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Health Doesn't Equal Weight

Various studies have examined beliefs about body weight, body weight controllability, and weight management, and found that individuals believe obesity is primarily caused by poor diet, and thinness is a result of self-control (Ravussin, 2020). The misconception that weight status alone can determine one’s health outcome reflects the deeply internalized nature of weight bias in modern society. Anyone who believes that an obese person could become thin by simply following a lifestyle of control fundamentally ignores the power of the energy-balance system centered in the hypothalamus (Aamodt, 2016).

The mechanisms involved in body weight regulation include physiological, biological, and genetic factors. Using twin studies, researchers have consistently found that “at least 40 % of the variability in BMI” is related to genetic factors involved in the “regulation of food intake and/or volitional activity.” (Ravussin, 2020). The body’s attempt to maintain homeostasis is one of the most fundamental concepts in biology, and this applies to our weight. The healthy weight an individual’s body aims for is called a setpoint weight, and like any biological force, and the system works tirelessly to bring his/her body back to a comfortable point (Bacon, 2010).

Research has consistently shown that when total body energy stores exceed the level that the body defends comfortably, “physiological changes that promote restoration of the set point ensue” (Ravussin, 2020). These changes include decreased appetite, increased energy expenditure and hormonal alterations, increased physical activity, among other factors (Ravussin, 2020). This weight restoration system also functions when energy stores are in a deficit, causing adaptive responses that inhibit ongoing weight loss and promotes fat regain (Ravussin, 2020).

More generally, the physiological mechanisms that defend one’s setpoint weight can be simplified to include alterations in one’s appetite, energy expenditure, or energy intake. Leptin, a “adipocyte-derived hormone, has a central role in regulating energy balance” through influencing one’s appetite. Leptin is produced in adipose fat tissue, so when fat cells increase in size, they trigger the release of various chemicals to turn down appetite, increase metabolism, and encourage physical activity to return fat cells to their previous size (Bacon, 2010). Conversely, as fat stores shrink when dieting, so does leptin production, and one’s appetite increases, metabolism decreases, and weight gain will ensue. In essence, leptin protects the body against weight loss in times of scarcity and limits weight gain in times of excess (Bacon, 2010).

On the opposite end of the spectrum, ghrelin is a hormone glibly referred to as the “hunger hormone” by scientists (Bacon, 2010). All day, ghrelin levels rise and fall in the body, and subconsciously trigger behaviors driving humans to eat. Ghrelin acts as an appetite trigger, and leptin turns down the intensity of the ghrelin response. When fat stores are high, leptin is produced and sends nerve messages to the brain that dampen the stimulating effect of ghrelin, or successfully suppress appetite. These two hormones are among many that mediate the body’s hunger system, and help preserve an individual’s setpoint weight.

One component of energy expenditure is exercise, and exercise is largely seen as a socially accepted means to weight loss. Exercise plays a significant role in metabolism and cardiovascular health, however, exercise alone accounts for minimal amounts of long-term weight loss and overall health (Bacon, 2010). Neuroendocrine pathways that produce or suppress hormones to regulate appetite and energy expenditure include anabolic hormones, including NPY, MCH, AgRP, ORX, and catabolic neuropeptides, including CRH, CART, and POMC (McMinn, 2001). When the body has a positive energy balance, neuroendocrine responses contribute to the adaptive changes opposing weight gain by promoting physical activity. To be continued....

Works Cited Aamodt, S. (2016). ​Why diets make us fat: The unintended consequences of our obsession with weight loss​. Melbourne: Scribe.

Bacon, L. (2010). ​Health at every size the surprising truth about your weight​. Dallas: Benbella Books.

Mcminn, J. E., Baskin, D. G., & Schwartz, M. W. (2000). Neuroendocrine mechanisms regulating food intake and body weight. ​Obesity Reviews,1(​ 1), 37-46. doi:10.1046/j.1467-789x.2000.00007.x

Ravussin, E., & Bogardus, C. (2000). Energy balance and weight regulation: Genetics versus environment. ​British Journal of Nutrition,83(​ S1). doi:10.1017/s0007114500000908