Alcohol and Caffeine

“Avoid alcoholic beverages, coffee and cola.” (City of Toronto, Heat Alerts and Extreme Heat Alerts, 2010)

“Don’t drink liquids that contain alcohol…these actually cause you to lose more body fluid.” (Center for Disease Control and Prevention, Tips for Preventing Heat-Related Illness, 2010)
Population-level heat advice, such as the quotes above, often includes recommendations to avoid alcohol and/or caffeine; however, these messages may be misleading. Here we evaluate the epidemiologic and physiologic evidence supporting such advice. 
There are a variety of postulated mechanisms by which alcohol and caffeine are thought to adversely affect health under conditions of heat stress. Primarily, there is concern that both substances cause diuresis resulting in increased urine output and subsequent dehydration. Alcohol consumption may lead to impaired judgment and the inability to adopt cooling behaviors. Further, alcohol may cause peripheral vasodilatation which may permit both heat loss and heat gain through the skin, as well as weakened cardiac contractility which may impair the body’s ability to compensate for heat-related stress. Caffeine may increase heart rate and metabolic rate, subsequently increasing body temperature. Beverages with alcohol and caffeine are relatively common; Table 1 presents a summary of the amounts of alcohol and caffeine in some beverages.
Evaluation of whether existing evidence supports recommendations to avoid consumption of caffeine and alcohol on hot days must consider how the studies are conducted. Epidemiologic studies, comparing alcohol and caffeine consumption among individuals in the general population who have experienced heat-related illness with those who have not, are a desirable source of evidence to guide population-level recommendations. However, due to lack of studies conducted in this manner, other methodologies may also provide valuable information. For example, studies that assess risk factors for heat illness in special populations (e.g., athletes, military personnel, other workers), studies that experimentally administer alcohol or caffeine to individuals and measure thermoregulation parameters, or other physiological mechanisms that are thought to be important in the response to heat (e.g., urine output) help to provide quantitative recommendations (i.e., the maximum amount of caffeine or alcohol exposure that is without harm). It should be noted that experimental studies seldom include the most vulnerable members of the population, such as the elderly and those with chronic illnesses.     
Table 1: Alcohol and caffeine content of common beverages1
Alcohol (g)
Caffeine (mg)
Coffee, brewed
250 ml
Tea, brewed
250 ml
250 ml
Beer, regular (5% alcohol by volume)
1 bottle     [431 ml]
Spirits (gin, rum, vodka, whiskey)
50 ml
Vodka cooler
1 bottle    [355 ml]
Wine: table, red or white
125 ml
Review of the Literature
Alcohol and Heat-related Illness
Epidemiologic studies
The epidemiologic literature assessing heat-related illness and alcohol is limited; there are no studies that assess recent alcohol consumption (in particular, the amount consumed) among the general public. There are population based case-control studies where individuals with, and without, heat-related illness are assessed for their usual pattern of alcohol (e.g., history of alcohol abuse), without specification of amount or timeline. For example, Kilbourne et al.2 studied 156 persons (73 fatal) with heatstroke in Missouri during the summer of 1980 and compared these cases to a group of 462 age, sex, and neighborhood-matched controls. Alcoholism was found to be associated with an increased risk of heatstroke (RR: 15, 95% CI: 1.9 to 120); the mechanism behind this association is uncertain as the researchers did not demonstrate a relationship between quantitative alcohol intake and heatstroke. Researchers suggest that increased risk of heatstroke among alcoholics might not be due to alcohol consumption, but rather to some other aspect of alcoholism (e.g., decreased ability to take protective measures because of impaired judgment). Misset et al.3 described risk factors for hospital mortality in a cohort of 345 heatstroke patients admitted to the intensive care unit (ICU) during the August 2003 heat wave in France. They found that survivors had a trend toward more frequent chronic alcohol abuse compared to non-survivors; 15.3% of non-survivors and 29.5% of survivors had chronic alcohol abuse, although this difference was not significant (p = 0.06). Authors conclude that alcohol abuse was not an independent predictor of mortality.
There are also a number of case studies that assess heat-related illnesses associated with individual alcohol consumption patterns. Interpretation of this data is difficult as the absence of a control group limits the assessment of whether the proportion of alcohol and caffeine consumers among cases differs from that of the general population. Hart et al.4 described the clinical characteristics of 28 patients with heatstroke, seen at a Dallas hospital during a heat wave in 1978; in 18% of patients, alcoholism was identified as a predisposing illness. Dematte et al.5 found that 28% of ICU patients with heatstroke in Chicago-area hospitals, during a 1995 heat wave, had a history of alcohol abuse. Austin and Berry6 selected 100 heatstroke patients from medical wards of a St. Louis hospital during the summers of 1952-1954. Of the patients who could give a history, 30% “admitted a record of alcoholic intake prior to the onset of their heatstroke”, although no amount is specified and the term alcoholism is used to refer to this group of patients. Therefore, it is unclear whether all of these patients had a history of alcoholism and consumed alcohol before the onset of heatstroke; 16% of patients with alcoholism died. 
