Sleep disturbances in alcohol-dependent (AD) individuals may persist despite abstinence from alcohol and can influence the course of the disorder.
Although the mechanisms of sleep disturbances of AD are not well understood and some evidence suggests dysregulation of circadian rhythms, dim light melatonin onset (DLMO) has not previously been assessed in AD versus healthy control (HC) individuals in a sample that varied by sex and race.
The authors assessed 52 AD participants (mean ± SD age: 36.0 ± 11.0 yrs of age, 10 women) who were 3–12 wks since their last drink (abstinence: 57.9 ± 19.3 d) and 19 age- and sex-matched HCs (34.4 ± 10.6 yrs, 5 women). Following a 23:00–06:00 h at-home sleep schedule for at least 5 d and screening/baseline nights in the sleep laboratory, participants underwent a 3-h extension of wakefulness (02:00 h bedtime) during which salivary melatonin samples were collected every 30 min beginning at 19:30 h. The time of DLMO was the primary measure of circadian physiology and was assessed with two commonly used methodologies.
There was a slower rate of rise and lower maximal amplitude of the melatonin rhythm in the AD group. DLMO varied by the method used to derive it. Using 3 pg/mL as threshold, no significant differences were found between the AD and HC groups. Using 2 standard deviations above the mean of the first three samples, the DLMO in AD occurred significantly later, 21:02 ± 00:41 h, than in HC, 20:44 ± 00:21 h (t = −2.4, p = .02).
Although melatonin in the AD group appears to have a slower rate of rise, using well-established criteria to assess the salivary DLMO did not reveal differences between AD and HC participants. Only when capturing melatonin when it is already rising was DLMO found to be significantly delayed by a mean 18 min in AD participants.
Future circadian analyses on alcoholics should account for these methodological caveats.
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Request Reprint E-Mail: daconroy@med.umich.edu
Although the mechanisms of sleep disturbances of AD are not well understood and some evidence suggests dysregulation of circadian rhythms, dim light melatonin onset (DLMO) has not previously been assessed in AD versus healthy control (HC) individuals in a sample that varied by sex and race.
The authors assessed 52 AD participants (mean ± SD age: 36.0 ± 11.0 yrs of age, 10 women) who were 3–12 wks since their last drink (abstinence: 57.9 ± 19.3 d) and 19 age- and sex-matched HCs (34.4 ± 10.6 yrs, 5 women). Following a 23:00–06:00 h at-home sleep schedule for at least 5 d and screening/baseline nights in the sleep laboratory, participants underwent a 3-h extension of wakefulness (02:00 h bedtime) during which salivary melatonin samples were collected every 30 min beginning at 19:30 h. The time of DLMO was the primary measure of circadian physiology and was assessed with two commonly used methodologies.
There was a slower rate of rise and lower maximal amplitude of the melatonin rhythm in the AD group. DLMO varied by the method used to derive it. Using 3 pg/mL as threshold, no significant differences were found between the AD and HC groups. Using 2 standard deviations above the mean of the first three samples, the DLMO in AD occurred significantly later, 21:02 ± 00:41 h, than in HC, 20:44 ± 00:21 h (t = −2.4, p = .02).
Although melatonin in the AD group appears to have a slower rate of rise, using well-established criteria to assess the salivary DLMO did not reveal differences between AD and HC participants. Only when capturing melatonin when it is already rising was DLMO found to be significantly delayed by a mean 18 min in AD participants.
Future circadian analyses on alcoholics should account for these methodological caveats.
Read Full Abstract
Request Reprint E-Mail: daconroy@med.umich.edu
