Auckland PSI^TM Institute

We hear it on the news every day. There is an obesity epidemic. We are obese. We just keep getting fatter and fatter. Who's responsible? We must find someone to blame. Why not blame the fat people? Many people in Western society seem to have opted for distancing ourselves from the intolerable and projecting it onto “fat” and "fat people". Our society's rage against fat as sin today may be comparable to the Victorian attitude about sex. Our desperation to avoid the stigma of fat is reflected in how we spend our money. In the United States alone,

"$33 billion annually (is spent) on weight loss products and services. This figure represents consumer dollars spent in the early 1990s on all efforts at weight loss or weight maintenance including low calorie foods, artificially sweetened products such as diet sodas, and memberships to commercial weight loss centers." ^1aColditz

After all, we can't control our age, our height, our colour, our socioeconomic status at birth, our parentage, our increasingly poisonous environment - we need something to claim control over - right? If we can't control our body weight, there's no hope for us - right? Wrong.

In determining normal weight versus overweight or obesity, it is problematic that “ideal” body weight is still being based on the weight and height chart developed by the insurance actuaries at Metropolitan Life Insurance Company^1b, based on the lowest mortality rate for men and women ages 25-59 in 1983. The scientific and statistical validity of this chart is highly questionable at best, considering that it disregards a wide range of the population (for example, those who don't buy life insurance, are under 25 or over 59), is purely based on correlations (which do not prove cause) and ignores many complex health variables. Varying metabolism, exercise and activity levels and regularity, and individual health, environmental, and genetic differences are not taken into account. Increasingly, studies are showing weight to be determined by all of these variables, many of which are not consciously controlled (²Coady, ³Hebebrand, ⁴Heitmann, ⁵U.S. Department of Health and Human Services, and ⁶Verga.

The Body Mass Index (BMI), a more modern version of the above standard-bearer for assessment of obesity, is similarly problematic. The BMI, like the Metropolitan Height and Weight charts, makes no distinction between muscle weight and fat weight:

"One problem with using BMI as a measurement tool is that very muscular people may fall into the “overweight” category when they are actually healthy and fit. Another problem with using BMI is that people who have lost muscle mass, such as the elderly, may be in the “healthy weight” category – according to their BMI – when they actually have reduced nutritional reserves. BMI, therefore, is useful as a general guideline to monitor trends in the population, but by itself is not diagnostic of an individual patient’s health status." ⁷National Institutes for Health, 2001)

And, according to ⁸Gallagher:

“… misclassification of fatness by BMI may occur in over one fourth of healthy adults.”

Unfortunately, BMI is now used both for medical diagnoses and self diagnoses every day in doctor's offices, bathrooms and gyms across the world.

Another problem causing confusion is that the distinction between compulsive overeating, or Binge Eating Disorder (BED), and obesity is rarely made. Most individuals, doctors included, equate the two, and prescribe weight loss diets for people deemed to be 'overweight" by these most subjective of assessment tools. Although most persons with BED are overweight, the reverse is not the case, because obesity has many causes other than compulsive overeating. For example, obese people have been found to expend less energy while sleeping and resting than those who are not obese, making it easier to gain weight on lower caloric intake than those with higher resting energy expenditure rates:

"Resting energy expenditure (REE) was investigated by indirect calorimetry in relation to body composition and to different degrees of obesity in order to assess if a defective energy expenditure contributes to extra body fat accumulation …. The analysis showed a negative impact of obesity on REE beyond body composition variables." (⁶Verga, p. 47)

Putting such a person on caloric restriction regimens is bound to fail, as their bodies will tell them that they are not getting enough to eat (they will have a constant nagging hunger that will only ease up when they eat). Checking for medications that cause weight gain, educating about food additives and trans fatty acids or transfats, and encouraging an increase in activity levels with guidance on how to incorporate regular exercise into daily routines is the only humane prescription for obesity when it is not related to overeating.

Additional causes of obesity unrelated to compulsive eating were also found by studies from the ⁷National Institutes for Health, and by ⁴Heitmann. Obesity has been shown to have a significant genetic component according to cross-sectional twin and family studies done by ²Coady. And this genetic component is compounded by the tendency of obese people to mate with each other, as they are often excluded from mainstream dating circles. From ³Hebebrand:

"Our results indicate that assortative mating is common among parents of extremely obese children and adolescents, ascertained between 1995 and 1997. In addition, the parental loading on the tenth decile is most prominent for the most obese children." (p. 345)

Moreover, recent research by ¹²Dallman suggests that high levels of stress over a long period of time (such as those caused poverty, chronic trauma and childhood abuse) can create changes in the brain that causes the body to redistribute its fat stores to the abdominal area and increases sucrose (sweets) appetite. Ironically, the stigma from being fat, especially as a child, and the consequent vulnerability to ongoing bullying and abuse by peers can set this viscous cycle in motion or exacerbate it early on.

