To ensure we offer contemporary continuing education opportunities, the CE credit associated with this video is no longer available, however, the video remains available for viewing.
The prevalence of obesity continues to climb in all age groups, and around the world. The standard paradigm assumes that we “eat too much and exercise too little, that obesity is due to two aberrant “behaviors”. However, are these behaviors cause or effect? Our research on children with brain tumors who develop hypothalamic damage and become obese after surgery or radiation, termed “hypothalamic obesity”, demonstrates that they have anatomic “leptin resistance”. In these subjects, excessive insulin release blocks leptin signaling to drive weight gain and hunger, while pharmacologic insulin suppression results in reduced food intake, increases spontaneous activity, and promotes weight loss. Why should insulin block leptin signaling? Leptin is a necessary signal to the VMH for the initiation of high-energy processes, such as puberty and pregnancy. If leptin always worked, then nobody could gain weight, and our reproductive capacity would be shot. Most obese people are hyperinsulinemic. But is that cause or effect? It is assumed that as you gain weight, cytokines are released from adipose tissue, which drive insulin resistance. However, our research demonstrates that dietary sugar is metabolized to fat in the liver, and it is this liver fat that drives insulin resistance unrelated to peripheral fat. Why should sugar drive insulin resistance? Naturally occurring sugar in fruit is what makes fruit palatable. But for our ancestors, fruit was readily available for one month per year, called “harvest time”. Then came four months of winter, and no food at all. We needed to stock up, to increase our adiposity in preparation for four months of famine. In other words, seasonal insulin resistance was evolutionarily adaptive; but year-round insulin resistance due to ubiquitous sugar availability has become maladaptive. It is assumed that people consume sugar because of its palatability. However, there is now evidence that sugar may be addictive in humans. Obese subjects will use sugar to treat psychological symptoms. Overweight women who were self-reported carbohydrate cravers reported greater relief from dysphoria in response to a carbohydrate-containing beverage as compared to a protein drink. Why are we drawn to sweet? Evolutionarily, sweetness was the signal to our ancestors that a given food was safe to eat because there are no sweet foods that are acutely poisonous (even Jamaican vomiting sickness only occurs after consumption of unripe ackee fruit, which is not sweet). Unfortunately, the food industry knows this and adds excess sugar to processed food to make us buy more. Thus, the behaviors associated with obesity are secondary to our biochemistry, and our biochemistry is secondary to our environment. Understanding these evolutionary precepts explain our obesity epidemic, and also point to environmental and policy solutions.
To view a complete description including abstract and learning objectives, please click here.