Sleeping Heart (Japanese Edition)

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A total of 98, subjects 41, men and 57, women aged 40 to 79 years from to and were followed until During a median follow-up of The respective multivariable hazard ratios were 2. Long sleep duration of 10 hours or longer was associated with 1. There was no association between sleep duration and cancer mortality in either sex. Association of sleep duration with mortality from cardiovascular disease and other causes for Japanese men and women: Thus, the association between short or long sleep duration and mortality from cardiovascular disease and other causes for Japanese men and women has remained unclear.

To examine the sex-specific associations of sleep duration and mortality from stroke, coronary heart disease, and other causes, as well as total mortality, we analyzed the extended follow-up data from a large-scale prospective study of approximately 98, Japanese men and women. The Japan Collaborative Cohort Study for Evaluation of Cancer Risk sponsored by Monbusho JACC study was conducted from to , when , subjects 46, men and 64, women aged 40 to 79 years and living in 45 communities across Japan participated in municipal health-screening examinations and completed self-administered questionnaires, including lifestyle data and medical histories of previous cardiovascular disease and cancer at baseline.

The details of the study procedure have been described previously. Of the , cohort participants, data from men and women were excluded because of missing information on sleep duration, as were data from subjects men and women who reported a history of cancer, stroke, or coronary heart disease.

Finally, a total of 41, men and 57, women were included in the study. For mortality surveillance in each of the communities, investigators conducted a systematic review of death certificates, all of which had been forwarded to the public health center in the area of residency. Mortality data were then centralized at the Ministry of Health and Welfare, and the underlying causes of death were coded for the National Vital Statistics according to the International Classification of Diseases , 10th revision ICD Therefore, all deaths that occurred in the cohort were ascertained by death certificates from a public health center, except for subjects who died after they had moved from their original community, in which case the subject was treated as withdrawals from observation when they moved out.

Stroke deaths were further subdivided into intraparenchymal hemorrhage I61 , subarachnoid hemorrhage I60 , and ischemic stroke I63 and I The follow-up is believed to be complete and accurate as a result of systematic examination of death certificates and residency status. By December 31, , except for 4 communities in which follow-up was terminated at the end of , 14, subjects were treated as withdrawals from observation when they died, and subjects were treated as withdrawals from observation when they moved out of the study community.

The median follow-up period for the participants was This study was approved by the ethics committees of the Nagoya University School of Medicine and the University of Tsukuba. The baseline data were collected by means of a self-administered questionnaire, which included sleep duration; demographic characteristics; and histories of hypertension, diabetes mellitus, and other chronic diseases, as well as habits related to smoking, alcohol consumption, diet, and exercise.

We obtained information about the average sleep duration on weekdays during the preceding year. The average sleep duration per day was classified into 7 categories: Fractions hours were rounded off eg, 7 hours represented responses from 6. Depressive symptom was assessed by using 4 psychological or behavior items 5: These 4 items were then combined into an overall index of depressive symptoms. The reproducibility and validity for dietary intake have been reported elsewhere. Statistical analyses were based on sex-specific mortality rates of disease outcomes and all cause during the follow-up period from — to to for 4 communities.

The person-years of follow-up were calculated from the date of filling out the baseline questionnaire to death, moving out of the community, or the end of follow-up, whichever came first.

Sex-specific age-adjusted mean values and prevalence of cardiovascular risk factors were calculated. These estimates were adjusted for age and other potential confounding factors by means of the Cox proportional hazards model. After a follow-up of 1,, person-years, the deaths of men and women: Table 1 shows sex-specific age-adjusted mean values or prevalence of risk characteristics at baseline by sleep-duration category. Compared with 7 hours of sleep, short or long sleep duration tended to be associated with older age and more depressive symptoms for both men and women.

Men and women with short sleep duration were more likely to have high perceived mental stress, whereas those with long sleep duration were less educated. Data are presented as percentage, except age, body mass index BMI , ethanol intake, and fresh fish intake, which are presented as mean. These associations, except for mortality from cancer, were slightly weaker but remained statistically significant after adjustment for cardiovascular risk factors and depressive symptoms.

HR refers to hazard ratio; CI, confidence interval.

