Obesity Research

Relationship of morningness-eveningness questionnaire score to melatonin and sleep timing, body mass index and atypical depressive symptoms in peri- and post-menopausal women.

Psychiatry Res. 2011 Jun 30;188(1):88-95. Epub 2011 Jan 14.
Relationship of morningness-eveningness questionnaire score to melatonin and sleep timing, body mass index and atypical depressive symptoms in peri- and post-menopausal women.


Previous work shows a relationship between measures of morning or evening preference (e.g., morningness-eveningness questionnaire (MEQ) scores) and melatonin and sleep timing, body mass index (BMI) and mood. This study explores the relationship of these factors to atypical depression (ATD) symptoms, particularly increased appetite and hypersomnia, in depressed and non-depressed peri- and post-menopausal women. Participants were 19 normal control subjects and 10 depressed patients, 46-72years of age. In a university hospital setting, we administered the MEQ and Structured Interview Guide for the Hamilton Depression Rating Scale, Seasonal Affective Disorders (SIGH-SAD version), which includes a measure of ATD, 3-5weeks before obtaining nighttime polysomnography and overnight plasma melatonin in dim light (<30lx). Scores on SIGH-SAD appetite-related items were significantly correlated with MEQ, dim light melatonin onset (DLMO) time and midsleep time (MST); BMI was related to MST, sleep end time, phase-angle differences between sleep and melatonin timing, and appetite measures. Results suggest that relative to women with earlier DLMOs and MSTs, depressed peri- and post-menopausal women whose DLMOs and MSTs are phase-delayed may experience increases in appetite, hypersomnia, and BMI. These symptoms might be relieved by sleep or light manipulations that advance melatonin and sleep timing parameters.

Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.

[PubMed – in process]
PMCID: PMC3100421
[Available on 2012/6/30]

Obesity and metabolic syndrome: Association with chronodisruption, sleep deprivation, and melatonin suppression.


Department of Cellular and Structural Biology, UT Health Science Center , San Antonio, Texas USA.


Obesity has become an epidemic in industrialized and developing countries. In 30 years, unless serious changes are made, a majority of adults and many children will be classified as overweight or obese. Whereas fatness alone endangers physiological performance of even simple tasks, the associated co-morbidity of obesity including metabolic syndrome in all its manifestations is a far more critical problem. If the current trend continues as predicted, health care systems may be incapable of handling the myriad of obesity-related diseases. The financial costs, including those due to medical procedures, absenteeism from work, and reduced economic productivity, will jeopardize the financial well-being of industries. The current review summarizes the potential contributions of three processes that may be contributing to humans becoming progressively more overweight: circadian or chronodisruption, sleep deficiency, and melatonin suppression. Based on the information provided in this survey, life-style factors (independent of the availability of abundant calorie-rich foods) may aggravate weight gain. Both epidemiological and experimental data support associations between disrupted physiological rhythms, a reduction in adequate sleep, and light-at-night-induced suppression of an essential endogenously produced molecule, melatonin. The implication is that if these problems were corrected with life-style changes, body-weight could possibly be more easily controlled.

Chronobiological aspects of nutrition, metabolic syndrome and obesity.

Adv Drug Deliv Rev. 2010 Jul 31;62(9-10):967-78. Epub 2010 May 24.

Chronobiological aspects of nutrition, metabolic syndrome and obesity.

Garaulet M, Madrid JA.

Department of Physiology, University of Murcia, Spain. garaulet@um.es


The present review starts from the classical physiological and nutritional studies related with food intake control, digestion, transport and absorption of nutrients. It continues with studies related with the metabolism of adipose tissue, and finish with modern experiments in genetics and molecular biology – all from a fresh, chronobiological point of view. Obesity will be explained as a fault in the circadian system, as pathology associated with “chronodisruption”. The main gaps in chronobiological research related to obesity will be also identified and chronobiological-based therapies will be proposed in order to allow the resetting of the circadian rhythm among obese subjects.

The chronobiology, etiology and pathophysiology of obesity.

Int J Obes (Lond). 2010 Jun 22. [Epub ahead of print]

The chronobiology, etiology and pathophysiology of obesity.

Garaulet M, Ordovás JM, Madrid JA.

