to improving the lives of individuals across mental illness.

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Participants

Participants were 163 inmates recruited from June 2002 to May 2007 as part of a larger longitudinal study ( Tangney, Mashek, and Stuewig 2007) at an urban adult detention center. Data were collected after entry into the jail (Time 1), again just before release to the community (Time 2), and then one year post-release (Time 3). Inmates were informed that participation was voluntary and that data were confidential, protected by a Certificate of Confidentiality from DHHS. Pre-release assessments (Time 2) were collected from 2002-2010, depending on inmates' release dates. Post-release assessments (Time 3) were collected from 2003 to 2010. Inmates received a $15-18 honorarium for completing the Time 1 assessment, $25 for the Time 2 assessment, and $50 for the Time 3 assessment.

Of the participants who consented to participate in the parent study ( N = 628), 120 were not eligible for longitudinal follow up because they were transferred, released, or bonded out before assessments could be completed. Of the 508 inmates enrolled in the longitudinal study, 86 people were disqualified because there were less than 6 weeks between intake and their release date and 12 people were considered not yet eligible for their pre-release assessment because they are still currently incarcerated. 410 inmates were eligible to be re-interviewed prior to their release from jail/prison (Time 2). Of these participants, we were unable to reach 116 participants in the allotted time frame for their Time 2 assessment (timed out), 5 refused to complete the assessment, 4 withdrew from the study, and one person did not have a release date, so was excluded, leaving 284 participants who completed a Time 2 assessment.

A total of 163 participants completed valid assessments of one or both of the stigma measures prior to release (Time 2). Because the stigma measures were added into the study after data collection had begun, 60 participants did not receive these measures. Due to study design/unexpected release, we collected an abbreviated version for 25 participants, and a missed version for 31 participants after the allotted time frame for the Time 2 assessment. Stigma measures were not included in these versions because they were collected after participants had been released, and therefore the prospective stigma measure did not make sense. An additional 5 people were excluded from analyses for having invalid data. shows a consort diagram for the Time 2 stigma measures. Participants ( N = 163) were about 33 years old on average ( range = 18.44 - 69.63) and primarily male (71.2%). This sample was racially/ethnically diverse (46.0% African American, 35.6% Caucasian, 6.1% Hispanic, 8.0% Mixed race/other race, 4.3% Asian/Pacific Islander).

This paper focuses on pre-release (Time 2) and post-release (Time 3) data. Missing data were handled using Full Information Maximum Likelihood (FIML). Thus, we were able to analyze the entire sample of individuals ( N = 371) who completed the post-release measures. FIML is highly encouraged when data are Missing at Random, which means that participants are not missing on items/variables for a reason that is relevant to the phenomenon being measured ( Schafer and Graham 2002; Little et al. 2013). In our sample, missingness is largely due to factors related to study design. Specifically, missingness was due to unexpected release from the jail, which occurred for various participants throughout the course of the study ( N = 56). Also, a proportion of data had already been collected at Time 2 before the stigma measures were introduced in our interview packet, resulting in missing data for 60 participants. In this case, the only identifiable variable related to missingness in our study was the date in which a person's interview occurred; because participants were recruited into the study randomly, we do not think that this influences our missingness in any consistent way ( Schafer and Graham 2002). All participants who had the opportunity to complete the stigma measures completed them; 5 individuals' stigma data were invalidated because they were erroneously administered outside the allowable timeframe or due to indications of invalidity from the PAI validity scales.

To increase our confidence that our data were missing at random, we analyzed whether participants who completed the stigma measures were different in important ways compared to the participants who did not complete the stigma measures. Specifically, we conducted t-tests comparing participants who completed the stigma measures ( N = 163) to those who did not ( N = 121), on demographics and outcome variables. Results of t-tests show no significant differences on any demographic variables, suggesting the groups were equivalent in race, age, gender, and years of education completed. There were no significant differences on any outcome variables, suggesting that the groups were equivalent in levels of post-release employment, community functioning, substance dependence, and mental health symptoms. Because missing data was unrelated to the variables being measured in our study, as well as any other consistent variable, it was estimated during analyses.

The FIML technique is considered to be a more accurate approach to missing data than the commonly used listwise deletion method ( Schafer and Graham 2002; Little et al. 2013). Listwise deletion of cases can strongly bias results because it deletes people who do not have complete data, which is not representative of the true population. It is almost impossible to predict whether listwise deletion will bias the results of any one study, and experts recommend not using the technique to avoid the possibility of bias ( Schafer and Graham 2002). Further, FIML was designed for estimation of entire waves of data when one wave is present and the other is missing, for example, when you estimate Y for people who have X ( Little and Rubin 1989). The same premise applies here, where we estimate X for participants who have Y. FIML uses all of the data available about a participant, including other measures at that timepoint (i.e. missing stigma data is estimated using other data on that person at Time 2) and outcome measures to determine the model parameters. Data values are not imputed in this technique, but rather the model parameters are estimated using all available information.

shows a consort diagram for Time 3 outcome measures. The sample analyzed in FIML was descriptively similar to the sample of 163 people ( Mean age = 33, range = 18.40 - 69.63; 70.1% male; 45.6% African American, 35.6% Caucasian, 7.0% Mixed race/Other race; 6.5% Hispanic, 3.5% Asian/Pacific Islander, and additionally there were 0.8% Mexican American, 0.5% Middle Eastern, 0.5% Native American participants in this larger sample).

Measures and Procedures

A battery of measures and demographic questionnaires were given at entry into the jail (Time 1); race was the only variable used from this timepoint. Other assessments relevant to this study were given prior to release from jail/prison (Time 2) and one year post-release (Time 3) timepoints. Time 2 assessments were conducted in the privacy of professional visiting rooms or secure classrooms, and included perceived stigma, shame-proneness, optimism, and criminal identity. Perceived and anticipated stigma were assessed with the Inmate Perceptions and Expectations of Stigma measure (IPES; Mashek et al. 2002) containing 12 items. Inmates were asked to indicate on a 7-point scale ("1" "totally disagree" to "7" "totally agree") their perceptions of how people in society feel toward criminals-e.g. "People on the outside think criminals are bad people" (6 items; alpha = .83). Participants were then asked to indicate how they thought they would be treated once released -e.g. "People in the community will accept me" (4 items; alpha = .88). Previous factor analyses ( Moore, Stuewig and Tangney 2013) indicated that this measure contained two factors: perceived stigma and anticipated stigma. Both scales were normally distributed (see ) and significantly correlated ( r = .36, p < .001).

Shame-proneness was assessed using the Test of Self-Conscious Affect-Socially Deviant (TOSCA-SD; Hanson and Tangney 1996). The TOSCA-SD is composed of 13 scenarios followed by a series of possible responses. Participants rated how likely they would be to respond in ways described (capturing shame and guilt responses). This measure has been shown to be reliable and valid with offenders ( Tangney et al. 2011). The shame-combined scale, including negative self-appraisal responses (e.g. "You would think, I'm inconsiderate") and behavioral avoidance responses (e.g. "You would leave as quickly as you could"), was used for these analyses. The TOSCA-SD shame-proneness scale had acceptable reliability (alpha = .77) and was normally distributed (see ). Optimism was assessed using 6 items from the Values in Action inventory (VIA; Peterson and Seligman 2001). This scale has been shown to be reliable and valid with inmates ( Heigel, Stuewig, and Tangney 2010). This scale assessed trait optimism (e.g. "I can always find the positive in what seems negative to others"). Responses were rated on a 5-point Likert scale where "1" was "not at all like me" and "5" was "very much like me" (alpha = .77). This scale was normally distributed (see ).

Two aspects of social identity were assessed. The Inclusion of Community in Self scale (ICS; Mashek, Cannaday, and Tangney 2007) assessed actual and desired connectedness with various target groups including the family, the criminal community, and the community at large. Responses were rated using six figures of circles overlapping to various degrees (representing not at all connected to as connected as possible). The item asking participants about their actual connectedness with the criminal community was used in the current analyses. The ICS has been determined to be valid with inmates, though test-retest data was not available to assess reliability ( Mashek et al. 2006). About 37 percent of participants indicated no connectedness to the criminal community, slightly skewing this variable (see ). Participants were also asked to what degree they agreed with the statement "I am a criminal" on a 6-point Likert scale from "1" "totally disagree" to "6" "totally agree." This variable was slightly kurtotic due to a concentration of data points at the low (especially) and high ends of the scale (see ).

Time 3 assessments were conducted by phone or (for those re-incarcerated) in person one year after inmates were released from jail/prison, and included employment, recidivism, mental health symptoms, substance dependence symptoms, and community functioning. Employment was assessed by asking participants whether they were unemployed, or had odd jobs, part-time (less than 35 hours), or full-time employment (more than 35 hours) in the year after release from jail, and how many weeks they worked in that year. The majority of participants (67.1%) reported having full-time employment in the year after release. A continuous variable ( total hours employed) was created by multiplying the number of hours expected for the type of employment (i.e. typical number of hours worked in full-time employment in the U.S. is 40 hours, part-time employment is 20 hours, and odd jobs is 5 hours) by the number of weeks participants were employed in the year after release. The distribution covered the full range and showed minimal skewness and kurtosis (see ), although there were substantial clusters at the extreme ends of the distributions reflecting unemployed and full-time employed participants.

Recidivism was assessed by both self-report and official records. Participants were asked whether they had been arrested for (self-reported arrests) and whether they had committed without being detected (self-reported offenses) each of 16 types of crime (i.e. theft, robbery, assault, murder, domestic violence, weapons offenses, major driving offenses, prostitution, drug offenses, sex offenses, fraud, kidnapping, arson, resisting arrest, miscellaneous, and other) during the year after their release. Official National Crime Information Center (NCIC) criminal records of arrests in the first year after release were collected as well (official arrests); 119 charge codes found on official records were categorized into the 16 types of crimes used for the self-report variables. To capture criminal versatility in these three sources, three variables were created to reflect the number of types of crimes (i.e. 0-16) that participants were arrested for (official arrests and self-reported arrests) and reported committing (self-reported offenses). Versatility (the number of different types of crimes) was employed rather than the frequency of arrest/offense because the latter is confounded by the type of crime, e.g., illegal substance use vs. violent offenses. The actual range for these variables were 0-5 for self-reported arrests, 0-6 for official records of arrest, and 0-9 for self-reported offenses. Because many participants reported/were found to have zero arrests and reported committing zero offenses, each variable was skewed (see ).

Eight items representing community participation/functioning were chosen from a measure of detailed demographic information given at the one year post-release assessment. Items included 1) residential stability, 2) homeownership, 3) current marital status, 4) largest source of support in the past year (i.e. job, family/spouse, friends, illegal activities, unemployment benefits, etc.), 5) valid driver's license, 6) financial support of children, 7) educational and vocational upgrades (i.e. taking vocational or college courses, graduating high school, getting GED, etc.), and 8) volunteerism in the community. Participant responses on each of the eight items were evaluated in terms of the level of adaptive functioning. We used the criminology literature to indicate certain responses as being adaptive, prosocial behaviors that are particularly useful for offenders' reintegration in the community. All other behaviors, including maladaptive ones and even neutral ones that could be adaptive or maladaptive depending on the situation, were considered fundamentally different and placed in another category.

Responses deemed to be adaptive were given a score of 1, and those that were either neutral or maladaptive were given a score of 0. Specifically, for residential stability, living in 1 or 2 places in the year post-release was considered adaptive and living in more than 2 places or being homeless was considered neutral/maladaptive. There is a general consensus in the literature of measuring residential stability with the number of places lived. For current marital status, being legally married was the only response considered adaptive. Social control theory (in criminology) states that the act of being legally married to someone is a community convention that is fundamentally different from other forms of cohabitation or relationships (Sampson and Laub 1993). It is believed that this represents a prosocial bond to the community that is not observed in cohabitating couples or other types of romantic relationships.

For largest source of financial support, a job or savings was considered adaptive and all other responses were considered neutral (i.e., family, spouse) or maladaptive (i.e. illegal activities). Research in criminology places great importance on the employment of ex-offenders after release from jail, and supporting oneself through a job or savings is considered the primary prosocial form of financial support. For financial support of children, supporting all of their children or more than their own children (i.e. a partner's children) was considered adaptive, not having children was considered neutral, and failing to financially support all of their children was considered maladaptive. In regards to supporting one's children, we do not think of it as penalizing those without children, but rather giving credit to those with children who also financially support their children. For educational and vocational upgrades, participating in any of the upgrades was considered adaptive and not participating in any was considered neutral/maladaptive. On yes/no questions, participants who reported owning their own home, having a valid driver's license, or volunteering in the community in the past year were given a score of 1 (adaptive) on those respective items. Scores were averaged across the eight dichotomous indicators to create a total functioning index. Because this is a formative construct composed of different areas of functioning that are not necessarily expected to be correlated with one another (i.e. having a valid driver's license may not necessarily be linked to financially supporting one's children), Cronbach's alpha was not calculated.

Levels of mental health symptoms were assessed with a shortened version of the Personality Assessment Inventory (PAI; Morey 2007), which included four scales: depression (DEP), anxiety (ANX), borderline features (BPD), and stress (STR). Item responses ranged from 1 = "False, not at all true" to 4 = "Very true." These scales use T-scores, which are normed on a sample of average adults; the ranges for each scale were 36T-90T for depression (24 items, α = .85), 34T-89T for anxiety (24 items, α = .89), 36T-94T for borderline features (24 items, α = .88), and 37T-91T for stress (8 items, α = .74). The PAI is a widely used, well-validated measure ( Morey 2007). These scales were all normally distributed (see ).

Using Simpson and Knight's (1998) Texas Christian University: Correctional Residential Treatment Form, Initial Assessment (TCU-CRTF), four substance dependence scales were created to capture symptoms of dependency on alcohol, marijuana, cocaine, and opiates in the first year post-release. Each variable was composed of items that assess each of the DSM-IV-TR substance dependence domains. Item responses ranged from 0 = "Never" to 4 = "7 or more times." Responses were averaged within domain and a total score was computed by taking the mean across the seven domains (six in the case of marijuana because withdrawal is not considered part of the criteria). Each scale had acceptable reliability (alcohol, 7 items, α = .93; marijuana, 6 items, α = .88; opiates, 7 items, α = .97; cocaine, 7 items, α = .98). Given the similarities between cocaine and opiates (illegal, highly addictive) and the low rate of opiate use in our sample, opiates and cocaine were combined into a category of hard drugs. Frequency and dependence of cocaine/opiate use was defined as the higher of the two ratings for either cocaine or opiates. As there were a large number of people with very few dependency symptoms, each variable was skewed (see ). The TCU has been shown to be reliable with jail inmates ( Stuewig et al. 2009).

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THE EFFECT OF STIGMA ON CRIMINAL OFFENDERS' FUNCTIONING: A LONGITUDINAL MEDIATIONAL MODEL*

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Participants were 163 inmates recruited from June 2002 to May 2007 as part of a larger longitudinal study ( Tangney, Mashek, and Stuewig 2007) at an urban adult detention center. Data were collected after entry into the jail (Time 1), again just before release to the community (Time 2), and then one year post-release (Time 3).

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Abstract

This study examined children's aggressive and assertive solutions to hypothetical peer scenarios in relation to parents' responses to similar hypothetical social scenarios and parents' actual marital aggression. The study included 118 9−10 year old children, and their mothers and fathers. Children's aggressive solutions correlated with same-sex parents' actual marital aggression. For children with mothers who exhibit low actual marital aggression, mothers' aggressive solutions to hypothetical situations corresponded with children's tendencies to propose aggressive but not assertive solutions. In a 3-way interaction, fathers' aggressive solutions to peer scenarios and marital aggression, combined, exacerbated girls' aggressive problem solving, but had the opposite effect for boys. Discussion addresses the complexity, particularly with respect to parent and child gender combinations, in understanding parents' aggressive influences on children's peer relationships.

Cross-contextual influences between family and peers have long been recognized ( Hartup, 1980; Parke & O'Neill, 1999), but clarification still is needed on ways that family relationships affect children's competency with peers. Children's observations of their parents in interpersonal contexts, particularly their parents' aggression, can influence the children's own social problem solving skills ( Dodge, Bates, & Pettit, 1990; Goodman, Barfoot, Frye, & Belli, 1999; MacBrayer, Milich, & Hundley, 2003). Social problem solving skills, in turn, can affect the children's peer relations ( Dodge & Pettit, 2003). Thus, children's solutions in socially challenging situations can be an important link between parent-child relations and peer relations. The present study investigates three ways that parents' aggression can influence children's social problem-solving. First, this study is designed to replicate and extend findings that link children's exposure to marital conflict and aggression to their social problem solving abilities (Goodman et al.; Rosenberg, 1987). Second, this study assesses connections between parents' aggressive responses to hypothetical social scenarios and children's problem solving responses. We examine separate and combined effects of marital aggression and parents' aggressive problem solving on children's aggressive and assertive problem-solving when they respond to hypothetical scenarios involving peer relations. Third, this study examines whether children who are exposed to marital aggression are more likely to encounter provocative and challenging peer situations.

Social learning theory offers a framework for understanding why parents' aggression is relevant to children's aggressive problem solving strategies. Social learning perspectives posit a complex array of variables, including consequences of the aggression and degree of identification with the aggressor, that coalesce to determine how parents' modeled aggressive behavior influences children's schema about the acceptability and effectiveness of aggressive strategies ( Bandura, 1977). The observation of one parent's aggression to the other is a highly unique situation for learning about aggressive problem solving. From a modeling perspective, observing parents' aggression with one another conveys a message about the appropriateness of aggression. Observing parents may encourage children to use aggression in wide ranging social situations ( Margolin, 1998). Investigators with samples of young children ( Graham-Bermann & Levendosky, 1998) as well as adolescents and young adults ( Cantrell, MacIntyre, Sharkey, & Thompson, 1995; Levendosky, Huth-Bocks, & Semel, 2002; McCloskey & Lichter, 2003) report that youths' exposure to marital aggression relates to their own aggressive behavior with peers.

