by Jesús Ramón Girando and Julia Libman
Polyphagy is defined as the pathological increase in the feeling of hunger and appetite that results in excess nutrient intake.
Physiology and pathophysiology
Polyphagia is probably based on an imbalance of the hypothalamic centers of satiety and diet (see chapters on Anorexia and Obesity). In the case of the polyphagia that accompanies diabetes mellitus without ketoacidosis, the decrease in the use of carbohydrates causes a state of hydrocarbon starvation and, by a not entirely clear mechanism, hypothalamic centers are affected, which is why there is an increased desire to eat. In this sense, it is interesting to remember that there are insulin receptors in the ventromedial zone of the hypothalamus, and that the presence of this hormone would be necessary for glucose to penetrate the cells of the center of satiety.
Experimental studies suggest that beta endorphin, an opioid peptide, plays a role in appetite control, and that it may be a factor leading to polyphagy, overfeeding, and obesity. Pituitary rats with genetic obesity contain more endorphin. Naloxone, a beta endorphin antagonist, cancels polyphagia in these animals.
Causes of polyphagia
Polyphagia can be secondary to poor eating habits, personal or family, psychiatric conditions or states of anxiety, and endocrine disorders such as diabetes and hyperthyroidism. In these last two cases it is associated with weight loss, as in some malabsorption conditions.
Interrogation and study methodology
The interrogation should evaluate the eating habits, the personality of the patient and the existence of concomitant clinical manifestations. The presence of a goiter with a picture of hypermetabolism, with or without ophthalmopathy, guides the investigation towards a hyperthiroidism. Uptake of Io 131 and the determination of tyroxin (T4) and triiodothyronine (T3) in plasma will confirm the diagnosis. The existence of diarrhea orients a picture of malabsorption, which requires a digestive study. Polyphagia associated with a family and / or obstetric history of diabetes, polyuria, and polidipsia, or signs of neuropathy or coronary heart disease, indicate decompensated diabetes without ketoacidosis. High blood glucose confirms the diagnosis.