Obesity is a serious concern because of the increased morbidity and mortality associated with adiposity. The traditional view of obesity is that lethargy and greed cause a positive energy balance, and this over the long-term translates into weight gain and accretion of body fat. The mainstream medical establishment would suggest that the treatment for such individuals is the forcing of a negative energy balance through vigorous exercise with calorie restriction. The problem with this theory is that the nutritional literature does not support this view point. For example, energy restriction has been shown to be ineffective at causing long-term weight loss and exercise is reported to stimulate appetite and increase energy intake. These factors explain the very high failure rate of individuals attempting to lose weight using the traditional paradigm as a model of treatment.
The main problem with the mainstream viewpoint on weight loss is that the cause and effect of weight gain has not been proven. It is true that a positive energy balance is associated with weight gain, but the cause and effect of the relationship is not straight forward. For example, while overeating and lack of exercise could be said to cause weight gain (the traditional viewpoint), it is just as true to say being overweight causes low energy levels and stimulates the appetite. Both of these scenarios maintain the association between weight gain and energy balance, but only the second explains the abject failure of diet and exercise regimens to produce effective long-term weight loss. The second scenario also nicely explains the positive weight loss results seen through eating high quality nutrient-rich diets even despite ad libitum feeding with no energy restriction.
Misunderstanding of the cause and effects of weight gain often leads to improper conclusions from data in research. This was illustrated in a paper published in the European Journal of Clinical Nutrition in 20081. In this study the researchers investigated the association between watching television with the subsequent increase in body mass index (BMI). The results showed that watching television more frequently at 11, 16 and 23 years was associated with a faster gain in BMI between 23 and 45 years in females, but not in males. Frequent television viewing at 16 years was associated with a faster gain in BMI between 16 and 45 years in both males and females. Television viewing at 23 years was associated with waist-to-hip ratios such that by 45 years, those watching television >4 hours per day had waist-to-hip ratios 0.03 to 0.04 higher than those watching television <1 hour per day.
While these results suggest that television viewing causes weight gain, care needs to be taken with interpretation of correlation statistics. The authors conclude that television viewing could be targeted in order to prevent obesity, making the assumption that the television watching was the cause of adiposity. However, this conclusion is based on the assumption that the cause of weight gain is lethargy. Similarly over simplistic unimaginative thinking has wasted years of research time trying to prove that lack of calcium in the diet in the cause of osteoporosis and that cholesterol in the diet the cause of cardiovascular disease. Logically, why should watching television make individuals overweight any more than reading a book, driving a car or sleeping? Logically it should not, and only preconceived bias that televisions is bad while reading is good, can shape such an obviously absurd viewpoint.
Let us for a minute assume that weight gain is caused not by lethargy and greed, but by a fructose-induced metabolic dysfunction in the insulin receptor, as has been shown in animal models. In this scenario, as blood sugar rises it is unable to enter the skeletal muscle due to defective insulin receptor function, and so glycogen stores become depleted. Instead, the glucose enters adipose tissue and is converted to triglycerides leading to increased adiposity. In addition, the insulin resistance raises fasting blood glucose levels and this decreases oxidation of free fatty acids in muscle. Muscle therefore become depleted of energy leading to a decrease in work output. At the same time, the dysfunctional insulin system disrupts negative feedback inhibition of appetite and satiety signals decrease. Would such an abnormal metabolism not make it more likely that an individual would sit in a chair and eat while watching television?
RdB