With a growing number of studies indicating an association between marital aggression and children's problematic behaviors with peers, researchers suggest that it is necessary to examine specific processes that link parents' direct displays of aggression to children's aggression with peers ( Grych & Fincham, 1990; Parke et al 2001). For example, in the larger field of marital conflict and children's peer relations, parents' expressions of negative emotions and regulation of negative affect emerge as important mediators of the link between parents' marital conflict and children's peer relations ( Lindsey, MacKinnon-Lewis, Campbell, Frabutt, & Lamb, 2002; Stocker & Youngblade, 1999). Thus, available evidence suggests that interparental conflict relates to children's peer behavior, but that association occurs in a context of more general displays of parents' displays of negative emotions. In addition, Eisenberg et al (2001) report parents' displays of negative emotions affect children's emotion regulation, which also affects children's social competencies. When parents display negative emotions toward other family members, children may come to believe that such emotions are socially acceptable, and even desirable.

Another way to explicate the association between interparental aggression and children's aggression with peers is to investigate the strategies youth and their parents generate when faced with challenging social situations. Only two studies have examined the question of whether children's exposure to interparental aggression influences children's problem solving strategies, not just their aggressive behaviors, with peers. Using a paper-and-pencil measure of problem-resolution strategies and social-cognitive skills, Rosenberg (1987) found that children who had witnessed battering tended to choose either passive or aggressive strategies to resolve interpersonal conflict. These children also were less likely to choose assertive strategies than were comparison children. More recently, Goodman et al. (1999) examined the relation between parents' marital aggression and the effectiveness of children's social problem-solving skills as assessed through children's interview responses to common social problems. These investigators reported that mothers' aggressive marital conflict tactics and conflict escalation related to children's use of less effective social coping strategies, primarily aggression with peers. Fathers' marital aggression, in contrast, did not account for significant variance in children's social coping effectiveness. This study assesses solutions to social problems as an index of social problem solving abilities, with ineffective solutions largely being aggressive solutions.

Studies of social problem solving skills frequently explore children's responses to hypothetical provocative social scenarios ( Dodge et al, 1990; Goodman et al., 1999; Quiggle, Garber, Panak, & Dodge, 1992). Responses to these scenarios can generalize to children's behavioral responses in naturalistic social situations. At the least they reveal how children interpret social problems and generate options in such situations. The rationale for studying children's aggressive and assertive problem solving comes from evidence that these responses generalize to children's behavioral responses in naturalistic social situations and play a role in children's overall adjustment ( Dodge, Petit, McClaskey, & Brown, 1986). Dodge and colleagues ( Dodge et al., 1990) show that children who generate aggressive responses to hypothetical situations tend to behave more aggressively in real life situations. Sandstrom (2004) found that aggressive strategies in response to peer provocation and rejection vignettes were associated with children's internalizing problems. On the other hand, assertive problem solving, which involves active attempts to manage or change stressful social situations is inversely related to emotional and behavioral problems ( Compas, Malcaren, & Fondacaro, 1988; Glyshaw, Cohen, & Towbes, 1989). Thus, the ability to generate and enact assertive, rather than aggressive, problem solutions appears to signify better developmental outcomes.

Parents' own social problem solving skills may contribute to children's aggressive versus assertive problem solutions. Investigations of other types of stressful situations, such as painful medical procedures ( Kliewer & Lewis, 1995), or post-divorce coping ( Miller, Kliewer, Hepworth, & Sandler, 1994) reveal that parents own problem solving can relate to children's reported strategies of how they make a problem better, or make themselves feel better ( Kliewer, Fearnow, & Miller, 1996). MacBrayer et al. (2003) directly investigated whether a mother's responses to hypothetical socially challenging scenarios relates to her child's social problem solving. To study the way that mothers might transmit hostile biases to their children, MacBrayer et al had mothers and children interpret and provide responses to provocative, ambiguous social problem scenarios. Their findings show significant correlations between mothers' and daughters' responses to the hypothetical problem scenarios. There were no significant correlations between mothers' and sons' responses. This study indicates that parental influences on children's aggression apply not only to overt aggression, but also to more subtle forms of relational aggression, such as rejecting, retaliating, and manipulative behaviors. Although this study included only mothers, the sex-specific findings highlight the need to include both fathers and mothers when examining parental influences in transmitting social problem solving strategies, particularly aggression. These results, however, underscore the relevance of directly assessing parents' own aggressive problem solving responses to hypothetical scenarios.

The present study is designed to examine the separate and interactive effects of marital aggression and parents' aggressive problem solving on children's aggressive and assertive social problem solving in response to peer scenarios. Based on the previous literature, we first hypothesize that marital aggression is positively related to children's aggressive social problem solving and negatively related to assertive problem solving. Second, we hypothesize that parents' own aggressive problem solving will be positively related to children's aggressive problem solving and negatively related to assertive problem solving. We included both mothers and fathers and tested these hypotheses separately for boys and girls to reveal potential sex-specific effects. Our research design also addresses the question of potential interactive effects between marital aggression and parents' own aggressive problem solving. This question is explored without specific hypotheses because previous literature does not inform us how the combination of exposure to marital aggression and parents' aggressive problem solving might affect children's problem solving.

The present study also examines the likelihood that children actually encounter the provocative social situations presented in this study. On the one hand, this question is a validity check on our procedures-are the hypothetical social scenarios representative of what children actually encounter in their lives? On the other hand, these data may reflect an important difference in the social experiences of children who are exposed versus not exposed to marital aggression. Several studies suggest that by adolescence, youth who have been exposed to marital aggression may be prone to peer rejection and may be selecting aggressive peers ( Ehrensaft, et al., 2003; Wolfe, Wekerle, Reitzel-Jaffe, & Lefebvre, 1998). The present study offers some preliminary data on whether pre-adolescent children from homes with versus without marital aggression report a higher likelihood of encountering provocative and rejecting social situations.

Method

Participants

The participants were 118 two-parent families, recruited through newspaper advertisements and/or fliers at local schools and community organizations. The criteria for participation were: a) the two parents and one target child were willing to participate; b) the child was aged 9 or 10; c) the two parents were residing in the same home with the child; d) the child was either these parents' biological child or had lived with them for three or more years; and e) all members of the family were able to complete the data collection in English.

Of the participating children, 51 (43%) were female and 67 (57%) were male. The average age was 10.0 years ( SD = .61). Their ethnicity was 21% African American, 25% Caucasian, 23% Hispanic/Latino, 8% Asian/Pacific Islander, and 26% mixed. Mothers' mean age was 38.5 years ( SD = 5.9; range = 25.6 to 53.5) and fathers' was 40.9 ( SD = 6.8; range = 24.3 to 55.5). Parents' education ranged from 7 to 20 years. For mothers (fathers), 8% (10%) had less than a high school education, 24% (29%) completed high school, 30% (22%) had some college, and 36% (40%) had a college degree or beyond. Mothers' (fathers') ethnicity was 31% (32%) Caucasian, 30% (27%) Hispanic/Latino, 24% (24%) African American, 10% (9%) Asian/Pacific Islander and 5% (8%) mixed. Twenty-three percent of mothers, 30% of fathers, and 2.5 % of the children were born outside the U.S. Combined family income averaged $67,810, (range = $8,700 to $165,000); 12% reported total family income < $25,000, 24% reported $25,000 − $50,000, 43% reported $50,000 − $100,000, and 21% reported ≥ $100,000.

Procedures

We collected these data during the first assessment of a larger study of children's violence exposure, family processes and children's adjustment. Both parents and the child participated in a 3−4 hour laboratory session administered by two graduate student experimenters. Families were compensated $100. In line with consent procedures that Margolin et al. (2005) recommend, the three family members jointly were involved in the consent procedures and in the decision to participate. Each family member was in a separate room to complete an individual battery of computerized and paper and pencil assessment measures. An experimenter read aloud all questions and answer choices to the child. An experimenter separately administered the problem solving interviews to each family member. These interviews were audio-taped for later coding. Due to experimenter error, one father was not interviewed.

Measures

Recent History of Interparental Aggression

The present study assesses both spouses' reports of husband-to-wife and wife-to-husband marital aggression during the previous year. The Domestic Conflict Inventory (DCI; Margolin, Burman, John, & O'Brien, 1990), revised in 2000, is a 61-item questionnaire that assesses partners' conflict tactics. This study uses the 14 physical abuse items, 11 of which are items from the Revised Conflict Tactics Scales ( Straus, Hamby, Boney-McCoy, & Sugarman, 1996). Each spouse completes the DCI twice--once for his or her own behavior and once for the partner's behavior. For each item, the respondent reports whether the spouse or self has ever engaged in the behavior. For the endorsed items, he or she reports how many times the behavior occurred during the past year by checking one of six frequency ranges: none (0), 1 per year (1), 2 to 5 per year (2), 6 to 12 per year (3), 2 to 4 per month (4), more than once per week (5). We handled disagreements between self-reports and spouse reports on specific behaviors by using the maximum of the two reporters. This solution is based on data that marital aggression tends to be under-reported ( Langhinrichen-Rohling & Vivian, 1994). Sums of maximum scores for husbands and wives yielded separate measures of husbands' aggression and wives' aggression for the past year. Margolin, John and Foo (1998) reported on the internal consistency and test-retest reliability. For DCI physical abuse items in the present study, internal consistency measured by Cronbach's alphas is .81 for husbands' physical aggression and .84 for wives' physical aggression. In this study, 26% of husbands and 35% of wives have at least one reported instance of physical aggression in the past year. Of those participants, the mean score for husbands is 2.94 ( SD = 2.6; range = 1−10) and for wives is 3.91 ( SD = 3.1; range= 1−13). The correlation between husbands' and wives' physical aggression in the past year is .53 ( p < .01).

Social Problem Solving Interviews and Coded Responses

The social problem solving interviews assessed children's and parents' open-ended responses to ambiguous and provocative hypothetical social situations. These procedures are similar to those in other studies on children's problem solving skills ( Dodge et al., 1986; Goodman, et al., 1999), but have not yet been used with adults. For children, this study used four scenarios involving potential social conflict with peers. Two additional scenarios involving interparental aggression were not used here due to low levels of children's aggressive solutions to these scenarios (1% of total solutions for girls; 2% for boys). For parents, this study used seven scenarios, four with peers and three with the spouse. After presenting each scenario, the experimenter asked the child or parent to describe up to three things that she or he would "do, say, or think in this situation". The experimenter prompted for at least three solutions, and wrote down the responses. Next, for the child only, the experimenter repeated the solutions, and asked the child to rate each response for: (a) effectiveness on a 5-point scale, where 0 represents not at all and 4 represents very effective; and (b) likelihood of performing each response on a 4-point scale where 0 represents extremely unlikely and 3 represents extremely likely. Children and adults alike gave ratings of the likelihood of having been in that specific scenario or a similar situation on a 5-point scale where 0 represents never and 4 represents all the time.

Two of the scenarios for children ( Someone takes your magazine; You are being teased) are patterned after the Alternative Solutions Test ( Caplan, Weissberg, Bersoff, Ezekowitz, & Wells, 1986). One is similar to the Quiggle, et al. (1992) protocol (A student bumps into you while you are standing in line). We wrote a fourth peer scenario involving social rejection for this study ( Your friend doesn't invite you to a party). Likelihood ratings indicate that most children had encountered each of the hypothetical situations at least once. Children's median ratings of likelihood of having experienced the situations were 1 ( almost never) on the 0−4 scale for two of the scenarios ( friend doesn't invite you to a party and a student bumps into you) and 2 ( sometimes) for the other scenarios ( someone takes your magazine and someone teases you).

Toward the goal of having similar procedures for assessing parents' and children's social problem solving, we used parallel ambiguous and potentially provocative scenarios for the parents. We modified some scenarios to be applicable to adults. For parents, the four peer scenarios are: Someone takes your newspaper; Someone yells at you for taking a parking space that person wants; Your friend doesn't invite you to a party; You hear other parents gossiping about you at a school function. In addition, we used three scenarios that involve conflict between spouses: Spouse comes home and starts criticizing you; Spouse ignores previous plans to watch television with you and is annoyed at being reminded of the plans; Spouse yells and insults you while in the car with your children. Parents' median ratings on the 0−4 scale of likelihood of encountering the situation were 2 ( sometimes) for the three scenarios involving spousal conflict, 0 for overhear gossip, and 1 for the three other scenarios involving peer conflict. Spousal conflicts depicted in the scenarios were a somewhat common occurrence, whereas peer conflicts were less common. Still, 93.5% of mothers (94.3% of fathers) had experienced at least one of the peer conflict scenarios, and 74.0% of mothers (85.4% of fathers) reported two or more experiences similar to the peer scenarios.

Based on audiotapes of the interviews and the experimenters' verbatim written notes of the problem solutions, we then divided each response into thought units to represent separate, discrete reactions (e.g., "I would yell at them and push them" was divided into two thought units, the first coded as verbal aggression and the second as physical aggression). Out of a multi-code system, we examined the aggressive and assertive codes, which are described in Appendix A. We collapsed four codes into an aggressive summary category to capture a range of behaviors spanning relational ( Crick & Grotpeter, 1995), verbal, and physical aggression. We collapsed three codes into an assertive category. Because participants provided different total numbers of solutions, the frequency for each category was represented by a percentage of the total number of responses given by each individual. Nine undergraduate research assistants learned the coding system by studying a codebook and meeting weekly for training. Coders demonstrated reliability by achieving Cohen's Kappas of .6 on practice data. The coding process involved listening to the tapes of the interviews while reading the experimenters' written notes. The coders continued to meet for practice and feedback on weekly reliabilities throughout the coding process. Two research assistants coded each participant's data.

summarizes mean percentages and reliabilities, calculated through intraclass correlation coefficients (ICC) for each summary category. ICC reliabilities ranges were .68 − .90 for parents and .90 − .97 for children. Based on the high ICCs, we used the mean percentage between the two coders for the analyses. Children's responses to the peer scenarios showed that assertive solutions were quite common, representing slightly over half of solutions. Aggressive strategies represented a smaller percentage of total strategies. However, 70% of children gave at least one aggressive solution, revealing a substantial amount of aggression. Parents' mean percentages of aggression reveal 2−3 times as many aggressive solutions in response to the spousal scenarios than peer scenarios. Mean percentages of parents' aggression are low, but the majority of parents report at least some aggression in response to the spousal scenarios. Approximately half of the fathers and one-third of the mothers report some aggression with peers.

Table 1

Results

Descriptive Information on Scenarios and Codes

We ran 2 (sex) × 2 (families with vs. without physical marital aggression) ANOVAs for children's and parents' data from the social problem solving interviews. We examined whether there are differences in the extent to which boys and girls from families with or without interparental physical aggression within the past year report having encountered the hypothetical peer scenarios. shows interaction effects between exposure to interparental aggression and children's sex for two scenarios. Post-hoc t-tests reveal that girls from maritally aggressive homes are more likely than girls from non-aggressive homes, t(1, 34) = −2.89, p < .01, or boys from either aggressive, t(1, 42) = 2.46, p < .05, or non-aggressive homes, t(1, 35) = 2.55, p < .05, to encounter the ambiguous situation of being bumped. Girls from maritally aggressive homes compared to those without aggression also are more likely to encounter the situation of not being invited to a party, t(1, 34) = −2.50, p < .05.

Table 2

We also ran 2 (child sex) by 2 (presence vs. absence of marital aggression) ANOVAs on children's ratings of the likelihood of using aggressive or assertive solutions, as well as on the children's effectiveness ratings of those solutions. To run these analyses, we collapsed ratings across scenarios. We calculated mean ratings for effectiveness of solutions coded as aggressive or assertive, and mean ratings for likelihood of actually enacting these solutions. We did not find main effects or interactions for child sex or parents' marital aggression on any of the 'likelihood of enacting' or 'effectiveness' ratings. The mean ratings for the whole sample for likelihood of using aggression and assertiveness, respectively, are 2.49 and 2.46 (between somewhat and extremely likely). The respective mean effectiveness ratings are 2.34 for aggression and 2.35 for assertion, also between somewhat and more than somewhat effective.

Another set of ANOVAs examined whether the percentage of proposed aggressive or assertive solutions differed by sex and presence versus absence of marital aggression. Analyses of children's aggressive solutions and assertive solutions showed no significant main effects or interactions for either of these coded responses. Analysis of mothers' and fathers' aggressive solutions in spousal scenarios showed main effects for sex, F(1,115) =6.65, p < .01, and for marital aggression F(1,115) = 7.57, p < .01. Mothers ( M = .17; SD = .18) gave more aggressive solutions than fathers ( M = .11; SD = .14). Parents who actually were physically aggressive in their marriage gave more aggressive solutions ( M= .34; SD = .25) than parents who were not actually aggressive ( M = .23; SD = .20). There was not a sex by marital aggression interaction for the spousal scenarios. Additionally, there were no main effects or interactions for parents' aggressive solutions to the peer scenarios.

Correlations between Parental Aggressive Problem Solving, Physical Marital Aggression, and Children's Aggressive and Assertive Solutions

presents Pearson's correlations between each of the parental influences on children's problem solutions and boys' and girls' aggressive and assertive solutions. Mothers' physical marital aggression within the past year is significantly correlated with girls' aggressive solutions to peer scenarios. Fathers' marital aggression in the past year is correlated with boys' aggressive solutions. We tested for differences in the correlations between boys and girls through r-to-z transformations, but found no significant differences.

