ORCID Profile
0000-0003-3397-543X
Current Organisation
University of the Witwatersrand
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Publisher: American Academy of Sleep Medicine (AASM)
Date: 09-03-2021
DOI: 10.5664/JCSM.9214
Publisher: Springer Science and Business Media LLC
Date: 29-03-2019
DOI: 10.1038/S41598-019-41712-1
Abstract: The PERIOD2 ( PER2 ) gene is a core molecular component of the circadian clock and plays an important role in the generation and maintenance of daily rhythms. Rs35333999, a missense variant of PER2 common in European populations, has been shown to associate with later chronotype. Chronotype relates to the timing of biological and behavioral activities, including when we sleep, eat, and exercise, and later chronotype is associated with longer intrinsic circadian period (cycle length), a fundamental property of the circadian system. Thus, we tested whether this PER2 variant was associated with circadian period and found significant associations with longer intrinsic circadian period as measured under forced desynchrony protocols, the ‘gold standard’ for intrinsic circadian period assessment. Minor allele (T) carriers exhibited significantly longer circadian periods when determinations were based on either core body temperature or plasma melatonin measurements, as compared to non-carriers (by 12 and 11 min, respectively accounting for ~7% of inter-in idual variance). These findings provide a possible underlying biological mechanism for inter-in idual differences in chronotype, and support the central role of PER2 in the human circadian timing system.
Publisher: Springer Science and Business Media LLC
Date: 15-12-2021
DOI: 10.1038/S41598-021-02021-8
Abstract: During lockdowns associated with the COVID-19 pandemic, in iduals have experienced poor sleep quality and sleep regularity, changes in lifestyle behaviours, and heightened depression and anxiety. However, the inter-relationship and relative strength of those behaviours on mental health outcomes is still unknown. We collected data between 12 May and 15 June 2020 from 1048 South African adults (age: 32.76 ± 14.43 years n = 767 female n = 473 students) using an online questionnaire. Using structural equation modelling, we investigated how insomnia symptoms, sleep regularity, exercise intensity/frequency and sitting/screen-use (sedentary screen-use) interacted to predict depressive and anxiety-related symptoms before and during lockdown. We also controlled for the effects of sex and student status. Irrespective of lockdown, (a) more severe symptoms of insomnia and greater sedentary screen-use predicted greater symptoms of depression and anxiety and (b) the effects of sedentary screen-use on mental health outcomes were mediated by insomnia. The effects of physical activity on mental health outcomes, however, were only significant during lockdown. Low physical activity predicted greater insomnia symptom severity, which in turn predicted increased depressive and anxiety-related symptoms. Overall, relationships between the study variables and mental health outcomes were lified during lockdown. The findings highlight the importance of maintaining physical activity and reducing sedentary screen-use to promote better sleep and mental health.
Publisher: Elsevier BV
Date: 10-2022
DOI: 10.1016/J.SMRV.2021.101571
Abstract: Antiretroviral therapy has significantly reduced morbidity and mortality in people living with HIV (PLWH). However, a direct consequence of higher survival is the development of ageing-related co-morbidities that have considerable potential to affect quality of life. Sleep disturbances in PLWH are a significant source of morbidity. A meta-analysis has estimated the prevalence of self-reported sleep disturbances in PLWH to be 58%, with commonly identified disturbances including insomnia, obstructive sleep apnoea and poor sleep quality. Not only do sleep disturbances impair daytime functioning, but chronic sleep disruption also associates with metabolic dysregulation and cardiometabolic disease. Therefore, an understanding of the pathogenesis of sleep disturbances in PLWH is important for reducing morbidity and improving quality of life. Several pathophysiological processes in HIV infection may cause sleep-wake dysregulation. In early infection stages, immunological changes such as expression of sleep-promoting cytokines could mediate sleep disturbances. Long term, chronic immune activation, in addition to side effects of antiretroviral therapy, may impact sleep homeostasis more severely, for ex le through increasing the risk of obstructive sleep apnoea. These sleep disturbances may further contribute to an inflammatory state, due to the bi-directional relationship between sleep and immunity. In summary, further elucidating the link between HIV, immune activation, and sleep is an underexplored avenue for minimising population morbidity and mortality.
