With a quick glance around, we can tell that the obesity epidemic is becoming more and more prevalent. And the greater our body weights become, the more we see the whole host of diseases that come along with obesity as well, including diabetes, heart disease, and even some types of cancer.
We like to think that preventing obesity is a simple matter of personal responsibility, and that if we only used our willpower, we could right the imbalance between our caloric intake and expenditure. But it is becoming increasingly clear that solving the obesity problem will require more than the customary fix of a little less chocolate cake and a little more time on the treadmill.
There are at least 32 gene variants that have been implicated as links to obesity, including one that decreases our propensity to choose healthy, low-fat foods. At various times, hormones in our gut, like glucagon-like peptide 1 and oxyntomodulin, are sending satiety signals to our brain, reducing our food intake, while others hormones, like ghrelin, are stimulating our appetites. The peptide hormone leptin, which is secreted by fat tissue and suppresses hunger, was once even a prime candidate for drug therapies — until we realized that blood concentrations of leptin actually increase with body fat and that most obese individuals have developed a resistance to the hormone.
Ashley Gearhardt, a clinical psychology doctoral student at Yale, also discovered that some people show both the neurological and behavioral signs of substance dependence in response to certain craveable types of food, such as ice cream, french fries, and candy, much like a smoker responds to cigarettes. What is intriguing, Gearhardt says, is that not all obese individuals exhibit “food addiction” and that not all lean individuals are free from these signs of dependence. But those who are addicted to food demonstrate the same neural response patterns to food cues as would be predicted for those with substance dependence.
Food addiction brings into question the role of our food environment, in which highly processed foods are advertised through “guerrilla marketing,” particularly to children. We do not yet understand all of the potential consequences that these highly marketed, rewarding foods may have, though Gearhardt suggests that they offer “the potential of hijacking control for at-risk individuals.” When faced with such an intense food environment, efforts at self-control may not be enough.
Striking as well are findings that obesity may even in fact have infectious origins, an idea encompassed in the term “infectobesity.” Already, six different pathogens have been indicted as causing obesity in animals, two of which are also associated with human obesity. Many more obese individuals than lean individuals harbor antibodies in their blood to the human adenovirus, or Ad-36, a pathogen responsible for causing respiratory tract infections, suggesting a link between human obesity and Ad-36.
An even more startling discovery supporting the idea of infectobesity was made in a recent study led by Dr. Jorge Henao-Mejia, Dr. Eran Elinav, and Mrs. Chengcheng Jin in the laboratory of Dr. Richard Flavell, a Sterling Professor of Immunobiology at the Yale School of Medicine and a Howard Hughes Medical Institute Investigator. Their study suggests yet another way in which obesity could be infectious: through gut microbiota, bacteria that live in our intestines. These bacteria populations are regulated by proteins called inflammasomes that are responsible for sensing particular stimuli and triggering an inflammatory response. The team observed that mice that were deficient in certain inflammasomes — and therefore had altered gut bacteria populations — exhibited a higher incidence of fatty liver disease and obesity when fed a high-fat diet. The same severity of disease was reproduced in healthy mice merely by cohousing the two populations, suggesting that the altered gut bacteria condition was infectious.
Elinav is quick to emphasize that this study does not suggest that gut microbiota cause obesity, but rather that it is the combination of diet, genetics, and microflora that promoted obesity in the mice. “This is another contributing mechanism [to obesity],” he explains, “ [but] the dietary component is of no less importance.” Both the high-fat diet and the genetic mutations in inflammasomes, by altering the gut microbiota, were necessary driving factors for the development of liver disease and obesity.
All of these findings add yet additional threads to what is becoming the more and more complex web of obesity, one in which we as humans are becoming increasingly trapped. Obesity is not a simple problem with a straightforward solution, and it does not look like we will be stumbling upon a quick fix anytime soon. But with the whole multitude of contributing factors — genetics, hormones, addiction, viruses, gut microbiota — we know that there is much more to be blamed in this epidemic than just that extra slice of chocolate cake.