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This article provides insight on to the different and contrasting components that make up the entire food system. The article gave me a better understanding as to how the food system works and what it actually means.

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Food System Basics

Food systems include the nuts and bolts of what it takes to move food from point A to point B along a supply chain. From labor and transportation to policies and climate, many factors influence how food gets from the farm to your fork.

We can also see food systems running at local, regional, national, or international levels. Production, processing, distribution, and consumption - food systems require many steps, each with a variety of inputs and outputs.

What Moves Food through the Food System?

In addition to the inputs and outputs listed for each step, the following are also present every step of the way:

Labor. Migrant farmworkers, farmer family members and community members, farmers' market staff, supermarket cashiers, meat plant workers, restaurant staff-it can require an incredible amount of human effort to get food from the field onto your plate. Providing workers a living wage and safe working conditions can help protect the people who make it possible for us to eat.

Energy. Try to picture all the fuel and electricity needed to power tractors, farm equipment, factories, delivery trucks, restaurants and grocery stores, and your kitchen appliance. The food system can be very energy-intensive, though some farmers like Milagro Farms seek to reduce dependence on fossil fuels by switching to renewable energy and finding sales outlets closer to home.

Waste. Food is packaged and repackaged as it moves through the food system, and there are losses at every step. Reducing packaging, recycling used packaging, and turning waste into biogas or compost can slash waste within the food system.

What Shapes the Food System?

These factors influence the food system as a whole:

Policy. Agricultural and food policyincludes the regulations producers need to follow to sell their goods, government aid to producers and consumers, trade agreements, and more. The last Texas legislative session led to some local food policy wins, such as limiting the permit fees farmers must pay for selling at multiple farmers' markets and making it easier to sell pickled and frozen fruits and vegetables. The current national farm bill increased funding for programs SFC champions, including conservation programs and SNAP.

Climate. Climate and weather patterns have always had a large impact on farming. There's no question the unpredictable weather patterns, extreme temperatures, floods, and droughts brought on by climate change add more uncertainty to the food system. Seed scientists are working to breed drought-resistant and heat-loving varieties that are adapted to local conditions. Many universities and research groups are searching for climate-smart ways to ensure that we can grow food and get it to those who need it for generations to come.

How You Can Strengthen Our Local Food System

Supporting our local food system can help our community become more resilient in the face of challenges like the current pandemic and climate change.

Shorter supply chains, less transportation, less processing, and more traceable and transparent production are all advantages of a local food system. Here are some tips for supporting a thriving Central Texas food system:

Buy local using our list of food access resources in Central Texas during COVID-19.

See if you qualify for food assistance, especially if your household income has dropped during the pandemic. With many local sales outlets accepting SNAP and WIC benefits, you can help keep food dollars local.

Further reading:

Thousands of Cars Line Up at One Texas Food Bank as Job Losses Hit Hard - NPR, 4/17/20

230,000 Texas Families Filed for SNAP Food Assistance in March, Twice as Many as Same Month Last Year - The Texas Tribune, 4/13/20

As Prices Fall, Texas Dairies Have to Keep Milking - KUT, 4/22/20

Market Disruptions, Low Prices Drive Texas Farmers to Plow Crops Under - San Angelo Standard-Times, 4/22/20

As COVID-19 Disrupts the Industrial Meat System, Independent Processors Have a Moment to Shine - CivilEats, 5/19/20

These 5 Foods Show How Coronavirus Has Disrupted Supply Chains - National Geographic, 5/19/20

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What Makes Up a Food System? Breaking it Down into 4 Parts

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What does our current food system look like, and how does it work? And if it's broken, how can we fix it? We take a look at the four main parts of our food system and the factors that influence them.

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Ogie goes into deep detail of the correlation between physical fitness and obesity, stating the importance that physical activity has on one's overall health. He addresses the main issue that most people have which is the mental block that occurs while pursing physical activity.

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Winning The Mental Battle of Physical Fitness and Obesity | Ogie Shaw | TEDxSpokane

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This TedTalk addresses how there may be more to weight loss than simply eating right and exercising. The speaker addresses how there is psychology behind it as well. The speaker did a great job explaining how psychology and health tie together

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The psychological weight loss strategy | Laurie Coots

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This article gives scientific insights from different perspectives on the different ways in which behavior works. This gave me a better understanding to human behavior in a more scientific way.

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When you try to understand people and explain why they do what they do, what frame do you use? The most common, intuitive (and highly useful) approach is the "belief-desire" frame. That is, people in everyday situations use both beliefs and desires to explain why people do what they do. For example, if we were to observe "Jon" leaving the house to go to the movies, we explain that action by assuming that Jon believes that the movie theater is playing a certain movie and seeing it is something he desires. We can be flexible with this frame. For example, if Jon were a movie critic, then we might presume his belief-desire state for seeing the movie is something different than if Jon were a teenager going to see the movie on a date with his new girlfriend.

Although belief-desire frames are helpful for everyday living, we need a more sophisticated, scientifically grounded frame for deeper understanding. The field of psychology has generated a wide variety of different paradigms, but unfortunately, these paradigms speak different languages and tell us different things about how to understand people. Skinnerian behaviorists claim that we need to get rid of terms like beliefs and desires, and empirically observe the kinds of effects that the environment has on the frequency of emitted behaviors. Cognitive psychologists use the language of information processing to explain beliefs and desires. Freudian theorists claim that conscious beliefs and desires ultimately play a pretty small role in explaining why people do what they do, and that the real drivers of human behavior are subconscious forces.

I am developing a more unified language for human psychology and psychotherapy. It takes the key insights from the cognitivists, behaviorists, psychodynamic theorists, and other paradigms (e. g., evolutionary psychology, Russian activity theory) and combines them into a more scientifically coherent (and comprehensive) system. When we look at human behavior via the unified system, three key processes frame our understanding.

The first key process is investment. The Unified Framework characterizes human behavior in terms of work effort directed toward effecting change. Whether Jon is headed out because he wants to see the movie, wants to critique the movie for his job, or wants to be with his girlfriend, his going to the movie is a form of investment. As suggested by the term investment, work efforts expended (which involve calculations about time, calories, opportunity costs, risks, and so forth) are directed toward particular outcomes. The return might be found in the joy he gets from the movie itself, from the fact that he completes an assignment for his job, or a kiss from his girlfriend at the end of it. Framed as such, we can then ask: Where do our tendencies toward investments come from? We are evolved primates, so evolution has primed us to value certain states of affairs (e.g., safety, territory, food, sex, higher social status) over others. In addition, people differ in terms of temperaments and dispositions, much of which is strongly influenced by genetics. Extroverted people find stimulating social situations more rewarding than introverted people. And, of course, one's learning history directly shapes the investment value system. If Jon loved the first two Star Wars movies, we are not surprised when we hear he has a strong desire to see the third.

The second key process is social influence. As Aristotle noted, we are an incredibly social animal, and one of the most important features of our environment is other people. And our action-investments rarely take place on an island, but they take place in the context of a social matrix. Social influence here refers to two things. First, it refers to the process by which one person's actions impact the investment of another person. In the current example, it would refer to the way it came about that Jon was going to the movies (did he ask her, she ask him, was there any tension in the process, etc). Important social influence processes involve competition, cooperation, and whether exchanges move people closer (i.e., become more dependent) or make them further apart (become more independent).

The second meaning of influence is as a resource. When considered as a resource, it refers to the capacity to move other people in accordance with our interests. Here it refers to the levels of respect and social value other people show us, the extent to which they listen, care about our well-being, and are willing to sacrifice for us. So, if Jon is attracted to his girlfriend and she agrees to go to the movie with him, that is an indicator of social influence as a resource. The harder Jon had to work to get her to go results in raising questions about his social influence. If she breaks up with him, that is a powerful indication of a loss of social influence.

The third core process is justification. In the language of the Unified Framework, "justification" is a broad concept that refers to both the systematic structure and the legitimizing function of verbal communication (including writing). You can think of justification as anything that involves questions and answers which lead to claims about what is and what ought to be. For example, if Jon explains to his girlfriend, "I saw the first two movies in the series and thought they were great," or says, "I am just happy to be with you, we can see whatever you want," both are "justifications." Likewise, if Jon (as a movie critic) gets a call and his editor asks if he has completed the write-up, there is a shared, if implicit, justification that Jon needs to do what his boss wants. Arguments, reasons for and against things, rationalizations, laws, and even scientific truth claims all are "justifications" in the unified language system. This blog is a justification for thinking about three core processes that explain why people do what they do.

If you want to achieve a better understanding of why people do what they do, consider starting with these three core processes. Human behavior is first and foremost a kind of "doing" or investing. Individuals do what they do because of either implicit or explicit cost-benefit analyses directed at certain outcomes. Then we can look to the social matrix to see the influence such investments might have on others or how the investment itself might be shaped by social influence factors. Finally, there is the explanatory system that people are using to make sense of the world around them and legitimize what they are doing and why. Keep in mind that even your analysis of the person's activity in terms of investment, influence, and justification is itself a kind of justification system. These processes line up quite well with common sense belief-desire psychology, and they are grounded in a scientifically unified view of human psychology.
Facebook Image: Vitaliipixels/Shutterstock LinkedIn Image: wavebreakmedia/Shutterstock

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When you try to understand people and explain why they do what they do, what frame do you use? The most common, intuitive (and highly useful) approach is the "belief-desire" frame. That is, people in everyday situations use both beliefs and desires to explain why people do what they do.

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This book summary describes, in depth, the major factors that influence body weight and what you can do to help maintain a weight or reach a goal weight.

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DEVELOPMENTAL DETERMINANTS

It has been postulated that there are times during people's lives when exposure to certain factors may increase their risk for the onset of obesity. These times have been termed "critical periods." If these critical periods, along with the influential factors, can be clearly defined, it may be possible to identify individuals at increased risk for the development and persistence of overweight and obesity in adulthood. The prenatal period, the period of adiposity rebound, and adolescence have been proposed as critical periods in childhood (Dietz, 1994); pregnancy and the immediate postpartum period have been proposed as critical periods for women in adulthood.

Prenatal Factors

Although the data are subject to a variety of interpretations, it has been documented in both animals and humans that females who are severely food restricted during the first one to two trimesters of pregnancy have progeny who have a higher prevalence of obesity, diabetes, insulin resistance, and hypertension later in life. Progeny of survivors of the Dutch famine in World War II demonstrated a higher prevalence of obesity and diabetes (Ravelli et al., 1976), although this conclusion was questioned by later studies (Jackson et al., 1996; Susser and Stein, 1994). Malnutrition in utero also has been reported to result in increased obesity and its complications later in life (Stanner et al., 1997). Lower birth weights also seem to be associated with increased upper body visceral adiposity in later life with its attendant increased risk of cardiovascular disease (Oken and Gillman, 2003; Rogers, 2003). Since individuals from a lower socioeconomic background are more likely to be exposed to malnutrition during gestation or early childhood, the prevalence of obesity in such subgroups might be expected to be higher.

Adiposity Rebound

Adiposity increases from birth until approximately 1 year of age, then declines to a minimum at approximately 6 years of age. The term "adiposity rebound" refers to the increase in body mass index (BMI) and body fat that occurs after this nadir in children between the ages of 5 and 7 years. Children experiencing adiposity rebound at an earlier age appear to have a three- to sixfold greater risk of increased adult BMI than do other children (Whitaker et al., 1998). He and Karlberg (2002) demonstrated, through the development of probability charts based on 3,650 children followed from birth to 18 years of age, that children who experienced this rebound before 8 years of age have a higher risk of adulthood obesity. However, Guo and coworkers (2000), using serial BMI data from the Fels Longitudinal study demonstrated that while there was no association between early age at adiposity rebound and adult BMI status in men, after controlling for effects of birth weight, adult physical activity, alcohol and cigarette use, there was approximately twice the risk for overweight with early rebound in women.

Causes of early adiposity rebound have been variously attributed to advanced skeletal maturity (Roland-Cachera et al., 1984; Williams and Dickson, 2002), high protein intake (Roland-Cachera et al., 1995), and parental BMI (Dorosty et al., 2000). Cameron and Demerath (2002) concluded after extensive review of the available scientific literature that the evidence is still not clear about whether age at adiposity rebound is a critical period for the development of obesity, but that early adiposity rebound might well be a statistical predictor of later obesity because of its strong relationship with early adiposity and accelerated maturation, both of which are established markers of later risk of obesity.

Adolescence

Although only 30 percent of adult obesity begins during childhood, 70 percent of the adult obesity that begins in childhood may start during adolescence (Dietz, 1994). Adolescent obesity is associated with a variety of adverse health effects in adulthood, including early mortality in men and increased risks of coronary heart disease, diabetes, and colorectal cancer (Miller, 1988; Must et al., 1992; Wylie-Rosett, 1988). Most of these risks were only slightly attenuated by adjustment for adult obesity, which suggests that obesity during adolescence may determine the risk of these later complications regardless of whether or not the individuals are obese adults.

