Etiology of obesity

Obesity results from an imbalance between energy intake and energy expenditure. That said, what influences the development of obesity? Why are so many Americans obese? The answer appears to be multifactorial, including: lifestyle, genetics, environment and neurobiology.

• Lifestyle choices that can affect the development of obesity include the type and amount of food intake and the amount of regular physical activity. As a result of consuming energy dense foods and a more sedentary habit, Swinburn, Sacks et al. estimate that the today's adult Americans have an energy surplus of ≈ 400 Calories/day greater than their 1970's counterparts.
• Genetic influences including multiple known variations in the fat mass and obesity-associated (FTO) gene have been associated with obesity. Individuals who are homozygous for certain FTO mutations have a greater risk of obesity then those who were heterozygous.* The literature strongly suggests that at least 22 other genes may influence a predisposition toward obesity.* Wardle J, Carnell S, et al. have estimated the heritability of BMI in children to be about 60% and individual variations to be 40%. Environmental factors can trigger the expression of these genetic predispositions.
• Environmental factors including food availability and pricing have been shown to influence the incidence of obesity. Sieden and Hawley et al. found a correlation between obesity and the dietary shifts from the traditional Samoan starchy food diet to one high in fat calories. From 1980 to 2010 the mean BMI rose 18% for Samoan males and females, 35-44 years old.*
  Powell, Han and Chaloupka found that "the relative costs of healthful vs. less healthful foods are higher and that this gap has increased over time". They also found that "the price of fast food but not the availability of fast food restaurants had a significant effect on teen BMI" and that the weight of teens in lower to middle socioeconomic status families was most sensitive to fast food prices.*
• Neurobiology of food addiction remains controversial, but "Drug abuse and addiction, and certain types of obesity can be understood as resulting from habits that strengthen with repetition of the behavior and that become increasingly harder for the individual to control despite their potentially catastrophic consequences." "Consumption of food, other than eating from hunger, and some drug use are initially driven by their rewarding properties, which in both instances involves activation of mesolimbic dopamine (DA) pathways." "Food activates brain reward circuitry both through palatability (involves endogenous opioids and cannabinoids) and through increases in glucose and insulin concentrations (involves DA increases)". Neuronal "circuits, which are modulated by DA, interact with one another so that disruption in one circuit can be buffered by another, which highlights the need of multiprong approaches in the treatment of addiction and obesity".*

A number of theories have been offered to explain how these factors work together to predispose humans toward overweight and obesity. The following are two examples:

• Glucostatic theory posits that a drop in glucose metabolism by neurons in the hypothalamus stimulates hunger and feeding behavior. Conversely, increased glucose metabolism by cells in the hypothalamus generates feelings of satiety and suppresses the desire for food. Chaput and Trembray (2009) found that glycemic reduction associated with post-gastric bypass, very low energy diets, carbohydrate-restricted diets and weight loss beyond 10% of body weight, destabilizes energy homeostasis inducing psychobiological vulnerability that favors weight regain.
• Leptin resistance is a common feature of obesity. Leptin is a hormone produced by adipose tissue. It is produced in proportion to adiposity and is often used as a proxy for a measure of total body fat. Circulating leptin serves to communicate the state of body energy stores to the central nervous system (CNS) in order to suppress food intake and permit energy expenditure. Leptin resistance has been shown to increase food intake along with decreased energy expenditure in both rodents and humans. Leptin receptors are known to be concentrated in areas of the hypothalamus that mediate hunger and feeding behaviors.*

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