Imposing actuarial based statistics normed on people who carried life insurance policies in 1983 on people who have been shunned for being different (fat) since childhood only reinforces the abusive cultural and familial messages that have already been internalized by most large people.

In any other "epidemic", would we blame the people who are "afflicted"? If not, then why is this one different? Perhaps because we prefer to believe that we all have conscious control over out weight.

Actually, it is our lifestyle, which is reinforced by the very structures we live and work in - our cities and towns and suburbs - that is the primary influence in this "epidemic". There was no such epidemic among hunter gatherers, and we are physiologically mostly the same now as we were 100,000 years ago. The three biggest environmental influences on obesity are: medication side effects, activity level and regularity of physical exercise, and food additives, such as transfats, that our bodies were not designed to digest. All of these factors are predominantly influenced by cultural forces - sedentary jobs, lack of leisure time, long sedentary commutes, the availability of fast foods to compensate for the lack of leisure time, medications to address the diseases caused by a sedentary yet overly busy lifestyle.

The Associated Press cites obesity expert ¹⁰Tom Farley, the author of Prescription for a Healthy Nation, who says "research in the field has moved away from the notion of personal responsibility to the idea of creating environments that foster healthy living....Physical activity has been engineered out of our world...It should be natural and normal to be physically active, instead of having to go to the gym."

"The solution to obesity is not that everyone should run a marathon," says ¹¹Michael Earls, co-author of a report by Trust for America's Health. "It's the little things that begin to make a dent in the problem, like taking the stairs instead of the elevator or riding your bike to work. If a city or town is built in such a way that it forces residents to drive long distances, instead of walking or cycling, then physical activity becomes something that has to be planned rather than an activity which can be woven into the fabric of everyday life," he said.

I would add to these suggestions that we, as a culture, should confront this needless cruelty in ourselves and each other, and transform our living environments into places that are accepting of differences. To do so, we might need to change the way we live, and stop relying on passive entertainment and fast foods paid for by industries that profit off of our self and body loathing. We might have to look to each other for recreation and community instead.

References:
²Coady, S.A., Jaquish, C.E., Fabsitz, R.R., Larson, M.G., Cupples, L.A., & Myers, R.H. (2002). Genetic variability of adult body mass index: a longitudinal assessment in Framingham families. Obesity Research, 10, 675-81.

^1aColditz, G.A. (1992). Economic costs of obesity. American Journal of Clinical Nutrition, 55, 503-507.

¹²Dallman, M.F., Pecorary, N., Akana, S.F., la Fleur, S.E., Gomez, F., houshyar, H., Bell, M.E., Bhatnagar, S., Laugero, K.D., and Manalo, S. (2003) Chronic stress and obesity: A new view of "comfort food". Proceedings of the National Academy of Sciences of the USA, 100/20, 11696-1170¹

¹¹ Trust for America's Health Report. (2005). F as in Fat: How obesity policies are failing in America.

¹⁰Farley, Tom, (2005). Prescription for a Healthy Nation : A New Approach to Improving Our Lives by Fixing Our Everyday World. Boston: Beacon Press

⁸Gallagher, D., Testolin, C., Heshka, S., & Heymsfield, S.B. (n.d.). Body mass index: Differential misclassification of under and over-fatness. New York City: Obesity Research Center, St.

³Hebebrand, J., Wulftange, H., Goerg, T., Ziegler, A., Hinney, A., Barth, N., Mayer, H., & Remschmidt, H. (2000). Epidemic obesity: are genetic factors involved via increased rates of assortative mating? International Journal of Obesity Related Metabolic Disorders, 24, 345-53

⁴Heitmann, B.L., Harris, J.R., Lissner, L., & Pedersen, N.L. (1999). Genetic effects on weight change and food intake in Swedish adult twins. American Journal of Clinical Nutrition, 69, 597-602.

^1bMetropolitan Life Insurance Company (1983). Metropolitan height and weight tables. New York: Author.

⁷National Institutes for Health (2001). Understanding adult obesity. NIH Publication No. 01-3680. Washington, DC: U.S. Government Printing Office.

⁵U.S. Department of Health and Human Services, Centers for Disease Control and Prevention (1996). Physical activity and health: A report of the surgeon general. Washington, DC: U.S. Government Printing Office.

⁶Verga, S, Buscemi, S., & Caimi, G. (1994). Resting energy expenditure and body composition in morbidly obese, obese and control subjects. Acta Diabetologia, 31(1), 47-51.

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