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ОглавлениеChapter 4 Alcohol and Diabetes
Marion J. Franz, MS, RD, CDE
Effects of Alcohol on Glycemia and Other Metabolic Outcomes
Effects of Alcohol on Diabetes Complications
Alcohol: Triglycerides, HDL Cholesterol, Blood Pressure, and Weight
Guidelines for Consuming Alcohol
Highlights Alcohol and Diabetes
• Moderate alcohol consumption (~15–30 g/day; one to two drinks) has minimal acute or long-term effects on blood glucose levels in people with type 1 or type 2 diabetes. Studies on alcohol consumption report a U- or J-shaped association, suggesting benefit from moderate consumption.
• Moderate consumption of alcohol by people with type 2 diabetes is associated with reduced risk of and mortality from coronary heart disease and lower total mortality rates. The mechanism for this benefit is unclear but is likely related to improvements in insulin sensitivity with consumption of moderate amounts of alcohol.
• If individuals with diabetes choose to drink alcoholic beverages, daily intake should be limited to an average of up to one drink per day for adult women and up to two drinks per day for adult men and no more than three drinks in any single day for women and no more than four drinks in any single day for men. Insulin or insulin secretagogue users, to prevent hypoglycemia, should consume alcohol with food.
• There are no data to support recommending alcohol use to people with or without diabetes who do not currently drink. Abstinence is recommended for people with risks related to alcohol consumption. However, for the majority of people with diabetes who choose to consume alcohol in moderation, alcohol consumption does not need to be discouraged.
Alcohol and Diabetes
Alcohol consumption in the United States is common. It is estimated that 76% of men and 65% of women consumed alcohol at least once in the last year. A large number of individuals exceed the recommended upper limits of average intake. An estimated 9% of men consumed an average of more than two drinks per day and 4% of women consumed an average of more than one drink per day (Report of the Dietary Guidelines Advisory Committee [DGAC] 2010). Surveys of Kaiser Permanente Northern California adult diabetes patients reported that just over 50% currently consumed alcohol, 22% had never consumed alcohol (abstainers), and 28% were former drinkers (Ahmed 2008). In the Third National Health and Nutrition Examination Survey (NHANES III), adults with diabetes also reported drinking half the amount of alcohol as adults without diabetes (Mackenzie 2006). The lower prevalence of alcohol consumption by people with diabetes may be the result of the higher prevalence of former drinkers among people with diabetes compared with the general population (28 and 15%, respectively) (Ahmed 2006), or alcohol consumption may have been discontinued because of declining health, perceived risk of alcohol on diabetes management, or physician advice to limit alcohol intake. If people with diabetes choose to drink alcoholic beverages, they need to know what effect it can have on blood glucose control and the management of their diabetes and how to drink safely.
The alcohol in beverages is ethanol (ethyl alcohol, C2H5OH), which is the intoxicating molecule present in distilled spirits, wine, and beer. It is the byproduct of the oxidation of sugars for energy by yeast enzymes (fermentation). The term “alcohol” will be used in this chapter. One drink is commonly defined as 12 oz regular beer, 8 oz malt liquor, 5 oz wine, or 1.5 oz 80-proof distilled spirits, each of which contains ~15 g alcohol.
The American Diabetes Association (ADA) nutrition recommendations state: “If adults with diabetes choose to drink alcohol, daily intake should be limited to a moderate amount (one drink per day or less for women and two drinks per day or less for men). Abstention from alcohol should be advised for people with a history of alcohol abuse or dependence, women during pregnancy, and people with medical problems such as liver disease, pancreatitis, advanced neuropathy, or severe hypertriglyceridemia” (ADA 2008).
This chapter begins with a summary of the metabolism of alcohol from the 1999 book American Diabetes Association Guide to Medical Nutrition Therapy of Diabetes (Franz 1999) and then proceeds with reviews and updates on the evidence for effects of alcohol on glycemia and other metabolic outcomes, its effect on diabetes complications, and summarizes recommendations for the consumption of moderate amounts of alcoholic beverages.
A literature search was conducted using PubMed MEDLINE, and additional articles were identified from reference lists. Search criteria included the following: alcohol research in human subjects with diabetes, English language articles, and publication after the completion of the 1999 chapter on alcohol. The initial search of potentially relevant articles identified 957 articles, of which 934 articles were excluded because titles or abstracts did not meet inclusion criteria. A total of 37 articles were retrieved for more detailed evaluation. Fourteen of these articles are included and 18 were added from the review of reference lists, making a total of 32 articles that met inclusion criteria. A total of 28 primary studies (15 epidemiological/observational studies and 13 clinical trials), 1 meta-analysis, and 3 reviews are included in Tables 4.1 and 4.2. All studies in the meta-analysis and reviews published after publication of the 1999 book (Franz 1999) are included in the tables.
