Incidence of Diabetes in Middle-Aged Men Is Related to Sleep Disturbances

Nilsson, Peter M.; Rööst, Mattias; Engström, Gunnar; Hedblad, Bo; Berglund, Göran

doi:10.2337/diacare.27.10.2464

Cited by 279 publications

(180 citation statements)

References 42 publications

(50 reference statements)

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“…The current data further indicate that not only reduced sleep duration but also reduced sleep quality may play a role in diabetes risk. Our laboratory findings are consistent with a body of epidemiologic evidence linking short or poor sleep and increased incidence of type 2 diabetes (17)(18)(19)(20)(36)(37)(38). Taken together, the current evidence suggests that strategies to improve sleep duration and quality should be considered as a potential intervention to prevent or delay the development of type 2 diabetes in at-risk populations.…”

Section: Discussionsupporting

confidence: 74%

“…It is possible that, under more chronic conditions, insulin secretion might increase to a level sufficient to compensate for the decrease in S.I. However, evidence to the contrary has been obtained in four independent prospective epidemiologic studies showing that poor sleep quality is associated with an increase in the risk of incident type 2 diabetes (17)(18)(19)(20). We observed an elevation in sympathovagal balance, which could be involved both in the decrease in S.I.…”

Section: Discussionmentioning

confidence: 41%

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Slow-wave sleep and the risk of type 2 diabetes in humans

Tasali

Leproult²,

Ehrmann³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

800

617

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There is convincing evidence that, in humans, discrete sleep stages are important for daytime brain function, but whether any particular sleep stage has functional significance for the rest of the body is not known. Deep non-rapid eye movement (NREM) sleep, also known as slow-wave sleep (SWS), is thought to be the most ''restorative'' sleep stage, but beneficial effects of SWS for physical well being have not been demonstrated. The initiation of SWS coincides with hormonal changes that affect glucose regulation, suggesting that SWS may be important for normal glucose tolerance. If this were so, selective suppression of SWS should adversely affect glucose homeostasis and increase the risk of type 2 diabetes. Here we show that, in young healthy adults, all-night selective suppression of SWS, without any change in total sleep time, results in marked decreases in insulin sensitivity without adequate compensatory increase in insulin release, leading to reduced glucose tolerance and increased diabetes risk. SWS suppression reduced delta spectral power, the dominant EEG frequency range in SWS, and left other EEG frequency bands unchanged. Importantly, the magnitude of the decrease in insulin sensitivity was strongly correlated with the magnitude of the reduction in SWS. These findings demonstrate a clear role for SWS in the maintenance of normal glucose homeostasis. Furthermore, our data suggest that reduced sleep quality with low levels of SWS, as occurs in aging and in many obese individuals, may contribute to increase the risk of type 2 diabetes.aging ͉ sleep quality ͉ sleep disordered breathing ͉ delta waves ͉ insulin resistance H uman sleep is composed of rapid-eye-movement (REM) sleep and stages 1, 2, 3, and 4 of non-REM (NREM) sleep. The deeper stages of NREM sleep, i.e., stages 3 and 4, also known as slow-wave sleep (SWS), are thought to be the most ''restorative.'' There is indeed evidence that SWS plays a role in waking neurobehavioral function (1), particularly in memory consolidation (2, 3), but whether SWS is also important for peripheral physiological function is not known. The initiation of SWS is temporally associated with transient metabolic, hormonal, and neurophysiologic changes, all of which could potentially affect glucose homeostasis. These include decreased brain glucose utilization, stimulation of growth hormone release, inhibition of corticotropic activity, decreased sympathetic nervous activity, and increased vagal tone. We therefore hypothesized that SWS plays a role in glucose regulation and that suppression of SWS may adversely affect glucose homeostasis.To test this hypothesis, we developed an experimental model in young healthy lean individuals that was designed to selectively suppress SWS and assessed the impact of this intervention on glucose homeostasis. The EEG was continuously monitored, and SWS was suppressed by delivering acoustic stimuli of varying frequencies and intensities. The intervention was designed to substitute deep NREM sleep, i.e., stages 3 and 4, with shallow NREM slee...

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Section: Discussionsupporting

confidence: 74%

Section: Discussionmentioning

confidence: 41%

Slow-wave sleep and the risk of type 2 diabetes in humans

Tasali

Leproult²,

Ehrmann³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

800

617

View full text Add to dashboard Cite

show abstract

“…For example, Cushing's syndrome, sleeping disorders, work stress and schizophrenia [30][31][32][33] appeared to be associated with an increased level of cortisol and also with an increased risk of type 2 diabetes and insulin resistance, although studies on sleep disorders showed inconsistent results regarding risk of diabetes [33][34][35][36][37].…”

