Forced Calorie restrictive diets that attempt to coerce the body into accepting a lower level of fat mass are dangerous and do not work. That they cause metabolic damage is well evidenced in the scientific literature. Such dietary regimens are deleterious to the health because excessive weight gain is actually a metabolic dysfunction whereby the hypothalamus becomes insensitive to leptin signaling. As leptin is responsible for relaying information about the size of the adipose tissue, this leptin resistance results in a situation whereby the hypothalamus is informed incorrectly that fat reserves are low and responds with adaptive changes to behaviour and metabolism. Fighting this homeostatic regulation with energy restriction simply causes the body to regulate metabolism as in the starvation state. As a result the skeletal muscle mass of the individual is reduced, because muscle is metabolically expensive to maintain.
In response to forced calorie restriction, the hypothalamus also decreases the amount of energy released from food as heat. This is thought to be due to a reduced level of circulating catecholamines that normally stimulate thermogenesis. The reduced thermic effect of food in combination with the reduction in resting metabolic rate (RMR) significantly increases the risk of weight regain following forced calorie restriction. To counter this effect, formerly obese individuals must consume less food than lean subjects in order to maintain correct weight. This is illustrated by data published in the American Journal of Clinical Nutrition in 19871. In this study, normal weight subjects had similar energy expenditures but higher energy intakes, compared to formerly obese subjects, suggesting that weight gain would be highly likely in the latter should they deviate from their energy restriction.
This data alone should be enough to disprove the tired old ‘eat-too-much, do-too-little’ paradigm of weight gain trotted out by the usual suspects in the medical establishment. That obese subjects prior to weight loss have increased RMR compared to normal weight individuals, but following weight loss to have lower RMR in combination with a blunted thermogenic response to food, is evidence that forced energy restriction is damaging to the metabolism. Because leptin resistance is the underlying cause of the energy dysfunction in obesity, it must be addressed before normal metabolic function be restored. This means reversing the insulin resistance that drives leptin resistance in the hypothalamus. High quality diets devoid of refined fructose and with high fibre to starch ratios are the solution to obesity, because fructose and refined carbohydrates are the main cause of insulin resistance in man.
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