Faculty of Biology, Department of Physiology, Campus of Espinardo, University of Murcia, Murcia, Spain.


The effect of circadian disruption (CD) on human health is an emerging issue. Many records link CD with diseases such as cancer, cardiovascular, cognitive impairment and obesity, all of them conducive to premature aging. The amount of sleep has declined by 1.5 h over the past century, accompanied by an important increase in obesity. Shift work, sleep deprivation and exposure to bright light at night increase the prevalence of adiposity. Animal models have shown that mice with Clock gene disruption are prone to developing obesity and MetS. This review summarizes the latest developments with regard to chronobiology and obesity, considering (1) how molecular clocks coordinate metabolism and the specific role of the adipocyte; (2) CD and its causes and pathological consequences; (3) the epidemiological evidence of obesity as a chronobiological illness; and (4) theories of circadian disruption and obesity. Energy intake and expenditure, relevance of sleep, fat intake from a circadian perspective and psychological and genetic aspects of obesity are examined. Finally, ideas about the use of chronobiology in the treatment of obesity are discussed. Such knowledge has the potential to become a valuable tool in the understanding of the relationship between the chronobiology, etiology and pathophysiology of obesity.International Journal of Obesity advance online publication, 22 June 2010; doi:10.1038/ijo.2010.118.

Significance and application of melatonin in the regulation of brown adipose tissue metabolism: relation to human obesity.

Obes Rev. 2010 Jun 16. [Epub ahead of print]

Significance and application of melatonin in the regulation of brown adipose tissue metabolism: relation to human obesity.

Tan DX, Manchester LC, Fuentes-Broto L, Paredes SD, Reiter RJ.

Department of Cellular and Structural Biology, the University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.


Summary A worldwide increase in the incidence of obesity indicates the unsuccessful battle against this disorder. Obesity and the associated health problems urgently require effective strategies of treatment. The new discovery that a substantial amount of functional brown adipose tissue (BAT) is retained in adult humans provides a potential target for treatment of human obesity. BAT is active metabolically and disposes of extra energy via generation of heat through uncoupling oxidative phosphorylation in mitochondria. The physiology of BAT is readily regulated by melatonin, which not only increases recruitment of brown adipocytes but also elevates their metabolic activity in mammals. It is speculated that the hypertrophic effect and functional activation of BAT induced by melatonin may likely apply to the human. Thus, melatonin, a naturally occurring substance with no reported toxicity, may serve as a novel approach for treatment of obesity. Conversely, because of the availability of artificial light sources, excessive light exposure after darkness onset in modern societies should be considered a potential contributory factor to human obesity as light at night dramatically reduces endogenous melatonin production. In the current article, the potential associations of melatonin, BAT, obesity and the medical implications are discussed.

Age-dependent association of exposure to television screen with children's urinary melatonin excretion?

Neuro Endocrinol Lett. 2006 Feb-Apr;27(1-2):73-80.

Age-dependent association of exposure to television screen with children`s urinary melatonin excretion?

Salti R, Tarquini R, Stagi S, Perfetto F, Cornélissen G, Laffi G, Mazzoccoli G, Halberg F.


Department of Pediatrics, University of Florence, Florence, Italy.


OBJECTIVES: Changes in magnetic field are associated with a decrease in nocturnal urinary melatonin excretion. Television screens emit low and very low frequency electromagnetic waves (radiofrequencies and light) and exposure to them may be associated with a decrease in 24-hour melatonin in children`s urine. Design and setting. An observational study in schools of Cavriglia, Italy, determined melatonin in 24-hour urines from 42 boys and 32 girls 6 to 13 years of age after one week of watching TV and after another week of abstaining from watching TV. RESULTS AND


MAIN FINDINGS: In a gender- and age-dependent fashion, exposure to a television screen was associated with lower urinary melatonin concentrations, affecting particularly younger children at a pubertal stage when important changes in melatonin`s time structure occur.

CONCLUSION: Additional work should test further relations to growth, maturation and development, focusing on any adverse effect from exposure to a television screen also on obesity from a neuro-hormonal viewpoint, quite apart from any decreased activity and/or other lifestyle alterations associated with watching TV.