While total fatness is an important consideration when evaluating developmental aspects of obesity, an additional consideration is adipose tissue distribution. Visceral adipose tissue has an independent effect on obesity-associated comorbidities (Emery et al., 1993) that is separate from that of total body fat, although the developmental aspects of visceral adipose tissue deposition have not been well studied. Among children, visceral adiposity appears to be associated with an increased risk of cardiovascular risk factors such as elevated triglycerides and reduced high-density lipoproteins that are independent of total body fat (Caprio et al., 1996; Gutin et al., 1994). However, the ages at which these relationships appear remain unclear. Cross-sectional studies suggest that visceral adipose tissue deposition is not marked before adolescence, but increases rapidly at that time.

Adulthood

The period after adolescence has not been intensively studied, although approximately two-thirds of adult obesity begins after adolescence. Whether additional critical periods exist in adulthood is less certain, but pregnancy and postpartum may constitute one such period for a subset of women (Williamson et al., 1994). Postpartum weight retention appears to range from 0.5 to 4.8 kg for most women (Johnston, 1991), but African-American mothers may be twice as likely to retain 9.1 kg (20 lb) or more postpartum than Caucasian mothers (Parker and Abrams, 1993). Boardley and colleagues (1995) found that African-American women ate more and were less physically active postpartum than were the Caucasian women in their sample. When the possible confounding factors of prepregnancy weight, gestational weight gain, prenatal physical activity, parity, and socioeconomic status were controlled, African-American women still retained more weight in the postpartum period than did Caucasian women. Results of several recent studies suggest that possible genetic factors may be involved in the tendency to retain weight postpartum. One study found that in women with normal prepregnancy BMIs, high first-trimester serum leptin concentrations (a protein hormone encoded by the obese gene) correlated with increased gestational weight gain and postpartum weight retention (Stein et al., 1998). In another study, women within 12 months of the birth of their first child who were homozygous for the 825T allele of the G-protein ß3, considered a "thrifty" genotype, had significantly higher BMIs and postpartum weight retention than women who did not carry the genotype (Gütersohn et al., 2000). No effect of the genotype was observed among women who had never given birth, suggesting a pregnancy-specific phenomenon. In addition, this relationship was only observed among women who engaged in low levels of physical activity, supporting the idea that physical activity may mitigate effects of genetic endowment on the potential for postpartum weight retention. Whether this particular genetic variation in this specific G protein is causally linked to the observed differences in BMI and weight retention or is merely a marker for the responsible mutation, as well as what the mechanism might be, are both questions that require further investigation (Feldman and Hegele, 2000).

GENETIC DETERMINANTS

The understanding of the genetic influences on overweight and obesity in humans has increased dramatically. Individuals show significant heterogeneity in their body weight and body fatness responses to altered energy balance, dietary components, and changing activity levels. It is now well-established that overweight and obesity have a significant genetic component, with estimates of the contribution of genetic variation to observed variation in obesity-related phenotypes (such as BMI, fat mass, and leptin levels) ranging from 30 to 70 percent (Comuzzie et al., 1993, 1994, 1996). However, little is yet known about the specific causes of heterogeneity (Pérusse and Bouchard, 1999). It seems clear that energy metabolism and neural control of appetite are involved in regulating body weight and may contribute to the etiology of obesity. Studies of resting metabolic rate show that the variation within families is less than the variation among families (Bogardus et al., 1986).

Several studies have evaluated the potential mechanisms by which genetic factors may contribute to obesity. One of the mechanisms by which differences in energy metabolism may contribute to obesity may involve defects in uncoupling proteins (UCP). Several types of uncoupling proteins have been identified. Fleury and colleagues (1997) first described human uncoupling protein 2 (UCP-2) and its links to obesity and hyperinsulinemia. Bouchard (1997) noted that markers near the UCP-2 gene in humans are linked to differences in resting metabolic rate. Thus, genetic differences in UCP-2, and perhaps other UCPs, may contribute to human obesity.

There is a group of at least 20 Mendelian syndromes in which obesity is a component, including Prader-Willi, Bardet-Biedl, Borjeson, Cohen, and Wilson-Turner (Gunay-Aygun et al., 1997; Reed et al., 1995). These genetic disorders are rare, and family studies do not suggest that the genes responsible for these syndromes are involved in the common forms of human obesity. For more than 99 percent of obese humans, the genetic basis of their obesity is unknown.

Animal Models of Genetic Obesity

The strongest evidence for genetic weight-regulating mechanisms is the recent elucidation of single gene defects that are associated with excessive weight gain in animals. Single gene mutations can indisputably cause obesity in both rodent models and in humans. In rodents, such mutations have been identified in at least five genes: the obese gene for the circulating adipose tissue-secreted factor leptin; the db gene for the receptor of leptin; the agouti yellow mutation, which controls hair color in mice through the production of melanin pigments (with its human equivalent, agouti signaling protein gene); the fat mutation in the carboxipeptidase E gene, which is a prohormone processing enzyme; and the tub mutation, the function of which has yet to be determined. Of the five gene products that currently have been associated with weight regulation, leptin is the best characterized. Genetic defects in leptin are associated with extreme obesity in both humans and laboratory animals. In addition, serum concentrations of leptin are elevated in close proportion to body fat in obese people with no defect in the leptin gene. Recent studies show that administration of recombinant leptin to lean and obese individuals results in dose-dependent weight loss (Heymsfield et al., 1999). Further research is needed to assess the potential role of leptin in obesity treatment.

Familial Aggregation of Risk for Obesity

Using the comprehensive Danish adoption registry, Stunkard and colleagues (1986) found that adopted children who were raised separately from their biological parents had body weights closer to those of their biological parents than to those of their adoptive parents. The children in this study were separated from their parents at a very early age, generally before 3 months, so the opportunity for the biological parents to instill eating and activity habits was very limited. Another study of adoptees showed a significant genetic influence on obesity, but none of the environmental indicators evaluated were found to contribute, although a number of the conditions considered have previously been associated with obesity (Sorensen et al., 1998). Stunkard and colleagues (1986) estimated that as much as 70 percent of the variance in the occurrence of obesity could be attributed to genetic factors, but other authors have postulated that as little as 20 percent of the variance is due to genetic factors. The general consensus is that genetic factors account for about 30 to 50 percent of the variance in the occurrence of obesity (Bouchard, 1997).

Twin studies provide the most impressive clinical evidence that genetic factors play an important role in the etiology of obesity in humans. Stunkard and colleagues (1990) studied identical and nonidentical twins who were reared together and others who were reared apart. They found a high correlation of body weight among identical twins, even if they were reared apart. Bouchard and colleagues (1990) studied twins who were isolated in the Canadian wilderness with no access to foods other than those provided by the investigators. Identical twins were overfed for a period of 100 days, and their gains in body weight and adipose tissue were evaluated. There was a closer association of both body weight and intra-abdominal adipose tissue (visceral fat) within twin pairs than among twin pairs.

The maximal heritability of obesity has been estimated to range from 30 to 50 percent, based on a review of family studies (Chagnon et al., 2000). Although extensive efforts have been made to identify mutations in the genes identified as obesity-associated in rodents and in other candidate genes for obesity in humans, to date only a handful of individuals have been identified with mutations in any of the genes that have produced obesity in rodents. Specifically, several humans have been identified with mutations in the leptin gene or its receptor, but no individuals have yet been found with mutations in the other genes identified in rodents.

In total, single gene mutations have been identified as responsible for obesity in 25 persons, with these mutations appearing in 7 genes (12 different mutations) (Pérusse et al., 1999) or in 5 genes (Chagnon et al., 2000). Studies of quantitative trait loci (QTL) in rodents have suggested at least 98 different QTLs associated with obesity (Chagnon et al., 2000).

Currently, the major effort in the search for specific genes that contribute to human overweight and obesity is based on the use of genome scanning. In genome scanning, linkage analysis is conducted to identify QTLs that affect the specific phenotype under study. The use of genome scanning has provided evidence of QTLs that influence body weight and the number of fat cells (Chagnon et al., 2000).

Comparison of the risks of obesity in spouses and in first-degree relatives has suggested that genetic factors may be of greater prominence in more severe obesity (Katzmarzyk et al., 2000). Among the members of families that contain at least one morbidly obese person, a major gene effect was transmitted in a codominant fashion, suggesting a gene-environment interaction (Rice et al., 1999). Both multifactorial and major gene effects have been suggested. Efforts are ongoing to identify the genetic and molecular basis of overweight and obesity, and it is likely that many genes (and within these genes and their promoters, many different mutations or variants) that are responsible for the genetic variation of obesity in humans will be identified.

The development of obesity likely involves a combination of shared environment and shared genetic propensities. The rapid increase in prevalence of obesity in the United States, as well as in many other countries, across all age groups may reflect a removal of environmental constraints (e.g., high levels of daily activity and food availability) on the expression of obesity genotypes. Knowledge of the genetic components of obesity is not likely to be useful to the military in the near term, but identification of markers of potential risk of obesity may well have implications for future screening.

AGE

Cross-sectional and longitudinal studies indicate a gradual increase in the average BMI of Americans up to the ages of 50 to 60 years (IOM, 1995). This trend is similar, with some variation, across males and females and across all evaluated ethnic groups. Population studies also indicate a decline in body weight and BMI among the elderly, usually in the seventh and eighth decades (IOM, 1995; Kuczmarski et al., 1994; NHLBI, 1998). The same trends have been identified in changes in total body fat and percent body fat (Chumlea et al., 2002). Overweight and obesity thus reach maximal rates among middle-aged adults. This pattern is shown in Figure 3-1.

The age-related body mass increase up to the fifth and sixth decades is accompanied by additional anatomical, structural, and body compositional changes. Stature declines from about age 30 onward, with rates in women faster than those in men and for postmenopausal women faster than their premenopausal counterparts. Declining stature accounts for a small portion of the age-related increase in BMI (Gallagher et al., 1996).

Many weight-management experts agree that body weight becomes progressively more difficult to maintain with age, but there appears to be little rationale for increasing the upper BMI range consistent with good health as individuals become older. Williams (1997) indicated that body weight and associated circumferences would increase with advancing age unless food intake is reduced and physical activity is substantially increased.

A large number of cross-sectional studies, however, do demonstrate that body fat increases with age, even after controlling for changes in body weight and physical activity levels (Baumgartner et al., 1995; Flynn et al., 1989; Forbes, 1987; Forbes and Reina, 1970; Gallagher et al., 1996, 1997; Noppa et al., 1980; Novak, 1972; Steen et al., 1979). Gallagher and colleagues (1996) demonstrated that the mean body-fat content in nonexercising civilian women with a BMI of 25 increased from 30 percent for those between the ages of 17 and 20 years to 36 percent for those ages 40 years and older. The implication of this is that lean body mass and, frequently, skeletal mass, decrease with age. Additionally, partitioning of adipose tissue between the subcutaneous and visceral compartments is also moderated by age (Borkan et al., 1983). Men have more visceral adipose tissue than do women at all ages, and the rate of visceral adipose tissue increase with age is greater in men than in women (Blaak, 2001).

In contrast to body fat, skeletal muscle mass declines with age beginning around the third decade of life (Dutta and Hadley, 1995). This observation is true not only for the general population, but it is also evident in military personnel (USAF, 1975). The rates of decline may accelerate after the onset of menopause in women (Aloia et al., 1991) and for both genders in the seventh and eighth decades (Flynn et al., 1989). Losses of skeletal muscle parallel changes in skeletal minerals with advancing age and are present even after controlling for loss in body weight (Gallagher et al., 2000). The mechanisms of body composition change with aging are multifactorial and include physical inactivity, diet, and hormonal and cytokine alterations. The loss of lean mass and gain in fat mass occur even with no apparent change in body weight. Since lean mass contributes the larger share of metabolic activity, total energy expenditure during rest or low activity will also decrease proportionally with the loss of lean mass.

Total energy expenditure and thus, energy requirements, decrease with advancing age (Tzankoff and Norris, 1978). Physical activity levels are lower in older individuals, which account for a portion of the energy expenditure reduction that comes with aging. Resting energy requirements are also lower in the elderly, due largely to decreases in all metabolically active tissues, including skeletal muscle, brain, and visceral organs. In laboratory animals, the heat produced by tissues per unit of mass decreases with age (a decrease in the specific resting energy expenditure of organs), but it remains uncertain whether this observation also applies to humans. The practice of resistance training by people over the age of 50 years may enhance fat-free mass, primarily skeletal muscle, and thereby help offset the age-related decline in resting metabolic rate (Hill and Saris, 1998; Tzankoff and Norris, 1977). In women, loss of ovarian function accounts for a lower rate of overall heat production compared with that observed in premenopausal women (Poehlman and Tchernof, 1998). Thus, both older men and women have lower rates of energy expenditure and, unless counterbalanced by increased physical activity and reduced food intake, older individuals, in general, will gain weight over time.

