Ethanol, contained in alcoholic beverages, increases plasma osmolarity, but because it freely traverses cell membranes, it does not affect serum tonicity. Therefore, it does not induce ADH secretion. Instead, the earliest work in this field showed that alcohol causes diuresis by inhibiting ADH.⁵ Another early study showed that for every 10grams of alcohol ingested, there would be an additional 100mL of urine output.⁶ Some thought that alcohol-induced diuresis was due to a loss of solutes, but Roberts⁷ proved that alcohol causes a diuresis even with concurrent ingestion of sodium chloride. A later study⁸ measured ADH levels after alcohol intoxication, and it did not show a correlation between alcohol and ADH levels; this study suggested there might be a direct toxic effect of alcohol on the renal tubules, though alcohol as an inhibitor of ADH is still the prevalent theory.⁹ Interestingly, ethanol has no effect on the renin angiotensin-aldosterone-system, as it has been shown to have no effect on aldosterone levels.¹⁰

Later research has shown that the diuretic effect of alcohol depends on several other factors. The higher the concentration of alcohol, the greater the diuresis.⁶ In addition, in chronic alcoholics, the diuretic effect of alcohol is reduced. This is probably multifactorial, due both to low solute intake and to tolerance to the diuretic effect. One study¹¹ showed that after exercise induced dehydration, alcohol will cause an increased urine output with augmented water losses as compared to a nonalcoholic beverage. Though the mechanism may not be fully understood, there is a measurable diuretic effect of ethanol on the kidneys, therefore ethanol would not be preferred as a beverage of choice to replete salt and water losses.

Sports drinks are another option to prevent dehydration. These beverages are designed to be consumed during sports activities or exercise. They typically contain sugars and electrolytes, including sodium, potassium, and magnesium. In a study of 400 farm workers in California, Moyce¹² found that the workers drank 0.2oz/kg of sugary drinks during their workday. Animal studies¹³ have shown acute kidney injury (AKI) associated with sugary beverages because the enzyme fructokinase is activated, leading to an inflammatory cascade, which causes tubulointerstitial kidney injury. In another mouse model, frequent dehydration led to hyperosmolarity, which triggered the endogenous production of fructose, which when metabolized by phosphofructokinase, led to kidney injury.¹⁴ If this mechanism were conserved in humans, it would militate against adding more fructose via supplements, however, in humans, multiple studies have not demonstrated that fructose induces AKI.¹⁵ One of these studies looked at the levels of KIM-1 and NGAL, urinary biomarkers for acute tubular necrosis, and found no difference in levels whether the subjects were hydrating with fructose-containing sports drinks or water.¹⁶ This latter study gives some support to proposing that high fructose containing drinks, though theoretically dangerous to renal function in animal models, may be safe for short term use in workers with cultural/personal aversion to unsweetened oral hydration.

Another important potential effect of sports drinks is that high glucose, hypertonic beverages cause a secretion of water into the intestinal lumen. Evans¹⁷ compared a hypotonic 2% glucose solution (111 mosms/kg) to a hypertonic 10% solution (565 mosms/kg). Despite predictable decreases in urine osmolality and increases in urine volume post ingestion, the magnitude of these changes was not correlated with the concentration of the ingested fluids. This suggests that concentrated glucose can reduce plasma volume transiently, but overall hydration status appears to normalize by 60 minutes after ingestion. Therefore, in a high risk environment, although subjects ingesting sugary drinks ultimately maintain euvolemia via ADH and aldosterone secretion, high glucose solutions are not preferred for rehydration due to the transient acute declines in plasma volume.

Finally, sports drinks with high glucose content can cause metabolic syndrome and predispose to diabetes with chronic use. The Union of European Football Associations (UEFA) recommends that its players ingest 6 mL/kg of fluid and 2g/kg of carbohydrates 3 hours before a match.¹⁸ It does not clarify which type of fluid. Wolyniec¹⁹ investigated whether hydrating with sports drinks that contain the popular sweetener xylitol, instead of sugar, would help amateur soccer players maintain hydration. She found that drinks sweetened with xylitol can cause diarrhea and lead to elevations in creatinine. This indicates that zero sugar sports drinks should not be recommended for maintaining hydration.

Public health messaging should be simple and broadly applicable. In consideration of concerns about the safety of high fructose drinks, xylitol-containing drinks, and the increased prevalence of metabolic syndrome in the US, rehydration with sugary beverages should not be encouraged, even though their short-term use could be beneficial.

Recommendations to avoid caffeine during strenuous activity are often justified by the diuretic effect reportedly associated with this substance. Caffeine is a methylxanthine, which inhibits adenosine, likely through blockade of the adenosine 1 receptor.²⁰ This is believed to result in decreased proximal sodium reabsorption in the renal tubules. The ensuing diuresis on its face would seem to militate against the use of caffeinated beverages as an appropriate hydration fluid. Studies have demonstrated, however, that the diuretic effect is only seen at extremely high doses and is most marked on initiation of ingestion with notable waning of effect with continued use.²¹

A recent trial²² evaluating effects on athletic agility of low dose caffeine, used a double-blind, cross-over design with nine moderately trained male soccer players who consumed caffeine (6mg/kg) or a placebo 60minutes before completing balance, reaction time, vertical jump, agility, 30m sprint, and ball-kicking speed tests. The caffeine had positive effects on many features of athletic performance including jump height (P=0.01) and power (P=0.08), and faster completion time according to the Illinois Agility Test (P=0.08) as compared to placebo. Of note, hydration status as measured by saliva assay demonstrated no significant negative effect following the ingestion of caffeine as compared to placebo. Caffeine intake significantly improved jump height, agility, and reaction time (P<0.05) but did not affect 30m sprint, ball-kicking speed, balance, and Rate of Perceived Exertion (RPE) values in soccer players (P>0.05). Although nonsignificant, caffeine intake also improved sprint (0.67%) and ball kicking (2.7%) performance percentages. Most significantly, caffeine consumption did not induce dehydration, and the athletes’ body hydration levels were normal.

Another investigation²³ studied seven endurance-trained, heat-acclimated cyclists who pedaled for 120minutes at 63%. VO₂max in a hot-dry environment (36°C; 29% humidity) on six occasions: 1) without rehydration; 2) rehydrating 97% of sweat losses with water; 3) rehydrating the same volume with a 6% carbohydrate-electrolytes solution; or combining these treatments with the ingestion of 6mg caffeine/kg body weight 45minutes before exercise. The study found no significant effect from caffeine on thermoregulation and heat dissipation but found increased sweat and urinary losses, though not sufficient to induce volume depletion or other negative effects. Prior studies, however, did not demonstrate the same degree of urinary and sweat losses.^24,25

A large meta-analysis²⁶ showed that caffeine had no harmful metabolic effects. In fact, the literature in neonates suggests caffeine had protective effects in preventing AKI under stress.

Taken together, these studies suggest that caffeinated beverages may enhance performance significantly and may result in diuresis, but the effect does not seem to result in harmful outcomes. Any negative effects may be limited to higher doses of caffeine and may also be attenuated by chronic use. These studies are limited by small sample sizes, and nonstandardized methods for assessing hydration and outcomes. Public health recommendations against caffeine are not warranted at this time.