GIN AND TONIC AND REACTIVE HYPOGLYCEMIA - WHAT IS IMPORTANT - THE GIN, THE TONIC, OR BOTH

The objectives of this study were to test the hypothesis that alcohol can cause reactive hypoglycemia by attenuating the release of counterr egulatory hormones. The subjects were eight healthy volunteers (five m en and three women, aged 20-40 yr). Each subject drank, using a random ized, double blind design 1) three large gin with regular tonics (0.5 g/kg alcohol and 60 g carbohydrate, mainly sucrose (G+T); 2) the same amount of alcohol with Slim-line tonic (0.5 g carbohydrate; G alone); and 3) regular tonic without alcohol (T alone). Glucose, insulin, and counterregulatory hormone levels and middle cerebral artery velocity ( MCAV), an index of cerebral blood flow, were measured. Alcohol levels averaged 60-70 mg/dL. Peak insulin levels were similar in both studies in which regular tonic was consumed (95% confidence interval for diff erence, -6 to 22 mu U/mL). After the ingestion of G+T, the blood gluco se nadir was lower compared to that with T alone (3.35 vs. 3.87 mmol/L ; P < 0.02) or G alone (3.35 vs. 3.95 mmol/L; P < 0.01). After drinkin g gin, subjects reported typical hypoglycemic warning symptoms unrelat ed to the prevailing glucose level. In both alcohol studies, there was marked blunting of GH release (P < 0.01). Despite a blood glucose nad ir of 3.35 mmol/L, plasma epinephrine levels rose only slightly from 2 67 to 455 pmol/L (P = NS) after G+T. Ingestion of alcohol also caused a transient rise in right MCAV (P < 0.05) followed by a late drop in v elocity in both cerebral hemispheres in the G+T study (P < 0.05). In o therwise healthy individuals a combination of gin and regular tonic ca n induce reactive hypoglycemia. Acute ingestion of alcohol impairs the epinephrine response and markedly suppresses the release of GH in res ponse to a fall in blood glucose levels.