This Japanese company pays its employees to get a good night's sleep

There was an increased risk of mortality from coronary heart disease for women with 4 or fewer hours and 5 hours of sleep, compared with those with 7 hours of sleep. After further adjustment for individual quantity of alcohol consumption as a continuous variable, the multivariable hazard ratio for male short sleepers was 1. As for total cardiovascular disease for women and noncardiovascular disease and all causes for men and women, there was a U-shaped relationship between sleep duration and mortality, with a nadir at 7 hours of sleep.

These associations were essentially unchanged when we excluded subjects whose events occurred within 5 years after baseline. Furthermore, the respective hazard ratios of mortality from all causes were 1. In this large-scale prospective study of Japanese men and women aged 40 to 79 years, we confirmed that, compared with 7 hours of sleep, short sleep duration of 4 hours or less was associated with a 2-fold increase in mortality from coronary heart disease for women and a 1.

To the best of our knowledge, ours is the first study to provide evidence of the association of short sleep duration with an increase in mortality from coronary heart disease for Asian women. Previous studies of Americans or Europeans support our findings. The Nurses' Health Study of 71, women aged 40 to 65 years reported that, compared with 8 hours of sleep, short sleep duration of 5 hours or less was associated with a 1. This finding contrasts with the result that risk of mortality from cardiovascular disease, other causes, and all causes were approximately half among women than among men.

The age-adjusted hazard ratios for women versus men were 0. Short sleep of 4 or fewer hours was found to be associated with increased risk of mortality from hemorrhagic stroke for men, although this association was not statistically significant.

However, when stratified by alcohol consumption habits, an increased risk of mortality from hemorrhagic stroke was observed among male drinkers with 4 or fewer hours and 5 hours of sleep. A cross-national study on sleep habits of approximately 35, men and women of 10 countries, including Japan, 10 showed that the prevalence of the use of alcohol as a sleep aid was the highest in Japan It is possible that the habit of using alcohol as a sleep aid enhances the risk of mortality from hemorrhagic stroke associated with short sleep duration.

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There is some evidence that may explain why short sleep duration is associated with an increase in mortality from coronary heart disease and total cardiovascular disease. Previous studies showed that short-term sleep deprivation leads to increased sympathetic nervous system activity, 12 , 13 elevated blood pressure, 12 , 14 elevated cortisol levels, 13 impaired glucose tolerance, 13 and increased inflammatory markers, 15 which may reflect and increase the risk of cardiovascular disease. Furthermore, recent epidemiologic studies have demonstrated that short sleep duration is associated with higher levels of hemoglobin A 1c , 16 total cholesterol, 17 and triglycerides, 17 higher blood pressure, 17 and increased incidence of hypertension.

This finding suggests other mechanisms for increasing nonspecific mortality, which need to be explored in further studies. The following limitations of our study need to be addressed. Sleep-disordered breathing, a known cause of daytime sleepiness, would be linked to increased sympathetic tone and glucose intolerance [ 7 ].

These mechanisms may be associated with the relationship between long sleep duration and DM. In summary, sleep loss was associated with DM via endocrine system disruption, which would, in part, affect our eating behavior and autonomic balance.

Question Details

Chart for the relationships between sleep deprivation and hypertension, diabetes mellitus, and coronary heart disease. Recent studies have shown that dysregulation of melatonin secretion may be associated with HT and IGT. The suprachiasmatic nucleus SCN in the hypothalamus, which serves as an essential component of the circadian clock, affects melatonin secretion. Light activates SCN neurons via retino-hypothalamic glutamate secretion. The SCN reaches autonomic neurons of the paraventricular nucleus PVN which projects to the intermediolateral column of the spinal cord IML where preganglionic sympathetic neurons are located that control the outflow to the pineal gland [ 49 - 51 ].

Injection of transneuronal tracers into various organs ranging from heart to ovaries and from white to brown adipose tissue resulted in the labeling of neurons in the SCN via the sympathetic and parasympathetic branches of the autonomic nervous system [ 55 - 58 ]. These data demonstrate that the SCN may transmit its circadian message, influencing the activity — rest cycle of peripheral organs, not only by the secretion of hormones that may freely pass all kinds of tissue barriers, such as melatonin, corticosterone, gonadal hormones and thyroid hormones but also by direct nervous system control of these organs.

