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This video is about how Tim Farris dealt with a lot of depression at some point in his life and how it runs in his family, but he doesn't let that stop him from living his life. He has learned to control his stress and stop letting fear get in the way of his goals.

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Tim Ferriss: Why you should define your fears instead of your goals

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The hard choices -- what we most fear doing, asking, saying -- are very often exactly what we need to do. How can we overcome self-paralysis and take action? Tim Ferriss encourages us to fully envision and write down our fears in detail, in a simple but powerful exercise he calls "fear-setting."

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Cognitive-Behavioral Therapy is a Success
Is Cognitive-Behavioral Therapy just as successful as medication?
The essay provides evidence that shows CBT is just as successful as taking medication which allows people who don't want to put chemicals in their body, or who have negative side effects to have an alternative method of getting better. There are many studies mentioned in this essay that has been done on people who experience struggles with the disorder and mental illnesses that prove CBT does work.

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After doing research and finding out that CBT helps people who have disorders, I decided to interview my friend who struggles with OCD. According to my friend, he confirms that “Taking medication for my OCD has a lot more negative effects on me than good ones, which is why I choose not to take it, even though my doctor insists I do.”

This quote he said is important because it shows that in some cases, taking a medication to relieve something, in his case-control his OCD, he has more negative side effects that cause multiple different issues than the initial issues he would have to face with OCD only.

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The academic journal by Zhang(s), Jin, and Zheng explains that CBT is a major factor that helps reduce the risk of relapsing when it comes to Major Depressive Disorder. This supports my claim that not only does CBT help with treating disorders, but it also helps with reducing the risk of relapse. "There were evidences that for MDD patients in remission, CBT was an effective intervention for relapse prevention at either short or long term follow-up" (Zhang(s), Jin, and Zheng).

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The academic journal by Liyanage, Suraweera, and Rodrigo explains how a young student Miss J battles with an atypical form of anorexia and underwent an enhanced form of Cognitive-Behavioral Therapy (CBT-E)  and was successfully treated by it. This supports my claim because CBT was able to treat a patient with an odd case of anorexia nervosa. "This case report suggests enhanced cognitive behavioral therapy is effective for atypical presentations of eating disorders in a nonwestern setting. Miss J presents with restrictive eating, the hallmark diagnostic feature of anorexia nervosa. However, in her case, restrictive eating is not driven by fear of weight gain which is known as nonfat phobic anorexia nervosa" (Liyanage, Suraweera, and Rodrigo).

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In the book "The Brain: The Story of You" by David Eagleman, he talks about how negative thoughts can lead to faster cognitive decline. This supports my claim because mental illnesses like Major Depressive Disorder and any form of anxiety is focused around negative thoughts which causes the brain to age faster, leading to long term issues. "...negative psychological factors like loneliness, anxiety, and depression, and proneness to psychological distress were related to more rapid cognitive decline" (Eagleman, 31).

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This is a very subjective question. Meaning it always depends on who you're asking. Because none of this has yet to be "proven" people will argue for This is a very subjective question. Meaning it always depends on who you're asking. Because none of this has yet to be "proven" people will argue for whoever's research and theories they agree with. I can give you some of my own personal (and I try really hard to be objective and steer clear of opinions, but that will always have a role so that's just my warning label of sorts, ha) but because this is such a big topic today it'd help if you were more specific... do you mean subconscious mind just basically like how we make decisions, fears, etc or do you want to go deeper meaning the abnormal subconscious mind and/or subconscious mind of trauma, etc. there are so many good out there. If you want recs let me know, but another good way to find is to do a bit of research online and/or going to a book store and looking at several books that deal with your specific questions... I hope this helps! ...more (less)

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This is a very subjective question. Meaning it always depends on who you're asking. Because none of this has yet to be "proven" people will argue for This is a very subjective question. Meaning it always depends on who you're asking.

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Describes that taking medication or going through Cognitive-Behavioral Therapy target the brain in different ways. This supports my claim because it shows that undergoing therapy targets the brain in a natural way while taking medication targets the brain to prevent negative thoughts, but has to be taken consistently in order to work. "For example, the mechanism behind the effectiveness of cognitive therapy for patients with MDD could be through an increase in prefrontal function, which is involved in cognitive control, while antidepressant medications operate more directly on the amygdala, which is involved in the generation of negative emotion" (Karlsson).