RACE/ETHNICITY

Whether there are racial/ethnic differences in response to the various components of weight management is a legitimate research question that has been explored to only a moderate extent. Data from National Health and Nutrition Examination Surveys (NHANES) clearly indicate that there are racial/ethnic differences in the prevalence of overweight and obesity. Flegal and coworkers (2002), reporting on 1999-2000 NHANES data, determined that in men 20 years of age and older, the prevalence of overweight (BMI ≥ 25) was 67.4 percent for non-Hispanic whites, 60.7 percent for non-Hispanic blacks, and 74.7 percent for Mexican Americans. The differences were not statistically significant, but sample sizes were relatively small. However, for women ages 20 years and older, the prevalence of overweight was 57.3 percent in non-Hispanic whites, 77.3 percent in non-Hispanic blacks, and 71.9 percent in Mexican Americans. The difference in prevalence between non-Hispanic white and non-Hispanic black women was statistically significant (Flegal et al., 2002). The causes of these differences in the prevalence of overweight have not been clearly identified, but are likely to be a combination of physiology, culture, and behavior.

The relationship of BMI to percent body fat is also affected by race/ ethnicity. Fernandez and colleagues (2003) recently reported the results of an analysis of 11 cross-sectional studies involving body composition assessments of African-American men and women, Hispanic-American men and women, and European-American men and women. The average age ranged from 42.6 to 50.8 years, and the average BMI ranged from 25.1 (European-American women) to 29.8 (African-American women). Total body fat was measured using dual-energy X-ray absorptiometry. There were no differences in the estimation of percent body fat from BMI for men across ethnic groups. However, for women with BMIs less than 30, Hispanic-American women had a significantly higher percent of body fat at a given BMI than did African-American or European-American women. However, at BMIs greater than 35, European-American women had a higher percent body fat than either of the other two groups of women. Some earlier studies have reported greater fat free mass in African-American women compared with Caucasian women with the same BMI, primarily due to the greater skeletal mass in African-American women (Gallagher et al., 1996; Ortiz et al., 1992).

A number of studies have examined possible physiological reasons for these race/ethnic differences. Foster and colleagues (1997) explored differences in resting energy expenditure (REE) between obese African-American women and Caucasian-American women. They found that REE was most closely correlated to body weight and that African-American women had lower REE than Caucasian-American women. Melby and coworkers (2000) examined behavioral and physiological characteristics related to obesity risk in young, sedentary, nonobese African-American and Caucasian-American women. The two groups were similar in age and anthropometric characteristics. Parameters examined included REE, respiratory exchange rates (RER), insulin sensitivity, and maximal oxygen consumption. REE was 3 to 4 percent lower in African-American women, but the difference was not statistically significant. However, the resting RER was significantly lower in African-American women. The African-American women also had significantly lower insulin sensitivity values that resulted in higher acute phase insulin response to glucose. Total daily energy expenditure and physical activity energy expenditure were significantly lower in the African-American women.

Tanner and coworkers (2002) recently identified a relationship between muscle fiber type and obesity. In a study of lean and obese African-American and Caucasian women, type I muscle fibers (slow twitch, oxidative muscle fibers) were significantly reduced in obese women compared with the lean women, and type IIb fibers (fast twitch, glycolytic muscle fibers) were significantly increased. These differences between lean and obese women were greater in African-Americans than in Caucasians. The type IIb phenotype is insulin resistant and deficient with regard to lipid disposal. The authors speculated that the prevalence of the type II fibers might result in partitioning lipid toward storage in skeletal muscle or adipose tissue rather than oxidation within the skeletal muscle, resulting in a positive fat balance.

A number of studies have also examined social and behavioral factors that may contribute to the difference in the prevalence of overweight between African-American and Caucasian women (Kumanyika et al., 1993; Stevens et al., 1994). Attitudinal and behavioral factors that limit the ability of some African-American women to lose weight or maintain weight loss have been identified. Regardless of whether or not they were overweight, African-American women were half as likely as Caucasian women to consider themselves overweight. There is a much greater cultural tolerance of overweight among African-Americans, and they have different body image perceptions. Although African-American women responded physiologically to a weight-reduction program in the same manner as Caucasian women, their drop-out rate from the program was double that of Caucasian women (Glass et al., 2002).

PHYSICAL ACTIVITY

While recent studies point to the importance of genetic factors in the etiology of obesity (Bouchard, 1997; Chagnon et al., 2000), the rapid rise in the prevalence of overweight and obesity in the last 20 years likely reflects major environmental shifts in exercise habits and food availability, which can be controlled.

Physical activity represents an important component of volitional energy expenditure. Modern transportation and other conveniences have reduced the need for energy expenditure in the form of physical exertion. Reductions in physical activity over the past several decades likely contribute to the evolution of the positive energy balance and weight-gain characteristics of all industrialized societies. Lack of physical activity begins in youth, with television watching time correlated with BMI, as well as with both prevalence and severity of overweight (Dietz and Gortmaker, 1985; Katzmarzyk et al., 1998; Tanasescu et al., 2000). A reduced emphasis on school physical education classes has been accompanied by a gradual decline in childhood fitness (Luepker, 1999). Indeed, physical inactivity is a major risk factor for development of obesity in children and adults (Astrup, 1999; Goran, 2001). Among adults who have maintained weight loss over time, a common factor is increased physical activity (Klem et al., 1997).

The effects of physical activity on weight and health may be influenced by age. Owens and coworkers (1992) evaluated the effects of physical activity on both weight change and the risk factors for cardiovascular disease during the perimenopausal period. Women who increased their activity levels during the 3-year study period (as measured using the Paffenbarger Physical Activity Questionnaire) had the smallest increases in body weight and the smallest decrement in high-density lipoprotein cholesterol.

Flatt (1987) has pointed out that to avoid increased fat deposition, both energy balance and macronutrient balance (especially fat balance) are necessary. When dietary fat is elevated, there is limited capacity to reduce total body fat by fat oxidation. Exercise, especially in bouts of 30 minutes of activity or more (Pate et al., 1995), can promote fat oxidation because the substrate that is preferentially oxidized switches from carbohydrate to fat. Thus, chronic extended bouts of exercise may, in effect, substitute for expansion of the adipose tissue, allowing the physically active individual to achieve fat balance while maintaining a lower body-fat mass than the sedentary individual (Flatt, 1987). Jakicic and coworkers (1995) initially demonstrated that over the short term, four 10-minute bouts of exercise per day, four times per week is more effective in reducing body weight than a single 30 to 40 minute period of exercise. However, the long-term data indicated that the short-term bouts of exercise were not as effective as the long bouts in reducing weight and maintaining weight loss (Jakicic et al., 1999).

Most fatty-acid oxidation in the human body occurs in muscle (Calles-Escandon and Poehlman, 1997). The intrinsic capacity of muscle to oxidize fat can be impaired by physical inactivity and possibly by loss of estrogen in women, but it is amenable to partial correction by exercise training (Calles-Escandon and Poehlman, 1997). A decrease in aerobic capacity and fat-free mass, rather than aging per se, is responsible for the decrease in fat oxidation seen in elderly women (Calles-Escandon and Poehlman, 1997). Exercise training increases oxidative disposal of fatty acids and improves muscle metabolism in both young and old individuals. However, the elderly do not increase fat utilization in response to exercise to the same extent as the young, despite performing exercise to the same intensity and for the same duration (Blaak, 2000; Calles-Escandon and Poehlman, 1997).

In a study of 970 healthy, female twins with a wide range of percent body fat, both total body fat and central adiposity were associated with physical activity (Samaras et al., 1999). Moderate-intensity sports of 1 and 2 hour durations accounted for within-pair differences of 1.0 kg and 1.4 kg, respectively, of total body fat. Among participants in whom one of a pair of twins was overweight, higher levels of physical activity were still associated with 3.96 kg lower total body fat and 0.53 kg lower central abdominal fat. In other words, even persons with an apparent genetic predisposition to adiposity showed an effect of physical activity on body-fat mass (Samaras et al., 1999). Studies of energy expenditure in individuals and families show that differences are greater between families than within families (Bogardus et al., 1986). Some differences in energy expenditure between families are due to genetic factors and some are due to differences in activity patterns.

Hormones affect the relationship of physical activity, body fat, and fat-free mass. Guo and coworkers (1999) found that associations between physical activity and fat-free mass were more pronounced in postmenopausal women than in premenopausal women, and that hormone replacement therapy had beneficial effects on body composition. Monozygotic twin pairs who were concordant for smoking and hormone replacement therapy status, but discordant for moderate-intensity activity, showed greater within-pair differences in total body fat than those who were concordant for activity level (Samaras et al., 1999), suggesting that the effect of physical activity is greater than that of hormonal status.

Habitual physical activity also affects other physical characteristics. Gilliat-Wimberly and coworkers (2001) found that an association exists between habitual physical activity and maintenance of resting metabolic rate in middle-aged women. Physical activity also may reduce the incidence of chronic diseases by favorably altering blood lipid profiles, reducing body fat, and improving lean body mass (Eliakim et al., 1997; Schwartz et al., 1991; Wei et al., 1997; Wilbur et al., 1999).

FOOD

Intake

In conjunction with the importance of physical activity levels, energy intake must be matched to energy expenditure. Positive energy balance results if energy intake is greater than energy expenditure. Increased energy consumption, decreased energy expenditure, or both can result in positive energy balance.

While the etiology of obesity is multifactoral, the common characteristic of all obese people is excessive energy storage in the form of body fat. Whether obese people consume more energy than do lean people has been a major source of controversy. Studies in modern respiratory chambers using doubly-labeled water have shown that weight-stable obese people have a higher resting metabolic rate and total 24-hour energy expenditure than do lean people (Jequier and Schutz, 1983; Ravussin et al., 1982; Zed and James, 1986), which demonstrates that average energy intake must indeed be higher in the obese. Some differences in energy expenditure, and consequently in energy intake, among families are due to genetic factors and differences in activity patterns. Social and cultural factors also contribute to individual food intake differences (de Castro, 1999).

Since the energy in food is derived from the macronutrients protein, fat, and carbohydrate (CHO), plus the optional energy source, alcohol, diets that are high in fat tend to be low in complex CHOs such as fiber. There is still considerable controversy over whether the role of diet composition or simply total energy intake is important in maintaining a healthy body weight.

Composition

A high energy intake or an energy intake that is not adjusted downward with declining physical activity or age-related decreases in lean body mass is associated with the development of overweight or obesity in susceptible individuals. In addition to total energy intake, the character of the diet may play a role in the etiology of obesity. High-fat diets may promote increased energy intake or may be associated with metabolic changes that promote the deposition of adipose tissue.

Dietary Fat

Research in both animals and humans suggests that high-fat (low in complex CHOs) diets promote obesity (Astrup et al., 2000; Bahceci et al., 1999; Blundell and Cooling, 2000; Cheverud et al., 1999; Maffeis et al., 2001). Because fat is more energy dense than other foods (9 kcal/g versus 4 kcal/g for protein and CHO), eating high-fat foods results in a greater energy intake than would eating a similar quantity of lower-fat foods. Fat modifies the taste of food and, in some people, promotes excess intake. Fatty foods tend to be easier to chew or may not require chewing, thus making larger quantities easier to eat in a shorter time than foods that require more mastication. Dietary fat also has a weaker satiation effect than CHOs, which results in the over consumption of fat (Rolls and Hammer, 1995; Rolls et al., 1999).

Some of the difference in weight gain on a high-fat versus a low-fat diet may be explained by differences in the metabolic processing of fat. Compared with dietary fat, CHOs require additional energy expenditure for digestion, assimilation, and conversion to fat. When energy intake exceeds expenditure, 23 percent of energy consumed is required to convert and store CHO as fat, compared with only 3 percent to store fat. Two studies in laboratory animals have demonstrated this effect of dietary fat on body weight and body composition (Donato and Hegsted, 1985; Lin et al., 1979).

The link between dietary fat and obesity in humans is not conclusive because of difficulties in accurately measuring or controlling the food intake and energy expenditure of individuals and the need to rely on estimates of body composition. Nonetheless, increasing evidence from clinical studies suggests that dietary fat promotes weight gain in humans as well as in animals. Studies in which people were overfed diets varying in the proportion of energy from fat (40 to 53 percent of kcal as fat) showed that high-fat diets promoted weight gain more efficiently than did lower-fat diets (Sims et al., 1973).

A positive correlation between the proportion of fat in the diet and the incidence of obesity has been noted among various cultures, as well as within ethnic groups that have migrated to the United States and adopted American dietary patterns (Curb and Marcus, 1991; Kushi et al., 1985). While these correlations all point to a causal role for dietary fat in obesity, they are subject to confounding variables such as differences in energy intake and expenditure, health status, and genetic and environmental influences. However, based on information such as that described above, Danforth (1985) recommended shifting to a higher-CHO and lower-fat diet to reduce the high prevalence of obesity in affluent societies such as the United States.

Obesity is more closely correlated with the level of dietary fat than with total energy intake (Dreon et al., 1988; Romieu et al., 1988). A low incidence of obesity has been observed among vegetarians who typically consume low-fat, high-CHO diets (Knuiman and West, 1982; Sacks et al., 1975). However, those who adhere to vegetarian diets for religious rather than nutritional reasons probably have a higher-fat diet (Dhurandhar and Kulkarni, 1993), and the prevalence of obesity among these types of vegetarians is high compared with that of omnivores (Dhurandhar and Kulkarni, 1992).