Donoghue et al.7 studied a cohort of miners with heat exhaustion. Nine percent admitted consuming alcohol in the previous 24 hours, although this may be an underestimation due to a workplace alcohol testing policy which does not allow alcohol consumption while on the job.
In summary, the body of epidemiologic evidence does suggest that a pattern of excessive alcohol consumption (e.g., alcoholism or chronic alcohol abuse) may be a risk factor for heat-related illness. Further, a history of excessive alcohol consumption may be an indicator of other characteristics which convey risk of heat-related illness. However, there is not sufficient evidence to draw conclusions about sub-chronic consumption or about isolated alcohol consumption prior to or during heat exposure.
Experimental studies
It is generally accepted that the primary mechanism by which alcohol increases diuresis is through inhibition of the effect of antidiuretic hormone (ADH) on the kidneys, thereby inducing diuresis.8 Experimental studies can assess the impact of alcohol on diuresis. For example, Eggleton9 found that urine excretion increased by 10 ml for every 1 g of alcohol consumed. In this case, a 350 ml bottle of beer that contained 14 g of alcohol would induce 140 extra ml of urine output. Note that a much smaller amount of spirits (50 ml) has 16 g of alcohol which would therefore induce greater diuretic effects with less consumption of fluids. Therefore, beer has a larger fluid-to-alcohol content and might pose comparatively less concern for fluid deficit, while spirits have a higher proportion of alcohol.10   
There are also experimental studies that administer alcohol with physical activity in the heat and assess thermoregulatory parameters. For example, Desruelle et al.11 administered either a relatively high dose of alcohol (1.2 g alcohol/kg, which would be approximately 84 g for a 70 kg person), or a placebo drink, to 8 subjects who then exercised in a warm environment (35ºC, 45% RH). There was no significant change in skin and body temperature or sweat rate; authors concluded that alcohol ingestion did not impair thermoregulatory responses in a warm environment.  
Hobson and Maughan12 examined the effect of ingesting 40 ml of 100% ethanol in a 1 L alcohol-free beer, compared to ingesting 1 L of alcohol-free beer, on urine production in 12 healthy males in both euhydrated and hypohydrated states. They found that the diuretic action of alcohol is blunted when the body is in a state of water deficit; they presume this occurs in order to restore fluid balance.
Caffeine and Heat-related Illness
No epidemiologic studies, assessing heat-related illness with consumption of caffeine, were identified. However, there are experimental studies that assess the impact of caffeine on diuresis, as well as assessments of physiological impacts of caffeine among athletes. A study by Neuhäuser-Berthold et al.13 investigated the influence of caffeine on diuresis, with the assistance of 12 healthy volunteers who regularly drank coffee. Volunteers were asked to abstain from consumption of methylxanthines (stimulants) for 5 days prior to the study. The first day of the study, volunteers were instructed to drink only the mineral water provided and fluid intake of each of the volunteers was carefully recorded. The next day, volunteers received 6 cups of coffee, containing 642 mg of caffeine, and mineral water as supplemental fluids. This resulted in a increase in 24-hour urine excretion of 753 ml (+/- 532 ml [p < 0.001]) and a negative fluid balance, suggesting large quantities of caffeine can drastically increase urine output, if a person has not consumed caffeine in the last week. Grandjean et al.14 administered water or water plus different combinations of beverages (carbonated, caffeinated caloric and non-caloric colas, coffee) to 18 healthy adult males and found that consuming caffeinated beverages did not significantly alter hydration status; there were no significant differences between individuals who consumed 253 mg caffeine/day, 114 mg caffeine/day, and only water. These results differ from those of Neuhäuser-Berthold et al.13; researchers14 suggest that since the subjects in the Neuhäuser-Berthold study had abstained from foods and beverages containing methylxanthines for five days prior, they had become caffeine naïve. They suggest that habitual caffeine drinkers become tolerant to caffeine thus diminishing its effect.14 Interestingly, Armstrong et al.15report that, in general, although there may be increased urine output acutely after caffeine ingestion, over a longer period this may be offset by decreased urine output; as a result, long-term hydration status may not change. 
Del Coso et al.16 found, among endurance athletes exercising in the heat, caffeine alone or in combination with water or a sports drink was not thermogenic (produce heat) and did not impair heat dissipation. However, it should be noted that rectal temperature was higher in persons who consumed caffeine plus a sports drink than with a sports drink alone and that caffeine increased urine flow and sweat electrolyte excretion, although not enough to affect dehydration or blood electrolyte levels. A detailed review by Armstrong et al.15 concluded that consumption of a moderate level of caffeine results in a mild increase of urine production and there is no evidence to suggest that moderate intake (<456 mg) induces chronic dehydration or negatively affects exercise performance, temperature regulation, and circulatory strain in the heat. Similarly, a review by Ganio et al.17 concluded that when caffeine consumption is less than 300-400 mg/day, there is no evidence to support caffeine restriction on the basis of impaired thermoregulation or changes in hydration status. 