Table 3

Mothers' aggressive solutions in spousal scenarios are negatively correlated with boys' assertive solutions and positively correlated with their aggressive solutions. Neither mothers' aggressive solutions with peers, nor fathers' aggressive solutions with spouse or peers, are significantly correlated with either boys' or girls' aggressive or assertive solutions. Using sums to examine additive effects, we found no correlations for the mothers' or fathers' total aggressive problem-solving.

We also examined within-person associations. For children, there are significant negative correlations between aggressive solutions and assertive solutions for boys, r = −.58, p < .01, and for girls, r = −.51, p < .01. There are no significant correlations between parents' marital aggression in the past year and their aggressive solutions in spousal scenarios ( r = .15 for mothers; r = .15 for fathers), or in peer scenarios ( r = .04 for mothers; .07 for fathers).

Regression Analyses Examining Interactions Between Parental Aggressive Problem Solving, Physical Marital Aggression, and Child Sex

We used hierarchical regression analyses to examine whether the 2-way and 3-way interactions between parents' marital aggression, parents' aggressive problem solving, and children's sex accounted for variance in children's problem solving. We ran four analyses to separately examine mothers' and fathers' aggressive solutions in the spousal and peer scenarios. We ran these four analyses for children's aggressive problem solving, and again for assertive problem solving. We entered main effects in the first step, 2-way interactions in the second step, and the 3-way interaction in the third step. We centered all predictor variables and used the product of centered variables to test interactions ( Aiken & West, 1991).

presents a summary of the 2-way and 3-way interaction effects in these regressions. For mothers, the 2-way interaction between marital aggression and aggressive solutions in spousal scenarios accounted for significant variance in children's aggressive and assertive problem solutions. For fathers, the 3-way interaction between marital aggression, aggressive solutions toward peers, and child sex accounted for significant variance in children's aggressive solutions.

Table 4

We plotted the significant interactions according to procedures described in Aiken and West (1991), in which regression lines are estimated at one SD above and below the mean for each independent variable. presents the slopes of the relations between mothers' aggressive problem solutions and children's problem solutions at values representing high or low levels of mothers' marital aggression within the past year. An analysis of the simple slopes predicting children's aggression indicates that the slope of the line representing children whose mothers use low actual marital aggression is significantly different from zero, B = −38.51, t(3,117) = −3.31, p < .01 and significantly different from the slope of the line of children of mothers with high actual marital aggression. Similarly, for children's assertion, the slope of the line of children exposed to low actual marital aggression is significantly different from zero, B = 23.95, t(3,117) = 2.63, p < .01, and different from the slope of the line of exposed children. When mothers exhibit low actual marital aggression, mothers' high levels of aggressive solutions in hypothetical spousal scenarios relate to children's high use of reported aggressive solutions and their low use of assertive solutions. In contrast, when mothers exhibit high actual marital aggression, children's aggressive problem solving is high and their assertive problem solving is low, regardless of the mothers' hypothetical solutions.

presents the relation between father's aggressive problem solutions and children's aggressive solutions. The figure presents separate slopes for girls and boys with fathers who exhibit high vs. low marital aggression. An analysis of simple slopes predicting children's aggression reveals that none of the slopes is significantly different from zero. T-tests comparing the slopes to one another reveal significant differences between boys with fathers who exhibit high marital aggression, B = −40.27, versus: (a) boys with fathers who exhibit low marital aggression, B = 9.38, t(1,25) = −6.13, p < .01; (b) girls with fathers who exhibit high marital aggression, B = −7.34 t(1,23) = −2.47, p < .05; and (c) girls with fathers who exhibit low marital aggression B = 33.61, t(1,38) = −7.90, p < .01. In addition, girls with fathers who exhibit high marital aggression also differ from (a) girls with fathers who exhibit low marital aggression, t(1,20) = −3.26, p < .01. Finally, boys and girls whose fathers exhibit low marital aggression differ from each other t(1,60) = −3.57, p < .01.

In general, boys gave fewer aggressive responses when faced with a father who exhibits high levels of actual marital aggression and who responds to hypothetical peer situations with levels of aggressive responses. Boys with fathers who exhibit low actual marital aggression, in contrast, reported a higher percentage of aggressive solutions in concert with the fathers' higher percentage of aggressive solutions. Girls respond with high percentages of aggressive solutions when their fathers exhibit high actual marital aggression and high percentages of aggressive problem solutions. Girls respond with few aggressive solutions if their fathers exhibit low actual marital aggression.

Finally, we checked for two types of additive effects. First we summed across responses to spousal and peer situations within each parent. There were no significant results on those analyses of each parent's total aggressive problem solving. Second, we also summed across mothers' and fathers' aggressive responses, and again found no significant results.

Discussion

The current study provides information on how different forms of parents' aggression relate to children's aggressive and assertive problem solving. Parents' reports of actual physical marital aggression during the past year were associated with children's aggressive problem solutions to provocative hypothetical peer scenarios. Parents' reports of aggression also relate to girls' likelihood of actually experiencing the peer situations. Mother-to-father physical aggression was significantly correlated with girls' aggressive problem solving, whereas father-to-mother physical aggression was correlated with boys' aggressive problem solving. Mother aggressive solutions were positively correlated with boys' aggressive solutions, and negatively correlated with boys' assertive solutions. The influence of parents' aggressive problem solving in hypothetical situations on children's aggressive problem solving was moderated, in certain analyses, by the presence of actual physical marital aggression. For families with high wife-to-husband actual aggression, aggressive problem solving in the hypothetical marital situations corresponded to high levels of children's aggressive problem solutions and to low levels of assertive solutions. For fathers, the primary finding was the 3-way interaction between child sex, husband-to-wife physical aggression, and fathers' aggressive solutions to hypothetical peer situations. In families with high husband-to-wife physical aggression, more aggressive problem solving by fathers corresponded with more aggressive solutions by girls but fewer aggressive solutions by boys. Because of the different patterns of effects for mothers and fathers, examining both parents together weakened rather than strengthened the findings.

Children's responses to the hypothetical peer situations show that, overall, children were highly likely to respond with assertive problem solutions. Assertive solutions, as defined here, reflect constructive, conflict mitigating strategies. In light of other research showing that stated strategies are related to actual behaviors and desired goals ( Chung & Asher, 1996; Dodge, et al. 1990), these data suggest that children typically are more likely to try to contain or resolve than to escalate conflict. Nonetheless, aggressive strategies with peers also comprised a notable proportion of children's responses with 70% of children responding with at least one strategy representing relational or physical aggression. Moreover, children rated the aggressive responses as moderately effective, and indicated that they were likely to actually exhibit the aggressive responses. This study only assessed aggression in reaction to the specified actions of others, which, according to Crick and Dodge (1996), may reflect deficits and distortions in taking in and interpreting information in social situations. Occasional aggressive responses to hypothetical situations and even low levels of actual aggressive behavior are anticipated at this stage of early adolescence. However, in light of the increase in deviant peer involvement and antisocial behavior in mid to late adolescence ( Broidy et al., 2003; Patterson & Yoerger, 2002), high levels of such responses or the continuation of responses into later adolescence may be problematic.

Marital Aggression and Children's Problem Solutions to Hypothetical Peer Situations

The results of the present study add further support to the possibility of aggressive reactions and potentially compromised peer relations for children exposed to marital aggression ( Kitzmann, Gaylord, Holt, & Kenny, 2003). The present study extends findings on the specific connection between exposure to interparental aggression and children's social problem solving skills. In comparison with results from Rosenberg (1987), the present study similarly finds links between interparental aggression and children's higher use of aggressive strategies, but finds less consistent results for reduced assertive strategies. In the present study, exposure to marital aggression does not necessarily impair children's assertive problem solving skills. This finding suggests that being exposed to aggressive models and using aggressive responses does not necessarily correspond to less facility with assertive responses, although perhaps the quality of the assertive responses should be further examined. The present study and the Goodman et al. (1999) study are similar in that both used community samples, and both examined husbands' and wives' marital conflict tactics in connection with young adolescents' social problem solving. Goodman et al. reported that mothers', but not fathers', self-reported marital aggression was associated with children's lower problem solving skills. Our findings support same-sex parent-child associations between parents' physical marital aggression and children's aggression.

Children have opportunities to observe both male and female models in the context of 2-parent families. It can be argued, on the one hand, that aggression exhibited by either parent against the other is salient in light of the child's close relationship to the perpetrator and recipient of the aggression. On the other hand, to understand gender-linked modeling of aggression, we also need to consider the societal sanctions for male and female aggression as well as the observed outcomes resulting from aggression ( Bussey & Bandura, 1999). More information still is needed to understand whether sex of child in combination with sex of parent play a role in how a child interprets and evaluates a parent's behavior. This combination may also play a role in the child's emotional reactions to the aggression.

Beyond modeling, an alternative explanation for the association between parents' marital aggression and children aggressive problem solving is that exposure to marital aggression might sensitize children to interpersonal conflict overall. Children may respond by feeling threatened, emotionally upset, or fearful of being drawn into a conflict ( Davies & Cummings, 1994; Grych & Fincham, 1993). The data provided here are consistent with the idea that exposure to aggression in the family context can generalize to aggressive responses in peer situations, but do not specify the mechanisms behind this link. The significant correlations between exposure to marital aggression and children's aggressive responses to the peer scenarios could reflect a) beliefs about the efficacy of aggressive reactions, b) an inability to generate benign explanations for the peer's behavior, c) a sense of threat due to ambiguous peer behavior, or d) urgency to end an uncomfortable situation. Further exploration of these types of cognitive and affective variables is needed to identify mediators of the connection between exposure to marital aggression and children's aggressive reactions.

In a related vein, several explanations could account for the finding that girls from maritally aggressive homes report a greater likelihood of having encountered peer rejection (not being invited to a party), and provocative peer behaviors (student bumps you). It is possible that the violence-exposed girls actually encounter the situations more frequently, and also possible that they are more sensitive to ambiguous situations and interpersonal slights. Either way, the potential for compounding effects cannot be ignored. The girls' experiences with peer rejection and provocation, and their tendencies to generate aggressive solutions to such situations, can lead to perpetuating cycles of problematic peer relations.

Parents' and Children's Problem Solutions to Hypothetical Situations

The reason we had parents respond to hypothetical provocative scenarios was to have a similar method for assessing parents' and children's problem solutions. As anticipated, the data revealed some similarities between parent and child responses to the scenarios. One mother, for example, said that she would "yell back" in response to spousal criticism. In response to teasing, her child said "tease him right back, get some of my friends to back me up, peg him with a ball". One notable difference, however, was that parents' aggression was almost exclusively verbal (2% physical for mothers; 4% for fathers), whereas 19% of children's aggressive responses involved physical aggression. Bivariate correlations reveal significant correlations in only one type of relationship. Mothers' aggressive problem solutions with the father are positively related to boys' aggressive problem solutions and negatively related to boys' assertive solutions.

The interaction effects in the regression analyses indicate that parents' aggressive problem solutions are best understood in the context of actual marital aggression. When mothers exhibit low actual marital aggression during the previous year, the mothers' high levels of hostile problem solving in response to hypothetical marital scenarios related to children's high levels of aggressive problem solving and low levels of assertive problem solving in peer scenarios. Yet, when mothers exhibit high marital aggression in the past year, mothers' own problem solving in the marital scenarios had no influence beyond that of the marital aggression. Goodman et al. (1999) similarly reported that, for families with the highest frequency of actual marital conflicts, children's problem solving effectiveness did not vary as a function of mothers' aggressive tactics. However, mothers' aggressive tactics were negatively associated with problem solving effectiveness in families with less actual marital conflict. In explaining why this finding held for mothers but not fathers, Goodman et al. suggested that mothers' aggressive tactics may be less arousing and threatening. Because the mothers' behaviors run counter to traditional gender expectations, they may be more salient and more likely to be imitated.

Fathers' aggressive problem solving is best understood through the 3-way interaction involving fathers' problem solving with peers, husband-to-wife marital aggression, and child sex. The combination of father's aggression toward the mother and his aggressive problem solving in hypothetical peer situations exacerbates girls' aggressive problem solving but has the opposite effect for boys. No hypotheses were proposed about different effects for girls and boys, as the previous literature on family violence exposure and youth aggression shows mixed effects or no differences for child sex ( Martin, 1990; McClosky & Lichter, 2003; Pagani et al 2004).

The current findings, with an interaction for child sex, introduce the possible explanation of differential socialization of boys and girls surrounding aggression. Young boys often receive conflicting messages about the appropriateness of aggression. Standing up for themselves in a physically aggressive manner with same-sex peers may be condoned whereas physical aggression with females is not. Thus, it is possible that a father's aggression across multiple contexts and particularly toward the mother communicates a message about undesirability of aggression to some pre-adolescent sons. However, these data also suggest that some girls may be motivated by an aggressive paternal model to react aggressively. Although we do not know what the girls hope to accomplish with their aggressive solutions, perhaps these are strategies to protect themselves. Girls who grow up with a father who is aggressive in multiple situations may identify with the mother. They may become sensitized to any form of being victimized, and thus generate aggressive responses to provocative situations. Attempts to explain these findings point out that there are multiple directions and pathways through which parents' aggression affects children's aggression. We need to understand more about the variability across children. We also need to look more systematically at these questions across developmental stages, as there is some evidence that sex differences related to interparental conflict aggression become more pronounced as youths progress through adolescence ( McCloskey & Lichter, 2003).

It is generally assumed that we can understand more about children's socialization by examining both maternal and paternal influences, and including both parents is a strength in any study. However, as Hinde (1999) notes, parental influences typically vary across different parent-child combinations. In the present study, we followed the tradition of separately examining mother-child and father-child influences, but also re-ran all the correlational analyses and regression analyses summing mothers' and fathers' scores to examine the combined impact of mothers' and fathers' aggression. Overall, there is no evidence from this study or other studies (e.g. Goodman et al., 1999) that additive effects reflecting more aggressive models relate to higher levels of children's aggressive problem solving. In light of the different patterns for mothers and fathers, we also ran the regression analyses including each parent as a separate predictor, looking for interactive effects. We did not find interactive effects between mothers' and fathers' aggressive solutions. Due to limited power for the 4-way interactions, this question should be examined further with a larger sample.

Limitations and Conclusions

An important consideration in this study is the complexity in understanding aggression, and the distinctions between thoughts and statements about aggression versus the actual performance of aggression. For example, we do not know whether children's problem solutions reported here are associated with their actual aggressive behaviors, although other studies ( Dodge, et al., 1990) do report such associations. There also are questions about coherence across measures of parents' aggression, and the extent to which the assessments of parents' aggression in the study relate to what the child actually observes. Although other studies indicate associations between parents' problem solutions in hypothetical situations and advice and coaching that parents actually communicate to children ( Kliewer, et al., 1996), we did not directly examine that question. Future studies could directly examine whether parents' articulated problem solutions to hypothetical situations relate to parents' intentional messages, e.g., their advice on how to handle aggressive peers. Future studies could also examine unintentional messages, e.g., children's observations of their parents' aggressive behavior when vying for a parking space. Another question of coherence in parents' aggression concerns the relationship between their actual marital aggression and their reported aggressive solutions. Between-group analyses show that parents with actual marital aggression, compared with those without marital aggression, are more likely to report aggressive problem solutions in the marital scenarios. However, correlation analyses find non-significant results between parents' aggressive solutions to the hypothetical marital conflicts and reports of actual physical marital aggression for wives and for husbands. These data point to the possibility that parents may articulate one message about aggression but demonstrate another message through their actual behavior.

Another consideration in interpreting the results of this study concerns the extent of physical aggression in the sample, which was a community sample of 2-parent families. In 26.7% of participating couples, at least one spouse exhibited physical marital aggression within the past year, and in 19.2% both spouses were physically aggressive. Still, because of our criterion that the parents were living together, our study did not include those children who had been exposed to high intensity physical aggression between parents who had subsequently separated. The criterion for participation thus may have attenuated the effects of violence exposure.

Another limitation of this study concerns the likelihood of additional sources of influence in children's aggression. Parents' harsh behavior to the child has been related to children's generation of aggressive problem solutions ( Dodge et al., 1990; Weiss, Dodge, Bates, & Pettit, 1992). Children's prior negative experiences with peers affect their expectancies of future interaction and likely influence their social problem solving with peers ( MacKinnon-Lewis, Rabiner, & Starnes, 1999). Children bring other characteristics that can moderate the relationship between parental models and peer interactions, such as emotion regulation skills and physiological reactivities ( Eisenberg, et al., 2001; Leary & Fainsilber Katz, 2004). These variables and genetic variables, such as the heritability of aggression and antisocial traits, potentially influence connections between parents' and children's generation of aggressive solutions. Questions about parental influence on children's aggressive problem solving also should be addressed with attention to developmental stage, as children's reactions to marital aggression and their identification with each parent vary across development.

Despite limitations, the results of this study provide a piece in the complicated puzzle of how parents influence children's aggressive and assertive problem solving with peers. Maccoby (1996) highlights the need for a "conceptual bridge" between intrafamily conflict and peer conflict. Parke and colleagues ( Parke, Burks, Carson, Neville, & Boyum, 1994) raise specific questions about how children transfer the strategies they acquire in the family context to peer relationships. The findings presented here call attention to mothers', as well as fathers' marital aggression as important influences in children's aggressive problem solving. The findings add to the small but growing literature suggesting that parents' own aggressive problem solving strategies have implications for the children's aggressive and assertive problem solutions with peers. Further research is needed to examine how parental influences might prime children to respond cognitively and emotionally in a conflict-escalating or de-escalating fashion. In light of the salience of peer relations for children's overall adjustment ( Bukowski & Adams, 2005), identifying ways that parents can bring about children's constructive responses to challenging peer situations warrants further attention.