Some studies have failed to demonstrate an association between fat intake and body weight in free-living populations. On the basis of food frequency questionnaires, Macdiarmid and colleagues (1994) stratified 1,800 people by their fat consumption (high was considered to be 45 percent or more kcal as fat and low was considered to be 35 percent or less kcal as fat) and found no statistically significant difference in age, BMI, or social class between the two groups. However, the high-fat group rated their general diet and health as poorer. The high-fat group also consumed significantly more protein and total energy, but less CHO and fiber; consumed meat and high-fat dairy products more frequently; and consumed fewer fruits, vegetables, and cereals.

Results of a small study suggest that the amount of energy required to maintain body weight may be related to the proportion of fat in the diet, regardless of an individual's weight status (Prewitt et al., 1991). These findings suggest that dietary fat may promote greater weight gain and body-fat accumulation than expected on the basis of energy intake alone. In contrast, Leibel and colleagues (1992) found no relationship between the ratio of dietary fat/CHO and the total energy required to maintain body weight. CHO ranged from 15 to 85 percent of total intake, and kcal from fat ranged from 0 to 70 percent of total intake. The disparity between findings of these two studies may be due to the shorter duration of the second study (33 days average and ranging from 15 to 56 days compared with 140 days in the Prewitt study). Differences among the normal-weight patients in the study of Prewitt and colleagues (1991) were not seen consistently before 13 to 16 weeks. Also, body composition was not assessed in the Leibel study, and results of animal studies suggest that isocaloric diets of varying fat content may produce differences in percent of body fat without changing body weight (Boozer et al., 1990, 1993).

The arguments for whether dietary fat promotes obesity were summarized in two recent, competing editorials. Willett (1998a, 1998b) argues that obesity has increased in the United States despite reductions in intake of dietary fat and that ecological studies have found no relationship between fat intake and obesity. In contrast, Bray and Popkin (1998) argue that individuals who gained weight may not have decreased (or may have increased) their intake of dietary fat. They also argue that ecological studies may not be appropriate to study the relationship between fat intake and obesity, that body weight is a poor measure of body fatness, and that most of the previous studies focused on outcomes other than obesity. Although the literature is not clear, results of studies on laboratory animals and the small number of human studies suggest that dietary fat does promote obesity. Recently, Astrup and colleagues (2002) reviewed evidence on the effects of low-fat diets. Four meta-analyses of weight change occurring on low-fat diets in intervention trials with overweight subjects were reviewed. These analyses consistently demonstrated significant weight loss in both normal-weight and overweight subjects.

Carbohydrates

Several rationales have been postulated for the use of high-protein, low-CHO diets: (1) intake of a high proportion of kcal as CHO has adverse physiological consequences, such as increasing insulin secretion, promoting fat deposition, and increasing serum triglycerides levels; (2) low-CHO diets can lead to a "ketogenic" state, which has been hypothesized to suppress appetite; (3) a high-protein diet preserves lean body mass during weight loss; and (4) the thermogenic effect of protein is the highest of the three macronutrients, resulting in increased energy expenditure for a similar intake.

There is at least some scientific rationale for the above hypotheses (Skov et al., 1999a, 1999b). A high-protein diet has been found to: stabilize blood glucose during nonabsorptive periods and reduce insulin response following test meals (Layman et al., 2003b), improve glucose oxidation (Piatti et al., 1994), decrease lipid oxidation (Piatti et al., 1994), produce positive changes in blood lipids (Layman et al., 2003b), and provide greater satiety than diets higher in CHO (Layman et al., 2003a). Although more research is needed on the subject of amino acid flux measurements and how it relates to blood glucose levels, data from Layman and colleagues (2003b) support the idea that the ratio of dietary protein and CHO can have a significant effect on metabolic balance and specifically on glucose homeostasis during weight loss.

The role of CHO in soft drinks in producing obesity is controversial. Some studies suggest that an increase in the consumption of soft drinks may have contributed to the increased prevalence of obesity (French et al., 2000; Troiano et al., 2000), whereas others do not support this hypothesis (Gibson, 2000; Macdiarmid et al., 1998; O'Brien et al., 1982).

Portion Size

There is little research available on the role of portion size in the increasing prevalence of overweight in the United States. However, common sense dictates that it is a contributing factor. For example, a single serving of meat is considered to be 3 to 4 oz based on the Dietary Guidelines and the U.S. Food Guide Pyramid. However, in restaurants (where Americans are spending a greater portion of their food dollars), an 8-oz portion of red meat would be considered a "petite" serving; the standard serving would be 12 to 16 oz. Thus, an individual consuming a 16-oz steak in a restaurant would be likely to report (if asked in a dietary survey) consuming a single serving of red meat, when in reality 4 to 5 servings were consumed.

The intake of soft drinks has increased dramatically in the last 40 years, as has the trend towards larger portion sizes (Hill and Peters, 1998). While a standard serving of a soft drink in 1960 consisted of one 6-oz serving, the standard size serving today is 12 oz, and many vendors sell 20-oz bottles almost exclusively. Fountain drinks have also increased to the "super-jumbo" 32- to 64-oz sizes. It is not unusual for individuals to consume some 500 to 1,000 kcal per day from soft drinks in addition to their usual solid-food diet.

The change to larger portion sizes has been particularly apparent in fast-food restaurants where portion size has been used as a competitive tool. Full-service restaurants also have adopted the practice of serving larger meals. Similar to the increase in soft drink portions sizes, fast-food restaurants now offer "super-size" portions for a minimal increase in cost. For example, a "jumbo super-size" order of a large hamburger, french fries, and soft drink at a fast-food restaurant may now contain more than 1,500 kcal for a single meal (Nielsen and Popkin, 2003; Young and Nestle, 2002, 2003). One of the distinguishing features of dining out in Europe compared with the United States is the difference in restaurant portion sizes, a factor that may contribute to the lower prevalence of obesity in Europe.

A recent trend analysis of portion size was conducted by Nielsen and Popkin (2003). Data were taken from four national food-consumption surveys covering the period 1977 to 1996. Food consumption was estimated as energy intake in kcal and as average portion sizes using food models to assist respondents in identifying portion size. Results demonstrated that for foods eaten both inside and outside the home, portions sizes have increased for salty snacks, desserts, soft drinks, fruit drinks, french fries, hamburgers, cheese-burgers, and Mexican food.

Meal Patterns and Eating Habits

Eating patterns that are appropriate for an active lifestyle may continue after the individual changes to a more sedentary lifestyle. Individuals for whom this observation has been made include athletes and a large percentage of people with increasing age and changing occupational responsibilities. Athletes who are in training expend large amounts of energy each day and, for many organized sports, are encouraged to eat large quantities to maintain their weight at an artificially high level. When activity declines, the eating pattern established during training may not be adjusted to meet the new lower energy needs. The same is true of military personnel. During initial entry training, advanced individual training, and special forces training, large amounts of energy are expended on a daily basis. By the time training is completed, individuals have been habituated to consume large amounts of food over a very short period of time.

In many occupations, tasks that require more physical activity are assigned to younger workers. As these workers age and acquire more responsibility, their work may become more sedentary, but eating patterns may not change. This pattern of decreased occupational energy expenditure with job promotion may be common in the military as well. Privates, airmen, and junior noncommissioned officers are more active than senior officers and noncommissioned officers. Despite strong commitments to engage in daily physical fitness, which may be unchanged or even increased in more senior individuals, the decrease in activities of daily living and job performance can lead to a positive energy balance unless particular care is taken to reduce energy intake.

The ubiquitousness of vending machines and fast-food outlets ensures constant access to foods at work-usually foods with a high caloric content largely in the form of fat or refined CHO. A major contributing factor to the epidemic of obesity in recent years is likely the rise in the proportion of meals eaten away from home (eating out), along with the increase in access to foods in virtually all locations. These changes have contributed in several ways to promoting obesity. Because more families include two-wage earners, adults spend more time out of the home and do not have time to prepare meals as they customarily did in the past. Meals consumed at restaurants tend to be larger and have a higher caloric content than those consumed at home, mainly because of higher fat content and larger portion sizes (Young and Nestle, 2003). In addition, a high percentage of meals eaten away from home are eaten in fast-food restaurants or consist of fast-food take-out. The presence of food in virtually every circumstance of daily life, from fast-food outlets to vending machines, encourages and allows individuals to consume multiple calorically dense meals and snacks per day (Bell et al., 1998; Rolls, 2000).

PHYSIOLOGICAL FACTORS

A number of phenotypic characteristics have been associated with the risk of weight gain, notably alterations in nonvolitional components of energy expenditure. Energy expenditure can be divided into three main components:

Resting metabolic rate (RMR), the rate of energy expended at rest, under thermo-neutral conditions, and in a post-absorptive state.

Thermic effect of feeding, the incremental increase in energy expenditure after a meal is consumed due to the energy costs of absorption and the transport of nutrients, as well as the synthesis and storage of protein, fat, and CHO. Some of the thermic effect of feeding may be mediated by sympathetic nervous system activity.

Energy expended for physical activity, including involuntary movements associated with shivering, fidgeting, and postural control.

RMR accounts for 60 to 75 percent of total energy expended in most adults. RMR is primarily related to the maintenance of fat-free mass, reflecting such activities as protein synthesis and breakdown, temperature and cellular homeostasis, and cardiovascular, pulmonary, and central nervous system function. Metabolism associated with visceral organ mass makes the largest contribution to RMR, followed by that of skeletal muscle mass and adipose tissue (Gallagher et al., 1998). RMR is consistently greater in men than in women due to the greater lean tissue mass of males. A low RMR relative to body size was found to predict weight gain (Ravussin et al., 1988) in both men and women, although some studies have not confirmed this observation (Weinsier et al., 2000). RMR begins to decrease with age in the middle of the fourth decade. Gilliat-Wimberly and coworkers (2001) found that an association exists between physical activity and maintaining RMR in middle-aged women.

The thermic effect of feeding usually accounts for 5 to 10 percent of daily energy expenditure and varies between lean and obese individuals (Astrup, 1996). Extensive studies have been inconsistent in supporting the view that excessive weight gain is secondary to a reduced thermic effect of food (Tataranni et al., 1995).

Recent studies support the view that small, nonvolitional physical activities such as fidgeting may account for individual differences in energy expended with changes in energy balance (Levine et al., 1999; Zurlo et al., 1992). Although relatively small in caloric magnitude, these activities may account for some of the between-individual differences observed in the regulation of body weight.

These three phenotypic energy expenditure characteristics serve as markers for potential weight gain over the long term. Many factors may contribute to these individual energetic differences, and the origin of these differences is the basis of intensive study.

ENVIRONMENTAL FACTORS

Smoking and Alcohol

Cigarette smoking increases metabolic rate and may limit food intake, and weight gain is a common consequence of smoking cessation (Perkins, 1993; Russ et al., 2001). The use of alcoholic beverages may also have an impact on body weight. Energy consumed as alcohol that is in excess of need is converted to and stored as fat. Drinking alcohol has been shown to be associated with a greater energy intake than drinking nonalcoholic beverages, perhaps due to increased appetite (Tremblay and St-Pierre, 1996; Tremblay et al., 1995).

A recent, large prospective study of a cohort of men ages 40 to 59 with a 5-year follow-up found that mean BMI increased significantly from the light-to-moderate to the very-heavy alcohol intake group. The study concluded that heavy alcohol intake (defined as ≥ 30 g/day of alcohol) contributed directly to weight gain and obesity, regardless of the type of alcohol consumed (Wannamethee and Shaper, 2003).

Pharmacological Agents That Produce Weight Gain

Numerous drugs can produce weight gain and fat gain. These include glucocorticoids (e.g., prednisone), hypoglycemic agents (e.g., insulin, sulfonylureas), certain antihypertensive agents (e.g., prazocin), anti-allergens (e.g., cyproheptadine), and numerous drugs that affect the central nervous system (e.g., thorazine, tricyclic antidepressants, valproic acid, lithium). Most of these drugs are used for diseases that mandate separation from the military, but there are a number of drugs that may be taken by military personnel that are not deemed a rationale for separation.

SOCIAL FACTORS

Americans live in a culture in which food is abundant. A well-developed and efficient food transportation and storage system assures a readily available and affordable food supply throughout the entire year.

The relative affluence of Americans has led to an increase in consumption of snack foods (Morgan and Goungetas, 1986) and an increase in the proportion of foods of animal origin compared with that of foods of plant origin (Senauer, 1986). Foods of animal origin are likely to be higher in energy and fat than comparable quantities of foods of plant origin.

The availability and abundance of food in the U.S. marketplace has accelerated dramatically in the past 30 years. The per capita energy content of food entering the American marketplace increased about 500 calories on a daily basis during this time period. In addition, fat intake has also increased steadily, although the relative intake of fat has been decreasing since the 1970s (Putnam and Allshouse, 1999). This decrease in fat intake has been associated with an increase in average total energy intake (Bray and Popkin, 1998). Food-supply studies indicate that the increase in the number of calories consumed is accompanied by a shift in macronutrient consumption that reflects an increase in refined CHO consumption and a decrease in consumption of fruits and vegetables (Putnam and Allshouse, 1999).