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Plastic changes in the brain have been difficult to study in humans, but there has been more success in animal studies. Changes in the brain in relation to experience have been detected at the cellular and molecular levels in animals using different experimental approaches. The advent of functional neuroimaging, including single photon emission CT (SPECT), positron emission tomography (PET), and functional MRI, has made it possible to study changes at the brain systems level (by measuring changes in brain blood flow or metabolisms) and, increasingly, also on the molecular level using SPECT and PET in the living human brain.
Brain system level studies on the effects of psychotherapy
So far, nearly 20 studies on brain changes after psychotherapy for depression, anxiety disorders, and borderline personality disorder have been published (Table). The first study was published nearly 20 years ago, in 1992. In this study, the researchers compared behavior therapy with fluoxetine treatment. Both treatment modalities demonstrated similar changes in the brain-especially in the caudate nucleus.

Drawn together, these system level studies suggest that cognitive-behavioral therapy (CBT), dialectic behavior therapy (DBT), psychodynamic psychotherapy, and interpersonal psychotherapy alter brain function in patients suffering from major depressive disorder (MDD), obsessive-compulsive disorder, panic disorder, social anxiety disorder, specific phobias, posttraumatic stress disorder, and borderline personality disorder (BPD). ³⁻¹⁶

The majority of these studies have reported similar brain changes after psychotherapy and medication. However, some recent studies have also shown clear differences among these treatment modalities. In the study by Goldapple and colleagues, ⁵ treatment response for CBT in patients with MDD was associated with increases in metabolism in the hippocampus and dorsal cingulate and decreases in the dorsal, ventral, and medial frontal cortex. This pattern was clearly distinct from the pattern caused by paroxetine, which included increases in metabolism in the prefrontal areas and decreases in the hippocampus and subgenual cingulate. In the recent study by Karlsson and colleagues, ¹⁷ clear differences emerged between short-term psychodynamic psychotherapy and fluoxetine among patients with MDD.
From brain changes to mechanisms of psychotherapy
In addition to just reporting the findings on brain changes as a result of psychotherapy, some of these studies have made it possible to construct models that explain the mechanisms behind the changes that result from the different psychotherapies. These models can then be compared with the psychological theories of these psychotherapies.

Many psychotherapies attempt to enhance patients' problem-solving capacities, self-representation, and regulation of affective states. The brain areas that play a role in these functions include the dorsolateral prefrontal cortex, ventral anterior cingulate cortex, dorsal anterior cingulate cortex, ventral and dorsal subregions of the medial prefrontal cortex, posterior cingulate cortex, precuneus, insular cortex, amygdala, and ventrolateral prefrontal cortex. (For a review, see Frewen et al. ¹⁸)

For example, the mechanism behind the effectiveness of cognitive therapy for patients with MDD could be through an increase in prefrontal function, which is involved in cognitive control, while antidepressant medications operate more directly on the amygdala, which is involved in the generation of negative emotion. ¹⁹

Because one of the major hypotheses regarding the effect of CBT on brain functioning concerns a more effective ("top-down") regulation of hyperexcitable limbic structures by prefrontal control systems, it seems that psychodynamic psychotherapy may also function, at least in part, via these mechanisms. The findings from a study by Beutel and colleagues ¹⁰ are in line with this hypothesis and demonstrate both a frontal deactivation and an amygdala-hippocampal hyperactivation seen in symptomatic patients with panic disorder. When their panic symptoms and anxiety levels were reduced following treatment, the frontal deactivation and amygdala-hippocampus hyperactivation were normalized.

