Suppression of plasma melatonin by a single dose of the benzodiazepine alprazolam in humans

McIntyre, Iain M.; Burrows, Graham D.; Norman, Trevor R.

doi:10.1016/0006-3223(88)90131-x

Cited by 54 publications

(20 citation statements)

References 18 publications

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“…It was proposed that valproate affects melatonin synthesis by its ability to enhance GABA signalling. It is of note that other GABA agonists, such as benzodiazepines, also acutely suppress nocturnal melatonin synthesis (McIntyre et al, 1988).…”

Section: Discussionmentioning

confidence: 99%

Effect of Sodium Valproate on Nocturnal Melatonin Sensitivity to Light in Healthy Volunteers

Hallam

Olver

Norman

2005

Neuropsychopharmacol

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Section: Discussionmentioning

confidence: 99%

Effect of Sodium Valproate on Nocturnal Melatonin Sensitivity to Light in Healthy Volunteers

Hallam

Olver

Norman

2005

Neuropsychopharmacol

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“…Special care was taken that subjects did not take any substances which are known to interfere with melatonin production and/or secretion, but which, among the general population, are sometimes not considered to be "medication," e.g., with respect to sleep: benzodiazepines (McIntyre et al 1988), antidepressants (Skene et al 1994), beta-blockers (Cowen et al 1985, and with respect to pain: anti-inflammatory drugs (Surrall et al 1987;Murphy et al 1994). Drugscreening in urine included benzodiazepines, barbiturates, cannabinoids, amphetamines, cocain and opiates.…”

Section: Study Populationmentioning

confidence: 99%

“…Patients, in whom diagnosis was RLS/ PLMD, underwent specific evaluation. Patients were only included when the disorder was considered to be idiopathic.Special care was taken that subjects did not take any substances which are known to interfere with melatonin production and/or secretion, but which, among the general population, are sometimes not considered to be "medication," e.g., with respect to sleep: benzodiazepines (McIntyre et al 1988), antidepressants (Skene et al. 1994), beta-blockers (Cowen et al 1985, and with respect to pain: anti-inflammatory drugs (Surrall et al 1987;Murphy et al 1994).…”

mentioning

confidence: 99%

A New Concept for Melatonin Deficit On Pineal Calcification and Melatonin Excretion

Kunz

1999

Neuropsychopharmacology

138

102

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Even though exogenous melatonin has proven to influence sleep and circadian parameters, low endogenous melatonin is not related to sleep disturbances, nor does it predict response to melatonin replacement therapy. In this manuscript, we present a new concept towards a definition of a melatonin deficit. The purpose of the study was to introduce a marker for an intra-individual decrease in melatonin production. Therefore, we developed a method to quantify the degree of pineal calcification (DOC) usingIn mammals, the circadian timing system has proven to be involved in the daily variation of almost any physiological and psychological variable evaluated so far (Weitzman et al. 1978;Wirz-Justice 1987;Johnson et al. 1992;Dijk and Czeisler 1995;Boivin et al. 1997). The rhythm of the circadian pacemaker comprised in the nuclei suprachiasmatici (SCN) becomes entrained to the environmental 24-hour rhythm, predominantly by two zeitgebers, light and melatonin (Dawson and Armstrong 1996).Melatonin influences the circadian phase in humans inversely compared to light. In particular, this drug delays circadian rhythms when administered in the morning and advances them when administered in the afternoon or early evening according to a phase response curve (PRC), which is nearly opposite in phase to the PRC's for light exposure (Lewy et al. 1992). Melatonin has proven to exert a chronobiotic mode of action (Dawson and Armstrong 1996) by its ability to facilitate the post-flight adaptation to jet-lag (Arendt et al. 1986), to phase advance the sleep of patients suffering from a phase-delay syndrome (Dahlitz et al. 1991;Tzischinsky et al. 1993), and to re-entrain the sleep-wake cycle of patients with a non-24-hour rhythm, such as in the blind, to the environmental light-dark cycle (Arendt et al. 1988;Lapierre and Dumont 1995;McArthur et al. 1996).However, in only one of the clinical studies (Haimov et al. 1995), in which exogenous melatonin proved usefulness, did low endogenous melatonin excretion predict response (Garfinkel et al. 1995;Hughes et al. 1998 Lushington et al. 1998;Youngstedt et al. 1998). Furthermore, normative data as to the amount of melatonin secretion demonstrate a huge inter-individual variability in humans (Dawson et al. 1992;Bergiannaki et al. 1995;Smith et al. 1997). Thus, existing normative data on melatonin excretion in a "healthy population" might only be considered normal in the sense that they are representative for the normal scatter. But since there is yet no pathology that can be attributed to either high or low melatonin levels, "normative" in this context may not necessarily indicate being healthy. The question arises, does a melatonin deficit or a hypopinealism exist at all?In a previously reported pilot-study we showed that the degree of pineal calcification (DOC) correlated positively to the incidence of chronic daytime tiredness as well as the subjective perception of sleep disturbances (Kunz et al. 1998). The basic assumption in that study was the hypothesis that an increasing degree of pineal c...

