Alcohol intake alters melatonin secretion both in healthy volunteers and in alcoholics in a variety of different situations (while drinking, during or after withdrawal, and with neurological complications).
The disturbance of circadian rhythms (Danel et al., 2001) may explain in part some mental disorders secondary to alcohol consumption. Two primary findings emerge from the studies of melatonin and alcohol consumption in healthy volunteers and in chronic alcohol-dependent drinkers in different situations (review in Danel and Touitou, 2004). The second major finding is that the nycthemeral rhythm of melatonin secretion is disrupted in some alcohol-dependent individuals. Melatonin concentrations were measured with a commercial enzyme-linked immunosorbent assay (ELISA) (Boeringer Mannheim, France) in a fully automated analyser (ES 700).
We used ANOVA with mixed linear models for paired comparisons to study the differences between the mean curves under two conditions (alcohol, without alcohol). Strictly nocturnal secretion of melatonin was seen in all subjects both during the alcohol-free session and during the alcohol session.
Our results thus shed new light on the observations in the literature about diurnal melatonin secretion in alcoholics. Majumdar and Miles (1987) were the first to report disturbances in the time of melatonin secretion in alcohol-dependent patients.
Now that we have shown that alcohol itself does not directly cause daytime melatonin secretion, we can hypothesize that disturbances in the timing of melatonin secretion in the literature are due to a shift in the circadian clock of melatonin secretion and appear to indicate possible internal desynchronization during chronic alcohol consumption. This alteration may reduce secretion or affect its circadian rhythm, thus causing daytime secretion in some alcoholics.
Examination of this hypothesis requires a study of the changes in melatonin secretion that may be due to alcohol consumption. None had a current or past diagnosis of alcohol, tobacco, or other substance abuse or dependency.

Melatonin circadian rhythm was studied during a single-blinded, randomized, crossover study that compared a 26 h alcohol session with a 26 h placebo session. While the curve during the alcohol session tended to show a delay in the onset of melatoninsecretion compared with the alcohol-free session, analysis of the data showed no statistically significant effect by alcohol on melatonin secretion (P = 0.45). Circadian melatonin secretion was observed in both sessions, with nocturnal secretion and no circulating melatonin during the day. We sought to determine if daytime melatonin secretion is caused directly by acute alcohol consumption or if it instead indicates a change in circadian synchronization.
It is not clear, however, whether daytime secretion of the hormone is caused directly by the acute alcohol consumption or instead it indicates a change in the alcoholic's circadian synchronization. Some subjects appeared to show a delay in the onset of melatonin secretion or in the time when the half-peak value was reached (subjects 1, 2, 3, 4, 6, and 10). They also reported the disappearance of the circadian rhythm of melatonin secretion during acute withdrawal. Although previous work indicates that alcohol inhibits melatonin secretion (Danel and Touitou, 2004), this experiment fail to show such inhibition. Another possible explanation is that the daytime melatonin secretion seen in alcoholics is due to chronically high blood alcohol levels that cause daytime melatonin secretion via mechanisms that have nothing to do with circadian timing. Because alcohol consumption as it occurs in alcoholics (continuous consumption of large amounts) has never been examined in healthy volunteers, we exposed 11 healthy volunteers to 256 g of alcohol over 24 h to study the circadian profiles of melatonin secretion.
This key article describing diurnal melatonin secretion was followed by three publications from an Italian team. Similar observations were made in two patients with delirium tremens (Mukai et al., 1998), for whom night-time and daytime serum melatonin concentrations were equivalent (samples taken every 4 h).
In such a case, the melatonin daytime secretion seen in alcoholics would be a cause rather than a consequence of desynchronization.

This difference was consistent in direction for all subjects, always a delay, either in the time that nocturnal melatonin secretion started or in the time that the half-peak value was reached. Two reported melatonin measurements in 10 alcohol-dependent patients, first during alcohol consumption and then after 2 weeks of abstinence. This suggests that the disordered circadian melatonin secretion seen in alcoholics indicates a shift in melatonin secretion rather than an acute effect of alcohol on this secretion, or alternatively, that it is a direct effect of chronic rather than acute exposure to high blood alcohol levels.
Alcohol consumption in heavy drinkers, on the other hand, often occurs over a much longer portion of the day and involves higher quantities.
One recent publication (Kuhlwein et al., 2003) reports a delay in the melatonin secretion of alcohol-dependent patients who had very recently stopped drinking, in the same direction as that we observed in 6 of our 11 subjects. To increase our understanding of the action of alcohol on melatonin secretion and in particular to determine whether alcohol enhances melatonin secretion during daylight hours, we conducted a blinded crossover study over a 26 h (circadian) period. That study, which sought to examine the relations between sleep disorders in alcohol-dependent patients soon after withdrawal and melatonin and cortisol concentrations, observed a delay in the nocturnal melatonin peak in 11 alcohol-dependent patients soon after withdrawal, compared with 10 age-matched controls.
In one session alcohol was administered regularly and repeatedly, and in the other, a placebo was administered.
This difference was due principally to high urinary melatonin levels in the daytime fraction.
The total dose administered represented an amount generally consumed daily by alcoholic subjects, i.e. Serum melatonin secretions were measured throughout the circadian cycle at 29 time points of the 26 h alcohol consumption session and the 26 h control session.

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