Affective hyperarousal is the hallmark of BPD and the main target for DBT. This would mean that DBT leads to a decrease in the activity in relation to emotional stimuli in the brain areas that serve these functions. This was indeed found in the study by Schnell and Herpertz, ¹⁵ whose findings suggest that after DBT, there is a decrease in hemodynamic response to negative stimuli in the right-sided anterior cingulate, the temporal and posterior cingulate cortices, and the left insula.
Molecular psychodynamics
All these studies, however, have investigated the brain changes on the whole brain systems level. To understand the more basic mechanisms related to psychotherapy, possible molecular and cellular changes should also be studied. So far, only 2 Finnish studies have measured molecular level changes after psychotherapy, and in this way directly tested the hypothesis put forth by Kandel ² that psychotherapy could lead to changes in gene expression through learning, by altering the strength of synaptic connections between nerve cells and inducing morphological changes in neurons. Interestingly, in both studies, the psychotherapy that was used was psychodynamic.

In the study by Lehto and colleagues, ²⁰ 19 depressive outpatients received psychodynamic psychotherapy for 12 months. Of the patients, 8 were classified as having atypical depression. Midbrain serotonin transporter and striatum dopamine transporter densities were recorded using SPECT brain imaging with the [123I]nor-Î²-CIT radioligand before and after psychotherapy. The researchers showed that midbrain serotonin transporter density significantly increased during psychotherapy in patients with atypical depression, but not among patients with standard depression. There were no changes in the levels of striatum dopamine transporter. Because of the subgroup finding, these results are difficult to interpret, and one of the shortcomings of this study is the lack of a control group.

In the other Finnish study, patients with MDD were randomized to receive either short-term psychodynamic psychotherapy or fluoxetine. Before being treated and after 4 months of treatment, they underwent a brain scan with PET using [carbonyl-11C]WAY-100635 (measures the density of serotonin type 1A [5-HT 1A] receptors) and [11C]raclopride (measures density of dopamine type 2/3 receptors). In the 2 published papers, the researchers reported that the clinical outcome in both treatment groups was similar in terms of standard symptom ratings (symptom remission was achieved in 59% of the patients and 77% of the patients met criteria for response). 17,21 However, an analysis of the change in the 5-HT 1A receptor density in the treatment groups revealed a significant increase in the psychotherapy group compared with the medication group, for which no change was detected (Figure). Fluoxetine increased [11C]raclopride binding in the lateral thalamus; no change was seen in the group that received psychotherapy.

Several previous studies have found changes in 5-HT 1A receptor binding in MDD that is not reversed by SSRI treatment. ²²⁻²⁷ This could mean that the recovery process in MDD after psychotherapy is different from recovery after medication. Currently, the clinical implications of these findings are unknown, but they may be related to the finding that suggests that the relapse rate for MDD is lower in patients treated with psychotherapy than in those treated with antidepressants. ²⁸
Conclusion
Although still preliminary, the studies using neuroimaging for measuring change caused by psychotherapy will in the long run lead to a more refined understanding of how different psychotherapies work. This may lead to a development in which specific modes of psychotherapy can be designed to target specific brain circuits. ¹ In addition, neurobiological research may help refine psychological theories about the change processes.