Publisher: Wiley
Date: 06-11-2022
DOI: 10.1111/JPI.12838
Abstract: The increasing number of people living with human immunodeficiency virus, HIV, (PLWH) have an elevated incidence of risk for noncommunicable comorbidities, the aetiology of which remains incompletely understood. While sleep disturbances are often reported in PLWH, it is unknown to what extent they relate to changes in the circadian and/or sleep homeostatic processes. We studied the relationship between sleep characteristics, circadian phase, and HIV status in older adults from the HAALSI (Health and Ageing in Africa: a Longitudinal Study of an INDEPTH Community in South Africa) subs le of the Agincourt Health and Demographic Surveillance System in South Africa ( n = 187, 36 human immunodeficiency virus positive [HIV+], age: 66.7 ± 11.5 years, range 45—93 years), where HIV prevalence is high and (in contrast to the global north) does not associate significantly with potentially confounding behavioural differences. In participants with valid actigraphy data ( n = 172), regression analyses adjusted for age and sex indicated that HIV+ participants had slightly later sleep onset ( β = .16, p = .039), earlier sleep offset times ( β = −.16, p = .049) and shorter total sleep times ( β = −.20, p = .009) compared to the HIV negative (HIV−) participants. In a subset of participants ( n = 51, 11 HIV+), we observed a later dim light melatonin onset (DLMO) in HIV+ (21:16 ± 01:47) than in HIV− (20:06 ± 00:58) participants ( p = .006). This substantial difference remained when adjusted for age and sex ( β = 1.21 p = .006). In 36 participants (6 HIV+) with DLMO and actigraphy data, median phase angle of entrainment was −6 min in the HIV+ group and +1 h 25 min in the HIV− group. DLMO time correlated with sleep offset ( ρ = 0.47, p = .005) but not sleep onset ( ρ = −0.086, p = .623). Collectively, our data suggest that the sleep phase occurred earlier than what would be biologically optimal among the HIV+ participants. This is the first report of a mistimed circadian phase in PLWH, which has important potential implications for their health and well‐being, especially given the well‐established relationships between circadian asynchrony and sleep deprivation with poorer health outcomes.
Publisher: American Diabetes Association
Date: 16-02-2016
DOI: 10.2337/DB15-0999
Abstract: The risk of type 2 diabetes (T2D) is increased by abnormalities in sleep quantity and quality, circadian alignment, and melatonin regulation. A common genetic variant in a receptor for the circadian-regulated hormone melatonin (MTNR1B) is associated with increased fasting blood glucose and risk of T2D, but whether sleep or circadian disruption mediates this risk is unknown. We aimed to test if MTNR1B diabetes risk variant rs10830963 associates with measures of sleep or circadian physiology in intensive in-laboratory protocols (n = 58–96) or cross-sectional studies with sleep quantity and quality and timing measures from self-report (n = 4,307–10,332), actigraphy (n = 1,513), or polysomnography (n = 3,021). In the in-laboratory studies, we found a significant association with a substantially longer duration of elevated melatonin levels (41 min) and delayed circadian phase of dim-light melatonin offset (1.37 h), partially mediated through delayed offset of melatonin synthesis. Furthermore, increased T2D risk in MTNR1B risk allele carriers was more pronounced in early risers versus late risers as determined by 7 days of actigraphy. Our results provide the surprising insight that the MTNR1B risk allele influences dynamics of melatonin secretion, generating a novel hypothesis that the MTNR1B risk allele may extend the duration of endogenous melatonin production later into the morning and that early waking may magnify the diabetes risk conferred by the risk allele.
Publisher: American Academy of Sleep Medicine (AASM)
Date: 11-2021
DOI: 10.5664/JCSM.9614
Location: France
No related grants have been discovered for Karine Scheuermaier.