Evidence suggests that consumption of a small to moderate amount of caffeine (2-3 cups of coffee or tea, among habitual caffeine drinkers) or alcohol (1 bottle of regular beer), over the course of a day, is unlikely to impair hydration status under normal conditions (i.e., in environments which are not excessively hot). Experimental evidence also suggests that thermoregulation in hot weather is also not impaired if consumption of alcohol and caffeine is moderate. Although there are limits to external generalizability (e.g., many of those affected by heat-illness, the elderly, and those with chronic illnesses were not included), these studies provide important physiological information:
  1. Both epidemiologic and experimental studies should be considered in evaluating the effect of alcohol and caffeine in hot environments. It is important to examine the study purpose and methods (including how alcohol/caffeine exposure is measured, and characteristics of the study sample) in order to assess generalizability of the findings to the general population and to vulnerable subgroups.   
  2. Studies among special populations (such as, athletes and outdoor workers) provide useful information.
  3. Epidemiologic evidence suggests excessive alcohol consumption may be a risk factor for heat-related illness or may be associated with other characteristics which convey risk.
  4. The available literature indicates that consumption of alcohol and caffeine, in small to moderate amounts on hot days, is unlikely to cause harm. These substances provide fluids and caffeine in moderation among habitual caffeine drinkers (approximately 300 mg/day or 3 regular cups of coffee) and alcohol in small amounts (approximately 1 beer) is unlikely to induce diuresis or other physiologic impairment. The consumption of alcohol in larger amounts should be avoided on hot days. 
  1. Epidemiologic studies that assess the amount of alcohol and caffeine consumption, as well as consumption timeline, among individuals in the general population who do and do not experience heat-illness.
  2. The effect of concurrent exposure to caffeine and to alcohol on the physiology of heat response in the elderly and other vulnerable populations. 
  1. Are there different susceptibilities to developing heat illness among different sub-groups (e.g., defined by gender or age) at the same levels of alcohol or caffeine consumption?
  2. How is thermoregulation, after alcohol and caffeine consumption, affected by cooling behaviors (e.g., the use of air conditioning)?
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  3. Misset B, De Jonghe B, Bastuji-Garin S, Gattolliat O, Boughrara E, Annane D, et al. Mortality of patients with heatstroke admitted to intensive care units during the 2003 heat wave in France: a national multiple-center risk-factor study. Crit Care Med. 2006;34(4):1087-92.
  4. Hart GR, Anderson RJ, Crumpler CP, Shulkin A, Reed G, Knochel JP. Epidemic classical heat stroke: clinical characteristics and course of 28 patients. Medicine (Baltimore). 1982;61(3):189-97.
  5. Dematte JE, O'Mara K, Buescher J, Whitney CG, Forsythe S, McNamee T, et al. Near-fatal heat stroke during the 1995 heat wave in Chicago. Ann Intern Med. 1998;129(3):173-81.
  6. Austin MG, Berry JW. Observations on one hundred cases of heatstroke. JAMA. 1956;161(16):1525-9.
  7. Donoghue AM, Sinclair MJ, Bates GP. Heat exhaustion in a deep underground metalliferous mine. Occup Environ Med. 2000;57(3):165-74.
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  9. Eggleton MG. The diuretic action of alcohol in man. J Physiol. 1942;101(2):172-91.
  10. Hajat S, O'Connor M, Kosatsky T. Health effects of hot weather: from awareness of risk factors to effective health protection. Lancet. 2010;375(9717):856-63.
  11. Desruelle AV, Boisvert P, Candas V. Alcohol and its variable effect on human thermoregulatory response to exercise in a warm environment. Eur J Appl Physiol. 1996;74(6):572-4.
  12. Hobson RM, Maughan RJ. Hydration status and the diuretic action of a small dose of alcohol. Alcohol Alcohol. 2010;45(4):366-73.
  13. Neuhäuser B, Beine S, Verwied SC, Lührmann PM. Coffee consumption and total body water homeostasis as measured by fluid balance and bioelectrical impedance analysis. Ann Nutr Metab. 1997;41(1):29-36.
  14. Grandjean AC, Reimers KJ, Bannick KE, Haven MC. The effect of caffeinated, non-caffeinated, caloric and non-caloric beverages on hydration. J Am Coll Nutr. 2000;19(5):591-600.
  15. Armstrong LE, Casa DJ, Maresh CM, Ganio MS. Caffeine, fluid-electrolyte balance, temperature regulation, and exercise-heat tolerance. Exerc Sport Sci Rev. 2007;35(3):135-40.
  16. Del Coso J, Estevez E, Mora-Rodriguez R. Caffeine during exercise in the heat: thermoregulation and fluid-electrolyte balance. Med Sci Sports Exerc. 2009;41(1):164-73.
  17. Ganio MS, Casa DJ, Armstrong LE, Maresh CM. Evidence-based approach to lingering hydration questions. Clin Sports Med. 2007;26(1):1-16.

October 2010