Family and Ethnicity

Eating is an intensely social activity, and many eating habits are acquired in a familial or ethnic setting. People tend to imitate the eating habits of their parents, so quantity and quality of foods eaten and meal patterns tends to be established early. Traditions that arise around eating patterns in a more agrarian or active society may favor excess consumption. Ethnic groups differ in their perceptions about appropriate body size and what constitutes overweight (Bhadrinath, 1990; Root, 1990).

Studies of changes in diet with immigration and acculturation show, for example, that Japanese who migrated to California and Hawaii have tended to abandon the traditional low-fat Japanese diet for American food patterns (Burchfiel et al., 1995; Curb and Marcus, 1991; Goodman et al., 1992; Hara et al., 1996; Ziegler et al., 1996). The result has been a marked increase in weight among these immigrants. Similarly, Japanese children who remain in Japan, but whose diet is increasingly western, are also getting heavier (Murata, 2000; Takada et al., 1998). Thus, dietary change is strongly associated with increased weight in both of these carefully studied population groups. The same phenomenon is observed in studies of South Asians who have migrated to the United Kingdom and who have modified their diet and physical activity patterns (McKeigue et al., 1992).

Socioeconomic Status

Social class and socioeconomic status (SES) influence the prevalence of overweight. In many countries of the world, lower SES is linked to increased body weight (Molarius et al., 2000). In contrast, in some developing countries and primitive societies, obesity is considered a sign of affluence or fertility (Molarius et al., 2000). However, some researchers who contend that obesity decreases economic status have disputed the belief that lower SES causes obesity in the United States. For example, one study reported that women who were overweight in late adolescence or early adult life were more likely to have lower income, greater levels of poverty, and decreased rates of marriage than were normal-weight women with comparable degrees of disability (Gortmaker et al., 1993).

The Potential Role of Viruses in the Etiology of Obesity

The possibility exists that at least some cases of human obesity are due to viral infection. Five viruses and scrapie agents cause obesity in animals (Bernard et al., 1988, 1993; Carp et al., 1998; Carter et al., 1983a, 1983b; Dhurandhar et al., 1990, 1992, 1997, 2000; Gosztonyi and Ludwig, 1995; Lyons et al., 1982; Nagashima et al., 1992). One of these viruses is a human adenovirus, Ad-36, which has been shown to produce a syndrome of increased body fat and paradoxically decreased serum cholesterol and triglycerides in chickens and mice (Dhurandhar et al., 2000). Preliminary data have been reported that demonstrated similar results in monkeys (Atkinson et al., 2000). Other preliminary studies suggest that humans with serum antibodies to Ad-36 have a higher BMI and lower serum lipids than do Ad-36 antibody-negative individuals (Atkinson et al., 1998).

Humans in Bombay, India, who had serum antibodies to SMAM-1, an avian adenovirus, were noted to be significantly heavier and to have lower serum lipids compared with antibody-negative individuals. Viral antigen was found in the serum of two of the individuals with SMAM-1 antibodies (Dhurandhar et al., 1997).

More research is needed to confirm the hypothesis generated from the above data that some cases of human obesity might be due to a viral infection. Since adenoviruses are common cold viruses, the possibility of the spread of Ad-36 and perhaps other obesity-producing viruses in the military community may be of significant concern.

SUMMARY

The brief review of factors influencing body weight presented in this chapter demonstrate that maintaining a healthy body weight is an extremely complex issue. Maintenance of fitness and appropriate body-fat standards by military personnel is affected by each individual's genetics, developmental history, physiology, age, physical activity level, environment, diet, ethnicity, and social background.

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There are numerous factors that can influence body weight. The individual has no control over some of these factors, including developmental determinants, genetic makeup, gender, and age. Other factors that influence body weight over which the individual has potential control include level of physical activity, diet, and some environmental and social factors.

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This article is helpful because it provides a list of benefits that add to what we learned in class regarding flexibility. Along with that, it provides some stretches that help with particular needs.

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Activities that lengthen and stretch muscles can help you prevent injuries, back pain, and balance problems.

A well-stretched muscle more easily achieves its full range of motion. This improves athletic performance - imagine an easier, less restricted golf swing or tennis serve - and functional abilities, such as reaching, bending, or stooping during daily tasks. Stretching can also be a great way to get you moving in the morning or a way to relax after a long day. Activities such as yoga combine stretching and relaxation and also improve balance, a wonderful combination.

However, note that experts no longer recommend stretching before exercise. Newer recommendations suggest that you start your workout routine with a warm-up, such as an easy walk or a sport-specific routine, such as serving some tennis balls and practicing ground strokes before a match. This gets blood and oxygen flowing to your muscles. After five to 10 minutes of warm-up, your muscles are warm and supple. This is a good time to stretch. You can even do your flexibility exercises as a post-workout cool-down.

To get more tips on starting a successful exercise program, buy Starting to Exercise, a Special Health Report from Harvard Medical School.

Disclaimer:

As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date of last review or update on all articles.

No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician.

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Benefits of flexibility exercises - Harvard Health

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Activities that lengthen and stretch muscles can help you prevent injuries, back pain, and balance problems....

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This article provides deeper insight into how aging effects muscles, joints, bones, skin and overall health. Furthermore, it provides the ways in which stretching exercises can benefit mobility as people age.

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Routine physical activity is an important part of healthy aging as it helps prevent several health problems, such as diabetes and heart disease.

Developing and maintaining your flexibility as you age can also be beneficial by reducing the risk of injury, maintaining good balance, and having a better range of motion. You will feel stronger once you gain a bit of flexibility, simply because that flexibility gives you the range of motion to let your muscles work more efficiently.

Maintaining flexibility will aid in muscle and joints health, which can keep older adults doing their favorite daily activities and remain independent.

If you are wondering if it's possible to become flexible as we age, the answer is YES! As we age, our bodies have a tendency to degenerate. We lose our skin's elasticity, our muscle tone, and bone density. Also, the water content in our tendons decreases and as a result, our tendons get stiffer. All these factors can contribute to the natural decrease in our flexibility.

The most common areas affected with decreased flexibility are often the shoulders and the hips. Other parts of the body that can be affected by the changes include the spine, neck, knees, ankles and any part of the body that has joints. This can result in chronic aches and pains.

1. Improves your ability to perform daily physical activities.

2. Decreases the risk of injuries such as fractures and muscle strains.

3. Improves balance which also decreases the risk of falling and injury.

4. Decreases chronic pain.

5. Improves your workouts due to better overall muscular performance.

6. Improves your posture which reduces hunching over.

7. Helps you keep a more youthful appearance.

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Many experts suggest that simple stretching techniques are best to help us ease into our workout routines and increase our flexibility.

Gaining flexibility takes time so be sure to go slowly, and pay attention to your body. One stretch doesn't fit everyone, but there are many variations that can be made. As you improve your flexibility, you'll be able to reach farther with the same stretch or add different stretches for the same muscle.

Stretching exercises are essential to help maintain flexibility and range of motion in joints. Yoga and Pilates are great forms of stretching exercise as they build core body strength and increase stability.

Additional tips to keep in mind:

1. Warm up the body by walking in place for five minutes. This will prepare your heart, muscles, and joints for activity.

2. Never force a stretch and do not bounce or jerk to get deeper into a stretch. Smooth and gentle movements are safer.

3. Don't lock your joints. Your arms and legs can be straight while stretching, but they shouldn't be stiff and locked. If it's more comfortable try bending your elbows and knees slightly.

4. Keep breathing. As with your movements, your breath should be slow and steady.

5. Aim to stretch every day. Try for 10 to 15 minutes a day, at least three days a week.

6. Don't forget recovery time. You will need to focus more on recovery after 50. Tissue recovery may take more time and more effort to support that recovery. Knowing how much recovery time that is needed often depends on your baseline fitness level.

In conclusion, age is only a number and doing nothing will not help the aging process in the least. For many older adults, maintaining mobility can be difficult. Muscles and joints weaken and range of movement deteriorates as we age.

Stretching benefits include the development and maintenance of strength, improving flexibility, and increased circulation and blood flow, all of which will provide a greater quality of life and healthy aging.

Contact ustoday to view our 4 convenient locations, view services and claim your complimentary 3-day trial membership!

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Why Flexibility Is So Significant As We Age

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Routine physical activity is an important part of healthy aging as it helps prevent several health problems, such as diabetes and heart disease. Developing and maintaining your flexibility as you age can also be beneficial by reducing the risk of injury, maintaining good balance, and having a better range of motion.

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This article provides the ways in which functional movement is crucial to day-to-day life. I also got insight into how physical therapy is very beneficial when improving movement of bones, joints and muscles.

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If you have started physical therapy, you are probably learning a lot of new terms. It can be challenging to keep up with sometimes, especially with phrases like "functional movement." What does that mean? And what does it have to do with you?

It is essential to understand what functional movement is to ensure your therapy will improve the most important movements you do in your day. We make sure our patients at EW Motion Therapy understand functional movement and how their therapy is helping them move better. Our ultimate goal for this article is to help you know what movements are considered functional and how you can improve them in your daily routine, even if you choose not to do therapy with us.

This article discusses functional movements, why they are important, how you can improve them, and how physical therapy can help. With this information, you can continue your treatment knowing you will substantially enhance your movement over time.

What makes a movement functional?

By definition, a functional movement is a movement sequence based on real-world situations. They are any movements you perform in multiple planes of motion with multiple joints to help you accomplish things more efficiently. Functional movements vary from person to person, based on your age and the activities you pursue. But common functional movements include things like sitting down, standing up, walking, tying shoes, and bending down to pick something up off the floor.

In other words, functional movements are the things you do during your day to help you accomplish essential tasks. Think about the movements required to put on your shoes in the morning. You have to be able to cross your legs, bend forward to put the shoe on, and balance while sitting without hand support, right? Each one of these movements make up the functional movement of putting on shoes.

Why is functional movement significant?

As the above example illustrates, functional movement is essential because difficulty with any of the parts required for a specific functional movement can cause great difficulty in managing crucial tasks. Knowing what tasks are difficult for you in your day can help you pinpoint the functional movements or parts of the movement you should work on.

If you have difficulty putting on shoes, it is much easier to think about the individual steps involved in that functional movement and pick which of those is the weak link in the process. Are you having trouble lifting your foot off the ground or crossing your leg? Depending on your answer to that question, you can develop more targeted strategies to improve those movements and accomplish those daily tasks more efficiently.

What can you do if you have a functional movement deficit?

When you realize you are having trouble doing something, the first step is identifying which functional movement you are having difficulty with. Then you need to answer the question of whether you have pain or whether you are a fall risk. If you have pain or think you might be a fall risk, consult your doctor. You should do this especially if your pain worsens over time, which could be a sign of a larger issue. However, suppose you do not have pain. In that case, a specialist like a physical therapist or occupational therapist can help assign exercises to improve those movements and get you moving better about your day.

How can physical therapy help improve functional movement?

Now you know more about what functional movement is and some steps you can take to identify and improve any deficits. If you choose to see a physical therapist, they will be able to take functional movements and break them down into their simplest parts while developing a strategy specifically for improving areas that need it. They will do some kind of functional movement screen, possibly something like the , to assess where you need to improve, and with your goals in mind, they will tailor a plan for you to move more efficiently.

It can be frustrating when you cannot accomplish tasks, either simple or very complex, during your day. We strive to help our patients at EW Motion Therapy move better, using our physical therapy background and years of experience, so that they can feel and live better than before. If you are interested in learning more about our physical therapy services, fill out the Request an Appointment form on our website, and someone from our staff will contact you within 48 hours with your next steps.

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What is Functional Movement? Why It's Important and How Physical Therapy Can Help

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What even is functional movement? We discuss which movements are functional and why it is important to improve them.

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This article delved into 4 major types of exercise that are important for different people and that provide the most benefits to the mind and body.

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Strengthening, stretching, balance, and aerobic exercises will keep you active, mobile, and feeling great.

Exercise is key to good health. But we tend to limit ourselves to one or two types of activity. People do what they enjoy, or what feels the most effective, so some aspects of exercise and fitness may be ignored. In reality, we should all be doing aerobics, stretching, strengthening, and balance exercises. Here, we list what you need to know about each exercise type and offer examples to try, with a doctor's okay.

1. Aerobic exercise

Aerobic exercise, which speeds up your heart rate and breathing, is important for many body functions. It gives your heart and lungs a workout and increases endurance. If you're too winded to walk up a flight of stairs, you need to see your doctor for a medical evaluation. If it's just because you are deconditioned, then you will need more aerobic exercise to help condition your heart and lungs and get enough blood to your muscles to help them work efficiently.