Alcohol is absorbed by a process of simple diffusion across the gastrointestinal mucosa of the stomach, duodenum, and jejunum and enters the portal circulation. It is one of the few substances that can be readily absorbed through the walls of the stomach into the bloodstream. With the ingestion of food, especially high-fat food, fewer alcohol molecules diffuse from the stomach. Ethanol does not require gastrointestinal digestion and may undergo first pass metabolism by gastric alcohol dehydrogenase (ADH). Adult men have greater gastric ADH activity then adult women; thus, alcohol bioavailability in men is reduced relative to that in women (Baraona 2001).
The primary mechanism by which the body disposes of alcohol is oxidation and use as a fuel source. Alcohol is the only nutrient that does not require insulin to be metabolized. The liver is the major organ for alcohol oxidation. The total quantity of alcohol and the rate of ingestion determine its effect. The liver contains three pathways for ethanol metabolism, each located in a different subcellular compartment: 1) the ADH pathway in the cytoplasm; 2) the microsomal ethanol-oxidizing system (MEOS) located in the endoplasmic reticulum; and 3) catalase, located in the peroxisomes. All three pathways result in the production of acetaldehyde, a highly toxic metabolite (Lieber 1976).
Alcohol is primarily oxidized to acetaldehyde and acetate and then to energy through the ADH pathway (Figure 4.1). Hepatic ADH is the rate-limiting enzyme and determines the action and timing of alcohol metabolism. If the limited number of ADH molecules in hepatocytes are occupied, excess alcohol molecules enter the general circulation and return to the liver when ADH molecules are free to process them. The detoxification rate of ethanol by hepatic ADH is thus limited to a processing rate of ~15 g/h (Goodsell 2006). Thus, longer time periods between ingestion of alcohol are essential so that oxidation can occur in the liver. Additionally, an alcohol-induced increase within the liver cell of the NADH/NAD ratio (NAD, nicotinamide adenine dinucleotide; NADH, reduced NAD) contributes to inhibition of gluconeogenesis. Acetate is released into the bloodstream and completes oxidation in other tissues. Alcohol oxidation is an effective source of energy because it is coupled with the synthesis of adenosine triphosphate.
Figure 4.1 Alcohol oxidation.
Alternatively, alcohol may also be metabolized via reactions in the smooth endoplasmic reticulum by the MEOS. The role of the MEOS is small, but may play a more predominant role at intoxicating levels of blood alcohol. Both the MEOS pathway and the smooth endoplasmic reticulum are also involved in the metabolism of many drugs, and this occurrence can potentially lead to adverse drug reactions. Only a small percentage of alcohol is oxidized via the catalase pathway.
Excessive alcohol that the liver cannot metabolize immediately enters the general circulation, where it becomes a part of all body fluids and enters into cells. Alcohol has a special affinity for the brain and quickly reaches the brain cells. At first, this results in a state of euphoria, often accompanied by release of inhibitions. However, longer-term alcohol use has a depressive effect on mental status.
In people with no history of chronic exposure to alcohol, it is estimated that ~75% of alcohol is oxidized by the ADH pathway, whereas 25% involves the MEOS. At high alcohol concentrations and longer duration of intake, as much as 80% of alcohol metabolism can proceed via a non-ADH pathway. Therefore, steady and prolonged alcohol consumption allows drinkers to tolerate larger amounts of alcoholic beverages. In addition to the MEOS pathway, there are increases in the ability of the hepatocytes to synthesize ADH to help clear the circulation of alcohol. As a result, the amount of alcohol that can be cleared in 1 h is doubled in an alcoholic (Lieber 1976).
EFFECTS OF ALCOHOL ON GLYCEMIA AND OTHER METABOLIC OUTCOMES
The 1999 chapter concluded that in short-term studies, in people with type 1 and type 2 diabetes, consumption of moderate amounts of alcohol had no acute postprandial impact on blood glucose and insulin levels in people with either type of diabetes (Franz 1999). However, for individuals with type 1 diabetes, a risk of late-onset hypoglycemia may exist. In individuals with type 2 diabetes, the risk of alcohol-induced acute hypoglycemia was modest (Franz 1999). Table 4.1 summarized studies published after 1999 on alcohol consumption and its effect on glycemia and other metabolic outcomes in people with type 1 and type 2 diabetes.
