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Post-fasting obesity

By Dr. Roberto Uliano

The causes of the yo-yo effect: adipose-specific thermogenesis

Yo-yo effect

In a dietary course we see a rapid decrease in body weight and a subsequent very slow, almost exhausting, phase of weight loss. This second phase is very critical for any weight loss program, as the patient gets tired of not getting results and, defeated, resumes habitual feeding, sometimes even in an excessive way, recovering the lost weight very quickly.

This mechanism, in scientific terms, is called " yo-yo effect " because, after a rapid weight loss, we see an equally rapid increase in weight. In most cases the patient will try to get back on the diet to reach the desired weight.

Slow metabolism

During a weight loss diet the body's metabolism decreases

Regardless of the psychological factors that lead to breaking a diet and resuming the previous diet, few people know that during the phases of food restriction, the body adapts and changes its metabolic efficiency, also trying to save energy through a decrease basal metabolism, cellular energy, and tissue reconstruction speed. It is as if the organism slowed down all its activities to save and not to succumb to the lack of food.

In 1950 Keys and his collaborators (so to speak the scholar of the Mediterranean diet) studied the effects of prolonged semi-fast and the subsequent re-feeding on conscientious objectors during the Second World War. They noted that in the re-feeding phase, when body fat was recovered 100%, the recovery of the lean mass was still at 40%. These results led to describing the preferential accumulation of fat as " post-fasting obesity ".

Fifty years later these results were confirmed by Weyer also in anorexia and in hypermetabolic pathologies. The slow recovery of the lean mass was due either to an inadequate intake of proteins or other necessary nutrients, or to a quantity of food taken energetically higher than the body's demands. In fact it was seen that this mechanism also recurred punctually with balanced diets, with the right intake of proteins or with low-fat diets. These experimental evidences lead to understand that there is a shift of the organism towards a greater metabolic efficiency in the moments of restriction that allows, however, the subsequent recovery of fat, to the detriment of the lean mass, in the re-feeding phase. What is the cause? it is adaptive thermogenesis that plays a crucial role in this mechanism .

Adaptive thermogenesis

Adaptive thermogenesis is a mechanism that produces heat in response to various environmental stresses such as cold, overeating and infections.

In the case of intense cold the heat is used to keep the temperature of the organs constant, while in the case of hyper-feeding this energy dissipation serves as a regulator of body weight.

Thermogenesis is under control of the sympathetic nervous system thanks to noradrenaline and thyroid hormones. To learn more: brown adipose tissue.

What happens, therefore, in the restriction phase and in the subsequent re-supply phase?

Until some time ago it was thought that the slowing of weight loss during a diet was due to the loss of lean mass and therefore to the slowing down of the metabolism.

In fact, the slowing down of metabolism is proportional to the loss of lean mass, so losing weight is natural to have a lower metabolism. The difference lies in the suppression of adaptive thermogenesis.

In the state of semi-fast characteristic of low-calorie diets, the body adapts by decreasing thermogenesis, thus eliminating the source of energy expenditure that allows a greater weight loss (it often happens that in the diets it feels cold).

The consequence is that weight loss stops.

Subsequently, during the re-feeding phase, thermogenesis under the control of the sympathetic nervous system is quickly reactivated to produce heat, so that the organs respond quickly to stressful stimuli, however another type of thermogenesis remains, suppressed by the muscle skeletal, defined adipose-specific thermogenesis, which depends on the reserves of adipose tissue.

This thermogenesis is a signal sent to the muscle in order not to activate protein synthesis (a very expensive energy process) and therefore to slow down the reconstitution of lean mass.

The downside is that the metabolism still remains at the semi-fasting stage and therefore still inefficient to support an excessive re-feeding. Only when the fat reserves are 100% recovered does muscle reconstitution and protein synthesis begin. This means it increases the likelihood of getting back the pounds lost and beyond.

Moreover in this phase there is a greater incidence of hypertensive risk and insulin resistance states, characteristic of diabetes.

The topic still has many points to look into, but it certainly lays the foundations for a different approach compared to the highly hypocaloric diets, an approach that revises both the metabolic aspect and the nutritional aspect in the treatment of obesity.