Aerobic exercise also helps relax blood vessel walls, lower blood pressure, burn body fat, lower blood sugar levels, reduce inflammation, and boost mood. Combined with weight loss, it can also lower "bad" LDL cholesterol levels. Over the long term, aerobic exercise reduces your risk of heart disease, stroke, type 2 diabetes, breast and colon cancer, depression, and falls.

Aim for at least 150 minutes per week of moderate-intensity activity. Try brisk walking, swimming, jogging, cycling, dancing, or classes like step aerobics.

Marching in place

Starting position: Stand tall with your feet together and arms at your sides.
Movement: Bend your elbows and swing your arms as you lift your knees.
March in a variety of styles:

March in place.

March four steps forward, and then four steps back.

March in place with feet wide apart.

Alternate marching feet wide and together (out, out, in, in).

Tips and techniques:

Look straight ahead and keep your abs tight.

Breathe comfortably, and don't clench your fists.

Make it easier: March slower and don't lift your knees as high.
Make it harder: Lift your knees higher, march faster, and really pump your arms.

2. Strength training

As we age, we lose muscle mass. Strength training builds it back. Regular strength training will help you feel more confident and capable of daily tasks like carrying groceries, gardening, and lifting heavier objects around the house. Strength training will also help you stand up from a chair, get up off the floor, and go upstairs.

Strengthening your muscles not only makes you stronger, but also stimulates bone growth, lowers blood sugar, assists with weight control, improves balance and posture, and reduces stress and pain in the lower back and joints.

A physical therapist or certified personal trainer can design a strength training program that you can do two to three times a week at a gym, at home, or at work. It will likely include body weight exercises like squats, push-ups, and lunges, and exercises involving resistance from a weight, a band, or a weight machine.

It's important to feel some muscle fatigue at the end of the exercise to make sure you are working or training the muscle group effectively.

Squat

Starting position: Stand with your feet shoulder-width apart, arms at your sides.
Movement: Slowly bend your hips and knees, lowering your buttocks about eight inches, as if you're sitting back into a chair. Let your arms swing forward to help you balance. Keep your back straight. Slowly return to the starting position. Repeat 8-12 times.

Tips and techniques:

Shift your weight into your heels.

Squeeze your buttocks as you stand to help you balance.

Make it easier: Sit on the edge of a chair with your feet hip-width apart and arms crossed over your chest. Tighten your abdominal muscles and stand up. Slowly sit down with control.
Make it harder: Lower farther, but not past your thighs being parallel to the floor.

3. Stretching

Stretching helps maintain flexibility. We often overlook that in youth when our muscles are healthier. But aging leads to a loss of flexibility in the muscles and tendons. Muscles shorten and don't function properly. That increases the risk for muscle cramps and pain, muscle damage, strains, joint pain, and falling, and it also makes it tough to get through daily activities, such as bending down to tie your shoes.

Likewise, stretching the muscles routinely makes them longer and more flexible, which increases your range of motion and reduces pain and the risk for injury.

Aim for a program of stretching every day or at least three or four times per week.

Warm up your muscles first, with a few minutes of dynamic stretches-repetitive motion such as marching in place or arm circles. That gets blood and oxygen to muscles, and makes them amenable to change.

Then perform static stretches (holding a stretch position for up to 60 seconds) for the calves, the hamstrings, hip flexors, quadriceps, and the muscles of the shoulders, neck, and lower back.

However, don't push a stretch into the painful range. That tightens the muscle and is counterproductive.

Single knee rotation

Starting position: Lie on your back with your legs extended on the floor.
Movement: Relax your shoulders against the floor. Bend your left knee and place your left foot on your right thigh just above the knee. Tighten your abdominal muscles, then grasp your left knee with your right hand and gently pull it across your body toward your right side.
Hold 10 to 30 seconds.
Return to the starting position and repeat on the other side.

Tips and techniques:

Stretch to the point of mild tension, not pain.

Try to keep both shoulders flat on the floor.

To increase the stretch, look in the direction opposite to your knee.

4. Balance exercises

Improving your balance makes you feel steadier on your feet and helps prevent falls. It's especially important as we get older, when the systems that help us maintain balance-our vision, our inner ear, and our leg muscles and joints-tend to break down. The good news is that training your balance can help prevent and reverse these losses.

Many senior centers and gyms offer balance-focused exercise classes, such as tai chi or yoga. It's never too early to start this type of exercise, even if you feel you don't have balance problems.

You can also go to a physical therapist, who can determine your current balance abilities and prescribe specific exercises to target your areas of weakness. That's especially important if you've had a fall or a near-fall, or if you have a fear of falling.

Typical balance exercises include standing on one foot or walking heel to toe, with your eyes open or closed. The physical therapist may also have you focus on joint flexibility, walking on uneven surfaces, and strengthening leg muscles with exercises such as squats and leg lifts. Get the proper training before attempting any of these exercises at home.

Standing knee lift

Starting position: Stand up straight with your feet together and your hands on your hips.

Movement: Lift your left knee toward the ceiling as high as is comfortable or until your thigh is parallel to the floor. Hold, then slowly lower your knee to the starting position.

Repeat the exercise 3-5 times.

Then perform the exercise 3-5 times with your right leg.

Tips and techniques:

Keep your chest lifted and your shoulders down and back.

Lift your arms out to your sides to help you balance, if needed.

Tighten your abdominal muscles throughout.

Tighten the buttock of your standing leg for stability.

Breathe comfortably.

Make it easier: Hold on to the back of a chair or counter with one hand.

Make it harder: Lower your leg all the way to the floor without touching it. Just as it is about to touch, lift your leg up again.

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The 4 most important types of exercise - Harvard Health

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Some aspects of exercise and fitness are ignored. In reality, everyone should do aerobics, stretching, strengthening, and balance exercises....

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This article helped give me more information on how crucial physical activity is when it comes to one's mental health. I learned more about how exercise releases endorphins which ultimately improves mood.

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The Mental Health Benefits of Exercise - HelpGuide.org

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From depression and anxiety to stress and ADHD, exercise is one of the most effective ways to improve your mental health. Learn how to get started.

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The Relationship Between Stress and Chronic Illness

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The Relationship Between Stress and Chronic Illness

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This article provides information on how extensive stress or chronic stress can ultimately lead to chronic illnesses such as diabetes, gastrointestinal problems, cardiovascular problems, and other conditions.

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American culture rewards people who deal with stress by working harder and faster to produce more in less time. Not surprisingly, the pace of our society has continued to accelerate over the years, leading to an alarming increase in stress-related illnesses.

The definition of stress could be rather difficult inasmuch as we all react to stress differently. What is stressful for one person may be pleasurable or have a mild effect on another. The American Institute of Stress defines it as a feeling of being overwhelmed or unable to cope with mental or emotional pressure, triggered by any change to which one must adapt, ranging from an extreme event like actual physical danger to the excitement of falling in love or accomplishing something.

In addition, stress may be experienced at various levels in physical, mental, or emotional tension. The reality is that stress is an unavoidable part of our everyday lives.

You may feel stressed about a variety of things, ranging from your performance in school to traumatic events such as the pandemic, a natural disaster, an act of violence, or a life-changing event like a divorce. No matter whether the stress you encounter results from a major event or an accumulation of everyday hassles, the impact stress will have in your life is mainly a result of your perception and response to it.

Harvard physiologist Walter B. Cannon set the groundwork for the further understanding of the effects of stress at a physiological level. He was the first to describe the "fight or flight" response as a sequence of biochemical changes that prepare you to deal with threat or danger.

From an evolutionary point of view, it was suggested that primitive people required a quick burst of energy to fight or flee when confronted with predators, like a saber-toothed tiger. Nowadays, we don't encounter such predators, but our "fight or flight" response may be activated when confronted with situations such as an extreme maneuver trying to avoid a car crash while driving or deciding how to react if being mugged.

Research studies on stress have provided further insight into what happens to our body during the "fight or flight" response. For example, any situation-whether real or imagined-could cause the cerebral cortex (which plays a key role in attention, perception, cognition, awareness, and thought, among other functions) to send an alarm to the hypothalamus (the main switch for stress response, positioned in the mid-brain) to then stimulate the sympathetic nervous system to make a series of changes in the body such as heart and breathing rates, or muscle tension and blood pressure increases. In addition, one's hands and feet may get cold as blood travels away from the extremities and digestive system into larger muscles to prepare to fight or run.

Unfortunately, when the "fight or flight" response switch is on for too long, like during times of chronic stress, we might experience long-term negative effects impacting digestion, reproduction, growth, and the responses of the immune and inflammatory systems.

Chronic stress happens when the stressors of life are unremitting and persistent. For example, stressors related to the global COVID-19 pandemic, which has led to some experiencing the loss of loved ones, fears of getting sick or dying, downsizing at work, loss of housing, or financial issues while dealing with a messy divorce. However, chronic stress is not limited to major events. It can also occur when smaller stressors accumulate over time and one is unable to effectively deal with them. The longer a person's stress response remains activated, the higher their risk of developing stress-related diseases.

Over 50 years of research on stress has shown evidence of the correlative impact chronic stress has on the onset of illnesses such as cardiovascular and gastrointestinal issues, as well as fatigue, hypertension, and diabetes.

Almost every system in the human body can be damaged by stress. Indeed, the cumulative effect of stress from years ago may still have a negative impact on you now.

The following are the 20 most common signs and symptoms of stress:

1. Frequent headaches, and jaw clenching or pain.

2. Tremors or trembling of lips, and hands.

3. Neck ache, back pain, muscle spasms.

4. Lightheadedness, faintness, dizziness.

5. Ringing, buzzing, or popping sounds.

6. Rashes, itching, hives, or "goosebumps".

7. Unexplained or frequent "allergy attacks".

8. Constipation, diarrhea, loss of control.

9. Difficulties breathing.

10. Sudden attacks of life-threatening panics.

11. Chest pain, palpitations, rapid pulse.

12. Excess anxiety, worry, guilt and nervousness.

13. Increased anger, frustration, and hostility.

14. Depression, frequent mood swings.

15. Increased or decreased appetite.

16. Insomnia, nightmares, disturbing dreams.

17. Difficulties concentrating, racing thoughts.

18. Constant tiredness, weakness, and fatigue.

19. Increased smoking, alcohol, or drug use.

20. Excessive gambling or impulse buying.

Stress can have a wide-ranging effect on emotions, mood, and behavior. Equally important are the effects on the body's various physiological systems, organs, and tissues.

The initial step in managing your stress effectively is to be aware of its four basic sources. First, the environment bombards you with different demands that require you to adjust. This could range from noise, traffic, weather or even pollution. The second refers to social stressors like work or college deadlines, financial issues, disagreements, demands for your time and attention from your family and work, or the loss of a loved one, among others. The third source of stress is physiological, which happens when we react to environmental and social threats. The fourth source of stress is your thoughts. Yes, your perception of who you are to the world, relationships, situations encountered in daily life. But most importantly, your inner stress management centers around your own " self-talk "-that is, how you speak internally to yourself, the quality of that conversation, and whether it is positive, negative, or irrational.

All these demands can trigger symptoms such as muscle tension, headaches, upset stomach, and anxiety. In addition, the physiological effects of stress can be impacted by other factors including lack of exercise and sleep, as well as poor nutrition.

Once you have identified the major sources of your stressed-related symptoms, you can make changes in your life to help alleviate your stress, such as ensuring better nutrition, sleeping habits, physical exercise, and the adoption of relaxation and stress-reduction techniques that not only relax the body but condition the mind to handle stress more effectively.

It is important to be aware that mind, body, and emotions are interrelated, so in order to obtain the best stress reduction results, at least one relaxation and stress-reduction technique should be incorporated in your overall stress management.

Mental health professionals can assist you in identifying the causes of stress in your life and guide you to the most appropriate techniques to reduce your stress-related symptoms by applying techniques like cognitive behavioral therapy (CBT) to help you reduce stress by changing the ways you think about stressful situations and develop coping strategies.

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The Relationship Between Stress and Chronic Illnesses

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This article shows the connection that stress has on the brain which then ultimately leads to negative effects on one's health.

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Today's life rhythms and demands are often challenging and require intense physical and psychological efforts in order to be sustained. An individual reacts to physical and mental strain that is potentially health threatening by activating interconnected neuroendocrine circuits. This response allows the body to face and deal with the challenge and re-establish homeostatic equilibrium. If the individual perceives a noxious stimulus as too intense, or its duration as too long, he may fail coping with it, and incur maladaptation. In this case, the stress response does not resolve into a state of balance (either similar or new, i.e., adapted, compared with the state before stress hits), neuroendocrine parameters remain altered, and illness may ensue.

It is clear that stress has both a physical (objective) and a psychological (subjective) component: the latter, as described by Koolhaas and colleagues, depends on the individual perception of its predictability and controllability [ 1]. The way a person can anticipate a certain stressor and then control it, largely defines the resulting stress response, how promptly and efficiently it is activated promoting adaptation, and how fast it is turned off once equilibrium has been recovered.

The time course of the stress response, characterized by measurable neuroendocrine and behavioral indexes, thus reveals whether a destabilizing stimulus is manageable, or conversely, cannot be handled and consequently becomes harmful.