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“…Measurement interference can arise from bleeding gums (Pullman et al, 2012), toothpaste (Figueiro & Rea, 2010), caffeine, tobacco and alcohol (Hartter et al, 2006;Zhou et al, 2009) leading to erratic values. Further, benzodiazepines (Hajak et al, 1996;McIntyre et al, 1988;McIntyre et al, 1993), beta blockers (Scheer et al, 2012;Stoschitzky et al, 1999;Vijayasarathy et al, 2010), nonsteroidal anti-inflammatory drugs (Murphy et al, 1996), anticoagulants (Zhou et al, 2009), diabetes medications (Nagorny & Lyssenko, 2012) and oral contraceptives (Hilli et al, 2008) have been associated with low melatonin values.…”

Section: Introductionmentioning

confidence: 99%

Melatonin rhythms in renal transplant recipients with sleep–wake disturbances

Burkhalter

Geest

Wirz‐Justice

et al. 2016

Chronobiology International

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We assessed salivary melatonin levels in renal transplant (RTx) recipients who participated in a randomised, multicentre wait-list controlled trial on the effect of bright light therapy on their sleep and circadian rhythms. A large proportion of RTx recipients in our cohort had unexpectedly low melatonin values, which precluded calculation of the dim-light melatonin onset (DLMO) as a circadian marker. Thus, the aim of this post hoc analysis was to describe the melatonin profile of home-dwelling RTx recipients diagnosed with sleep-wake disturbances (SWDs). The participants were characterised by means of sleep questionnaires, validated psychometric instruments [Pittsburgh sleep quality Index (PSQI), Epworth sleepiness scale (ESS), Morningness-Eveningness Questionnaire (MEQ) and Depression, Anxiety and Stress Scale (DASS)] in addition to melatonin assay in saliva. Data were analysed with descriptive statistics and group comparisons made with appropriate post hoc tests. RTx recipients [n = 29 (aged 54.83 ± 13.73, transplanted 10.62 ± 6.84 years ago)] were retrospectively grouped into two groups: RTx recipients whose dim light melatonin onset (DLMO) could be calculated (n = 11) and those whose DLMO could not be calculated (n = 18). RTx recipients having a measurable DLMO had a number of differences from those without DLMO: they were younger [46.4 ± 14.9

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Suppression of plasma melatonin by a single dose of the benzodiazepine alprazolam in humans

Cited by 54 publications

References 18 publications

Effect of Sodium Valproate on Nocturnal Melatonin Sensitivity to Light in Healthy Volunteers

Effect of Sodium Valproate on Nocturnal Melatonin Sensitivity to Light in Healthy Volunteers

A New Concept for Melatonin Deficit On Pineal Calcification and Melatonin Excretion

Melatonin rhythms in renal transplant recipients with sleep–wake disturbances

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