Table 4.1 Alcohol Consumption and Its Effect on Glycemia and Other Metabolic Outcomes in Persons with Type 1 and Type 2 Diabetes
A large cross-sectional study of adults with diabetes (n = 38,564) reported that alcohol consumption was linearly and inversely associated with A1C levels; however, with three or more drinks per day, A1C levels began to increase (Ahmed 2008). Similar findings were reported in NHANES III, in which adults with diabetes who had ≥30 drinks of alcohol per month, compared with nondrinkers, had average A1C levels 1.2% lower than other adults with diabetes (Mackenzie 2006). However, increasing risk for poor adherence to diabetes self-care behaviors with increasing alcohol consumption, starting with individuals who consume one drink per day, has also been reported (Ahmed 2006). Therefore, it is important that health care providers ask people with diabetes about alcohol consumption and encourage moderate and sensible use, shown to have potentially beneficial effects on glycemic control (van de Wiel 2004).
Type 2 Diabetes
Two clinical trials examined the effect of alcohol in individuals with type 2 diabetes (Shai 2007; Bantle 2008). Adults with type 2 diabetes (n = 109) who abstained from alcohol were randomly assigned to drink wine (13 g alcohol; ~5 oz) or nonalcoholic beer (controls) each day for 3 months. In individuals drinking wine, fasting plasma glucose (FPG) decreased ~22 mg/dL, but no effect on postprandial glucose levels was observed. In the controls, FPG and postprandial glucose levels did not change. Interestingly, patients in the alcohol group with the higher baseline A1C levels had greater decreases in FPG and reported improvements in their ability to fall asleep (Shai 2007). In the second study, adults with type 2 diabetes drank either wine (24 g alcohol; ~8.5 oz) or grape juice with their evening meal, with no acute effect on glucose or insulin levels. Wine (18 g alcohol; ~6.5 oz) or abstinence was continued for 30 days, with wine having no effect on glucose or lipids but insulin sensitivity improving (Bantle 2008). A systematic review of earlier, small, acute studies also concluded that moderate consumption of alcohol does not acutely impair glycemic control in individuals with type 2 diabetes and may actually result in a small decrease in glucose concentrations (Howard 2004). However, chronic ingestion (>45 g/day) has been shown to cause deterioration in glucose control; the effects from excess alcohol are reversed, however, after abstinence for a number of days.
In individuals with diet-treated type 2 diabetes, meals with or without alcohol were followed by either rest or 30 min of exercise, and the combination of moderate exercise with or without alcohol did not cause hypoglycemia (Rasmussen 1999). In a second study, in people with diet-treated type 2 diabetes, alcohol or water were ingested before insulin-induced hypoglycemia to determine the influence of alcohol on glucose counterregulation and recovery from insulin-induced hypoglycemia. Alcohol had no effect on recovery from hypoglycemia, although it decreased peak glucagon response (Rasmussen 2001).
Type 1 Diabetes
Previous studies reported no acute effect of moderate alcohol intake with a meal on blood glucose levels in people with type 1 diabetes. However, a risk of late-onset hypoglycemia was reported (Franz 1999). Inhibition of gluconeogenesis, reduced hypoglycemia awareness due to cerebral effects of alcohol, and/or impaired counterregulatory responses to hypoglycemia have been reported as possible causes. Five of six men with type 1 diabetes had dinner at 6:00 p.m. followed by drinking wine (70 g alcohol, 20 oz) or water at 9:00 p.m. After drinking wine, treatment for hypoglycemia was required after breakfast; growth hormone was significantly reduced, with no other differences in insulin or other hormone levels (Turner 2001). Similarly, in adults with type 1 diabetes, hypoglycemia (blood glucose 50 mg/dL) resulted in lower peak growth hormone levels compared to placebo; however, this result was also associated with a decrease in insulin sensitivity (Kerr 2007). In a study similar to the Turner study, individuals with type 1 diabetes drank either orange juice or vodka with their evening meal. After drinking alcohol, based on continuous glucose monitoring data, individuals reported more than twice as many hypoglycemic episodes throughout the next 24 h than after drinking orange juice (Richardson 2005).
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.