This implies that not all stimuli that elicit strong neuroendocrine responses are real stressors, but only those that exceed the individual's ability to change and adapt.

Cortical centers in the brain sense a disturbing stimulus and respond by activating pathways that through the limbic system stimulate peripheral networks, including the sympathetic-adrenal-medullary axis and the renin-angiotensin system, and later the hypothalamic-pituitary-adrenal (HPA) axis [ 2]. A cascade of events follows that results in the orchestration of a complex response. Adrenaline and other hormones, and neuropeptides are produced and regulate cardiovascular and metabolic functions (inducing, for instance, increases in heart rate, breath frequency, glucose release) for a prompt response concerted to overcome the challenge.

If the distressing stimulus persists, the HPA axis kicks in to sustain the immediate reaction mediated by the centrally activated peripheral systems. The HPA response starts with the hypothalamus delivering corticotropin-releasing hormone to the pituitary and culminates with the stimulation of the adrenal cortex by the pituitary-derived adrenocorticotropic hormone to produce glucocorticoids (GCs). Most organs and tissues, including sympathetic nerves, immune cells and several brain regions express GC receptors and are responsive to GCs induced by stress. Consequently, these hormones participate in the regulation of disparate stress-associated processes, from the modulation of cardiovascular effects and the immune function, to the eventual dampening of the stress response through inhibition of the HPA axis when adaptation is attained.

In situations in which the stressor is overwhelming and cannot be resolved, stress becomes chronic. In this case, the GC-dependent negative feedback mechanism that controls the stress response does not work, GC receptor resistance develops, and the systemic levels of the molecular mediators of stress remain high, compromising the immune system and damaging in the long-term multiple organs and tissues [ 3].

What is the actual impact of chronic stress on health?

When considering the numerous cellular targets of the chemical mediators of stress, one would expect that protracted, stress-dependent neuroendocrine dysregulation may damage directly or through functional circuits practically all organs and tissues. To clarify this assumption and identify the biochemical pathways significantly impaired by chronic stress to the extent of producing illness, researchers have on one hand searched for putative morphological tissue alterations associated with stress, and on the other analyzed the molecular mechanisms of action of the main stress hormones.

Effects of chronic stress on brain structure

It has been shown that chronic stress is linked to macroscopic changes in certain brain areas, consisting of volume variations and physical modifications of neuronal networks. For example, several studies in animals have described stress-related effects in the prefrontal cortex (PFC) and limbic system, characterized by volume reductions of some structures, and changes in neuronal plasticity due to dendritic atrophy and decreased spine density [ 4]. These morphological alterations are similar to those found in the brains of depressed patients examined postmortem, suggesting that they could also be at the basis of the depressive disorders that are often associated with chronic stress in humans. This hypothesis is supported by imaging studies that evidenced structural changes in the brain of individuals suffering from various types of stress-related disorders, such as those linked to severe traumas, major negative life events or chronic psychosocial strain. In particular, Blix and colleagues observed atrophy of the basal ganglia and significantly reduced gray matter in certain areas of the PFC in subjects afflicted with long-term occupational stress [ 5]. In general, the consequences of these alterations in a brain region can expand to other functionally connected areas, and potentially cause those cognitive, emotional and behavioral dysfunctions that are commonly associated with chronic stress, and that may increase vulnerability to psychiatric disorders.

Interlink between the brain & the immune system

The understanding of the molecular circuits that underlie brain architectural changes and medical conditions linked to chronic stress is just at the beginning. Research in this area has centered primarily on the signaling functions of those molecules that are directly induced by stress through the activation of the sympathetic-adrenal-medullary and HPA networks, focusing on their possible cellular targets. Since receptors for stress neuropeptides and hormones are broadly expressed in immune cells [ 6], most studies have concentrated on the effects of stress on the immune system (IS). In fact, psychological stress can induce the acute phase response commonly associated with infections and tissue damage, and increase the levels of circulating cytokines and of various biomarkers of inflammation [ 2]. As suggested by Maier and Watkins, the interlink between the stress response and inflammation elicited by the IS can be explained from the evolutionary perspective by considering that the stress response is an adaptive process developed by co-opting the IS mechanisms of defense [ 7]. In this frame, a psychological stressor, perceived by the brain as 'danger', that is, potentially harming, sets in motion a neuroimmune circuit that stimulates the IS to mount a protective reaction intended to prevent damage, repair it and restore homeostasis.

This neuroimmune communication is bidirectional because the cytokines produced by stress-stimulated immune cells also convey a feedback to the nervous system, further modulating the release of stress hormones in the brain, as well as brain activity that regulates behavior and cognitive functions. In a situation of chronic stress, the neuroimmune axis can be overstimulated and breaks down, thus causing neuroendocrine/immune imbalances that establish a state of chronic low-grade inflammation, a possible prelude to various illnesses [ 8].

Diseases whose development has been linked to both stress and inflammation include cardiovascular dysfunctions, diabetes, cancer, autoimmune syndromes and mental illnesses such as depression and anxiety disorders.

Persistent, abnormal levels of cytokines and stress chemical mediators in the brain may also damage the parenchyma and cause neuronal death, thus contributing to the brain structural changes associated with chronic stress that are described above [ 9].

Despite the large number of studies that have addressed the biological effects of chronic stress and their impact on human health, the emerging picture still merely outlines the biochemical and functional responses of the nervous and immune systems to long-term stress, highlighting some nodes of information exchange between the two networks, but still lacking essential elements concerning additional cellular players, and functional and molecular mechanisms.

Some recent studies have, however, significantly improved our knowledge of how chronic stress promotes two of the diseases that have long been associated with it: atherosclerosis and depression.

Effects of chronic stress on hematopoietic stem cells in cardiovascular diseases

Heidt and colleagues demonstrated how stress increases the levels of circulating inflammatory leukocytes by direct stimulation of hematopoietic stem cell proliferation [ 10]. In this new pathway, stress induces the release of noradrenaline by sympathetic nerve fibers targeting blood vessels in the bone marrow of mice. The catecholamine then acts on mesenchymal stem cells located in the hematopoietic niche, which express high levels of the β3 adrenergic receptors. One of the consequences of this interaction is the downregulation of the chemokine CXCL12, a known target of noradrenaline, which is normally produced by several types of niche cells, including mesenchymal stem cells. This releases the inhibition typically exerted by CXCL12 on the proliferation of hematopoietic stem and progenitor cells and on leukocyte migration, thus promoting cell division and leukocyte mobilization into the bloodstream.

Predictably, the inflammatory response induced by the activation of this neuroimmune pathway may have adverse health effects, in particular by exacerbating pre-existing medical conditions. Specifically, the study demonstrated that this mechanism became activated when atherosclerosis-prone mice ApoE-/- were subjected to long-term stress, leading to enhanced recruitment of inflammatory cells in atherosclerotic plaques, higher levels of proteases and increased plaque fragility. Most interestingly, β3-adrenergic receptor blockers opposed leukocyte production and mobilization, thus counteracting plaque inflammation.

When shifting their attention to human subjects, the scientists determined that individuals under considerable occupational stress had significantly more circulating leukocytes compared with when they were not working, suggesting that the neuroimmune mechanism they discovered might be set off by chronic stress and sustain an inflammatory reaction also in humans. If demonstrated, this would open the way to conceptually new therapeutic possibilities not only for atherosclerosis and its related complications, but also for other stress-related diseases that are aggravated by chronic inflammation.

Mechanisms of chronic stress-associated depression & brain-skeletal muscle communication

The mechanisms by which stress chemicals may induce depression are mostly undetermined. Research in this field is starting to define how multiple, independent, though often interconnected biochemical pathways affected by chronic stress concur to promote this disease.

Ota and colleagues have identified a molecular mechanism triggered by chronic stress that contributes to neuronal atrophy in specific brain areas, an anomaly that is typically observed in depressed patients, independent of the cause of depression [ 11]. In their study, they observed that persistent high levels of GCs, resulting from stress-induced hyperactivation of the HPA axis, stimulate the production of the molecule REDD1 in the PFC of rodents subjected to prolonged stress. REDD1 is generally induced by a variety of stressors - from energy stress, to hypoxia, to DNA damage - in most tissues and inhibits the kinase mTORC1, thus altering the phosphorylation state and function of its targets. In the brain, the interference of REDD1 with mTORC1 signaling ultimately impinges on neuronal protein synthesis, spine formation and synaptic plasticity. The inhibition of mTORC is pivotal for synaptic impairment and appears to be a central endpoint of molecular pathways turned on by chronic stress. In fact, also the decrease of brain-derived neurotrophic factor levels in response to chronic stress disrupts mTORC1 function.

Proinflammatory cytokines induced by stress are also involved in the development of chronic stress-associated depression [ 12]. The acute phase response generally triggered by a harmful factor implies the so-called sickness behavior that includes symptoms similar to those typical of depressive disorders, like social withdrawal, decreased physical activity, fatigue, somnolence, mood and cognitive alterations. This adaptive response is orchestrated by cytokines, and is meant to divert an individual from normal activities in order to save energy, thus facilitating a reaction against the challenge, and subsequent recovery. In the case of chronic inflammation that may set in with prolonged stress, persisting cytokine signaling in the brain prevents the resolution of sickness behavior that consequently can degenerate into depression. The biochemical mechanisms underlying cytokine-induced depression are not well defined, but they may involve alterations of serotonin and glutamatergic transmission, and induction of GC resistance [ 12].

One of the pathways that are implicated drives the oxidation of tryptophan (a precursor of serotonin) to Kynurenin (Kyn) and results in the brain production of several neuroactive molecules ( Figure 1 ) [ 12]. The enzymes tryptophan 2,3-dioxygenase and indoleamine 2,3-dioxygenase trigger the Kyn pathway in the liver and extrahepatically respectively, and can both be activated by chronic stress: tryptophan 2,3-dioxygenase in fact responds to GCs, while indoleamine 2,3-dioxygenase is induced by proinflammatory cytokines. The Kyn pathway not only affects the brain levels of serotonin and thus serotonergic transmission and its mood and behavioral effects, but it is also responsible for the production of tryptophan metabolites that have neuroinflammatory properties or can affect glutamatergic neurotransmission in the brain either positively or negatively. It follows that a shift in the pathway that favors the production of 3-hydroxykynurenine - an inducer of reactive oxygen species and inflammation - and quinolinic acid - an N-methyl-d-aspartate receptor agonist - over the antioxidant and N-methyl-d-aspartate receptor inhibitor kynurenic acid, may promote depression [ 12].

There is evidence that physical exercise can sustain brain health by regulating the production of neurotrophic factors, neurotransmitters, as well as inflammatory molecules. This can translate in a general enhancement of cognitive abilities, a reduced risk of neurodegenerative diseases and a mitigation of depression [ 13].

An interesting study has recently demonstrated that a key mechanism by which physical exercise counteracts chronic stress-dependent depression is the modulation of the Kyn pathway of tryptophan degradation [ 14]. In this work, Agudelo and colleagues demonstrated that skeletal muscle contraction during protracted training induces locally the interaction of the transcriptional coactivator PGC-1α1 with the transcription factors PPARα/δ, thus increasing in the muscles the expression and activity of a set of kynurenin aminotransferases (KAT). KATs catalyze the peripheral transformation of tryptophan-derived Kyn into kynurenic acid, causing a drop in the levels of circulating Kyn. Since Kyn can cross the blood-brain barrier, its peripheral catabolism has the effect to reduce also its brain concentration and so the production of neurotoxic molecules along the 3-hydroxykynurenine and quinolinic acid branch of the degradation pathway. In mice, under conditions that mimic chronic stress, the overexpression in skeletal muscles of PGC-1α1 prevents neuroinflammation, synapses impairment and depression-like behaviors that are instead observed in control animals. Similarly, the scientists found that exercise training stimulates the PGC-1α1-KAT pathway also in humans, and through this mechanism, potentially regulates those Kyn-dependent toxic effects in the brain that contribute to chronic stress-associated depression.

By identifying new signaling cascades implicated in the regulation of depression caused by chronic stress, Ota's and Agudelo's studies suggest novel areas of investigation for therapy development. Drugs that inhibit REDD1 effects on mTORC1, or that modulate brain levels of Kyn by enhancing its peripheral metabolism could improve the treatment of depression maybe also when it is not stress related. Since depressed individuals are usually reluctant to carry out regular physical exercise, drugs that mimic exercise training and reduce the plasma concentration of Kyn by acting peripherally would be of particular interest.

Biological & social implications of the latest findings in chronic stress research

These studies significantly improve our understanding of the interactions between the nervous systems and peripheral tissues and organs, and how their alterations can cause illness ( Figure 2 ). An important discovery is that if on one hand chronic stress can cause immune dysfunctions, that is, impair a peripheral function, on the other hand proper stimulation of a peripheral tissue like skeletal muscles can relieve stress symptoms and protect the brain, possibly favoring recovery. This suggests that programs of physical exercise should be formally proposed as a preventive measure to people known to be exposed to intense stress (eg., work-related stress), and could be prescribed as a form of therapy in combination with other treatments to ease mood and cognitive deficits caused by chronic stress.

