Author
Helen J. Burgess
Other affiliations: University of Oxford, Max Planck Society, University of Chicago ...read more
Bio: Helen J. Burgess is an academic researcher from Rush University Medical Center. The author has contributed to research in topics: Circadian rhythm & Melatonin. The author has an hindex of 39, co-authored 100 publications receiving 4557 citations. Previous affiliations of Helen J. Burgess include University of Oxford & Max Planck Society.
Topics: Circadian rhythm, Melatonin, Medicine, Actigraphy, Morning
Papers published on a yearly basis
Papers
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TL;DR: Consensus-based guidelines are presented for collecting and analyzing melatonin for studies that are conducted in the natural living environment, the clinical setting, and in-patient research facilities under controlled conditions.
Abstract: Melatonin synthesis from the pineal gland is regulated by the circadian pacemaker located in the suprachiasmatic nuclei and by ocular light exposure. Melatonin has a circadian rhythm that peaks during the night in normally entrained individuals. In the absence of light and other synchronizing signals, the rhythm of melatonin production persists with an elevation that occurs during the subjective, as opposed to the actual, night. There is a relatively direct anatomic pathway between the suprachiasmatic nuclei and the pineal gland, and comparatively few exogenous factors are known to affect melatonin concentrations (see Table 1 from Arendt, 2005, for a summary of these factors).1 As a result, the rhythm of melatonin production has been shown to reflect both the phase and, if collected over more than 1 cycle, the period of the endogenous circadian oscillator, thus providing a reliable means to estimate the timing of the internal circadian clock located in the suprachiasmatic nuclei.
The circadian melatonin rhythm is currently the most commonly used circadian phase marker in humans.2–4 A variety of methods for sampling and analyzing melatonin have been described, but there are no established guidelines on when and how these various methods should be used. The multitude of assessment methods described can be confusing to those seeking to assess circadian rhythms in their own patients. Furthermore, the variety of melatonin phase markers reported in the literature increases the difficulty of comparing results from different studies, and the lack of comparable normative values impedes evaluation of results from clinical populations.
This workgroup was formed following an Associated Professional Sleep Societies workshop on the use of melatonin as a circadian phase marker. Our goal was to achieve consensus for collecting and analyzing melatonin, thereby assisting clinicians and researchers in determining which method of measuring melatonin is most appropriate for their particular needs, as well as facilitating the comparison of data among researchers and clinicians. We present here a consensus statement on the preferred uses of urine, saliva, and blood samples and discuss the advantages and disadvantages of each approach. Also discussed are factors that may affect the measurement of melatonin and the different circadian phase markers that might be derived from these methods.
407 citations
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15 Oct 2015-Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine
TL;DR: A systematic literature review and meta-analyses were performed and the GRADE approach was used to update the previous American Academy of Sleep Medicine Practice Parameters on the treatment of intrinsic circadian rhythm sleep-wake disorders as discussed by the authors.
Abstract: A systematic literature review and meta-analyses (where appropriate) were performed and the GRADE approach was used to update the previous American Academy of Sleep Medicine Practice Parameters on the treatment of intrinsic circadian rhythm sleep-wake disorders. Available data allowed for positive endorsement (at a second-tier degree of confidence) of strategically timed melatonin (for the treatment of DSWPD, blind adults with N24SWD, and children/ adolescents with ISWRD and comorbid neurological disorders), and light therapy with or without accompanying behavioral interventions (adults with ASWPD, children/adolescents with DSWPD, and elderly with dementia). Recommendations against the use of melatonin and discrete sleep-promoting medications are provided for demented elderly patients, at a second- and first-tier degree of confidence, respectively. No recommendations were provided for remaining treatments/ populations, due to either insufficient or absent data. Areas where further research is needed are discussed.
276 citations
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TL;DR: The efficacy of appropriately timed bright light exposure and exogenous melatonin administration for producing circadian adaptation to night work and the impact of individual differences on possible circadian interventions and issues associated with the use of bright light interventions in the field are discussed.
239 citations
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TL;DR: Examining individual differences in a large sample of complete melatonin profiles not suppressed by light found an earlier occurrence of the onset of melatonin secretion was associated with an earlier wake time, more morningness and the absence of a bed partner.
Abstract: The aim of this study was to examine individual differences in a large sample of complete melatonin profiles not suppressed by light and search for possible associations between the amount and timing of melatonin secretion and a multitude of lifestyle variables. The melatonin profiles were derived from saliva samples collected every 30 minutes in dim light from 85 healthy women and 85 healthy men aged 18-45 years. There was a large individual variability in the amount of melatonin secreted with peak values ranging from 2 to 84 pg/ml. The onset of melatonin secretion ranged from 18:13 to 00:26 hours. The use of hormonal birth control, reduced levels of employment, a smaller number of days on a fixed sleep schedule, increased day length and lower weight were associated with an increased amplitude of melatonin secretion. The use of hormonal birth control, contact lenses, a younger age, and lower ratings of mania and paranoia were associated with a longer duration of melatonin secretion. An earlier occurrence of the onset of melatonin secretion was associated with an earlier wake time, more morningness and the absence of a bed partner. Lifestyle and behavioral variables were only able to explain about 15% of the individual variability in the amount of melatonin secretion, which is likely because of a substantial genetic influence on the levels of melatonin secretion.
225 citations
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TL;DR: Neither questionnaire should be exclusively used to time light or exogenous melatonin treatment, as this could result in the mistiming of these treatments relative to the DLMO, thereby potentially worsening circadian misalignment.