ALCOHOL: TRIGLYCERIDES, HDL CHOLESTEROL, BLOOD PRESSURE, AND WEIGHT
Concern has been expressed that excessive intake of alcohol may result in hypertriglyceridemia, hypertension, and weight gain in individuals with diabetes even though, at moderate levels of consumption, this does not result in higher risk of CHD or total mortality (Koppes 2006). A limited number of studies have examined the effect of alcohol consumption on triglycerides, blood pressure, and weight in people with diabetes. Advice to avoid alcohol is often given to people with diabetes because of the assumption that even moderate amounts of alcohol will raise triglycerides and blood pressure and contribute to weight gain. However, the limited available research does not support this advice.
Triglycerides
In people without diabetes, some evidence exists to suggest that moderate intake of alcohol has no detrimental effects on triglyceride levels, even in people who are hypertriglyceridemic. Two observational studies suggested moderate consumption of alcohol had beneficial effects on triglyceride and HDL cholesterol levels. Analysis of NHANES III data from 8,125 participants revealed that mild-to-moderate alcohol consumption (1–19 drinks of alcohol per month) was associated with a lower prevalence of the metabolic syndrome and was significantly and inversely associated with three of its components—elevated triglycerides, low serum HDL cholesterol, and hyperinsulinemia (Frieberg 2004). In a study of 14,077 British women, women consuming 1–14 drinks of alcohol per week, compared to nondrinkers, had a reduction in CHD associated with the lowest triglyceride levels and highest levels of HDL cholesterol (Nanchahal 2000).
Although excessive alcohol intake, high intake of saturated fatty acids, and elevated glucose concentrations are reported to be the cause of secondary hypertriglyceridemia (especially in people with obesity) (Chait 1972), clinical trials show that the effect of moderate alcohol intake on triglycerides in people with or without hypertriglyceridemia is limited. When two alcoholic drinks or water per day for 2 weeks were consumed by people with fasting triglyceride levels of 200–750 mg/dL or by people with normal triglyceride levels (90 mg/dL), there were no significant differences reported between the effect of alcohol or the effect of water on triglyceride levels. The authors concluded that acute alcohol intake is not an important determinant of triglyceride concentrations in individuals with hypertriglyceridemia (Pownall 1999). In fact, moderate alcohol intake may actually have a beneficial effect on triglyceride levels. In a trial of healthy women, either none, one, or two drinks per day of alcohol were consumed for 8 weeks. Fasting triglyceride levels were significantly reduced by 7.8% after consumption of one drink per day and by 10.3% with two drinks per day. Fasting insulin levels decreased by 19.2% and insulin sensitivity increased by 7.2% (Davies 2002).
Only a few studies conducted in people with diabetes are available. In men with type 2 diabetes, light drinkers (<14 drinks per week) had an average triglyceride level of 115 mg/dL compared to 132 mg/dL in nondrinkers and 170 mg/dL in heavy drinkers (>14 drinks per week). Thus, triglyceride levels were significantly higher in heavy drinkers than in nondrinkers and light drinkers (Wakabayashi 2002). Subjects with type 2 diabetes either consumed wine (6.5 oz) with the evening meal or abstained for 30 days, and alcohol had no effect on triglycerides or total, LDL, or HDL cholesterol (Bantle 2008). Clearly, to answer the question of alcohol and its effects on triglyceride levels, additional clinical trials are needed, especially in individuals with diabetes. However, in individuals with high triglyceride levels (>500 mg/dL), complete abstinence is recommended along with reduced saturated fat intake to reduce the risk of pancreatitis (Miller 2011).
HDL Cholesterol
In an epidemiological study, in subjects without diabetes, 30 g alcohol a day was reported to increase HDL cholesterol by ~4 mg/dL; this, along with other positive biological marker effects, was calculated to lower risk of CHD by ~25% (Rimm 1999). In a study in people with diabetes that included the relationship of alcohol intake and HDL cholesterol, each additional drink per day was also related to increases in HDL cholesterol (~2.0 mg/dL) (Shai 2004). In a year-long study, people with type 2 diabetes ate a Mediterranean diet with either one daily 4 oz glass of wine or no alcoholic beverage; at year-end drinking wine with the Mediterranean diet resulted in a significant increase in HDL cholesterol (34.8 mg/dL) compared to the Mediterranean diet without alcohol (Marfella 2006). However, in a 30-day study, wine (24 g alcohol) with the evening meal or abstinence had no effect on HDL cholesterol (Bantle 2008). Thus, the effect of alcoholic beverages on HDL cholesterol in people with diabetes is unclear.