And, SCN neurons are labeled via both the sympathetic and parasympathetic systems, indicating that the SCN may indeed support both the activity and rest periods of the circadian cycle. The SCN-PVN-autonomic axis affects hormone secretion and the sensitivity of the target organs to these hormones through neuronal mechanisms. For example, anatomical and physiological evidence shows that the SCN influences the level of insulin secretion from the pancreas [ 59 - 61 ]. Additionally, when the SCN stimulates glucose secretion from the liver, at the same time it stimulates glucose uptake by other tissues [ 61 ].

This timely orchestrated action of the SCN on glucose metabolism prepares the body, just before waking, for the coming period of activity. Disruption of this orchestration may be associated with the pathophysiology of HT and DM. For a long time, physiological studies have indicated that patients suffering from these diseases exhibit disturbed circadian rhythm [ 62 , 63 ].

Severe decreases in staining for several SCN neurotransmitters in hypertensive patients revealed an anatomical basis for these disturbances [ 64 ]. This intriguing observation suggests that SCN activity is changed by a different autonomic feedback in HT. Furthermore, recent evidence supports the notion that circadian disturbances can be detected before the development of HT or DM [ 65 , 66 ]. In the evening of the day after sleep deprivation, sympathetic nervous system activity and BP are elevated. These increases may be associated with the increased risk of CHD.

On the other hand, because sleep deprivation is related to reduced salt excretion or IGT, excessive intake of calories or salt should be avoided by people who are not getting enough sleep. In addition, since alcohol intake with sleep deprivation tends to elevate BP the next evening, people also should avoid drinking alcohol after not getting enough sleep. However, there is little evidence to support the notion that a sympathetic system blockade could be truly beneficial to such populations. Recently, Scheer et al. Repeated melatonin intake reduced nocturnal systolic and diastolic BP by 6 and 4 mmHg, respectively Fig.

The treatment did not affect heart rate. Repeated but not acute melatonin intake also improved sleep. These findings suggested that support of the circadian pacemaker function may provide a new strategy for the treatment of essential hypertension. Means of ambulatory blood pressure after repeated melatonin and repeated placebo sadministration. The light-gray background indicates the average period in bed. From Scheer et al. Similarly, Cagnacci et al. In a randomized, double-blind, placebo-controlled crossover study, 9 females with normal BP and 9 females who were treated essential hypertensives received a 3-week course of melatonin 3 mg or placebo intake 1 hr before going to bed.

ABP was measured to evaluate BP reduction with melatonin intake. In comparison with placebo, melatonin administration did not influence diurnal BP but did significantly decrease nocturnal systolic and diastolic BP, by 3. Additionally, Grossman et al. The 38 treated hypertensive patients 16 females with nocturnal hypertension were randomized in a double-blind fashion to receive either controlled-release melatonin 2 mg or placebo 2 hrs before bedtime for 4 weeks.

Simko and Paulis [ 71 ] summarized a potential role of melatonin in antihypertensive treatment. The nighttime production of melatonin is found to be reduced in hypertensive individuals. Melatonin administration decreased BP in several animal models of hypertension, in healthy men and women, and in patients with arterial HT.

The most promising results were achieved in patients with nondipping nocturnal BP.

Simko and Paulis [ 71 ] considered several potential mechanisms of BP reduction in melatonin, as follows. Melatonin can, via its scavenging and antioxidant nature, improve endothelial function via the increased availability of nitric oxide, thereby exerting vasodilatory and hypotensive effects, it can also interfere with the peripheral and central autonomic nervous systems, with a subsequent decrease in the tone of the adrenergic system and an increase in the cholinergic system.

Sleep periods that are neither too short nor too long may be important to keep us healthy. National Center for Biotechnology Information , U. Journal List Curr Cardiol Rev v. Author information Article notes Copyright and License information Disclaimer. This is an open access article distributed under the terms of the Creative Commons Attribution License http: This article has been cited by other articles in PMC.