Abstract: The dim light melatonin onset (DLMO) is the most reliable measure of central circadian timing in humans. However, it is not always possible to measure the DLMO because sample collection has to occur in the hours before usual sleep onset, it requires staff support and considerable participant effort, and it is relatively expensive. Questionnaires that ask people about the timing of their behavior, such as their sleep, may provide an easier and less expensive estimate of circadian timing. The objective of this analysis was to compare the MEQ score derived from the Morningness-Eveningness Questionnaire (MEQ) and the MSFsc derived from the Munich ChronoType Questionnaire (MCTQ) to the DLMO in the largest sample to date (N = 60). Our hypothesis was that MSFsc would correlate more highly with the DLMO than MEQ score. Our sample of 36 healthy controls and 24 patients with delayed sleep phase disorder ranged in age from 18 to 62 years. All participants slept at times of their own choosing for a week before the assessment of their DLMO. The DLMO correlated significantly with both the MEQ score (r = -0.70, p < 0.001) and MSFsc (r = 0.68, p < 0.001). A linear regression using MEQ, MSFsc, and age to predict the DLMO explained 60% of the DLMO variance. The strongest predictor of the DLMO was MSFsc (beta = 0.51, p = 0.001), followed by MEQ (beta = -0.41, p = 0.004), and age (beta = 0.26, p = 0.013). The beta values for MSFsc and MEQ score were not statistically different from each other. Nonetheless, around a 4-h range in the DLMO was observed at a given MEQ score and a given MSFsc, indicating that neither questionnaire should be exclusively used to time light or exogenous melatonin treatment, as this could result in the mistiming of these treatments relative to the DLMO, thereby potentially worsening circadian misalignment.
222 citations
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TL;DR: There is growing evidence that neuroticism is a psychological trait of profound public health significance, a robust correlate and predictor of many different mental and physical disorders, comorbidity among them, and the frequency of mental and general health service use.
Abstract: The personality trait of neuroticism refers to relatively stable tendencies to respond with negative emotions to threat, frustration, or loss. Individuals in the population vary markedly on this trait, ranging from frequent and intense emotional reactions to minor challenges to little emotional reaction even in the face of significant difficulties. Although not widely appreciated, there is growing evidence that neuroticism is a psychological trait of profound public health significance. Neuroticism is a robust correlate and predictor of many different mental and physical disorders, comorbidity among them, and the frequency of mental and general health service use. Indeed, neuroticism apparently is a predictor of the quality and longevity of our lives. Achieving a full understanding of the nature and origins of neuroticism, and the mechanisms through which neuroticism is linked to mental and physical disorders, should be a top priority for research. Knowing why neuroticism predicts such a wide variety of seemingly diverse outcomes should lead to improved understanding of commonalities among those outcomes and improved strategies for preventing them.
1,412 citations
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TL;DR: It is demonstrated that insufficient sleep and irregular sleep-wake patterns, which have been extensively documented in younger adolescents, are also present at alarming levels in the college student population.
1,360 citations
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TL;DR: Data support an association between smoking and Crohn's disease whereas smoking cessation, but not current smoking, is associated with an increased risk of ulcerative colitis.
Abstract: IBD, comprising Crohn's disease and ulcerative colitis, is a chronic immunologically mediated disease at the intersection of complex interactions between genetics, environment and gut microbiota. Established high-prevalence populations of IBD in North America and Europe experienced the steepest increase in incidence towards the second half of the twentieth century. Furthermore, populations previously considered 'low risk' (such as in Japan and India) are witnessing an increase in incidence. Potentially relevant environmental influences span the spectrum of life from mode of childbirth and early-life exposures (including breastfeeding and antibiotic exposure in infancy) to exposures later on in adulthood (including smoking, major life stressors, diet and lifestyle). Data support an association between smoking and Crohn's disease whereas smoking cessation, but not current smoking, is associated with an increased risk of ulcerative colitis. Dietary fibre (particularly fruits and vegetables), saturated fats, depression and impaired sleep, and low vitamin D levels have all been associated with incident IBD. Interventional studies assessing the effects of modifying these risk factors on natural history and patient outcomes are an important unmet need. In this Review, the changing epidemiology of IBD, mechanisms behind various environmental associations and interventional studies to modify risk factors and disease course are discussed.
1,125 citations
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TL;DR: Chronic sleep loss, behavioral or sleep disorder related, may represent a novel risk factor for weight gain, insulin resistance, and Type 2 diabetes.
Abstract: Chronic sleep loss as a consequence of voluntary bedtime restriction is an endemic condition in modern society. Although sleep exerts marked modulatory effects on glucose metabolism, and molecular mechanisms for the interaction between sleeping and feeding have been documented, the potential impact of recurrent sleep curtailment on the risk for diabetes and obesity has only recently been investigated. In laboratory studies of healthy young adults submitted to recurrent partial sleep restriction, marked alterations in glucose metabolism including decreased glucose tolerance and insulin sensitivity have been demonstrated. The neuroendocrine regulation of appetite was also affected as the levels of the anorexigenic hormone leptin were decreased, whereas the levels of the orexigenic factor ghrelin were increased. Importantly, these neuroendocrine abnormalities were correlated with increased hunger and appetite, which may lead to overeating and weight gain. Consistent with these laboratory findings, a growing body of epidemiological evidence supports an association between short sleep duration and the risk for obesity and diabetes. Chronic sleep loss may also be the consequence of pathological conditions such as sleep-disordered breathing. In this increasingly prevalent syndrome, a feedforward cascade of negative events generated by sleep loss, sleep fragmentation, and hypoxia are likely to exacerbate the severity of metabolic disturbances. In conclusion, chronic sleep loss, behavioral or sleep disorder related, may represent a novel risk factor for weight gain, insulin resistance, and Type 2 diabetes.
1,090 citations