Appendix

Appendix A

Demanding Behavior

Making demands or asking strongly for something.

"Tell her to back off" "Give me back my newspaper!" (P)

Spiteful Behavior

Acting out of spite, passive aggression, making passive-aggressive or sarcastic comments.

"Get him expelled" "Say 'Gee, I'm glad you had a nice day'" (P)

Verbal Aggression

Yelling, name calling, verbal threats, revenge or retaliation.

"I'd get a baseball bat and warn them that I'll hit them" "I'd match his criticism" (P)

Physical Aggression

Physically hostile infringements on the person or possessions; hitting, grabbing.

"Bump him" (C)

Assertive Cooperative

Higher order solutions, which meet the subject's needs, but also consider the other's feelings and needs a. Compromising - taking the other person into account when solving the problem.

"Ask if we can take turns reading the magazine." (C)

Assertive Prosocial

Addressing problem in a good-natured, kind or nice manner or making a polite request with prosocial words such as "please" or "thank-you" or providing an explanation or rationale for behavior.

"I would explain that the magazine was mine and I did not mean to leave it...could I please have it back?" (C)

Assertive Direct

Confronting person or issue, information seeking. Being direct, getting to the point through the use of statements or questions.

"I would ask for my magazine back." (C)

Footnotes

¹ Due to a change in interview procedures, we did not collect ratings on aggressive responses from the first 13 children.

References

Broidy LM, Nagin DS, Tremblay RE, Bates JE, Brame B, Dodge KA, et al. Developemental trajectories of childhood disruptive behaviors and adolescent delinquency: A six-site, cross-national study. Developmental Psychology. 2003;39:222-245. [[PMC free article] [PubMed] Google Scholar]

Dodge KA, Pettit GS. A biopsychosocial model of the development of chronic conduct problems in adolescence. Developmental Psychology. 2003;39:349-371. [[PMC free article] [PubMed] Google Scholar]

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Parents' Aggressive Influences and Children's Aggressive Problem Solutions with Peers

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This study examined children's aggressive and assertive solutions to hypothetical peer scenarios in relation to parents' responses to similar hypothetical social scenarios and parents' actual marital aggression. The study included 118 9−10 year old children, and their mothers and fathers. Children's aggressive solutions correlated with same-sex parents' actual marital aggression.

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CON 3

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Diagnosing mental illness isn't like diagnosing other chronic diseases. Heart disease is identified with the help of blood tests and electrocardiograms. Diabetes is diagnosed by measuring blood glucose levels. But classifying mental illness is a more subjective endeavor. No blood test exists for depression; no X-ray can identify a child at risk of developing bipolar disorder. At least, not yet.

Thanks to new tools in genetics and neuroimaging, scientists are making progress toward deciphering details of the underlying biology of mental disorders. Yet experts disagree on how far we can push this biological model. Are mental illnesses simply physical diseases that happen to strike the brain? Or do these disorders belong to a class all their own?

Eric Kandel, MD, a Nobel Prize laureate and professor of brain science at Columbia University, believes it's all about biology. "All mental processes are brain processes, and therefore all disorders of mental functioning are biological diseases," he says. "The brain is the organ of the mind. Where else could [mental illness] be if not in the brain?"

That viewpoint is quickly gaining supporters, thanks in part to Thomas R. Insel, MD, director of the National Institute of Mental Health, who has championed a biological perspective during his tenure at the agency.

To Insel, mental illnesses are no different from heart disease, diabetes or any other chronic illness. All chronic diseases have behavioral components as well as biological components, he says. "The only difference here is that the organ of interest is the brain instead of the heart or pancreas. But the same basic principles apply."

A new toolkit

Take cardiology, Insel says. A century ago, doctors had little knowledge of the biological basis of heart disease. They could merely observe a patient's physical presentation and listen to the patient's subjective complaints. Today they can measure cholesterol levels, examine the heart's electrical impulses with EKG, and take detailed CT images of blood vessels and arteries to deliver a precise diagnosis. As a result, Insel says, mortality from heart attacks has dropped dramatically in recent decades. "In most areas of medicine, we now have a whole toolkit to help us know what's going on, from the behavioral level to the molecular level. That has really led to enormous changes in most areas of medicine," he says.

Insel believes the diagnosis and treatment of mental illness is today where cardiology was 100 years ago. And like cardiology of yesteryear, the field is poised for dramatic transformation, he says. "We are really at the cusp of a revolution in the way we think about the brain and behavior, partly because of technological breakthroughs. We're finally able to answer some of the fundamental questions."

Indeed, in recent years scientists have made many exciting discoveries about the function - and dysfunction - of the human brain. They've identified genes linked to schizophrenia and discovered that certain brain abnormalities increase a person's risk of developing post-traumatic stress disorder after a distressing event. Others have zeroed in on anomalies associated with autism, including abnormal brain growth and underconnectivity among brain regions.

Researchers have also begun to flesh out a physiological explanation for depression. Helen Mayberg, MD, a professor of psychiatry and neurology at Emory University, has been actively involved in research that singled out a region of the brain - Brodmann area 25 - that is overactive in people with depression. Mayberg describes area 25 as a "junction box" that interacts with other areas of the brain involved in mood, emotion and thinking. She has demonstrated that deep-brain stimulation of the area can alleviate symptoms in people with treatment-resistant depression (Neuron, 2005).

Maps of depression's neural circuits, Mayberg says, may eventually serve as a tool both for diagnosis and treatment. Understanding the underlying biology, she adds, could help therapists and psychopharmacologists decide which patients would benefit from more intensive therapy, and which aren't likely to improve without medication. That would be a welcome improvement, she says. "Syndromes are so nonspecific by our current criteria that the best we can do now is flip a coin. We don't do that for any other branch of medicine," she says.

Yet despite the progress and promise of her research, Mayberg isn't ready to concede that all mental illnesses will one day be described in purely biological terms. "I used to think you could localize everything, that you could explain all the variants by the biology," she says. "I think in a perfect world you could, but we don't have the tools to explain all those things because we can't control for all of the variables."

One of the biggest problems, she says, is that mental illness diagnoses are often catchall categories that include many different underlying malfunctions. Mental illnesses have always been described by their outward symptoms, both out of necessity and convenience. But just as cancer patients are a wildly diverse group marked by many different disease pathways, a depression diagnosis is likely to encompass people with many unique underlying problems. That presents challenges for defining the disease in biological terms. "Depression does have patterns," Mayberg says. "The caveat is different cohorts of patients clearly have different patterns - and likely the need for different specific interventions."

Software malfunction

When it comes to mental illness, a one-size-fits-all approach does not apply. Some diseases may be more purely physiological in nature. "Certain disorders such as schizophrenia, bipolar disorder and autism fit the biological model in a very clear-cut sense," says Richard McNally, PhD, a clinical psychologist at Harvard University and author of the 2011 book "What is Mental Illness?" In these diseases, he says, structural and functional abnormalities are evident in imaging scans or during postmortem dissection.

Yet for other conditions, such as depression or anxiety, the biological foundation is more nebulous. Often, McNally notes, mental illnesses are likely to have multiple causes, including genetic, biological and environmental factors. Of course, that's true for many chronic diseases, heart disease and diabetes included. But for mental illnesses, we're a particularly long way from understanding the interplay among those factors.

That complexity is one reason that experts such as Jerome Wakefield, PhD, DSW, a professor of social work and psychiatry at New York University, believe that too much emphasis is being placed on the biology of mental illness at this point in our understanding of the brain. Decades of effort to understand the biology of mental disorders have uncovered clues, but those clues haven't translated to improvements in diagnosis or treatment, he believes. "We've thrown tens of billions of dollars into trying to identify biomarkers and biological substrates for mental disorders," Wakefield says. "The fact is we've gotten very little out of all of that."

To be sure, Wakefield says, some psychological disorders are likely due to brain dysfunction. Others, however, may stem from a chance combination of normal personality traits. "In the unusual case where normal traits come together in a certain configuration, you may be maladapted to society," he says. "Call it a mental disorder if you want, but there's no smoking-gun malfunction in your brain."

You can think of the brain as a computer, he adds. The brain circuitry is equivalent to the hardware. But we also have the human equivalent of software. "Namely, we have mental processing of mental representations, meanings, conditioning, a whole level of processing that has to do with these psychological capacities," he says. Just as software bugs are often the cause of our computer problems, our mental motherboards can be done in by our psychological processing, even when the underlying circuitry is working as designed. "If we focus only at the brain level, we are likely to miss a lot of what's going on in mental disorders," he says.

The danger in placing too much attention on the biological is that important environmental, behavioral and social factors that contribute to mental illness may be overlooked. "By over-focusing on the biological, we are doing patients a disservice," Wakefield says. He sees a red flag in a study by Steven Marcus, PhD, and Mark Olfson, MD, that found the percentage of patients who receive psychotherapy for depression declined from 53.6 percent in 1998 to 43.1 percent in 2007, while rates of antidepressant use stayed roughly the same ( Archives of General Psychiatry, 2010).

A nuanced view

The emerging area of epigenetics, meanwhile, could help provide a link between the biological and other causes of mental illness. Epigenetics research examines the ways in which environmental factors change the way genes express themselves. "Certain genes are turned on or turned off, expressed or not expressed, depending on environmental inputs," McNally says.

One of the first classic epigenetics experiments, by researchers at McGill University, found that pups of negligent rat mothers were more sensitive to stress in adulthood than pups that had been raised by doting mothers (Nature Neuroscience, 2004). The differences could be traced to epigenetic markers, chemical tags that attach to strands of DNA and, in the process, turn various genes on and off. Those tags don't just affect individuals during their lifetime, however; like DNA, epigenetic markers can be passed from generation to generation. More recently, the McGill team studied the brains of people who committed suicide, and found those who had been abused in childhood had unique patterns of epigenetic tags in their brains ( Nature Neuroscience, 2009). "Stress gets under the skin, so to speak," McNally says.

In McNally's view, there's little danger that mental health professionals will forget the importance of environmental factors to the development of mental illness. "I think what's happening is not a battle between biological and non-biological approaches, but an increasingly nuanced and sophisticated appreciation for the multiple perspectives that can illuminate the etiology of these conditions," he says.

Still, translating that nuanced view to improvements in diagnosis and treatment will take time. Despite decades of research on the causes and treatments of mental illness, patients are still suffering. "Suicide rates haven't come down. The rate of prevalence for many of these disorders, if anything, has gone up, not down. That tells you that whatever we've been doing is probably not adequate," Insel says.

But, he adds, there's good reason to hold out hope. "I think, increasingly, we'll understand behavior at many levels, and one of those will be physiological," Insel says. "That may take longer to translate into new therapies and new opportunities for patients, but it's coming."

In the meantime, according to Insel and Kandel, patients themselves are clamoring for better biological descriptions of mental disorders. Describing mental illnesses as brain malfunctions helps minimize the shame often associated with them, Kandel says. "Schizophrenia is a disease like pneumonia. Seeing it as a brain disorder destigmatizes it immediately."

Certainly, Kandel adds, social and environmental factors are undeniably important to understanding mental health. "But they do not act in a vacuum," he says. "They act in the brain."

It's too soon to say whether we'll someday have a blood test for schizophrenia or a brain scanning technique that identifies depression without any doubt. But scientists and patients agree: The more we understand about our brain and behavior, the better. "We have a good beginning of understanding of the brain," says Kandel, "but boy, have we got a long way to go."
Kirsten Weir is a freelance writer in Minneapolis.

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Diagnosing mental illness isn't like diagnosing other chronic diseases. Heart disease is identified with the help of blood tests and electrocardiograms. Diabetes is diagnosed by measuring blood glucose levels. But classifying mental illness is a more subjective endeavor. No blood test exists for depression; no X-ray can identify a child at risk of developing bipolar disorder.

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Many people with serious mental illness are challenged doubly. On one hand, they struggle with the symptoms and disabilities that result from the disease. On the other, they are challenged by the stereotypes and prejudice that result from misconceptions about mental illness. As a result of both, people with mental illness are robbed of the opportunities that define a quality life: good jobs, safe housing, satisfactory health care, and affiliation with a diverse group of people. Although research has gone far to understand the impact of the disease, it has only recently begun to explain stigma in mental illness. Much work yet needs to be done to fully understand the breadth and scope of prejudice against people with mental illness. Fortunately, social psychologists and sociologists have been studying phenomena related to stigma in other minority groups for several decades. In this paper, we integrate research specific to mental illness stigma with the more general body of research on stereotypes and prejudice to provide a brief overview of issues in the area.

The impact of stigma is twofold, as outlined in Table ​Table1. 1 . Public stigma is the reaction that the general population has to people with mental illness. Self-stigma is the prejudice which people with mental illness turn against themselves. Both public and self-stigma may be understood in terms of three components: stereotypes, prejudice, and discrimination. Social psychologists view stereotypes as especially efficient, social knowledge structures that are learned by most members of a social group ( 1- 3). Stereotypes are considered "social" because they represent collectively agreed upon notions of groups of persons. They are "efficient" because people can quickly generate impressions and expectations of individuals who belong to a stereotyped group ( 4).

PUBLIC STIGMA

Stigmas about mental illness seem to be widely endorsed by the general public in the Western world. Studies suggest that the majority of citizens in the United States ( 13, 15- 17) and many Western European nations ( 18- 21) have stigmatizing attitudes about mental illness. Furthermore, stigmatizing views about mental illness are not limited to uninformed members of the general public; even well-trained professionals from most mental health disciplines subscribe to stereotypes about mental illness ( 22- 25).

Several themes describe misconceptions about mental illness and corresponding stigmatizing attitudes. Media analyses of film and print have identified three: people with mental illness are homicidal maniacs who need to be feared; they have childlike perceptions of the world that should be marveled; or they are responsible for their illness because they have weak character ( 29- 32). Results of two independent factor analyses of the survey responses of more than 2000 English and American citizens parallel these findings ( 19, 33):

1. fear and exclusion: persons with severe mental illness should be feared and, therefore, be kept out of most communities;

2. authoritarianism: persons with severe mental illness are irresponsible, so life decisions should be made by others;

3. benevolence: persons with severe mental illness are childlike and need to be cared for.

Although stigmatizing attitudes are not limited to mental illness, the public seems to disapprove persons with psychiatric disabilities significantly more than persons with related conditions such as physical illness ( 34- 36). Severe mental illness has been likened to drug addiction, prostitution, and criminality ( 37, 38). Unlike physical disabilities, persons with mental illness are perceived by the public to be in control of their disabilities and responsible for causing them ( 34, 36). Furthermore, research respondents are less likely to pity persons with mental illness, instead reacting to psychiatric disability with anger and believing that help is not deserved ( 35, 36, 39).

The behavioral impact (or discrimination) that results from public stigma may take four forms: withholding help, avoidance, coercive treatment, and segregated institutions. Previous studies have shown that the public will withhold help to some minority groups because of corresponding stigma ( 36, 40). A more extreme form of this behavior is social avoidance, where the public strives to not interact with people with mental illness altogether. The 1996 General Social Survey (GSS), in which the Mac Arthur Mental Health Module was administered to a probability sample of 1444 adults in the United States, found that more than a half of respondents are unwilling to: spend an evening socializing, work next to, or have a family member marry a person with mental illness ( 41). Social avoidance is not just self-report; it is also a reality. Research has shown that stigma has a deleterious impact on obtaining good jobs ( 13, 42- 44) and leasing safe housing ( 45- 47).

Discrimination can also appear in public opinion about how to treat people with mental illness. For example, though recent studies have been unable to demonstrate the effectiveness of mandatory treatment ( 48, 49), more than 40% of the 1996 GSS sample agreed that people with schizophrenia should be forced into treatment ( 50). Additionally, the public endorses segregation in institutions as the best service for people with serious psychiatric disorders ( 19, 51).

STRATEGIES FOR CHANGING PUBLIC STIGMA

Change strategies for public stigma have been grouped into three approaches: protest, education, and contact ( 12). Groups protest inaccurate and hostile representations of mental illness as a way to challenge the stigmas they represent. These efforts send two messages. To the media: STOP reporting inaccurate representations of mental illness. To the public: STOP believing negative views about mental illness. Wahl ( 32) believes citizens are encountering far fewer sanctioned examples of stigma and stereotypes because of protest efforts. Anecdotal evidence suggests that protest campaigns have been effective in getting stigmatizing images of mental illness withdrawn. There is, however, little empirical research on the psychological impact of protest campaigns on stigma and discrimination, suggesting an important direction for future research.

Stigma is further diminished when members of the general public meet persons with mental illness who are able to hold down jobs or live as good neighbors in the community. Research has shown an inverse relationship between having contact with a person with mental illness and endorsing psychiatric stigma ( 54, 57). Hence, opportunities for the public to meet persons with severe mental illness may discount stigma. Interpersonal contact is further enhanced when the general public is able to regularly interact with people with mental illness as peers.

SELF-STIGMA

Low self-esteem versus righteous anger describes a fundamental paradox in self-stigma ( 64). Models that explain the experience of self-stigma need to account for some persons whose sense of self is harmed by social stigma versus others who are energized by, and forcefully react to, the injustice. And there is yet a third group that needs to be considered in describing the impact of stigma on the self. The sense of self for many persons with mental illness is neither hurt, nor energized, by social stigma, instead showing a seeming indifference to it altogether.

We propose a situational model that explains this paradox, arguing that an individual with mental illness may experience diminished self-esteem/self-efficacy, righteous anger, or relative indifference depending on the parameters of the situation ( 64). Important factors that affect a situational response to stigma include collective representations that are primed in that situation, the person's perception of the legitimacy of stigma in the situation, and the person's identification with the larger group of individuals with mental illness. This model has eventual implications for ways in which persons with mental illness might cope with self-stigma as well as identification of policies that promote environments in which stigma festers.

