Portal de Periódicos da CAPES

Metabolic and Endocrine Pathology during Hangover

1977; Springer Nature; Linguagem: Inglês

10.1007/978-1-4615-9038-5_28

2214-8019

Reino Ylikahri, Matti Huttunen,

High Altitude and Hypoxia

The role of several metabolic and endocrine factors in the pathogenesis of hangover has been studied in healthy human volunteers under experimental conditions. Significant changes in the blood concentrations of acetaldehyde, glucose, lactate, ketone bodies and free fatty acids were found during hangover, but none of these changes correlated with the intensity of hangover. Plasma electrolyte concentrations were not changed during hangover, except for a mild metabolic acidosis which had a significant correlation with the intensity of hangover. The metabolic changes, including acidosis, could be prevented by the administration of fructose. However, fructose had no effect on the intensity of hangover. The basal concentrations of the anterior-pituitary hormones, i. e., thyroid stimulating hormone (TSH), luteinizing hormone (LH), growth hormone (GH) and prolactin (PRL), in plasma were not significantly altered during hangover. The secretion of TSH and LH induced by the administration of the releasing hormones (TRH and LHRH) was not affected by alcohol intoxication or hangover, but the TRH-induced release of PRL was totally blocked during hangover. This may indicate increased dopaminergic activity in the hypothalamus during hangover. The plasma concentration of Cortisol was elevated and that of testosterone decreased during hangover, but these changes are probably only unspecific reactions to the stress. It is concluded that the metabolic and endocrine factors studied by us probably do not have any major role in the pathogenesis of hangover. However, the observed changes in the secretion of PRL may reflect the primary neural events involved in the induction of hangover.