***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Aims Alcohol and hypoglycaemia independently affect cognitive function . This may be relevant for insulin‐treated diabetic patients who drive motor vehicles . The aim of this study was to examine the effect of mild hypoglycaemia ( 2.8 mmol/l ) with modest alcohol intoxication ( levels below UK driving limits ) on intellectual performance in patients with Type 1 diabetes The aim of the present study was to evaluate the acute effect of ethanol on insulin sensitivity , and glucose , insulin , free fatty acid ( FFA ) , and triacylglycerol responses in ten patients with non-insulin-dependent ( type 2 ) diabetes . In the test study an oral dose of 0.66 g ethanol/kg followed by continuous intravenous infusion of 0.1 g ethanol/kg per h was given to maintain a constant ethanol level in the blood . In the control study identical volumes of oral water and intravenous saline ( 9 g NaCl/l ) were given . After 90 min insulin sensitivity was determined by the hyperinsulinaemic , euglycaemic clamp technique . Ethanol caused no change in blood glucose or insulin concentrations . The FFA level was suppressed by ethanol while the triacylglycerol level was unaffected . The insulin sensitivity was not affected by ethanol . No major acute effect of ethanol on the glycaemic control in fasting type 2 diabetic patients was found in comparison with what is seen in healthy people . The present study , along with the sparse literature , indicates that the ability of ethanol to induce hypoglycaemia is attenuated or absent in diet-treated type 2 diabetes . Furthermore , we found no change in insulin sensitivity . Consequently , the risk of acute ethanol-induced aberrations in carbohydrate metabolism in diet-treated type 2 diabetes seems to be less than previously expected , when alcohol is not taken as a part of a meal Drinking ethanol is widely believed to predispose to hypoglycaemia in patients with Type 1 diabetes , the suggested mechanism being suppression of hepatic gluconeogenesis . The hypoglycaemic effect of ethanol was investigated by measuring steady‐state glucose infusion rate during a hypoinsulinaemic ( mean plasma insulin 14 ± 1.3 ( SEM ) mU I‐1 ) , euglycaemic ( blood glucose 5 mmol I‐1 ) clamp . Nine patients with Type 1 diabetes fasted overnight and then had , in single‐blind fashion , ethanol 0.5 g kg‐1 by intravenous bolus followed by 0.25 g kg‐1 h‐1 or matched volumes of saline . After 1 h of ethanol or saline , all infusions were stopped and blood glucose monitored for a further 90 min . A 60‐min ethanol infusion leading to a steady‐state blood concentration of 26.2 ± 1.4 mmol I‐1 ( 120.7 mg % ) did not alter the glucose infusion rate needed to maintain euglycaemia ( 1.22 ± 0.12 mg kg‐1 min‐1 before and 1.23 ± 0.12 during ethanol infusion ) , the initial rate of fall of blood glucose  ( ethanol 0.039 mmol I‐1 min‐1 vs control ( 0.033 ) , the lowest blood glucose ( 4.43 mmol I‐1 vs 4.31 ) , or the rate of blood glucose recovery  ( ethanol 0.050 mmol I‐1 min‐1 vs control 0.054 ) . We conclude that a moderate amount of ethanol , administered intravenously under controlled conditions , does not lead to hypoglycaemia in patients with Type 1 diabetes who have fasted overnight Summary Both hypoglycaemia and alcohol consumption affect cognitive function but it is unclear whether moderate drinking alters awareness of hypoglycaemia . We have examined this in a single blind r and omised hyperinsulinaemic clamp study in eight non-diabetic subjects and seven Type 1 ( insulin-dependent ) diabetic patients . After 30 min of euglycaemia ( blood glucose 4.5 mmol/l ) subjects drank either 0.75 g/kg ethanol or a placebo drink after which blood glucose was lowered to 2.5 mmol/l for 40 min . Awareness of hypoglycaemia , reaction time and physiological responses were measured before and after ethanol . At a blood glucose concentration of 4.5 mmol/l , ethanol ( producing peak blood levels of 20–25 mmol/l ) caused a transient increase in systolic blood pressure ( p<0.05 ) , a sustained increase in heart rate ( p<0.01 ) and a slowing of reaction time in both normal subjects and diabetic patients . During hypoglycaemia in both groups , the slowing of reaction time and increase in sweating were more marked after ethanol than placebo ( both p<0.05 ) , while the increase in finger tremor ( p<0.05 ) was blunted after ethanol , in both groups . Counter regulatory hormone secretion was not affected by ethanol . Despite increases in symptoms during hypoglycaemia , only 2 of 15 individuals “ felt hypoglycaemic ” after ethanol compared to 11 out of 15 after placebo . We conclude that after moderate drinking non-diabetic subjects and Type 1 diabetic patients are less aware of hypoglycaemia despite exaggerated physiological changes The objectives of this study were to test the hypothesis that alcohol can cause reactive hypoglycemia by attenuating the release of counterregulatory hormones . The subjects were eight healthy volunteers ( five men and three women , aged 20 - 40 yr ) . Each subject drank , using a r and omized , 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 difference , -6 to 22 microU/mL ) . After the ingestion of G+T , the blood glucose 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 drinking gin , subjects reported typical hypoglycemic warning symptoms unrelated to the prevailing glucose level . In both alcohol studies , there was marked blunting of GH release ( P < 0.01 ) . Despite a blood glucose nadir of 3.35 mmol/L , plasma epinephrine levels rose only slightly from 267 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 velocity in both cerebral hemispheres in the G+T study ( P < 0.05 ) . In otherwise healthy individuals a combination of gin and regular tonic can induce reactive hypoglycemia . Acute ingestion of alcohol impairs the epinephrine response and markedly suppresses the release of GH in response to a fall in blood glucose levels We have recently shown , in studies with patients with Type 1 ( insulin dependent ) diabetes , that alcohol intake at 2100 hrs significantly reduced blood glucose values after 10 - 12 hours , compared with control studies with no alcohol . We hypothesised that this was due to the following effects of alcohol : 1 . Alcohol metabolism increases NADH , leading to a reduction in hepatic gluconeogenesis ; and 2 . increased glycogen phosphorylase activity depletes hepatic glycogen stores ; 3 . After the alcohol is metabolised , hepatic insulin sensitivity is increased , leading to the restoration of glycogen stores and reduction in blood glucose levels , and 4 . consequently , after several hours , glycogen stores and insulin sensitivity return to normal . A model describing these changes ( DiasNet-Alcohol ) was implemented into the DiasNet model of human glucose metabolism . Our study suggests that the DiasNet-Alcohol model gives a reasonable approximation of the effect of alcohol on blood glucose concentration observed in our study and supports our hypothesis for the mechanism behind these effects in Type 1 diabetes 
    Output:
    
All associations recommend that ethanol should only be consumed with food intake .
The majority of included studies showed that ethanol intake increased the risk of hypoglycemia in patients with T1D .