CONCLUSIONS

Researchers are beginning to apply what social psychologists have learned about prejudice and stereotypes in general to the stigma related to mental illness. We have made progress in understanding the dimensions of mental illness stigma, and the processes by which public stereotypes are translated into discriminatory behavior. At the same time, we are beginning to develop models of self-stigma, which is a more complex phenomenon than originally assumed. The models developed thus far need to be tested on various sub-populations, including different ethnic groups and power-holders (legislators, judges, police officers, health care providers, employers, landlords). We are also learning about stigma change strategies. Contact in particular seems to be effective for changing individual attitudes. Researchers need to examine whether changes resulting from anti-stigma interventions are maintained over time.

All of the research discussed in this paper examines stigma at the individual psychological level. For the most part, these studies have ignored the fact that stigma is inherent in the social structures that make up society. Stigma is evident in the way laws, social services, and the justice system are structured as well as ways in which resources are allocated. Research that focuses on the social structures that maintain stigma and strategies for changing them is sorely needed.

References

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Articles from World Psychiatry are provided here courtesy of The World Psychiatric Association

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Understanding the impact of stigma on people with mental illness

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Many people with serious mental illness are challenged doubly. On one hand, they struggle with the symptoms and disabilities that result from the disease. On the other, they are challenged by the stereotypes and prejudice that result from misconceptions about mental illness.

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J Pers Soc Psychol. Author manuscript; available in PMC 2015 Jul 22.

Published in final edited form as:

Abstract

The current research provides a framework for understanding how concealable stigmatized identities impact people's psychological well-being and health. The authors hypothesize that increased anticipated stigma, greater centrality of the stigmatized identity to the self, increased salience of the identity, and possession of a stigma that is more strongly culturally devalued all predict heightened psychological distress. In Study 1, the hypotheses were supported with a sample of 300 participants who possessed 13 different concealable stigmatized identities. Analyses comparing people with an associative stigma to those with a personal stigma showed that people with an associative stigma report less distress and that this difference is fully mediated by decreased anticipated stigma, centrality, and salience. Study 2 sought to replicate the findings of Study 1 with a sample of 235 participants possessing concealable stigmatized identities and to extend the model to predicting health outcomes. Structural equation modeling showed that anticipated stigma and cultural stigma were directly related to self-reported health outcomes. Discussion centers on understanding the implications of intraindividual processes (anticipated stigma, identity centrality, and identity salience) and an external process (cultural devaluation of stigmatized identities) for mental and physical health among people living with a concealable stigmatized identity.

Keywords: stigma, psychological distress, courtesy stigma, mental illness, identity

Recent reviews in psychology and sociology and from the Department of Health and Human Services have concluded that stigma has large and varied effects on people's life outcomes (e.g., Major & O'Brien, 2005; U.S. Department of Health and Human Services [DHHS], 1999; Williams, Neighbors, & Jackson, 2003). The goal of the current research is to propose and test a novel model for understanding how stigma impacts psychological and health well-being among people who live with a concealable stigmatized identity. Concealable stigmatized identities are vastly understudied in comparison to visible stigmatized identities. Despite the acknowledgment that stigma can have a variety of negative effects, there is currently no conceptual framework to understand how possessing a concealable stigmatized identity impacts psychological and physical distress. We seek to fill that gap.

Because stigma is socially constructed, we believe it is critical to examine both intraindividual and external stigma processes that can impact well-being. Whereas most psychological research has focused solely on the psychological processes internal to individuals that enable stigmatization to lead to psychological distress, here we focus on the impact of both intraindividual processes (i.e., anticipated stigma, centrality, and salience) and an external process (i.e., cultural stigma). In doing so, we adopt a broader approach to studying the impact of stigmatization than what has previously been attempted.

We propose that for people living with a concealable stigmatized identity, both psychological distress (as measured by levels of depression and anxiety) and health (as measured by self-report of illness symptoms) can be predicted by examining four important stigma-related components. First, at the intraindividual level, how much devaluation and prejudice does a person expect to occur if the identity is revealed? We predict that greater anticipated stigma will be related to increased distress. Next, how central is the concealable stigmatized identity to the self? Identities can be more or less self-definitional, and for concealable stigmatized identities we predict that greater centrality will be related to more distress. Last, how salient is the concealable stigmatized identity? Some people may rarely think about the identity, whereas others may think about it several times a day. We predict that increased salience will be related to increased distress. Finally, at the external, or cultural, level, different types of identities are culturally devalued to different degrees. We predict that possessing an identity with greater cultural stigma attached to it will be related to more psychological distress. Note that level of cultural stigma is determined by the community or culture in which a person is living, not by the individual him- or herself.

By simultaneously examining the relationships between these four constructs-anticipated stigma, centrality, salience, and cultural stigma-and psychological distress (in Study 1) and both psychological distress and health outcomes (in Study 2), we present a model that has both theoretical and practical implications. Although each of the four constructs has, individually, been theorized to affect people living with stigmatized identities, this research marks the first time they have been examined simultaneously, thereby allowing a fuller theoretical picture of how stigma operates in people's lives. More practically, this knowledge may help elucidate the pathways through which stigma can lead to health disparities ( Muehrer, 2002), thereby leading to better interventions to reduce the negative impact of stigma.

Concealable Stigmatized Identities

A concealable stigmatized identity is an identity that can be kept hidden from others but that carries with it social devaluation ( Crocker, Major, & Steele, 1998). Specifically, an identity is stigmatized if it is considered a mark of failure or shame, tainting the self in the eyes of others ( Goffman, 1963). The term covers a broad range of identities, including history of mental illness, rape, molestation, epilepsy, domestic violence, previous incarceration, HIV/AIDS, and substance abuse (see Pachankis, 2007, for a review). Although these attributes differ considerably in their etiology, course, and treatment, there are important similarities among all of these concealable stigmatized identities. Each is socially devalued and may render an individual vulnerable to prejudice and discrimination solely on the basis of this attribute (e.g., loss of status, employment discrimination, personal rejection). These identities also have negative stereotypes associated with them (e.g., mental illness's association with danger and instability; rape's association with promiscuity and moral impurity).

Associative Stigma

An additional distinction concerning concealable stigmatized identities is whether the identity is personal versus associative. A personal concealable stigma is an identity that the self possesses, such as one's own history of mental illness. In contrast, an associative stigma (also known as a courtesy stigma or affiliate stigma) is a stigma that a person possesses because of his or her close connection to a stigmatized other ( Birenbaum, 1970; Goffman, 1963). Research has shown that parents of disabled children; spouses, siblings, and children of the mentally ill; and caregivers of people living with AIDS all report feeling stigmatized, including feelings of shame, the need to keep the identity concealed, and the belief that others avoid (or may avoid) them due to their associative stigma ( Corrigan & Miller, 2004; Mickelson, 2001; Wight, Aneshensel, Murphy, Miller-Martinez, & Beals, 2006). In the current research we examined whether our model applies to both personal and associative concealable stigmatized identities.

Stigma and Psychological Distress

Stigma scholars have long linked stigmatized identities to increased psychological distress. Although early theorizing assumed uniformly negative outcomes for people in stigmatized groups (e.g., Allport, 1954; Erickson, 1956), current stigma research has recognized that there is immense variability in how people cope with and respond to stigmatized identities (see Major, 2006, for a review of this new perspective on stigma). Thus, for example, among visibly stigmatized racial minorities, African Americans routinely report higher self-esteem than do European Americans ( Gray-Little & Hafdahl, 2000), but Hispanics, Asian Americans, and Native Americans report lower self-esteem than do European Americans ( Twenge & Crocker, 2002). Research on the relationship between concealable stigmatized identities and psychological distress has been somewhat more consistent, with rape, childhood sexual abuse, and mental illness related to increased psychological distress (e.g., Brewin, Andrews, & Valentine, 2000; Link, Struening, Neese-Todd, Asmussen, & Phelan, 2001). However, even these relationships have been critiqued and questioned ( Corrigan & Watson, 2002; Rind, Tromovitch, & Bauserman, 1998). The enormous variability of psychological distress within stigmatized groups has led stigma researchers across domains to assert that simply examining the link between a social identity and psychological distress is no longer useful in trying to explain who is vulnerable to distress ( Friedman & Brownell, 1995; Twenge & Crocker, 2002). Instead, it is crucial to understand how the psychological meaning of the identity works in tandem with stigma to make a person more or less vulnerable to distress.

Although stigma can affect many different types of life outcomes (e.g., employment, housing, educational achievement), psychologists have primarily focused on psychological outcomes such as self-esteem, life satisfaction, happiness, depression, and anxiety. Because these measures tend to be highly correlated, they are often made into composites of "psychological well-being" or "psychological distress." In the current research we focused on depression and anxiety as a composite measure of psychological distress. We chose these measures because they are often used in stigma research (see Mak, Poon, Pun, & Cheung, 2007, for a review), thereby making our work comparable with other research in the area. We also chose them because level of psychological distress is an important and powerful variable. Depression and anxiety are often comorbid with a variety of health conditions (e.g., cardiovascular disease, diabetes) and are related to exacerbation of medical symptoms and decreased healthy behaviors ( Katon & Ciechanowski, 2002). Thus, in choosing psychological distress as our outcome variable, we were guided both by its overall importance to psychological and physical well-being and by its theorized link to stigma.

Current Concepts and Models

Direct Effects of Stigma-Related Factors

Drawing on research conducted across a variety of different concealable stigmatized identities (e.g., mental illness, HIV/AIDS, childhood sexual abuse), we first define each of our four stigma identity-related factors-anticipated stigma, centrality, salience, and cultural stigma-and outline our predictions for how each of these separate factors can directly impact psychological distress when considered alone. In the sections that follow, we present a more complex framework that (a) examines how these factors can influence psychological distress when considered simultaneously and (b) accounts for both the direct and indirect (i.e., mediated) effects of these variables (see ). Finally, we extend this framework to consider how these factors influence both psychological distress and health (see ).

Anticipated Stigma

What do people think will happen if others learn of their concealable stigmatized identity? The concern that others will look down upon, shun, or discriminate against them is at the heart of anticipated stigma. Anticipated stigma refers to the degree to which individuals expect that others will stigmatize them if they know about the concealable stigmatized identity. Unlike people with visible stigmatized identities, who regularly interact with others who know of their stigmatized identity, people with concealable stigmatized identities may not know exactly how others will react if they reveal the identity. They do know, however, the negative stereotypes about their group. As Link and colleagues ( Link, 1987; Link, Cullen, Struening, & Shrout, 1989) have discussed in regard to mental illness stigma, people often learn negative stereotypes before they acquire a stigmatized identity, and it is difficult to unlearn those stereotypes once one gains the identity. Thus, people with concealable stigmatized identities know the negative stereotypes about their groups and may even recall times when they themselves have discriminated against people with their identity. Moreover, because their identity is hidden, people with concealable stigmatized identities may often be in the position to directly witness disparagement of their stigmatized group ( Wahl, 1999). It is not surprising, therefore, that people with concealable stigmatized identities are concerned about what will happen if they reveal their identity.

Previous research on anticipated stigma- often termed felt or perceived stigma- has consistently shown that the more people believe that others devalue their group, the worse their reported psychological well-being. This effect has been shown with several concealable stigmatized identities, including mental illness (e.g., Link, 1987; Link et al., 1989, Link & Phelan, 2001; Rosenfield, 1997), epilepsy ( Westbrook, Bauman, & Shinnar, 1992), and HIV status ( Katz & Nevid, 2005). Notably, for mental illness, the effect of perceived stigma on psychological distress occurs over and above any positive effects of mental illness treatment and continues long after the initial labeling of a mental illness disorder ( Link, Struening, Rahav, Phelan, & Nuttbrock, 1997; Markowitz, 1998).

Measures of anticipated stigma in the literature, however, have often conflated several different types of beliefs (e.g., internalized shame, one's own beliefs about stereotypes, social rejection, and beliefs about others' possible attitudes and actions) into one measure termed perceived stigma. For example, Link's (1987) perceived Devaluation-Discrimination scale includes items such as "Most people believe that a man who has been hospitalized for a mental illness is dangerous" ( Link, 1987; Link et al., 1997). Such items measure knowledge of stereotypes, but they do not directly measure whether the person with mental illness (or other concealed stigmatized identity) believes that others will devalue them if they reveal their concealed identity. It is this personal sense of anticipated stigma that we examined in the current research. Our measure of anticipated stigma explicitly asked people how likely they believed a variety of negative outcomes would occur if they revealed their stigmatized identities, making it a more direct and theoretically clear measure of anticipated stigma. We predicted that the more people anticipated negative consequences if they revealed their concealed stigmatized identities, the more distress they would report.

Centrality

A second factor that may allow a concealable stigmatized identity to impact psychological and health well-being is how central the identity is to the self. Just as people vary in the extent to which they anticipate stigmatizing reactions to their identity, they vary in whether the identity is considered to be critical to their self-definition. Although some previous research has examined the role of centrality of concealable stigmatized identities, it has focused predominantly on centrality's effects on disclosure decisions among people who are concealing sexual minority status ( Griffith & Hebl, 2002; Ragins, 2008). To our knowledge, all other previous research on the role of centrality in psychological distress has focused on visible identities (primarily race). In both cross-sectional and longitudinal studies, greater centrality of ethnic identity has been related to lower levels of psychological distress among African Americans (e.g., Sellers, Caldwell, Schmeelk-Cone, & Zimmerman, 2003; Sellers, Smith, Shelton, Rowley, & Chavous, 1998; Yip, Seaton, & Sellers, 2006). On the contrary, work examining other stigmatized identities, including women and Latinos, as well as some additional work done with African Americans, has shown either a negative or null relationship between centrality-also called identity importance or group identification-and psychological well-being (e.g., Eccleston & Major, 2006; Major, Quinton, & Schmader, 2003; McCoy & Major, 2003).

In the current research we predicted that greater centrality of the identity would be related to increased psychological distress. While previous research has suggested that identities that are more central to the self may have benefits for psychological well-being because they offer people a source of social support and can provide external attributions for negative events (e.g., Bourguignon, Seron, Yzerbyt, & Herman, 2006; Crocker & Major, 1989; Cross, 1991), we predicted that this is not the case for those whose identity is concealable. Given that people with concealable stigmatized identities are less likely to spend time with similar others ( Frable, Platt, & Hoey, 1998), the buffering effects of identity centrality on psychological well-being are not often open to those with concealable stigmatized identities. Thus, we hypothesized that higher levels of identity centrality would predict higher rates of psychological distress among people with concealable stigmatized identities.

Salience

Stigmatized identities also vary in the extent to which they are salient to the holders of the identities. For some people, the identity will cross their minds only once a year, and few situations will make the identity salient ( Quinn, Kahng, & Crocker, 2004). For others, the identity may be chronically accessible and occupy their thoughts quite often. To the extent that people are frequently thinking about the concealed identity, the stigma is a more important and salient part of their lives. Thus, our measure of salience is a straightforward frequency measure asking how often people think about their concealable stigmatized identity. We did not ask what people were thinking about or how they were feeling when they were thinking about the identity. We were interested in sheer salience of the identity to the self. We predicted greater salience would be related to increased psychological distress.

There are no current measures of stigma salience for concealed identities, but there has been research on two related concepts. Both stigma consciousness ( Pinel, 1999) and race-based rejection sensitivity ( Mendoza-Denton, Downey, Purdie, Davis, & Pietrzak, 2002) highlight individual differences in people's thoughts and expectations about whether situations are related to their stigmatized identity. However, both of these measures capture constructs substantially different from mere salience of the identity. Stigma consciousness measures the extent to which people believe their group membership is being used to judge or evaluate them (e.g., women wondering if men interpret their actions in a gendered way because they are women). The race-based rejection sensitivity measure is designed to examine whether people in specific situations in which their identity is known to others expect and are concerned about stereotype-related treatment (e.g., African Americans wondering if store clerks think they will shoplift). This measure is more akin to our anticipated stigma measure but is dependent on assessing stereotype-relevant situations for visible identities. Neither of these measures are frequency measures per se, and both would be difficult to adapt for identities that remain concealed in most situations. A comparison of these measures directly highlights the differences in the day-to-day experiences of concealable versus visible stigmatized identities. As noted by Goffman (1963), people with visible stigmas are managing situations, whereas people with concealed stigmas are managing information about the self.

Cultural Stigma

Different stigmatized identities carry with them different levels of social devaluation. This level of devaluation is culturally constructed, in that it originates outside the self and is not connected to any idiosyncratic characteristics beyond the stigma label. Unlike the intraindividual identity-related variables discussed thus far- anticipated stigma, centrality, and salience-level of cultural stigma is determined externally from the person possessing the identity. Although social scientists have emphasized that stigma is constructed through social relationships, cultures, and institutions ( Hebl & Dovidio, 2005; Link & Phelan, 2001), level of cultural stigma has rarely been examined as a predictor of psychological distress.

In the current research we take a novel approach to capture levels of cultural stigma. To obtain a truly external measure of cultural stigma, we asked a separate sample of participants-a sample that could be considered the cultural peers of our main sample of people with concealable stigmatized identities-to rate how negatively people with each of the concealable stigmatized identities are viewed. We then used these ratings of cultural stigma as a predictor of psychological distress. This process of using external aggregate ratings is similar to work done by Cutrona and colleagues ( Cutrona et al., 2005; Cutrona, Wallace, & Wesner, 2006), in which aggregate ratings of neighborhood distress and census ratings of neighborhood poverty were used along with intraindividual-level risk factors (e.g., personality, socioeconomic status) to predict psychiatric disorders. We hypothesized that level of cultural stigma would affect psychological distress such that those with more socially stigmatized identities would report more distress, over and above the distress related to the internal factors of anticipated stigma, centrality, and salience. This is an important step to take stigma out of the individual and place it back into the larger culture, where it originated.

