Genetic, Traumatic and Environmental Factors in the Etiology of Obesity

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Abstract
From the point of view of mechanism, it appears that hyperphagia may be the result of: (1) Either hypoglycemia or blocks of carbohydrate metabolism, in particular, of the hexokinase reaction, leading to metabolic hypoglycemia of the latero-anterior hypothalamic centers ("feeding center"). Abnormalities of carbohydrate metabolism may be due in turn to endocrine imbalance, where the pituitary, the adrenal cortex, the adrenal medulla, the pancreatic islets, the thyroid and indirectly the gonads may be involved. Equilibrium between the 2 pancreatic hormones may be of particular importance. (2) Increased lipogenesis, decreased rates of mobilization of fat and metabolic inertia of depot fats, due to tissue factors (enzymatic) or to endocrine or nervous influences on these tissues. (3) Immobilization, which brings the organism below the threshold of proportional response of energy intake to energy expenditure. (4) Autonomic disturbances, such as are produced by central-anterior hypothalamic lesions, and probably by lesions of the thalamus and of association fibers from the frontal lobes. The mechanism of this type of hyperphagia is poorly understood. (5) Activation, or release of inhibition, of the feeding centers, unaccompanied by metabolic disturbances. Both the depression of the central (obesity) centers and the activation of the lateral (feeding) centers may be partially under the dependence of cortical factors. (6) Psychosomatic factors either mediated through autonomic or nervous disturbances, or acting exclusively at the cortical level. Obesity is the result of prolonged action of one or several of these factors. This analytical approach appears to permit some differentiations of the increased risks which are characteristically linked with obesity.

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