Section: Discussionmentioning

confidence: 99%

Depression as a risk factor for the onset of type 2 diabetes mellitus. A meta-analysis

et al. 2006

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Aims/hypothesis: Evidence strongly suggests that depression and type 2 diabetes are associated, but the direction of the association is still unclear. Depression may occur as a consequence of having diabetes, but may also be a risk factor for the onset of type 2 diabetes. This study examined the latter association by reviewing the literature and conducting a meta-analysis of longitudinal studies on this topic. Methods: Medline and PsycInfo were searched for articles published up to January 2005. All studies that examined the relationship between depression and the onset of type 2 diabetes were included. Pooled relative risks were calculated using fixed and random effects models. To explore sources of heterogeneity between studies, subgroup analyses and meta-regression analyses were performed. Results: Nine studies met our inclusion criteria for this meta-analysis. The pooled relative risk was 1.26 (1.13-1.39) using the fixed effects model and 1.37(1.14-1.63) using the random effects model. Heterogeneity between studies could not be explained by (1) whether studies controlled for undetected diabetes at baseline; (2) the method of diabetes assessment at followup; (3) the baseline overall risk of diabetes in the study population; and (4) follow-up duration. Conclusions/ interpretation: Depressed adults have a 37% increased risk of developing type 2 diabetes mellitus. The pathophysiological mechanisms underlying this relationship are still unclear and warrant further research. A randomised controlled study is needed to test whether effective prevention or treatment of depression can reduce the incidence of type 2 diabetes and its health consequences.

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“…[54][55][56] A growing body of epidemiological evidence supports an association between short sleep duration and the risk of obesity [57][58][59][60][61] and type 2 diabetes. [62][63][64][65][66] The potential mechanisms by which sleep deprivation may predispose to obesity are: (1) an alteration of the neuroendocrine control of appetite characterized by a decrease in the levels of the anorexigenic hormone leptin and an increase in the levels of the orexigenic hormone ghrelin; (2) an increased opportunity to eat; (3) an altered thermoregulation; and (4) an increased fatigue leading to reductions in physical activity. 67 Furthermore, physiological data suggest that short-term partial sleep restriction leads to striking alterations in metabolic function including decreased carbohydrate tolerance and insulin resistance.…”

Section: Short Sleep Duration: Association With Glucose Homeostasismentioning

confidence: 99%

The glucostatic theory of appetite control and the risk of obesity and diabetes

Chaput

Tremblay

2008

Int J Obes

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More than 50 years ago, Jean Mayer proposed that changes in blood glucose concentrations or arteriovenous glucose differences are detected by glucoreceptors that affect energy intake. According to this theory, an increase in blood glucose concentrations results in increased feelings of satiety whereas a drop in blood glucose concentrations has the opposite effect. The pioneering work of Mayer has recently received support from our group as low glycemia has been shown to be linked with body weight gain prospectively and has been considered as a strong predictor of the amount of weight regained after weight loss. This state of mild hypoglycemia also predicts the increase in depressive symptoms with weight loss and a greater propensity to glucose intolerance and type 2 diabetes, particularly for individuals having short sleep durations. Furthermore, knowledgebased work has been shown to induce a significant increase in spontaneous energy intake being related to changes in glycemic control. In accordance with the glucostatic theory, this oriented review suggests that factors favoring a trend toward hypoglycemia and/or glucose instability might induce excess energy intake, overweight and impaired glucose tolerance. Data also raise the possibility that fat gain might be protective against mild hypoglycemia by providing compensation to the stimuli promoted by a modern environment. Keywords: body weight; glycemia; glucose homeostasis; glucose intolerance; metabolism; weight gainThe identification of the biochemical basis for hunger and meal initiation, and of the signals controlling these neurobiological processes have been the subject of extensive research and debate for some decades regarding the control of food intake. These studies led to the classical lipostatic, 1 aminostatic, 2 and thermostatic 3 theories of food intake control as well as more recent hypotheses. [4][5][6] However, all of these theoretical ideas were preceded by the notion that glucose uptake and utilization played a central and metabolically privileged role in the control of hunger, satiety and the regulation of body energy balance. Although these notions were first discussed and suggested by Carlson in a classic text published in 1916, 7 they were formalized by Jean Mayer into the classical glucostatic theory in the mid 1950s. 8,9 The glucostatic theory of food intake control postulated that reduced glucose utilization in critical brain regions leads to perception and expression of hunger, and increased glucose utilization in these same glucosensitive sites leads to decreased hunger and cessation of eating. Mayer proposed that decreased glucose utilization or 'metabolic hypoglycemia', the point at which the peripheral arteriovenous difference in blood glucose becomes negligible and glucose is no longer entering 'metabolizing cells', was the signal for meal initiation. In his 1955 paper, Mayer explicitly argued that the glucostatic theory would account for the short-term control of hunger and food intake, whereas he invoked a lipostatic mechanism...

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Incidence of Diabetes in Middle-Aged Men Is Related to Sleep Disturbances

Cited by 279 publications

References 42 publications

Slow-wave sleep and the risk of type 2 diabetes in humans

Slow-wave sleep and the risk of type 2 diabetes in humans

Depression as a risk factor for the onset of type 2 diabetes mellitus. A meta-analysis

The glucostatic theory of appetite control and the risk of obesity and diabetes

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