Summary

In the current work, we examine the direct and independent effect of each of our stigma-related variables on psychological distress for people with concealable stigmatized identities. There are varying levels of empirical and theoretical support for each of the intraindividual variables (anticipated stigma, centrality, and salience), but they have never been tested simultaneously. To our knowledge, utilizing an external measure of cultural stigma has not previously been examined. Also, because previous research has primarily focused on visible identities, several of the variables were modified (anticipated stigma, centrality) or specifically developed (salience, cultural stigma) for concealable stigmatized identities. The test of the direct effects model allows both a theoretical and practical advancement in the understanding of the experiences of people who live with concealable stigmatized identities.

Mediated Models Predicting Psychological Distress and Health Outcomes

We believe that in order to fully understand the negative effects of stigma, it is important to consider both the direct and indirect processes through which stigma results in deleterious psychological and health outcomes. That is, although it is important to understand the relative impact of each factor independently, these factors coexist within individuals and are likely to influence each other. Below we outline our framework for considering both the direct and indirect effects of these factors on psychological distress (see ) and both psychological distress and illness symptoms (see ).

Mediated Model Predicting Psychological Distress

In order to understand this complex process, we first started with the assumption that people who live with a concealable stigmatized identity contend with two basic types of stigma: anticipated stigma, which is an intraindividual process, and cultural stigma, which is an external process. Anticipated stigma has been consistently linked to deleterious psychological effects (see Mak et al., 2007, for a review), but the reasons why this occurs are not fully known. In the mediated model that we tested in the current work, we examined how anticipated stigma can affect well-being indirectly through both centrality and salience.

In Study 1, we predicted that greater levels of anticipated stigma would be related to greater centrality of the identity. Although there has been no research on this relationship for people with concealable stigmatized identities, there has been an ongoing debate on a similar topic within research on racial identity. Specifically, there are opposing viewpoints on whether greater centrality of racial identity leads to more perceived stigma and, ultimately, more distress or whether more perceived and experienced stigma leads to greater centrality (e.g., Branscombe, Schmitt, & Harvey, 1999; McCoy & Major, 2003). For concealable stigmatized identities, we hypothesized that because most people have little day to-day experience with discrimination because their identity is concealed, it makes more theoretical sense that it is their own anticipation of devaluation and rejection that will increase the importance of the identity for the self. That is, to the extent that people believe they will be rejected by others, the identity becomes more important in defining the self. In a similar vein, we hypothesized that greater anticipated stigma would be related to increased salience of the identity. Again, to the extent that people believe that greater rejection and devaluation will occur if others know about the identity, the identity will be on their minds more frequently. In summary, people who anticipate more stigma may also, in turn, find the identity to be of greater magnitude for the self-it will be more central and salient and may, therefore, lead to compromised well-being.

We predicted that cultural stigma would directly affect psychological distress. We expected that cultural stigma would impact well-being due to the myriad subtle changes and slights that occur because one possesses a devalued identity. These faint-and for people with concealable stigmatized identities, fairly infrequent- degradations in treatment or relationships are hard for an individual to identify and do not necessarily consciously filter through individuals' psyches (see Link & Phelan, 2001, for a discussion of how stigma changes life outcomes). Thus, we predicted that levels of cultural stigma would have only direct effects on well-being, without working indirectly through centrality and salience.

Mediated Model Predicting Health

In Study 2, we extended the model tested in Study 1 to examine both psychological distress and health outcomes (see ). Members of stigmatized groups tend to have more negative health outcomes across a variety of indicators when compared with members of nonstigmatized groups ( DHHS, 1999). Within research on racial stigma, there has been a consistent link between perceptions of discrimination and negative health outcomes, as well as reported experiences of discrimination and negative health outcomes ( Williams, Neighbors, & Jackson, 2003). We predicted, on the basis of these findings, direct effects for both anticipated and cultural stigma on increased illness symptoms within our sample. That is, to the extent that people were worried about social rejection and discrimination (anticipated stigma) and were, indeed, devalued due to their identity (cultural stigma), they would report more illness symptomatology. In addition, increased psychological distress has been consistently and strongly comorbid with negative health indicators ( Katon & Ciechanowski, 2002). Thus, in our current model we expected that psychological distress would be strongly related to increased illness symptomatology.

In summary, in Study 2 we tested a model predicting both psychological and health outcomes simultaneously. We expected that, in line with predictions from Study 1, anticipated stigma would be both directly related to psychological distress and indirectly related to it through its effect on centrality and salience. In addition, we predicted that both anticipated stigma and cultural stigma would be directly related to self-reported health outcomes. Finally, we predicted that in line with a large and consistent literature, psychological distress would be strongly related to more negative health outcomes.

Study 1

In Study 1, we measured the intraindividual constructs of anticipated stigma, centrality of the concealed identity to the self, and salience of the identity to self in a sample of 300 people living with concealable stigmatized identities. We also measured psychological distress, as indexed by depression and anxiety. In order to create an external measure of cultural stigma, we collected data from a second sample in which we had participants-who were not selected for having a concealable stigmatized identity-rate the level of devaluation associated with each of the identities reported in the first sample.

In our analyses, we first examine the independent, direct effects of each variable on psychological distress. Then, we consider both the direct and indirect effects of these variables on psychological distress within the model presented in . Additionally, we provide tests of potential alternate models. Finally, we examine whether the model applied equally well to people with associative versus personal concealable stigmatized identities. Previous research has shown that although people with associative stigma reported feeling stigmatized, the level of distress was not as high as for people with a personal concealable stigmatized identity. In the current research we examine (a) whether there are differences in the reported distress level and (b) whether those differences are mediated by the lower levels of anticipated stigma, centrality, and salience that people with an associative stigma (compared with personal stigma) are likely to possess.

Method

Participants

People concealing a stigmatized identity are difficult to identify. In order to find participants potentially concealing a stigmatized identity, we included two questions in a mass prescreening session held during the 1st week of the semester during introductory psychology classes at the University of Connecticut. Participants were first asked if they possessed an identity that they regularly kept hidden from others. If they answered yes, they were further queried on whether they believed that if they revealed the identity to others, the reaction would be "mostly negative," "mostly surprised," or "mostly positive." Over the course of two semesters, we screened a total of 2,057 students with these questions. Of these, 746 (36%), noted that they were concealing an identity that they believed others would react to negatively or with surprise. We deliberately used these broad criteria in order to obtain a variety of concealed identities. These 746 students were eligible to sign up for our study as one of many listed in our web-based participant pool system. There was no particular incentive for them to sign up for our study versus any other study occurring in the participant pool.

A total of 377 participants signed up and completed the survey. Of these, 300 participants indicated a codable stigmatized identity and were included in analyses. More information about the identities is given below. Participants completed the survey as partial fulfillment of a course requirement. Participants were predominantly female (73.3%) and Caucasian (85.4%), and the mean age was 18.59 years ( SD = 1.08).

Procedure

The first page of the survey gave a neutral explanation of a concealed identity ("Almost all people have parts of their history or personal identity that they regularly keep concealed from other people. In the questions that follow, we are interested in learning more about the experience of both concealing and revealing 'hidden' experiences or identities"), followed by examples of positive, negative, and neutral identities. We reminded them that they were selected because they had indicated in the prescreening that they had something about themselves that they regularly kept hidden. The participants were then asked to describe their concealed identity in their own words and were told that this identity would be referred to as their "concealed identity" in the survey. They were also told that if they had multiple concealed identities, they should choose only one on which to report.

Participants then completed a battery of measures related to both concealed identity and psychological distress (described below). Two presentation orders of these materials were created such that half of the participants completed the questions about the concealed identity first followed by the psychological distress measures, and the other half completed the measures in the reverse order. All participants were assured of their anonymity, and each participant completed the survey alone in a small cubicle.

Measures

Nature of the concealed identity

Two raters coded the open-ended responses describing the concealed identity into one of the following categories: (a) mental illness (e.g., depression, obsessive compulsive disorder), (b) weight/appearance concerns (e.g., eating disorder), (c) sexually related activity (e.g., fetishes, affairs), (d) medical conditions (e.g., diabetes, epilepsy), (e) history of rape, (f) history of childhood sexual abuse, (i) sexual orientation, (j) family member with medical or psychological issues (e.g., cancer, mental illness), (k) family member with addiction (e.g., alcoholism, gambling), (l) abusive family (e.g., domestic violence), (m) drug use, (n) criminal actions (e.g., stealing), (o) abortion, (p) lies about background or personal information, (q) death of a family member, (r) adoption, and (s) uncodable (e.g., question was not answered or did not include enough information for the coders to categorize it). Interrater reliability was high (κ = .93), and discrepancies were resolved through discussion. Because the last four categories above- concerning lying ( n = 10), family member death ( n = 19), adoption ( n = 4), and being uncodable ( n = 44)-were not clearly stigmatized identities (i.e., they do not taint the whole person in the eyes of others or carry with them consensual negative stereotypes), we did not include these participants' data in the analyses.

Anticipated stigma

To measure the extent to which people thought they would be socially stigmatized if they revealed their identity, we presented a 15-item scale with the following directions: "If others knew your concealed identity, how likely do you think the following would be to occur?" Answers were rated on a 1 ( not at all likely) to 7 ( very likely) Likert scale. The scale contained the nine-item "day-to-day" discrimination scale from Kessler, Mickelson, and Williams (1999, p. 214), with items such as "Getting poorer service than others do at restaurants or stores" and "People threatening or harassing you," as well as six additional items we thought would be likely to capture the type of social devaluation about which college students would be concerned: "People not wanting to date you," "Current friends stop hanging out with you," "Friends avoiding you," "Roommates wanting to move out of apartment or dorm room," "People not wanting to get to know you better," and "People not wanting to get involved in an intimate relationship with you" (α = .95).

Identity centrality

We used the Importance to Identity sub-scale of the Collective Self-Esteem scale ( Luhtanen & Crocker, 1992) to examine the centrality of the concealed identities to self. This four-item scale has been widely used across different types of identities ( Luhtanen & Crocker, 1992; Sellers et al., 1998) and was modified to pertain to concealed identity (e.g., "My concealed identity is an important reflection of who I am"). Each item was answered on a 7-point response scale that ranged from 1 ( strongly disagree) to 7 ( strongly agree). Questions were coded so that higher scores reflected greater centrality (α = .76).

Identity salience

A one-item measure asked participants to indicate the extent to which they generally think about their concealed identity. Response options were almost never, several times a year, once a month, once a week, a few times a week, once a day, and many times each day. Participants checked the frequency level that best described their situation. We then converted this categorical measure into a continuous measure representing number of thoughts per day. Specifically, "almost never" = 0 times per day; "several times a year" = 3/365; "once a month" = 12/365; "once a week" = 52/365; "a few times a week" = (4 × 52)/365; "once a day" = 1; "many times a day" = 5.

Psychological distress

In line with previous work on stigma and psychological distress, we defined distress as a combination of depression and anxiety (e.g., Kessler et al., 1999; Major & Gramzow, 1999; Sellers et al., 2003). Items from the State-Trait Anxiety Inventory-Trait (STAI-T) scale and the Center for Epidemiological Studies-Depression scale (CES-D) were standardized and combined to create a composite measure of psychological distress. The CES-D is a 20-item self-report measure of depressive symptomatology ( Radloff, 1977). It is one of the most used and validated measures of depression ( Shafer, 2006). Participants indicated the extent to which they felt each symptom during the past week on a 4-point scale ranging from 0 ( Rarely or none of the time) to 3 ( Most or all of the time). Scale reliability for this sample was high (α = .91). The STAI-T is a 20-item self-report measure of trait levels of anxiety that has also been widely used and validated ( Spielberger, Vagg, Barker, Donham, & Westberry, 1980). Each item was rated on a 1 ( not at all) to 5 ( very much) scale, and scale reliability for this sample was high (α= .92). The two scales were correlated at r = .79, and the reliability of the composite measure was α = .95.

Cultural stigma

In order to collect an external measure of cultural stigma, we had a separate group of 114 participants complete a survey about their beliefs and views of different stigmatized groups. Participants were predominantly female (72.8%), Caucasian (79.8%), and 19.4 years of age ( SD = 1.9). Undergraduate students were recruited from several large classes at the University of Connecticut to complete the survey. Thus, this sample constituted a sample of peers for the concealed identity sample.

We collected ratings from this separate group of participants in order to determine the relative level of devaluation of each type of concealable stigmatized identity in our main sample. Participants were first asked to think about a particular group (e.g., "People who have a history of mental illness," "People who have had an abortion," "People who have been raped"). Then they were asked to respond to the question "How do you think people with this identity are generally viewed by others?" on a 1 ( very positive) to 7 ( very negative) scale in reference to each of the 13 concealed identities in the main sample plus 1 visible identity (African American ethnicity) for comparison. Note that the rating always focused on the people rather than an event or experience.

All participants rated all of the identities, and presentation of the identities was randomized across participants. We specifically phrased this question to downplay socially desirable responding and to capture consensual ratings of stigma. Participants in this study could be considered "raters" or "judges" of identity negativity (i.e., we had 114 judges of 13 different targets). We computed an intraclass correlation (ICC) to examine rater reliability ( Shrout & Fleiss, 1979) and found the ratings reliable (ICC = .99). We used the mean rating of each identity as our measure of cultural stigma. Notably, all of the concealed identities were judged to be as negative or more negative than possessing an African American racial identity, and all were above the midpoint of the scale, with means ranging between 4.10 (for people with a hidden medical condition) to 6.40 (for people with a history of criminal activity).

Additional measures

The survey contained, in addition to the main variables of interest, several additional measures. We adapted the Ruminative Responses Scale ( Treynor, Gonzalez, & Nolen-Hoeksema, 2003) to ask participants how often they tended to ruminate about their concealed identity (10 items; α = .89). Rumination is a maladaptive coping strategy whereby people have a tendency to focus on their own negative thoughts and feelings, resulting in increased depression ( Nolen-Hoeksema, 1991; Nolen-Hoeksema & Morrow, 1991). In the current study, we examined whether our measures of anticipated stigma, centrality, and salience predicted depression, controlling for the tendency to ruminate on the self. Participants were also asked to indicate the length of time they had possessed their concealed identity, which ranged from less than a year (5.6%) to their entire lifetime (11.8%), with a mean of approximately 5 years. Finally, we also asked a variety of questions, primarily open-ended, around beliefs about disclosure, which are not discussed here.

Results

We examined whether the order of questionnaires affected the variables by conducting independent t tests on each of the variables of interest (centrality, salience, anticipated stigma, and distress). There were no significant effects of order (all p s > .10).

Categories and Descriptives

As can be seen in the first column of , the most frequent concealed identity within the sample was mental illness, followed by appearance concerns.

Table 1

The first column of shows the mean levels and standard deviations for each of the variables. There is no theoretical reason why men and women should differ on these variables, and indeed they do not. There were no gender differences in mean levels of depression, anxiety, anticipated stigma, centrality, or salience (all ps > .33). There was a small gender difference on the cultural stigma ratings (men = 5.18, women = 4.99), t(298) = 2.00, p = .05, but this difference was not replicated in Study 2.

Overall, participants showed a great deal of variability in the extent to which they deemed the identity central to the self. The mean fell in the middle of the scale with a 1.5-point standard deviation. Thus, the sample includes participants for whom the concealed identity ranged from not at all definitional of the self to extremely central to the self. Likewise, the frequency with which the identity was on the minds of the participants varied greatly. Some participants rarely thought of the identity: 32% of the sample reported they thought of the identity once a month or less, whereas 34% of the sample reported they thought of their identity once a day or more. Participants reported relatively low levels of anticipated stigma, reflecting their beliefs that they were unlikely to suffer from overt discrimination.

Finally, distress was quite high in the sample. The mean on the depression scale was 20.63. A frequency analysis showed that 59% of the sample fell at or over a score of 16, which is used as the clinical cutoff point for depression diagnosis ( Radloff, 1977). Surveys of the general population have found mean CES-D scores around 9 ( Weissman, Sholomskas, Pottenger, Prusoff, & Locke, 1977), although surveys of young adults have sometimes shown a mean closer to 15 ( Radloff, 1991).

Predicting Distress

(above the diagonal) shows the bivariate correlations between the variables. As predicted, anticipated stigma, identity centrality, salience of identity thoughts, and cultural stigma were all positively related to psychological distress.

Table 3

Examining the direct effects of stigma-related factors

Although previous research and theory has discussed each variable individually as a predictor of distress, no previous research has examined all four variables simultaneously. Given that many of the variables were correlated with each other, a linear regression predicting distress in which all predictors were entered simultaneously was conducted. In this way, the unique effect of each stigma variable could be examined. All of the intraindividual variables (anticipated stigma, centrality, salience) were entered on the first step, followed by cultural stigma on the second step. As seen in , anticipated stigma, centrality, and salience were each significant predictors of distress. Supporting our hypotheses, more anticipated stigma, increased centrality, and increased salience were each uniquely related to increased distress. In the second step of the regression, cultural stigma significantly added to the variance accounted for in distress. Thus, cultural stigma-a variable completely external to the participants-impacted distress. There was practically no change in the betas of the intraindividual variables, indicating that cultural stigma was a relatively separate source of distress. The full model was significant, F(4, 295) = 35.38, p < .001, accounting for a third of the variance in distress ( R ² = .32). Thus, results supported our hypothesis that these four variables are unique predictors of distress for people with concealable stigmatized identities.

