It is a sobering fact that more than a third of America’s adults are obese, along with nearly 18% of US children. Weight gain is more complex than a simple mathematical equation (Caloric Intake > Caloric Expenditure = Weight Gain).
A constellation of genetics, environment, and behavior contribute to obesity. In this article, we’ll explore these factors and the research around them.
In the mid-1990s, research revealed the presence of the obesity gene—known as the ob gene—and its related protein, leptin, a hormone produced by fat cells. These discoveries were initially thought to be the answer to the obesity epidemic, but in fact they provoked even more questions related to the complex feedback signaling system that involves adipose (fat) tissue and the brain.
Animal studies have shown that leptin has two effects: reduction of caloric intake and enhancement of energy use. In other words, it burns fat (Jequier E & Tappy L, Physiol Rev 1999;79(2)451–480).
In human studies, a congenital deficiency in leptin results in marked obesity, hyperinsulinemia, insulin resistance, and hyperphagia (increased hunger), a common presentation of obese patients. This actual genetic mutation, however, is quite rare. Most obese people are actually hyperleptinemic—or have an abundance of leptin, not a deficiency.
Other rodent models of obesity have led to the discovery of even more genetic mutations related to obesity. One is the “fat mutation” of the gene coding for the protein carboxypeptidase E (CPE). CPE plays a role in the synthesis of appetite suppressing chemicals, and this mutation can cause weight gain by decreasing their production.
Animal models of obesity and genes are groundbreaking, but how do they affect heritability? One study that looked at the early life risk factors of obesity found that maternal and paternal body mass index (BMI), as well as maternal gestational weight gain, contribute to obesity (Bammann K, PloS ONE 2014;9(2):e86914). Studies of adopted children and twins have also shown that human obesity has a genetic component.
The heritability of BMI is 25%–40% (Bouchard C. Genetics of obesity in humans: current issues. In: The Origins and Consequences of Obesity. Chichester, UK: Wiley, 1996, p.108 –117). Age-related changes in body fatness and total body fat during young adult life are also heritable.
This is not an all or nothing game, though. The genes involved in weight gain only increase the susceptibility of an individual to the development of obesity. Simply having the genes does not guarantee one will be obese.
It’s been traditionally thought that during infancy and early childhood, we have an innate sense of satiety (or the feeling of knowing you’ve had enough to eat). One study of infant appetite, food responsiveness, and growth in twins found that infants with lower satiety and higher food responsiveness were heavier than their twin by three months of age, when both were exclusively breastfed (van Jaarsveld CHM et al, JAMA Pediatrics 2014;online ahead of print). These findings suggest something more than just genetics is contributing to the development of appetite and early rapid weight gain, both of which are associated with increased lifetime risk of obesity.
Mothers’ parenting may play a role in this. Since the foundation for eating habits is laid in early childhood, another study explored the role of maternal feeding practices in relation to weight gain and obesity-promoting eating patterns in two-year-old children (Rodgers RF et al, Int J Behav Nutr Phys Act 2013;10:24). The study looked at parental feeding efforts including intake monitoring, restriction of calories and variety, pushed feeds, and reward-based practices (eg, “you get dessert if you finish your whole dinner!”).
All of these methods, though pursued in the child’s best interest, actually encourage negative eating behaviors in children. Interestingly, restricting snacks between meals and limiting access to high-fat foods may not work either, as they often have the unintended result of “obesogenic eating behaviors” like habitual gorging and emotional eating even when a child is not hungry (Faith MS et al, Obes Res 2004;12(11):1711–1722).
The authors also report that maternal emotional feeding practices predicted children’s emotional eating and tendency toward high calorie, low nutrition snacks in response to external cues. These miscues and external influences of using “treats” as a reward or to correct negative behaviors in children may lead to abnormal weight gain, dysfunctional relationships with food, and generalized coping difficulties.
Since emotional eating in children has been associated with overweight and binge eating disorder in adolescence, recognition of this maternal-child relationship is a key treatment strategy for prevention of child obesity (Braet C et al, J Health Psychol 2008,13(6):733–743; Stice E et al, Health Psychol 2002;21(2):131–138).
Certain personality traits may be an early indicator of genetic vulnerability to a variety of pathological behaviors, including binge-eating episodes (Koren R et al, Twin Res Hum Genet 2014;17(2):65–71). In fact, one study demonstrated that patients with classic eating disorders (anorexia nervosa, bulimia, and binge eating) had higher sensitivity to punishment than controls, which echoes the internalizing tendencies of these patients (Harrison A et al, Psychiatry Res 2010;177(1–2):1–11).
Another study investigated whether personality is associated with fluctuations in weight over time. This study found that those individuals who scored high in neuroticism or low in conscientiousness are more susceptible to becoming overweight or obese because of associated subcharacteristics of these traits, such as high impulsivity and low self-discipline (Sutin AR et al, J Pers Soc Psychol 2011;101(3):579–592). This configuration of traits makes these individuals vulnerable to temptation and makes it more difficult to stay on task during stressful times or life’s difficulties.
Not only are people with high neuroticism and low conscientiousness vulnerable to becoming overweight and obese, but they are also in peril because of other high-risk behaviors that contribute to poor health. These individuals are inclined to smoke, abuse drugs, be sedentary, and binge eat and drink (Rush CC et al, Psychol Addict Behav 2009;23(1):140–145). They also struggle with weight regulation (the tendency for weight to yo-yo) and major comorbidities, including hypertriglyceridemia, hypertension, and even elevated inflammatory markers.
Thus, their personality leads to low “willpower” and perseverance skills, which are necessary for success with consistent diet and exercise to achieve and maintain a healthy weight. Undoubtedly, these behaviors have been modeled or learned from early childhood. They establish a strong risk for obesity from day one in individuals with the genetic potential for obesity and neurotic, impulsive, sensitive, and high-achieving personalities.
TCRBH’s Take: Obesity is caused by a complex interplay of nature and nurture. Unfortunately, we can’t help our obese clients change their genes, but we can help them with strategies to change ingrained attitudes and relationships with food that may trace all the way back to childhood. We can also be aware that certain personality types may be more likely to be obese and need more help controlling impulses and high-risk behaviors.
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