Abstract Sleep loss is a common condition in developed countries, with evidence showing that people in Western countries are sleeping on average only 6. Sleep duration, hypertension, coronary heart disease, diabetes mellitus. Increased risk of CHD in subjects with 5 or fewer, 6, 7, and 9 or more compared with those with 8 hours of sleep. Increased odds ratios of AMI in subjects with 5 or fewer compared with those with 6 to 8 hours of sleep.

Increased odds ratios of DM and IGT in subjects with 5 or fewer, 6, and 9 or more compared with those getting 7 to 8 hours of sleep. Increased risk of DM in subjects with 5 or fewer, 6, and 8 or more compared with those getting 7 hours of sleep. Open in a separate window. Sleep Duration and HT The prevalence of HT has increased over the past decade despite improvements in awareness, treatment, and control of this disease [ 12 ].

Sleep Duration and CHD Short sleep duration imposed on a group of healthy subjects increased sympathetic nervous system activity and blood pressure elevation. Sleep Duration and DM Spiegel et al. Melatonin intake reduced systolic and diastolic blood pressure during sleep by 3. The reduction in nocturnal systolic BP was significantly greater with melatonin than with placebo. Long working hours and occupational stress-related cardiovascular attacks among middle-aged workers in Japan.

National Sleep Foundation Sleep Survey. National Sleep Foundation; We are chronically sleep deprived. Are we chronically sleep deprived? Sleep in America Poll The effects of sleep deprivation and shift work. J Clin Hypertens Greenwich Obesity, sleep apnea, and hypertension. Sleep apnea and cardiovascular disease. Disorders of glucose metabolism in sleep apnea.

Mortality risk associated sleeping patterns among adults. Short and long sleep and sleeping pills. Hajjar I, Kotchen TA. Trends in prevalence, awareness, treatment, and control of hypertension in the United States, Short sleep duration as a risk factor for hypertension. Effects of a restricted sleep regimen on ambulatory blood pressure monitoring in normotensive subjects. Effects of insufficient sleep on ambulatory blood pressure in hypertensive patients: Effect of insufficient sleep on blood pressure monitored by a new multibiomedical recorder.

Increased sympathetic and decreased parasympathetic cardiovascular modulation in normal humans with acute sleep deprivation. Association between nocturnal vagal tone and sleep depth, sleep quality, and fatigue in alcohol dependence. Irwin MR, Ziegler M. Sleep deprivation potentiates activation of cardiovascular and catecholamine responses in abstinent alcoholics.

INTRODUCTION

Effects of sleep and circadian rhythm on human circulating immune cells. Effects of sleep on the production of cytokines in humans.

Partial sleep deprivation reduces natural killer cell activity in humans. Partial night sleep deprivation reduces natural killer and cellular immune responses in humans. Effect of sleep and sleep deprivation on catecholamine and interleukin-2 levels in humans: J Clin Endocrinol Metab. Effect of sleep loss on C-reactive protein, an inflammatory marker of cardiovascular risk. J Am Coll Cardiol. Buell P, Breslow L. Mortality from coronary heart disease in California men who work long hours. Exhaustion, psychological stressors in the work environment, and acute myocardial infarction in adult men. Relation between job strain and myocardial infarction: Theorell T, Rahe RH.

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Sleep Duration as a Risk Factor for Cardiovascular Disease- a Review of the Recent Literature

A prospective study of sleep duration and coronary heart disease in women. Impact of sleep dept on metabolic and endocrine function. Association of sleep time with diabetes mellitus and impaired glucose tolerance. Sleep duration as a risk factor for the development of type 2 diabetes. Sleep loss results in and elevation of cortisol levels the next evening.

Disruption of the nocturnal testosterone rhythm by sleep fragmentation in normal men. Endogenous sex hormones and cardiovascular disease in men: A prospective population based-study.

Insulin resistance, body fat distribution, and sex hormones in men. Interrelation between plasma testosterone and plasma insulin in healthy adult men: Testosterone, sex hormone-binding globulin, and the development of type 2 diabetes in middle-aged men: Low levels of sex hormone-binding globulin and testosterone are smaller, denser low density lipoprotein in normoglycemic men.

J Clinic Endocrinol Metab. Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Hypertenison and associated metabolic abnormalities: N Engl J Med. Characterization of the multisynaptic neuronal control of the rat pineal gland using viral transneuronal tracing.

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