Table 4

Examining the mediated model

A second goal with the current data was to consider both the direct and indirect effects of these factors on psychological distress. We theorized that, as shown in , anticipated stigma would have a direct effect on distress but would also work indirectly through its relationships with centrality and salience. Cultural stigma was predicted to have only a direct effect on distress. Using Amos 6.0 software ( Arbuckle, 2005), we utilized structural equation modeling to test the model. Direct maximum likelihood estimation of missing data was used to allow information from the full sample ( N = 300) to be used in the structural analyses. Each of our variables was represented as a measured variable in the model. The exogenous variables (anticipated stigma and cultural stigma) were correlated in order to represent the causal influences of variables not measured in the model ( Kline, 2005). Finally, we assessed model fit with four indexes: chi-square, root-mean-square error of approximation (RMSEA; Steiger, 1998), comparative fit index (CFI; Bentler, 1990), and the Akaike information criterion (AIC; Akaike, 1987). A nonsignificant chi-square value, an RMSEA value of .06 or lower, and a CFI value greater than .95 indicate good fit ( Hu & Bentler, 1999). Because we also wanted to be able to compare alternative, nonhierarchical models to our hypothesized model, we also reported the AIC, which is a goodness-of-fit measure that is adjusted to penalize for model complexity. Thus, when comparing alternative, nonhierarchical models, the one with the lower AIC is preferred ( Hu & Bentler, 1995).

We first tested the saturated model. Consistent with our hypotheses, the paths from cultural stigma to centrality and salience were nonsignificant (all ps > .49) and were deleted from the model. The trimmed model (see ) fit the data well, χ ²(2) = 0.59, ns, CFI = 1.0, RMSEA = .00, AIC = 36.6, and all remaining paths were significant (all p s < .05). There was a significant direct effect of cultural stigma on psychological distress. Anticipated stigma had a direct effect on distress, but it also had indirect effects on psychological distress through centrality and salience. Taken together, the model that provided the best fit for our data indicates that anticipated stigma associated with one's concealed identity impacts psychological distress directly and indirectly on the basis of the extent to which the identity is central and salient to the self. Cultural stigma, or degree of actual social devaluation associated with one's concealed identity, directly affects one's experience of psychological distress.

Alternative explanations

With correlational data it is impossible to definitively determine direction of causality or to rule out all possible alternative third-variable explanations. We can, however, offer additional analyses to identify plausible alterative models and compare such models to our hypothesized model in order to help draw useful conclusions from our data ( Tomarken & Waller, 2003).

First, it is possible that the directions of the causal relationships between the variables in the proposed model were different from how we theorized them to occur. In order to examine this alternative hypothesis, we tested the fit of a model in which centrality, salience, and cultural stigma were exogenous variables, and we examined the direct and indirect effects of these two variables on anticipated stigma and distress. Path coefficients largely replicated the original model, but this alternative model showed slightly worse fit for the data, χ ²(1) = 2.61, ns, CFI = .99, RMSEA = .07, AIC = 40.6. In addition, the AIC for the alternative model was higher (40.6 vs. 36.6), indicating that our hypothesized model is preferred.

Second, it is possible that our model may fit well for only particular subgroups of participants. One such alternative is that the model fitted for only the mental illness group. To test for the possibility that those in the mental illness group (who were also likely high in depression and anxiety) were driving our results, we tested an alternative model without them. This model fit equally well, χ ²(2) = 0.21, ns, CFI = 1.00, RMSEA = 0.0, AIC = 36.2. All of the path coefficients were of similar weight, and all remained significant. Thus, our original hypothesized model fit equally well for people whose concealable stigmatized identity was not mental illness.

Likewise, given that our sample was predominantly female, it may also be plausible that this model fit the data better for women than for men. Thus, we ran the model separately for men and women. Our hypothesized model fit well for both women, χ ²(2) = 1.32, ns, CFI = 1.00, RMSEA = 0.0, AIC = 37.3, and men, χ ²(2) = 0.40, ns, CFI = 1.00, RMSEA = .00, AIC = 36.4, when examined separately.

Finally, a third alternative explanation is that there was some general personality factor or style-such as a proneness to be more negative, anxious, or neurotic-that was predicting both distress and the stigma variables. While we cannot rule out all possibilities, we did collect a measure of rumination. Rumination is a style of thinking in which people chronically brood on negative thoughts. Consistent with previous research (e.g., Nolen-Hoeksema, Stice, Wade, & Bohon, 2007), the relationship between rumination and distress was quite strong in our sample ( r = .61). To help rule out the possibility that such a personality variable might account for the relationships found between our identity-related stigma variables and distress, we conducted an additional linear regression. In the first step, we entered rumination. As expected, rumination was a strong predictor of distress (β = .61, p < .001). In the second step, we entered our identity-related variables: anticipated stigma, centrality, salience, and cultural stigma. If a negative coping style such as rumination explained the relationship between the identity variables and distress, the relationship between the identity variables and distress should drop to nonsignificant. They did not. Each of the variables remained significant predictors of distress at p < .05, with the exception of cultural stigma, which slipped to p = .06. Thus, even controlling for a major psychological vulnerability factor toward depression and negative thought, anticipated stigma, centrality, salience, and cultural stigma remained predictive of psychological distress.

Examining Associative Stigma

Our final set of hypotheses for these data examined whether there were differences in the reported distress level for people with associative versus personal stigma and whether these differences were mediated by the lower levels of anticipated stigma, centrality, and salience that people with an associative stigma (compared with personal stigma) are likely to possess. As predicted, compared with those with a personal stigma, participants with an associative stigma reported significantly less distress, less anticipated stigma, lower identity centrality, and less salience (see for means and standard deviations). Next, we examined whether the identity variables (centrality, salience, and anticipated stigma) were associated with distress for those with an associative stigma. Examining correlations for those with an associative stigma only, we found that centrality ( r = .35), salience ( r = .32), and anticipated stigma ( r = .37) were all significantly related to distress ( p < .01). Thus, despite the lower levels of distress, the relationships between the identity variables and distress were similar for people with an associative stigma and people with a personal stigma. Cultural stigma was not significantly predictive of distress ( r = .11, ns), but this was not surprising given there were only three different types of associative stigma (family members with mental illness, family members with addiction, and family members with abusive relationships), and all had fairly similar cultural stigma ratings (4.11 to 4.88).

Table 5

Finally, we examined whether the association between stigma type (associative vs. personal) and distress was mediated by the identity variables. As shown above, we know that possessing an associative stigma (vs. possessing a personal stigma) is associated with (a) less distress and (b) lowered mean levels of each of the identity variables. In addition, (c) each of the identity variables is significantly correlated with distress. In order to examine mediation with multiple mediators ( Kenny, Kashy, & Bolger, 1998), in the final step we examined whether the relationship between stigma type (associative vs. personal) and distress would be eliminated when the mediating variables are included. We conducted a linear regression predicting distress in which the categorical variable of stigma type (coded 0 = associative stigma, 1 = personal stigma) was entered in the first step, and the three identity variables (centrality, salience, and anticipated stigma) were entered in the second step. As predicted, stigma type was significant in the first step (β = .16, p < .01), but this relationship dropped to zero (β = -.01, ns) when the identity variables were entered, each of which were significant predictors of distress.

Because we were examining multiple correlated mediators, we used a method developed by Preacher and Hayes (2008) to produce the path coefficients presented in . Bootstrapping and use of multivariate coefficient products resulted in practically identical results. We first examined whether the total effect of stigma type on distress ( B = 0.24, p < .01) was accounted for by the mediators when they were considered as a group. When the three mediators were included, the direct effect of stigma type on distress was reduced to zero ( B = −0.02, ns), mirroring the effect shown when using simultaneous regression above. shows that each path coefficient was significant at p < .01. In addition to accounting for a significant amount of the distress as a group, each of the indirect paths could be examined. The indirect effects for each path were computed while controlling for the effects of the other mediators. Each indirect effect was significant ( p < .01), with a point estimate of .12 for anticipated stigma, .08 for centrality, and .07 for salience. In summary, people with an associative stigma reported less distress than did those with a personal stigma, and this difference was completely mediated by the higher levels of anticipated stigma, identity centrality, and identity salience of people with personal concealed stigmatized identities.

Discussion

In the current study we sought to test a model for predicting psychological distress for people with concealable stigmatized identities. To our knowledge, this is the first test of a framework combining both intraindividual variables and an external variable for predicting distress. In support of our hypotheses, the extent to which people anticipate social devaluation if the identity is revealed, the more central the identity is to the self, the more salient the identity is, and the extent to which the identity is considered culturally stigmatized each uniquely predicted variance in psychological distress in a sample of participants with a wide variety of concealable stigmatized identities.

In order to gain insight into the processes of how stigma can ultimately impact distress levels, we used structural equation modeling to simultaneously examine the direct and indirect effects of anticipated and cultural stigma on distress through centrality and salience. As predicted, we found that cultural stigma-a measure of devaluation completely external to the study participants- had a direct effect on distress but no indirect effects through centrality or salience. Anticipated stigma, however, had a more complicated relationship to distress. The direct effect from anticipated stigma to distress remained strong, but anticipated stigma also worked indirectly through its relationships with centrality and salience. Thus, people who anticipate social devaluation and rejection if they reveal their identity also report greater centrality and salience of the identity, which in turn relate to increased reports of distress. To our knowledge, these results are the first to provide a general framework for understanding the mechanisms through which stigma impacts the lives of those who live with a concealable stigmatized identity.

Our sample also afforded us the chance to examine associative stigma. Three of the identities in our sample stemmed from associations with stigmatized family members, including family members with mental illness, addictions, and abusive relationships. Although the magnitude of the correlations between each of the stigma variables (anticipated stigma, centrality, and salience) and distress were the same for people with personal stigma versus associative stigma, people with an associative stigma reported less anticipated stigma, centrality, salience, and distress. Further, we found that the difference in level of distress was completely mediated by anticipated stigma, centrality, and salience. Thus, our theoretical framework holds across a broad spectrum of concealable stigmatized identities, including those characterized as either personal or associative stigmas.

Study 1 provided initial support for our framework examining how anticipated stigma, centrality, salience, and cultural stigma relate to psychological distress in a sample of people with concealable stigmatized identities. These findings are important because they extend previous theorizing to the context of concealable stigmatized identities and allow researchers to further understand the phenomenological experience of living with such an identity. However, given the novelty of our approach, we wanted to replicate our general pattern of findings in a second sample of people with concealable stigmatized identities. Further, we chose to extend the model by examining the effects of stigma on health.

Study 2

Stigma has been frequently linked to poorer health outcomes (for reviews, see Major & O'Brien, 2005; Williams et al., 2003). Stigma's role in negative health consequences is multiply determined, including indirect effects on health through psychological distress (i.e., the two are often strongly comorbid) and direct effects on health through increased stress of both experiences of discrimination and institutionalized discrimination built into the health care system.

In Study 2, we tested a model in which anticipated stigma, centrality, salience, and cultural stigma predicted psychological distress and illness symptoms (see ). Consistent with the results from Study 1, we expected to replicate the pattern of direct and indirect effects between the stigma-related variables and psychological distress. We also predicted, on the basis of a large body of work showing that psychological distress and negative health outcomes are highly comorbid (e.g., Gallo, Armenian, Ford, Eaton, & Khachaturian, 2000; Knox et al., 2006; Penninx et al., 1998), a strong direct relationship between the experience of psychological distress and illness symptoms.

Our hypotheses for the relationships between anticipated stigma, centrality, salience, and cultural stigma and illness symptoms were more tentative because they had not been previously examined. Because previous research has shown effects of perceived prejudice and experienced discrimination on health (e.g., Katz & Nevid, 2005; Kessler et al., 1999), we hypothesized that both anticipated stigma and cultural stigma would have direct effects on the experience of health problems. We had no a priori reason to predict that centrality and salience would have direct effects and thus predicted that they would only indirectly affect health outcomes through the experience of psychological distress.

In sum, by testing the pattern of relationships shown in , we aimed to replicate the pattern of findings in Study 1 and to examine how these stigma variables impact health outcomes for people living with a concealable stigmatized identity.

Method

Participants

We used the same recruitment strategy as noted in Study 1. However, we used a new method to determine eligibility: Students were presented with a checklist and were asked to indicate whether they were currently concealing any of the 13 identities we examined in Study 1. A total of 3,956 students were prescreened with the checklist over the course of 3 semesters. Of these, 1,063 (27%) reported possessing a concealable stigmatized identity and were eligible to sign up for the study. Because the study was completely anonymous, we did not link participants' answers in prescreening to their data collected in the study. Once participants came to the study, they were asked to describe their concealed identity in their own words, just as was done in Study 1. A total of 272 participants completed the survey. Of these, 235 participants indicated a codable stigmatized identity and were included in analyses. Participants completed the survey as partial fulfillment of a course requirement. Participants were predominantly female (63.0%) and Caucasian (82.6%), and the mean age was 18.87 years ( SD = 1.38).

Procedure

Procedures of Study 2 replicated those of Study 1. Participants were first given the same explanation of a concealed identity. The participants were then asked to describe their hidden experience or identity in their own words and were told that it would be referred to as their "concealed identity" in the survey.

Measures

Nature of the concealed identity

Although participants were eligible to complete this study only if they indicated during the prescreening session that they had one of the 13 different types of stigmas we examined in Study 1, participants were again asked to write about their concealed identity in an open-ended essay. Two raters coded these open-ended responses into one of the 13 types of identities we examined in Study 1 (see the second column of for the full list and frequency counts). Responses that were considered uncodable (e.g., the question was left blank or the response did not include enough information for the coders to categorize it) or that did not fall into these 13 categories because they were not clearly stigmatized (e.g., death of a family member, past failures on important exams, hidden temper) were excluded. Interrater reliability was again high (κ = .89), and discrepancies were resolved through discussion. As with Study 1, participants indicated living with their concealed identities for a mean length of time of approximately 5 years.

Anticipated stigma

In order to assess the extent to which people thought they would be socially stigmatized if they revealed their identity, we had participants complete the same 15-item scale used in Study 1 (α = .96).

Identity centrality

We used the same modified version of the Importance to Identity subscale of the Collective Self-Esteem scale ( Luhtanen & Crocker, 1992) used in Study 1 to examine the centrality of the concealable stigma to self (α = .74).

Identity salience

Participants completed the same one-item measure used in Study 1 to assess the frequency with which they reported thinking about their concealed identity. Again, responses were converted to a response rate of times per day for analyses.

Psychological distress

Only the 20 items from the CES-D were used as a measure of psychological distress for this study (α = .93).

Illness symptoms

The Pennebaker Inventory of Limbic Languidness (PILL; Pennebaker, 1982) was used to assess current illness symptoms. The PILL is a 54-item assessment of common physical symptoms and sensations (e.g., chest pain, nausea, coughing), and validation studies show that scores on the PILL are related to the actual number of physician visits within the past year, the number of days that activities of daily living have been limited due to health problems, and the number of work absences due to health problems ( Pennebaker, 1982). Participants were asked to rate the frequency with which they had experienced each symptom on the following 5-point Likert scale: 1 ( have never/almost never experienced symptom), 2 ( less than 3- 4 times per year), 3 ( every month), 4 ( every week), 5 ( more than once each week). The PILL is scored by summing the total number of symptoms that participants indicated experiencing once every month or more (i.e., scores of 3, 4, or 5). Consistent with findings from prior research that has utilized the PILL (e.g., Pennebaker, 1982; Richards, Beal, Seagal, & Pennebaker, 2000; Sloan, Marx, & Epstein, 2005), the internal reliability of this scale was high (α = .95).

Cultural stigma

Because our sample in Study 2 consisted of the same types of concealable stigmatized identities that we assessed in Study 1, we used the same ratings of cultural stigma that were reported in Study 1.

Results

Descriptive information about the sample is given in -. Generally, means and standard deviations for all variables were similar to those found in Study 1. Again, for the sake of completeness we examined whether there were differences between men and women in the mean levels of each of the variables. Men and women did not significantly differ in level of depression, health outcomes, anticipated stigma, centrality, or cultural stigma (all ps > .47). There was a marginal difference in salience levels reported (men = 1.86, women = 2.44), t(228) = −1.9, p = .06.

Again, there was a great deal of variability in centrality, with mean level of centrality just above the midpoint of the scale. The salience of concealed identity also ranged across the whole scale, although overall salience was higher in this study compared with that in Study 1. Approximately 16% of the sample reported thinking about the identity once a month or less, whereas 58% reported thinking about the identity once a day or more. Mean levels of anticipated stigma were again relatively low. Scores on the depression inventory revealed relatively high levels of depression, with 66% of the sample falling above the cutoff point of 16 used to diagnose depression ( Radloff, 1977). Participants reported a mean sum of 17.28 ( SD = 11.10) on the PILL, which is similar to the mean sums reported in the original validation study for the PILL ( M = 17.9, SD = 4.5; Pennebaker, 1982) and subsequent research utilizing this measure ( M = 21.6, SD = 11.2; Sloan et al., 2005) among college samples.

Predicting distress and health

Again we used structural equation modeling to test a model of the direct and indirect effects of anticipated stigma, centrality, and salience on distress and illness symptoms. Direct maximum likelihood estimation of missing data was used to allow information from the full sample ( N = 235) to be used in the analyses. Each of our variables was represented as a measured variable in the model. Anticipated stigma and cultural stigma again acted as the only exogenous variables in the model, and they were again correlated in order to represent the causal influences of variables not measured in the model ( Kline, 2005). We first tested the full, saturated model. Unlike in our Study 1 model, the paths from anticipated stigma to salience, and from cultural stigma to distress, were nonsignificant (all ps > .40), so they were deleted from the model. Additionally, as predicted, the paths from cultural stigma to centrality, centrality to illness symptoms, and salience to illness symptoms were also nonsignificant (all ps >.40), so they were also deleted from the model. The trimmed model (see ) fit the data well, χ ²(5) = 3.07, ns, CFI = 1.0, RMSEA = .00, AIC = 47.07, and all remaining paths were significant (all ps < .05) except for the path from salience to depression, which was marginally significant ( p = .08). The model accounted for 19% of the variance in depression and 19% of the variance in reported illness symptoms.