Hypertension
The 2010 Report of the Dietary Guidelines Advisory Committee concluded that “strong evidence indicates that moderate alcohol consumption does not elevate risk of either hypertension or stroke. It is also well documented that alcohol consumed in excess of moderate causes an increase in blood pressure and stroke” (DGAC Report 2010). There are limited available data on moderate alcohol consumption and hypertension in people with diabetes. In individuals with diabetes, a J-shaped relationship was observed between alcohol intake and blood pressure (Pitsavos 2005), and in another study, moderate drinking compared to no alcoholic beverage had no effect on blood pressure (Marfella 2006).
Weight Gain
The 2010 report of the DGAC also examined the relationship between alcohol intake and weight gain and concluded that “moderate evidence suggests that among free-living populations, moderate drinking is not associated with weight gain. However, heavier consumption over time is associated with weight gain” (DGAC Report 2010). The report does note that regardless of the alcoholic beverage, all contain calories that are not a good source of nutrients and, when consumed beyond an average of two drinks a day, may lead to weight gain. Below this level of consumption, the evidence suggests that individuals who drink in moderation do not gain weight at a faster rate than nondrinkers. Table 4.3 contains a list of alcoholic beverages and their caloric content. No studies examining the effect of alcohol consumption on weight have been done in people with diabetes.
Table 4.3 Percentage and Grams of Alcohol and Calories in Alcoholic Beverages
GUIDELINES FOR CONSUMING ALCOHOL
Information regarding benefits and contraindications should be given to individuals with diabetes so that they can make their own decisions regarding consumption of alcoholic beverages. For the majority of people, moderate consumption with food will have minimal, if any, acute or long-term effects on blood glucose levels and may have beneficial effects on insulin sensitivity and create a decreased risk for CHD.
Abstention from alcohol should be advised for individuals who cannot restrict their drinking to moderate levels; children and adolescents; individuals taking prescription or over-the-counter medications that can interact with alcohol; and individuals with medical problems such as liver disease, pancreatitis, advanced neuropathy, or severe hypertriglyceridemia. In addition, alcohol should be avoided by women who are pregnant or nursing or who are unsure if they are pregnant and by individuals who plan to drive, operate machinery, or take part in activities that require attention, skill, or coordination. Risk of unintentional injuries and breast and colon cancer should also be taken into consideration (DGAC Report 2010). No one should drink alcohol before driving.
The data do not support recommending alcohol consumption to individuals with or at risk for diabetes who do not currently drink (ADA 2008), since only observational and small clinical trials documenting the effects of alcohol are available. On the other hand, for many with diabetes, consumption of moderate amounts of alcohol does not need to be discouraged.
If alcohol is consumed, it should be consumed in moderation and only by adults. The Dietary Guidelines for Americans, 2010, defines moderate alcohol consumption as average daily consumption of up to one drink per day for women and up to two drinks per day for men and no more than three drinks in any single day for women and no more than four drinks in any single day for men (DGAC Report 2010). They also advise to drink alcohol with food to slow alcohol absorption.
The type of alcohol-containing beverage consumed does not make a difference. Because alcohol does not affect blood glucose levels or require insulin to be metabolized, occasional use of alcoholic beverages can be considered an addition to the regular meal plan, and no food should be omitted. If consumed on a regular basis, calories from alcoholic beverages may need to be considered. Although regular beer does contain carbohydrate, because of the risk of hypoglycemia (likely due to reduced gluconeogenesis by alcohol), it is prudent that individuals not count the carbohydrate from alcohol when determining insulin boluses. Light beer may be a better choice. In addition, individuals with diabetes may not realize that wine and distilled spirits contain negligible amounts of carbohydrate.
For people using insulin or insulin secretagogues, alcohol should be consumed with food to prevent hypoglycemia. Evening consumption of alcohol by insulin users may increase the risk of nocturnal and fasting hypoglycemia. Hypoglycemia during the morning after consuming alcohol the evening before can be avoided by awakening at the usual time, eating a usual breakfast, and frequently testing blood glucose levels.
Drinking excessive amounts of alcohol and/or “binge” drinking can increase risk for lactic acidosis, which can be fatal. Although lactic acidosis associated with metformin is rare, patients who routinely drink more than moderate amounts of alcohol or with a history of binges of alcohol intake may not be good candidates for metformin therapy.
For all people with diabetes, meals and snacks should be eaten on time and selected with usual care. Alcohol can have a relaxing effect and may dull judgment. The decision to drink or not drink alcoholic beverages must be made by the individual with diabetes. Individuals should be educated about the effects of alcohol on metabolic parameters and health if they are to make the best decision for their health and well-being.
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Marion J. Franz, MS, RD, CDE, is a Nutrition/Health Consultant at Nutrition Concepts by Franz, Inc., Minneapolis, MN.
