The Obesity Paradox (Addendum)

The obesity paradox describes the apparent contradiction that despite a large energy intake and massive fat reserves, the obesity disease is perceived by the hypothalamus as one of starvation. This explains the total failure of calorie restriction and exercise to cause weight loss in obesity, a situation akin to feeding a starving man less food and making him work hard in a field. The reason for the obesity paradox stems largely from the leptin and insulin resistance that develops from low quality foods that typify the Western diet. Leptin and insulin act as afferent signals to the hypothalamus and under normal circumstances provide information on the state of adipocyte storage size (leptin) and on the short-term availability of glucose in plasma (insulin). When these signals become muted through insensitivity in the receptors of the hypothalamus, the situation is interpreted as one of low levels of both leptin and insulin. This causes the hypothalamus to respond as if fat stores were low and as if blood sugar levels were in a fasting state.

Under these conditions, forcing the issue with calorie restriction and physical activity is counter productive. It is also morally wrong, just as it would be to force a starving man to build a bridge across a river or plough a field. The physiological responses to forced calorie restriction or physical activity by the starving man are not dissimilar to those of the obese man. Energy expenditure is restricted significantly by the hypothalamus, including reductions in the thermic effects of food and activity, in addition to a downregulation of the resting metabolic rate. In terms of the former, this is achieved by restrictions in the release and circulation of catecholamine hormones, while the later is achieved through down regulation of the circulating levels of the active T3 thyroid hormone. In addition, the protein of the body becomes a source of fuel and the alanine cycle is upregulated to supply the liver with a source of amino acids that can be converted to glucose. The end result is a tenacious effort to maintain body fat, and all the while protein is being burned as a fuel.

This explains the large loss of protein seen initially during dieting. It is observed that much of the weight loss seen in low calorie diets in the initial stages is skeletal muscle, something that can lead to semi-permenant down-regulation of the resting metabolic rate, the damage from which can last for years. The loss of protein is problematic because skeletal muscle mass is inversely associated with mortality. As protein is lost, not just skeletal muscle is catabolised, but also protein from organs and vital structures. This loss of body protein increases the risk of death considerably because protein can be lost from cardiac muscle and this greatly increases the risk of arrhythmias. For example, in a study published in the American Journal of Clinical Nutrition1, researchers re-examined the medical data on obese dieters who died during a very low calorie diet comprising of collagen hydrolysates taken from between 2 to 8 months. The data showed that the survival times of the patients were related to their initial body mass index and therefore their initial fatness.

Obese subjects are known to have higher resting metabolic rates compared to normal weight individuals because they have more skeletal muscle mass. It therefore makes sense that the more overweight subjects survived for longer because under conditions of protein catabolism they had larger stores of protein. The subjects likely died because they lost too much cardiac protein and this caused heart failure in the subjects, and it is likely that the more overweight subjects took a longer time to reach this point because of their higher skeletal muscle masses. This shows the futility of trying to force weight loss while the hypothalamus is in the process of conserving energy. Effective weight loss is only achieved through removal of the metabolic dysfunction that causes the leptin and insulin resistance. Because this leptin and insulin resistance is caused by a low quality Western diet, it stands to reason that the cure is a high quality traditional diet, something that has been shown to cause weight loss even in the absence of physical activity or calorie restriction.

RdB

1van Itallie, T. B. and Yang, M. 1984. Cardiac dysfunction in obese dieters: a potentially lethal complication of rapid, massive weight loss. American Journal of Clinical Nutrition. 39: 695-702

About Robert Barrington

Robert Barrington is a writer, nutritionist, lecturer and philosopher.
This entry was posted in Cardiovascular Disease, Insulin Resistance, Leptin Resistance, Mortality, Obesity, Traditional Diets, Weight Loss, Western Diet. Bookmark the permalink.