We then replicated the series of alternative models we tested in Study 1. We tested the fit of a model in which centrality, salience, and cultural stigma each acted as exogenous variables, and we examined the direct and indirect effects of these three variables on anticipated stigma and distress. Path coefficients largely replicated the original model, and this alternative model provided adequate fit for the data, χ ²(5) = 4.13, ns, CFI = 1.0, RMSEA = .00, AIC = 48.13. The chi-square, CFI, and RMSEA fit indexes of this alternative model were similar to those obtained in our hypothesized model, although the AIC for the alternative model was slightly higher (48.13 vs. 47.07), indicating that our hypothesized model was preferred.

We also tested an alternative model without participants who reported a mental illness. This model fit similarly well, χ ²(5) = 6.78, ns, CFI = .98, RMSEA = .05, AIC = 50.79. All of the path coefficients were of similar weight, and all remained significant. Thus, our original hypothesized model fitted equally well for people whose concealable stigmatized identity was not mental illness.

Likewise, given that our sample was predominantly female, it may also be plausible that this model fit the data better for women than for men. Thus, we ran the model separately for men and women. Our hypothesized model fit well for both women, χ ²(5) = 4.06, ns, CFI = 1.00, RMSEA = .00, AIC = 48.08, and men, χ ²(5) = 6.52, ns, CFI = .94, RMSEA = .06, AIC = 50.52, when examined separately. Although the fit statistics were lower for the men-only model than for the women-only model, these statistics indicate that their data did fit the model on the basis of conventional values.

Discussion

We sought to replicate the basic pattern of results of Study 1 and use our conceptual framework to examine self-reported illness symptoms. Study 2 again demonstrated that anticipated stigma, centrality, and salience directly predicted distress. Anticipated stigma also affected distress indirectly through centrality but not through salience. Interestingly, cultural stigma did not directly predict psychological distress but it did predict illness symptoms.

As expected, distress (as measured by depression) was the strongest predictor of illness symptoms. Anticipated stigma also had a direct effect on illness symptoms, signifying that the more people believed others would devalue them if their identity were known, the more illness symptoms they experienced. Moreover, cultural stigma directly predicted illness symptoms-people who possessed identities that were more culturally devalued reported greater illness symptoms. However, contrary to our expectations, anticipated stigma was not significantly related to salience, and cultural stigma had a small but significant effect on one intraindividual variable, salience, which was marginally related to distress. Taken together, the results present a framework for understanding how intraindividual factors and external stigma can impact both psychological distress and health for people living with concealable stigmatized identities.

General Discussion

Despite the fact that both researchers and practitioners have acknowledged that stigma is a powerful predictor of life outcomes ( Link & Phelan, 2006; Major & O'Brien, 2005; DHHS, 1999), current research lacks a thorough understanding of how stigma affects psychological and health well-being. Furthermore, social psychological research examining the effects of stigma has been largely one-sided, focusing predominantly on visible stigmas such as race and gender (for reviews, see Crocker et al., 1998; Major & O'Brien, 2005). In the current research, we proposed, and found support for, a conceptual framework that can be used to examine how both intraindividual factors (i.e., anticipated stigma, centrality, and salience) and an external factor (i.e., level of cultural stigma) are related to psychological distress and illness symptoms for people who live with a concealable stigmatized identity.

Study 1 demonstrated that anticipated stigma, centrality, salience, and cultural stigma each independently relate to greater psychological distress among people who live with concealable stigmatized identities. Study 1 also showed that the effect of anticipated stigma on distress occurred through its impact on centrality and salience. Thus, the intraindividual experience of stigma had both direct and indirect effects on psychological well-being.

Study 2 largely replicated these results. Again, we demonstrated that anticipated stigma, centrality, and salience had a direct effect on psychological distress, although the effect of salience on distress was weaker than that of the other variables. Further, Study 2 results demonstrated that the effect of anticipated stigma on distress also occurs indirectly, although its effects occurred via only centrality and not salience. Importantly, in order to get a more holistic sense of how stigma impacts people's psychological and health well-being, we examined how these processes impact both psychological distress and illness symptoms. These results demonstrated that anticipated stigma does have a direct and negative effect on both psychological and health well-being and that cultural stigma has a direct effect on health well-being. However, the effect of the other intraindividual processes- centrality and salience-may impact health only indirectly, by predisposing people to experience more psychological distress.

Results from the current research give greater theoretical insight into the role of stigma in the lives of people living with a concealable stigmatized identity. We took a multidimensional approach to examining the effect of stigma on psychological distress by assessing both anticipated and cultural stigma. Examining anticipated stigma is particularly important for people with concealable stigmatized identities. If their identity is truly concealed from most people they come into contact with, then they may have experienced little direct discrimination. Instead, knowing that their identities are devalued and potentially being exposed to hostile talk and attitudes about their identity by unknowing others (e.g., Wahl, 1999) will lead them to anticipate that others will devalue them if their identities become known. Although participants' reported levels of anticipated stigma were relatively low (they did not think it was highly likely that others would discriminate against them if they revealed the identity), they were a strong predictor of psychological distress and directly predicted poorer health functioning. Similar to identity threat ( Steele, Spencer, & Aronson, 2002), stigma has an insidious, undermining effect even in the absence of direct discrimination. The worry and concern about possible devaluation alone can lead to negative outcomes.

In addition, our measure of anticipated stigma addressed some of the conceptual murkiness of previous measures. In our measure we ask directly, "If others knew your concealed identity, how likely would the following be to occur ...," followed by a host of potential types of discrimination and social rejection. Previous research has tended to ask to what extent people know the stereotypes about their group or agree with the stereotypes rather than ask whether they think discrimination is likely to happen to them personally. We believe this is a real strength of the measure and more directly taps the way that a concealed stigmatized identity impacts the self. People often do not know what will happen when they reveal the identity, but their concerns about it will likely affect their behavior.

Stigma does not take place solely within the individual; instead it originates from the social devaluation attached to a particular identity within the society. Although social scientists recognize the social construction of stigma, we rarely attempt to measure it. In the current work, we developed a novel measure of cultural stigma in which we obtained ratings of relative devaluation of each of the identities represented in our samples, and then we used the external stigma ratings to predict distress and health. We found that this external measure of stigma was related to distress (in Study 1) and health (in Study 2), even controlling for the effects of the intra-individual variables. By demonstrating the power of cultural stigma, we hope to highlight that stigma does not occur solely within the individual.

In addition to developing new measures of anticipated and cultural stigma, we sought to address a theoretical quandary about centrality. We found that centrality is positively related to distress, signifying that the more central the identity is to the self, the more distress is reported. Although people with visible stigmas may reap psychological benefits from identity centrality because they can utilize mechanisms that provide group-based social support and attributional processes (e.g., Crocker & Major, 1989), according to our data identity centrality seems to render people who live with a concealed identity more vulnerable to distress. That is, because they may anticipate and experience prejudice due to their identity but cannot necessarily use their group-based identity to buffer themselves from these negative outcomes, people whose concealed identities are central to their self-definition may be increasingly susceptible to psychological distress. This finding points to the necessity for more nuanced work on different types of stigmatized identities. While we believe many of the concerns and experiences of people living with concealed versus visible identities overlap, the dimension of visibility may shape identity and coping in some fundamentally different ways ( Quinn, 2006).

Results also showed that people whose concealed stigmatized identity is highly salient in their daily lives report increased psychological distress. Previous experimental works shows that actively hiding a salient stigmatized identity results in more cognitive work due to increased concern with controlling and suppressing thoughts about the stigmatized identity ( Smart & Wegner, 1999). Likewise, dealing with increasingly negative and intrusive thoughts about an identity ( Major & Gramzow, 1999) is related to more distress. Thus, the current work maps onto previous work showing that the more frequently a person is thinking about a stigmatized identity, the more distressing the identity is likely to be. More research is needed to answer whether the distress results from the increased cognitive work of hiding information ( Smart & Wegner, 1999), from the potential feelings of shame or inauthenticity that come from hiding an important part of the self ( Kelly, 2002), or from a close relationship between identity frequency and intrusive thoughts about being stigmatized ( Major & Gramzow, 1999). Moreover, while we treated salience as a trait-level variable, it is likely that particular situations make the identity more or less salient. Thus, identity salience may fluctuate more than do centrality or anticipated stigma on a day-to-day basis. It is also possible, however, that people learn to avoid contexts that are related to the identity, thereby working to keep the level of salience relatively stable.

Beyond adding to the literature on anticipated stigma, cultural stigma, centrality, and salience, we also examined associative stigma in Study 1. Although the concept of associative, or courtesy, stigma has been around in the psychological literature since at least the 1960s, and the larger concept of family stigma (e.g., that disgraced family members taint the honor of the whole family) is strong in many cultures around the world, there has been little research on the psychological ramifications. In our sample, three of the concealed identities stemmed from associations with stigmatized family members, including family members with mental illness, addictions, and abusive relationships. As with people reporting personal stigmas, those reporting associative stigmas were also affected by the anticipated stigma, centrality, and salience of the identity. The differences in mean levels of centrality, salience, and anticipated stigma also lend concurrent validity to these measures. That is, if they are important variables related to stigmatized identities, they should be lower for people with less stigmatized identities and higher for people with more stigmatized identities. That is exactly what we found.

Limitations

There are several limitations to the current research. First, because we focused on explicating general processes, and because we have only small numbers of many of the identities, it is not possible to test our model on each specific identity. Thus, we must be cautious about whether these variables will be equally predictive for different concealable stigmatized identities. Future research could examine identities separately as well as add identity-specific variables to increase prediction (e.g., level of sexual assault activism for people who have experienced rape). The fact that the centrality, salience, and anticipated stigma variables predicted distress for both personal and associative stigmas supports the generalizability of the work across a range of identities. However, because the research was done with a college population, future work needs to examine whether the models generalize to both a broader adult population and to more specific and marginalized populations who may already be bearing the brunt of other stigmatized conditions such as homelessness and poverty.

Our primary goal in the current work was to establish a conceptual framework for understanding which factors may undermine psychological and health well-being for people with concealable stigmatized identities and to provide data to substantiate the basic structure of this model. In this work, we examined the utility of our basic conceptual model by imposing a set of causal relationships on our data and examining whether these relationships adequately fit the data across two separate samples. Results indicate that this basic structure adequately represented the relationships among these variables across both studies. However, it is important to keep in mind the limitations of structural equation modeling. The nature of these relationships represents the specific covariance structure of our data, a structure that may have some degree of variability depending on the makeup of the sample in question. This variability is likely one reason why the impact of cultural stigma on psychological distress did not replicate in Study 2. The relationships between cultural stigma and other variables are especially tied to the composition of the identities that our participants possessed and the degree to which these identities were socially stigmatized. Thus, given that the proportion of each type of identity (and its concomitant social stigmatization) varied from Study 1 to Study 2, this variability will inevitably influence the results of our analyses. Therefore, although we expect that future work will replicate the basic pattern of results that we have obtained across two separate samples, the specific path weights and relative fit of this model in other samples will ultimately depend on the unique covariance structure of those data.

Another limitation to the current research is its cross-sectional nature. With correlational data collected at only one point in time, it is not possible to establish causal direction. It is possible that people who are already distressed report more identity centrality, more salience, and anticipate more stigma from others. Although we tried to rule out several alternative models with additional analyses, a longitudinal design in which we collect distress and health data over multiple time periods is needed to further address questions of directionality. We expect that the relationship is likely bidirectional over time.

We examined several theoretically derived predictors of distress, but there are at least two important variables not included in our current model. The amount of discrimination actually experienced over the lifetime is likely to predict distress. Previous research has shown that people with mental illness report greater depression when they have had experiences of discrimination ( Markowitz, 1998) and rejection ( Link et al., 1997). Experiencing discrimination due to sexual orientation is positively related to loneliness and depression and negatively related to self-esteem ( Diaz, Ayala, & Bein, 2004; Ramirez-Valles, Fergus, Reisen, Poppen, & Zea, 2005). Thus, to the extent that people have revealed their identities to others, experiences of discrimination will be important to include in future work.

The current model also does not address issues around disclosure experiences. Previous research on disclosure of stigmatized identities (e.g., HIV, sexual orientation, child abuse, sexual assault, and mental illness) has shown that revealing the stigmatized identity can have a number of both positive (e.g., greater cognitive resolution, increased relationship closeness, and decreased feelings of isolation) and negative (e.g., increased trauma-related symptoms, loss of relationships, physical harm) consequences (e.g., Cain, 1991; Derlega, Winstead, Greene, Serovich, & Elwood, 2004; Gidron, Peri, Connolly, & Shalev, 1996; Herek, Gillis, Cogan, & Glunt, 1997; Lepore, Fernandez-Berrocal, Ragan, & Ramos, 2004). Thus, explaining disclosure and connecting it to other stigma-related feelings and cognitions is a particularly ripe area for future research.

Conclusion

At the broadest level, living with stigma- both visible and concealable- encompasses issues of identity and self-definition (centrality, salience, collective esteem), treatment and relationships (anticipated stigma, experienced stigma), outcomes (psychological distress, health, achievement, employment), and the social context in which people live (cultural stigma). Our work underscores the notion that the influence of these factors on well-being is neither simple nor direct. Some people exhibit distress; others do not. Some situations result in negative outcomes; some do not. The good news of stigma research is that many people, despite living in a culture that often devalues them, can be happy, resilient, and well adjusted. Ultimately, the goal for researchers is to be able to predict which people within stigmatized groups will be vulnerable or resilient and why. In this article, we have examined how this complex constellation of processes unfolds among those who possess a concealable stigmatized identity. In doing so, we have provided a conceptual framework that we hope will stimulate research efforts designed to understand the impact of stigmatized identities on all facets of well-being.

Acknowledgments

This research was supported by a University of Connecticut Research Foundation grant to Diane M. Quinn, and preparation of the article was supported in part by predoctoral Ruth L. Kirschstein National Research Service Award 1F31MH080651 to Stephenie R. Chaudoir. We thank Jennifer Crocker, Valerie Earnshaw, Rachel Kallen, and Jeffrey Sanchez-Burks for their comments on drafts of the article and Shondell Diaz, Karen Grudzinski, Zahra Nims, and Sarah Pennington for help with data collection and coding.

Footnotes

¹Throughout the article we use the term concealable stigmatized identities. We feel this term is most appropriate for two reasons. First it denotes that the person has an identity that is stigmatized by the broader culture. That is, the person does not have a "natural" or "innate" stigma but instead some sort of experience or attribute that has been culturally construed as stigmatized-a stigmatized identity. In this way we hope to both call attention to the cultural construction of stigma and avoid further dehumanizing people with stigmatized identities. Second, we use the word identity instead of mark, attribute, or label because we believe that part of the power of stigma is how it affects the self. Indeed, the presumption behind almost all psychological work on stigma is that the power of stigma is the power to change the self and identity. However, as we make clear in the sections on centrality and salience, simply possessing a stigmatized identity does not mean that it is central to the person's self-definition. Instead, people can and do vary in whether they feel the stigmatized identity is an important part of the self.

² The prediction is based on the assumption that the person regularly keeps the stigmatized identity concealed or closeted. To the extent that a person is "out" and the identity is no longer concealed, processes more akin to those of visible stigmatized identities may be applicable.

³ Because of the nature of concealed stigmatized identities, we designed this study to be as noncoercive as possible. We wanted participants to be able to easily not answer the questions or discuss their concealed stigmatized identity if they did not feel comfortable. We also did not want them to feel further stigmatized by participating. Thus, we built several safeguards into the design. The first was the description of a "concealed identity," which was deliberately written with neutral language and accompanied by both positive and negative concealed identities so that participants would not feel "marked" by being in the study-and so that if they wanted to write down some other, more neutral identity, they could. Second, in both studies, the data were submitted truly anonymously. We did not collect any identifying information with the data and we did not link the survey answers back to prescreening responses. Third, participants completed the survey in individual cubicles such that they would not feel that others knew they were in the study or wondered what they might have written about. Finally, we did carefully gauge their reactions at the end of the study for any indications of emotional upset, and we gave them a chance to write privately about what they thought of the study. There were no indications of negative reactions.

⁴ We also conducted the linear regression with gender and time since stigma onset in the first step. These variables were not significant predictors of distress and did not change the beta weights or significance of the rest of the variables.

⁵Given that the cultural stigma-psychological distress relationship did not replicate in Study 2, we tested whether this null relationship was due to the fact that we assessed only depression in Study 2 rather than the depression-anxiety composite measure of distress used in Study 1. We reanalyzed our model from Study 1, using only depression as our primary outcome (rather than a composite of both depression and anxiety). This model yielded similar fit, and the relationship between cultural stigma and depression remained significant (β = .12, p < .05). Using anxiety only (rather than the composite) as our primary outcome also yielded similar fit and a marginally significant relationship between cultural stigma and anxiety (β = .09, p = .08). Thus, the nonreplication of the cultural stigma to psychological distress relationship in Study 2 does not appear to have been driven by the fact that we did not include anxiety in this outcome.

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# data[].attributes.attachment_link.title
Living With a Concealable Stigmatized Identity: The Impact of Anticipated Stigma, Centrality, Salience, and Cultural Stigma on Psychological Distress and Health

# data[].attributes.attachment_link.description
J Pers Soc Psychol. Author manuscript; available in PMC 2015 Jul 22. Published in final edited form as: The current research provides a framework for understanding how concealable stigmatized identities impact people's psychological well-being and health.