In people with type 1 diabetes, both mild alcohol intoxication and hypoglycemia (blood glucose ~43 mg/dL) were associated with deterioration in reaction time and other tests of cognitive function, and the total impairment was greater when both were experienced together (Cheyne 2004). The authors emphasize the importance of individuals testing blood glucose levels before driving and not driving when mildly hypoglycemic, even if asymptomatic. Individuals also must be aware that the effects of alcohol and hypoglycemia on cognitive function are additive and significant even after small quantities of alcohol. It is important to completely avoid alcohol when driving.
Elevated total ketone body concentrations are characteristic of both diabetic ketoacidosis (DKA) and alcoholic ketoacidosis (AKA). However, DKA compared to AKA is characterized by a higher glucose concentration and a lower b-hydroxybutyrate–to–acetoacetate and lactate-to-pyruvate ratios. Hormonal profiles are similar with decreased insulin levels and elevated levels of counterregulatory hormones (Umpierrez 2000). Liberal lunchtime ingestion of alcohol by patients with type 1 diabetes compared to placebo resulted in postprandial b-hydroxybutrate levels being elevated with alcohol and suppressed with placebo (Kerr 2009). The authors suggest that “binge” drinking may increase the risk of significant ketosis, especially if insulin administration is erratic. They recommend that patient education materials contain information to highlight these potential problems.
Summary
In people with type 2 diabetes, acute or longer-term moderate consumption of alcoholic beverages appears to have no detrimental effect on glucose control, whereas longer-term consumption of alcohol may actually improve fasting glucose levels and insulin sensitivity. Alcohol consumption also does not influence responses to exercise or hypoglycemia.
In people with type 1 diabetes, moderate consumption of alcohol appears to have minimal, if any, acute effect on glucose levels and insulin needs. However, of concern is the occurrence of late-onset hypoglycemia, likely due to reduced growth hormone levels after alcohol consumption. Thus, it is important that individuals repeatedly self-monitor blood glucose levels after drinking alcoholic beverages to determine if treatment for hypoglycemia is needed. Also of concern is the additive effect of alcohol and hypoglycemia on cognitive function and the need to avoid alcohol when planning to drive.
EFFECTS OF ALCOHOL ON DIABETES COMPLICATIONS
The protective effect of alcohol against coronary heart disease (CHD) in the general population is well established. Over 40 studies in diverse populations have documented a 10–40% reduction in risk associated with one to three drinks per day (Rimm 1999). The mechanisms responsible for the effect of alcohol in individuals without diabetes are reported to be increased HDL cholesterol, decreased platelet aggregation, decreased clotting factors such as fibrinogen, improvement in markers of inflammation and endothelial dysfunction (increased tissue plasminogen activator and decreased plasminogen activator inhibitor 1), and enhanced insulin sensitivity (Tanasescu 2001a; Koppes 2006). Studies on alcohol consumption and diabetes complications are summarized in Table 4.2.
Table 4.2 Alcohol Consumption and Diabetes Complications
Importantly, in men and women with diabetes, moderate alcohol intake is also associated with a lower risk of CHD (Ajani 2000; Solomon 2000; Tanasescu 2001b; Wakabayashi 2002; Pitsavos 2005), lower mortality risk from CHD (Valmadrid 1999; de Vegt 2002), and lower total mortality risk (Diem 2003). A systematic review demonstrated that among people with diabetes, moderate alcohol consumption is associated with a 34–55% decrease in risk for CHD and a 55–79% decrease in risk for death from CHD (Howard 2004). In a meta-analysis, statistical pooling of studies comparing alcohol consumers to non-consumers showed a reduced relative risk (RR) for incident CHD (RR = 0.57). RR for CHD mortality was reduced in alcohol consumption categories until ≥18 g/day (RR = 0.75), after which it increased. RR for total mortality was lower in the <6 g/day category (RR = 0.64) (Koppes 2006).
In contrast, one study reported that all levels of alcohol consumption in people with diabetes compared to nondrinkers were associated with more atherosclerosis (as measured by high-resolution b-mode ultrasound of carotid arteries). However, in people with normal and impaired glucose tolerance, compared to nondrinkers, alcohol consumption was associated with less atherosclerosis (Cooper 2002).
Researchers have attempted to determine potential mechanisms for the overwhelming association of alcohol with decreased risk for CHD and mortality in people with diabetes. Alcohol intake in the Health Professionals Follow-Up Study of men with type 2 diabetes was associated with increased HDL cholesterol and adiponectin and decreased levels of fibrinogen and other markers of inflammation and endothelial dysfunction (Shai 2004). However, in a cross-sectional study measuring degree of atherosclerotic progression in people with type 2 diabetes, light drinking but not heavy drinking was associated with decreased atherosclerotic progression, but changes in serum HDL cholesterol and plasma fibrinogen levels were not involved in this beneficial effect (Solomon 2000). In two studies, acute alcohol consumption (40 g) improved insulin sensitivity in individuals with and without type 2 diabetes (Avogaro 2004; Schaller 2010). In individuals with type 2 diabetes, alcohol consumption also significantly reduced acute free fatty acid levels (Avogaro 2004) and acutely increased artery vasodilation (Schaller 2010). In a crossover trial, individuals drank wine (18 g alcohol) with meals or abstained for 30 days; consumption of alcohol had no effect on lipids, including HDL cholesterol, or glucose, but did lower fasting serum insulin levels (Bantle 2008). In a year-long study, individuals were randomized to moderate daily wine (11 g alcohol) with meals or none after a first nonfatal myocardial infarction (MI). Compared to the controls, wine consumption significantly reduced oxidative stress markers and proinflammatory cytokines as well as improving cardiac function after MI (Marfella 2006).
Risk of microvascular complications related to alcohol consumption was examined in two studies. In the EURODIAB Prospective Complications Study, in people with type 1 diabetes, moderate alcohol consumption was associated with risk of proliferative retinopathy, neuropathy, and macroalbuminuria in a U-shaped manner. Moderate consumers (30–79 g alcohol/week) had the lowest risk of microvascular complications; alcohol consumption also was not associated with occurrence of ketoacidosis or hypoglycemia (Beulens 2008). In the AdRem Study, in people with type 2 diabetes, moderate alcohol consumption, compared to not drinking at all, was not associated with presence or progression of diabetic retinopathy, but was associated with a higher risk of deterioration of visual acuity—the magnitude increased with increasing amount of alcohol (Lee 2010).
Summary
In people with type 2 diabetes, moderate alcohol consumption is associated with decreased CHD and mortality risks and decreased total mortality. The type of alcoholic beverage does not influence beneficial effects (Valmadrid 1999; Howard 2004; Shai 2004; Koppes 2006). The observed mortality risk reduction related to moderate alcohol consumption in people with type 2 diabetes is largely attributed to the reduced risk of CHD. The most consistent mechanism for the beneficial effects of alcohol is an increase in insulin sensitivity. However, improvements in markers of inflammation and endothelial dysfunction are also reported. Improvements in HDL cholesterol and fibrinogen have been mixed.
In individuals with type 1 diabetes, moderate alcohol consumption is associated with lower risk of microvascular complications. In individuals with type 2 diabetes, moderate alcohol consumption was not associated with retinopathy.