References:
References
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2. Kandel ER. A new intellectual framework for psychiatry. Am J Psychiatry. 1998;155:457-469.
3. Brody AL, Saxena S, Stoessel P, et al. Regional brain metabolic changes in patients with major depression treated with either paroxetine or interpersonal therapy: preliminary findings. Arch Gen Psychiatry. 2001;58:631-640.
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6. Baxter LR Jr, Schwartz JM, Bergman KS, et al. Caudate glucose metabolic rate changes with both drug and behavior therapy for obsessive-compulsive disorder. Arch Gen Psychiatry. 1992;49:681-689.
7. Nakatani E, Nakgawa A, Ohara Y, et al. Effects of behavior therapy on regional cerebral blood flow in obsessive-compulsive disorder. Psychiatry Res. 2003;124:113-120.
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9. PraÅ¡ko J, HorÃ¡cek J, ZÃ¡lesky R, et al. The change of regional brain metabolism (18FDG PET) in panic disorder during the treatment with cognitive behavioral therapy or antidepressants. Neuro Endocrinol Lett. 2004;25:340-348.
10. Beutel ME, Stark R, Pan H, et al. Changes of brain activation pre- post short-term psychodynamic inpatient psychotherapy: an fMRI study of panic disorder patients. Psychiatry Res. 2010;184:96-104.
11. Furmark T, Tillfors M, Marteinsdottir I, et al. Common changes in cerebral blood flow in patients with social phobia treated with citalopram or cognitive-behavioral therapy. Arch Gen Psychiatry. 2002;59:425-433.
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13. Straube T, Glauer M, Dilger S, et al. Effects of cognitive-behavioral therapy on brain activation in specific phobia. Neuroimage. 2006;29:125-135.
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23. Sargent PA, Kjaer KH, Bench CJ, et al. Brain serotonin 1A receptor binding measured by positron emission tomography with [11C]WAY-100635: effects of depression and antidepressant treatment. Arch Gen Psychiatry. 2000;57:174-180.
24. Bhagwagar Z, Wylezinska M, Taylor M, et al. Increased brain GABA concentrations following acute administration of a selective serotonin reuptake inhibitor. Am J Psychiatry. 2004;161:368-370.
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29. Nakao T, Nakagawa A, Yoshiura T, et al. Brain activation of patients with obsessive-compulsive disorder during neuropsychological and symptom provocation tasks before and after symptom improvement: a functional magnetic resonance imaging study. Biol Psychiatry. 2005;57:901-910.
30. Sakai Y, Kumano H, Nishikawa M, et al. Changes in cerebral glucose utilization in patients with panic disorder treated with cognitive-behavioral therapy. Neuroimage. 2006;33:218-226.
31. Apostolova I, Block S, Buchert R, et al. Effects of behavioral therapy or pharmacotherapy on brain glucose metabolism in subjects with obsessive-compulsive disorders as assessed by brain FDG-PET. Psychiatry Res. 2010;184:105-116.

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Plastic changes in the brain have been difficult to study in humans, but there has been more success in animal studies. Changes in the brain in relation to experience have been detected at the cellular and molecular levels in animals using different experimental approaches.

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Describes that more research is being done by scientists to prove that the brain changes when going to behavioral therapy, just like it changes when taking medication. This supports my claim because it backs up my thesis that behavioral therapy is just as effective as drug therapy (taking medication to treat the illness). “Like drug therapy, behavior modification therapy produces metabolic and functional changes in the brains of people with obsessive-compulsive disorder, scientists are reporting today” (Blakeslee).

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Credit... The New York Times Archives

This is a digitized version of an article from The Times's print archive, before the start of online publication in 1996. To preserve these articles as they originally appeared, The Times does not alter, edit or update them.

Occasionally the digitization process introduces transcription errors or other problems. Please send reports of such problems to archive_feedback@nytimes.com.

Like drug therapy, behavior modification therapy produces metabolic and functional changes in the brains of people with obsessive compulsive disorder, scientists are reporting today.

It is the first time that behavior therapy, a method that changes the way people think about uncomfortable thoughts or feelings, has been shown to physically alter brain function in a mental disorder, said Dr. Daniel X. Freedman, a psychiatrist at the University of California at Los Angeles and editor of The Archives of General Psychiatry, which is publishing the report.

The research strongly supports the idea that a specific brain circuit is responsible for obsessive compulsive disorder, or O.C.D., and raises hopes that other mental problems, like phobias, will similarly respond to behavior therapy, said Dr. Lewis Baxter, an associate professor of psychiatry and behavioral sciences at U.C.L.A. who led the new research.

Obsessive compulsive disorder afflicts 1 in 40 people and is more common than diabetes or asthma. People who have the disorder are besieged by unpleasant, unwanted, senseless thoughts or sensations which usually involve hygiene, violence or sex, and they feel compelled to act out these thoughts without deriving any enjoyment or reward.

"We are enthusiastic about Dr. Baxter's work," said Dr. Judith Rappaport, chief of the child psychiatry branch at the National Institute of Mental Health in Bethesda, Md. Many complex behaviors may be hardwired from birth in complex neurochemical circuits that can go awry, she said. Caution Is Urged

But Dr. Thomas R. Insel, a neurophysiologist at the mental health institute, warned that the imaging technique used in the study was extremely unreliable. To demonstrate functional brain changes before and after treatment, patients were injected with a radioactive sugar that passed into their brains from the bloodstream. Brain areas that were more metabolically active, and hence used more sugar, lit up under scanning devices.