In addition, Heidt's study suggests another intriguing possibility: if chronic stress can stimulate hematopoietic stem and progenitor cells through the activation of the peripheral nervous system, it is plausible that it can activate also other types of stem cells in other tissues by a similar mechanism. Bidirectional communication could in principle exist between the nervous system and every organ and tissue, and represents a general mechanism of nervous control of tissue homeostasis. A few recent studies have provided evidence that supports this hypothesis [ 15-16]. One of the resulting and provoking implications is that chronic stress could promote cancer development also by direct induction of uncontrolled cell proliferation.

The recognition that chronic stress can cause serious diseases has intensified research to determine the biochemical perturbations that compromise homeostasis to a degree that prevents spontaneous recovery. The picture is very complex because chronic stress appears to affect organ and system functions at multiple levels. Yet, it is by pinpointing specific biochemical processes affected by chronic stress that it will be possible to envisage solutions to stimulate resilience and control stress-dependent diseases.

It is clear that in the case of illnesses caused by heightened occupational stress, priority should be given to preventive interventions with the purpose of creating and maintaining work conditions respectful of human physiological, emotional and social needs: in other words, the work environment should stimulate growth and productivity while supporting each individual in their challenges. If certain measures could be implemented through official regulations that assure, for example, fair contracts, training, and sensible work schedules in relation to the type and load of responsibilities and the levels of physical and mental engagement implied by the job, others are less manageable because they strictly depend on human factors. Elements like discordant interactions with coworkers and superiors' demands beyond formal agreements, that are quite common in very competitive work environments, can sharpen tensions and exaggerate the psychosocial strain to the point of causing illness, yet they usually remain overlooked and uncontrolled [ 17].

Footnotes

Financial & competing interests disclosure

The author has no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.

Open Access

This work is licensed under the Creative Commons Attribution 4.0 License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

Articles from Future Science OA are provided here courtesy of Future Science Group

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The effects of chronic stress on health: new insights into the molecular mechanisms of brain-body communication

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Today's life rhythms and demands are often challenging and require intense physical and psychological efforts in order to be sustained. An individual reacts to physical and mental strain that is potentially health threatening by activating interconnected neuroendocrine circuits. This response allows the body to face and deal with the challenge and re-establish homeostatic equilibrium.

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This TedTalk discusses how consistent stress increases the amount of cortisol that is produced in the brain which has many negative factors such as affecting brain size, decreasing focus and concentration and decrease connections within neurons.

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How stress affects your brain - Madhumita Murgia

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This article describes how exercise not only can decrease the chance of chronic illness but can also assist people in improving their health when they have chronic illness. The article dives into how different exercises (strength training, cardio, and flexibility/balance) can aid in the improvement of overall health.

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Exercise and chronic disease: Get the facts

If you have a chronic condition, you might have questions about exercising. How often can you exercise? Which exercises are safe? Understand the basics about exercise and chronic disease.
By Mayo Clinic Staff
If you have a chronic disease - such as heart disease, diabetes, asthma, or back or joint pain - exercise can have important health benefits. However, it's important to talk to your doctor before starting an exercise routine. He or she might have advice on what exercises are safe and any precautions you might need to take while exercising.

Find out what you need to know about exercise and chronic disease.

How can exercise improve a chronic condition?

If you have a chronic condition, regular exercise can help you manage symptoms and improve your health.

Aerobic exercise can help improve your heart health and endurance and aid in weight loss. High-intensity interval training is generally safe and effective for most people and can take less time. In high-intensity interval training, you alternate exercising at high levels of intensity and exercising at a less intense level for short periods of time. Even activities such as walking at higher intensities count.

Strength training can improve muscle strength and endurance, make it easier to do daily activities, slow disease-related declines in muscle strength, and provide stability to joints.

Flexibility exercises may help you to have optimal range of motion about your joints, so they can function best, and stability exercises may help reduce the risk of falls.

For example:

Heart disease. Regular exercise can help improve your heart health. Recent studies have shown that interval training is often tolerated well in people with heart disease, and it can produce significant benefits.

For people with high blood pressure, exercise can lower your risk of dying of heart disease and lower the risk of heart disease progressing.

Diabetes. Regular exercise can help insulin more effectively lower your blood sugar level. Physical activity can also help you control your weight and boost your energy. If you have type 2 diabetes, exercise can lower your risk of dying of heart disease.

Asthma. Often, exercise can help control the frequency and severity of asthma attacks.

Back pain. Regular low-impact aerobic activities can increase strength and endurance in your back and improve muscle function. Abdominal and back muscle exercises (core-strengthening exercises) may help reduce symptoms by strengthening the muscles around your spine.

Arthritis. Exercise can reduce pain, help maintain muscle strength in affected joints and reduce joint stiffness. It can also improve physical function and quality of life for people who have arthritis.

Cancer. Exercise can improve the quality of life for people who've had cancer, and it can also improve their fitness. Exercise can also lower the risk of dying from breast, colorectal and prostate cancer.

Dementia. Exercise can improve cognition in people with dementia, and people who are active on a regular basis are at less risk of dementia and cognitive impairment.

What exercises are safe?

Your doctor might recommend specific exercises to reduce pain or build strength. Depending on your condition, you might also need to avoid certain exercises altogether or during flare-ups. In some cases, you might need to consult a physical or occupational therapist before starting to exercise.

If you have low back pain, for example, you might choose low-impact aerobic activities, such as walking and swimming. These types of activities won't strain or jolt your back.

If you have exercise-induced asthma, be sure to keep an inhaler handy while you exercise.

If you have arthritis, the exercises that are best for you will depend on the type of arthritis and which joints are involved. Work with your doctor or a physical therapist to create an exercise plan that will give you the most benefit with the least aggravation on your joints.

How often, how much and at what intensity can I safely exercise?

Before starting an exercise routine, it's important to talk to your doctor about how long your exercise sessions can be and what level of intensity is safe for you.

In general, try to accumulate about 30 minutes of physical activity a day at least five days a week. For example, try walking briskly for about 30 minutes most days of the week. You can even break physical activity up into short chunks of time spread out through the day. Any activity is better than none at all.

If you're not able to do this much activity, do as much as you can. Even an hour a week of physical activity can have health benefits. Start with moving more and sitting less, and work your way up to moving more each day.

If you haven't been active for a while, start slowly and build up gradually. Ask your doctor what kind of exercise goals you can safely set for yourself as you progress.

Do I need to take special steps before getting started?

Depending on your condition, your doctor might recommend certain precautions before exercising.

If you have diabetes, for example, keep in mind that physical activity lowers blood sugar. Check your blood sugar level before any activity. If you take insulin or diabetes medications that lower blood sugar, you might need to eat a snack before exercising to help prevent low blood sugar.

If you have arthritis, consider taking a warm shower before you exercise. Heat can relax your joints and muscles and relieve any pain you might have before you begin. Also, be sure to choose shoes that provide shock absorption and stability during exercise.

What kind of discomfort can I expect?

Talk to your doctor about what kind of discomfort you might expect during or after exercise, as well as any tips for minimizing your pain. Find out what type or degree of pain might be normal and what might be a sign of something more serious.

If you have heart disease, for example, signs or symptoms that you should stop exercising include dizziness, unusual shortness of breath, chest pain or an irregular heartbeat.

What else do I need to know?

Starting a regular exercise routine can be tough.

To help you stick with your routine, consider exercising with a friend. You might also ask your doctor to recommend an exercise program for people who have your condition, perhaps through a local hospital, clinic or health club.

To stay motivated, choose activities that are fun, set realistic goals and celebrate your progress.

Share any concerns you might have about your exercise program - from getting started to keeping it up - with your doctor.

Show references

See more In-depth

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What you need to know about exercise and chronic disease

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If you have a chronic condition, you might have questions about exercising. How often can you exercise? Which exercises are safe? Understand the basics about exercise and chronic disease. By Mayo Clinic Staff If you have a chronic disease - such as heart disease, diabetes, asthma, or back or joint pain - exercise can have important health benefits.

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This article delves into the meaning behind Complementary, Alternative, or Integrative Health and the different ways in which it is used to benefit people's mind and body.

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We've all seen the words "complementary," "alternative," and "integrative," but what do they really mean?

This fact sheet looks into these terms to help you understand them better and gives you a brief picture of the mission and role of the National Center for Complementary and Integrative Health (NCCIH) in this area of research. The terms "complementary," "alternative," and "integrative" are continually evolving, along with the field, but the descriptions of these terms below are how we at NIH currently define them.

Complementary Versus Alternative

According to a 2012 national survey, many Americans-more than 30 percent of adults and about 12 percent of children-use health care approaches that are not typically part of conventional medical care or that may have origins outside of usual Western practice. When describing these approaches, people often use "alternative" and "complementary" interchangeably, but the two terms refer to different concepts:

If a non-mainstream practice is used together with conventional medicine, it's considered "complementary."

If a non-mainstream practice is used in place of conventional medicine, it's considered "alternative."

Most people who use non-mainstream approaches also use conventional health care.

In additional to complementary and alternative, you may also hear the term "functional medicine." This term sometimes refers to a concept similar to integrative health (described below), but it may also refer to an approach that more closely resembles naturopathy (a medical system that has evolved from a combination of traditional practices and health care approaches popular in Europe during the 19th century).

Integrative Health

Integrative health care often brings conventional and complementary approaches together in a coordinated way. It emphasizes a holistic, patient-focused approach to health care and wellness-often including mental, emotional, functional, spiritual, social, and community aspects-and treating the whole person rather than, for example, one organ system. It aims for well-coordinated care between different providers and institutions.

The use of integrative approaches to health and wellness has grown within care settings across the United States. Researchers are currently exploring the potential benefits of integrative health in a variety of situations, including pain management for military personnel and veterans, relief of symptoms in cancer patients and survivors, and programs to promote healthy behaviors.

Types of Complementary Health Approaches

Complementary health approaches include natural products and mind and body practices.

This group includes a variety of products, such as herbs (also known as botanicals), vitamins and minerals, and probiotics. They are widely marketed, readily available to consumers, and often sold as dietary supplements.

According to the 2012 National Health Interview Survey (NHIS), which included a comprehensive survey on the use of complementary health approaches by Americans, 17.7 percent of American adults had used a dietary supplement other than vitamins and minerals in the past year. These products were the most popular complementary health approach in the survey. (See chart.) The most commonly used natural product was fish oil.

Researchers have done large, rigorous studies on a few natural products, but the results often showed that the products didn't work for the conditions studied. Research on others is in progress. While there are indications that some may be helpful, more needs to be learned about the effects of these products in the human body, and about their safety and potential interactions with medicines and other natural products.

Mind and body practices include a large and diverse group of procedures or techniques administered or taught by a trained practitioner or teacher. The 2012 NHIS showed that yoga, chiropractic and osteopathic manipulation, and meditation are among the most popular mind and body practices used by adults. According to the 2017 NHIS, the popularity of yoga has grown dramatically in recent years, from 9.5 percent of U.S. adults practicing yoga in 2012 to 14.3 percent in 2017. The 2017 NHIS also showed that the use of meditation increased more than threefold from 4.1 percent in 2012 to 14.2 percent in 2017.

Other mind and body practices include acupuncture, relaxation techniques (such as breathing exercises, guided imagery, and progressive muscle relaxation), tai chi, qi gong, hypnotherapy, Feldenkrais method, Alexander technique, Pilates, Rolfing Structural Integration, and Trager psychophysical integration.

The amount of research on mind and body approaches varies widely depending on the practice. For example, researchers have done many studies on acupuncture, yoga, spinal manipulation, and meditation, but there have been fewer studies on some other practices.

Other Complementary Health Approaches

Some complementary approaches may not neatly fit into either of these groups-for example, the practices of traditional healers, Ayurvedic medicine, traditional Chinese medicine, homeopathy, naturopathy, and functional medicine.

NCCIH's Role

NCCIH is the Federal Government's lead agency for scientific research on complementary and integrative health approaches.

NCCIH's Mission and Vision

The mission of NCCIH is to define, through rigorous scientific investigation, the usefulness and safety of complementary and integrative health interventions and their roles in improving health and health care.

NCCIH's vision is that scientific evidence informs decision making by the public, by health care professionals, and by health policymakers regarding the use and integration of complementary and integrative health approaches.

To learn more, visit the NCCIH Facts-at-a-Glance and Mission webpage.

For More Information

This publication is not copyrighted and is in the public domain. Duplication is encouraged.

NCCIH has provided this material for your information. It is not intended to substitute for the medical expertise and advice of your health care provider(s). We encourage you to discuss any decisions about treatment or care with your health care provider. The mention of any product, service, or therapy is not an endorsement by NCCIH.

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Complementary, Alternative, or Integrative Health: What's In a Name?

# data[].attributes.attachment_link.description
We've all seen the words "complementary," "alternative," and "integrative," but what do they really mean? This fact sheet looks into these terms to help you understand them better and gives you a brief picture of the mission and role of the National Center for Complementary and Integrative Health (NCCIH) in this area of research.