But, Dr. Insel said, metabolic changes in one region of the brain may not have any links to a mental function and they may not even be related to the brain. Several years ago, he said, researchers claimed that a certain part of the brain "lit up" during panic attacks. But followup studies using more precise mapping techniques found that the "lit" areas reflected increased blood flow to the patients' jaw muscles, which clamped down during panic attacks.

Nevertheless, Dr. Baxter's study is important, Dr. Insel said, because two very different therapies had similar effects on identical brain regions. This points to but does not prove the existence of a single brain circuit underlying obsessive compulsive disorder, he said. Techniques of the Study

The study followed two groups of patients for 10 weeks, scanning their brains before and after treatment. One group took the drug Prozac, an antidepressant. The other met twice a week with a behavior therapist who taught them to recognize each obession, acknowledge it and learn to accept the urge without carrying it out. For example, people who feared contamination and constantly washed were made to tolerate dirt on their hands for over an hour each day. Gradually, the thoughts did not have the same imperative, Dr. Baxter said, adding, "People tell us the obessions don't capture their minds or beings in the same way."

After treatment, seven of the nine people treated with drugs and six of the nine in behavior therapy showed significant changes in the brain area where habit learning and complex movements are centered .

This region, the right caudate nucleus, was less active after both kinds of treatment, Dr. Baxter said. People with the most improvement in behavior showed the greatest amount of brain change. The five patients who failed to respond to either treatment did not show any brain changes, nor did two healthy volunteers who agreed to be scanned twice, he said. A Circuit in the Brain

The study points to a single brain circuit underlying obsessive compulsive disorder, Dr. Baxter said. This circuit has three correlated parts, which are hyperactive in untreated patients with the disorder.

The circuit begins in the orbital region of the frontal cortex, just above each eye. In evolutionary terms, it is an old part of brain involved in emotions, anger and worry, Dr. Baxter said. Here arise unconscious thoughts involving bodily excretion, disgust, aggression, sexual urges, violence and a host of disturbing impulses. Nerve fibers in the orbital region carry such impulses to the caudate nuclei lower in the brain for possible action.

Normally, Dr. Baxter said, the impulses are filtered out and not acted upon. The caudate nuclei serve as a "gate" that only lets the most powerful and important impulses through. "If I dropped you in a mountain of cow manure, you should feel uncomfortable until you wash," he said. "Some disturbing thoughts and threats should capture our attention and drive us to act on them until the danger has passed."

In a normal person, the spring on the gate is tight enough so that only significant impulses and thoughts can break through, Dr. Baxter said, but in obsessive compulsive disorder the gate is broken. Disturbing, worrying thoughts leak through and capture the rest of the circuit, a major brain relay station called the thalamus that reaches out to drive activity throughout the brain. As troublesome thoughts capture the person's mind, the loop tends to amplify itself, Dr. Baxter said.

After either drug or therapy treatment, the three parts of the circuit are no longer correlated, Dr. Baxter said. The whole system quiets down. Data From Second Study

At the mental health institute, Dr. Susan Swedo, chief of the unit in behavioral pediatrics, has followed patients with the disorder for one year after similar drug therapy. She found striking changes in the frontal orbital cortex and, unlike Dr. Baxter, no change in the caudate nucleus. Her study is described in today's issue of The Archives of General Psychiatry.

Both Dr. Swedo and Dr. Baxter said that their findings were probably compatible. It may be that after 10 weeks, changes occur in the caudate and after a year they occur in the orbital cortex, Dr. Baxter said. Both areas are hyperactive in patients with the disorder and less active after treatment.

Behavior therapy affects the same brain circuit, Dr. Baxter said. It may induce learning, which alters brain anatomy and hence brain function. But it is impossible to prove, with current imaging techniques, that anatomy has been affected, he said. "We can only infer functional change and that the brain changes when it learns."

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Behavior Therapy Can Change How the Brain Functions, Researchers Say

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This is a digitized version of an article from The Times's print archive, before the start of online publication in 1996. To preserve these articles as they originally appeared, The Times does not alter, edit or update them. Occasionally the digitization process introduces transcription errors or other problems. Please send reports of such problems to archive_feedback@nytimes.com.