Literature Review

Sleep Deficiency and Deprivation Leading to Cardiovascular Disease

Article· Literature Review (PDF Available)inInternational Journal of Hypertension 2015(1):1-5 · October 2015with 48 Reads
DOI: 10.1155/2015/615681
Sleep plays a vital role in an individual’s mental, emotional, and physiological well-being. Not only does sleep deficiency lead to neurological and psychological disorders, but also the literature has explored the adverse effects of sleep deficiency on the cardiovascular system. Decreased quantity and quality of sleep have been linked to cardiovascular disease (CVD) risk factors, such as hypertension, obesity, diabetes, and dyslipidemia. We explore the literature correlating primary sleep deficiency and deprivation as a cause for cardiovascular disease and cite endothelial dysfunction as a common underlying mechanism.
Review Article
Sleep Deficiency and Deprivation Leading to
Cardiovascular Disease
Michelle Kohansieh1and Amgad N. Makaryus2
1Stern College for Women, Yeshiva University, New York, NY 10016, USA
2Department of Cardiology, North Shore-LIJ Health System, Hofstra North Shore-LIJ School of Medicine,
Nassau University Medical Center, East Meadow, NY 11554, USA
Correspondence should be addressed to Amgad N. Makaryus;
Received  November ; Revised  May ; Accepted  May 
Academic Editor: Markus P. Schlaich
Copyright ©  M. Kohansieh and A. N. Makaryus. is is an open access article distributed under the Creative Commons
Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is
properly cited.
Sleep plays a vital role in an individual’s mental, emotional, and physiological well-being. Not only does sleep deciency lead
to neurological and psychological disorders, but also the literature has explored the adverse eects of sleep deciency on the
cardiovascular system. Decreased quantity and quality of sleep have been linked to cardiovascular disease (CVD) risk factors, such
as hypertension, obesity, diabetes, and dyslipidemia. We explore the literature correlating primary sleep deciency and deprivation
as a cause for cardiovascular disease and cite endothelial dysfunction as a common underlying mechanism.
1. Introduction
Sleep is an essential part of human health and well-being.
Sleep plays a vital role in an individual’s mental, emotional,
and physiological health. Not only does sleep deciency lead
to neurological and psychological disorders, but also vast
amounts of literature have explored the adverse eects of
sleep deciency on the cardiovascular system. Decreased
quantity and quality of sleep, whether due to sleep disorders
or just through lack of proper sleep patterns, have been linked
to cardiovascular disease (CVD) risk factors, such as hyper-
tension, obesity, diabetes, and dyslipidemia []. Studies
have shown that short durations of sleep are associated with
greaterriskofdevelopingordyingfromCVD[]. While
secondary causes of sleep deciency leading to CVD have
been well described such as obstructive sleep apnea, here we
explore the literature correlating primary sleep deciency and
deprivation as a cause for cardiovascular disease through an
underlying mechanism of endothelial dysfunction.
2. Sleep Deficiency and Deprivation:
Defining the Problem
Sleep deprivation and deciency have a high prevalence in
western societies. e National Sleep Foundation reported
that less than half (%) of all Americans receive a good
night’s sleep almost every night []. According to the National
Institute of Health, sleep deciency is a broad concept that
occurs (a) if an individual does not get enough sleep (sleep
deprivation), (b) if an individual’s sleeping habits are out
of sync with the body’s natural circadian rhythm (sleeping
quantity of sleep is diminished due to a sleep disorder or
external factors []. Our review will focus on four specic
variations of sleep deciency: insomnia, acute total sleep
deprivation (TSD), partial sleep deprivation (PSD), and night
shi workers.
Acute TSD refers to the avoidance of sleep for a period
of at least one night. PSD, or sleep restriction, refers to
the reduction in the total sleep time relative to one’s usual
baseline during a -hour period. PSD is the most common
form of sleep deprivation encountered in everyday life in
modern societies []. Insomnia is dened as a predominant
associated with one or more of the following symptoms:
diculty initiating sleep, diculty maintaining sleep char-
acterized by frequent awakenings or problems returning to
sleep aer awakenings, or early morning awakenings with
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International Journal of Hypertension
Volume 2015, Article ID 615681, 5 pages
International Journal of Hypertension
follows a work schedule that is outside the typical “ to ”
business day. According to the Bureau of Labor Statistics,
millions of Americans are considered shi workers, including
doctors and nurses, pilots, bridge builders, police ocers,
customer service representatives, and commercial drivers.
rhythm, are sleep deprived, and experience frequent sleep
disturbances [,].
3. Establishing the Link between
Sleep Deficiency/Deprivation and
Cardiovascular Disease
3.1. Endothelial Dysfunction. e endothelium is the thin
layer of cells that covers the internal surface of blood vessels,
cardiac valves, and several body cavities. ese cells play a
vital role in maintaining homeostasis by sensing changes in
hemodynamic forces and blood-borne signals. In response
to homeostatic changes, endothelial cells elicit relaxation and
contractions of the underlying vascular smooth muscle cells
releasing vasoactive substances. Among those substances,
nitric oxide (NO) plays a key role [].
When an imbalance of the actions of the endothelium
toward reduced vasodilation and increased vasoconstriction
as well as increased prothrombotic properties occurs, it is said
that endothelial dysfunction is present. Arterial endothelial
dysfunction is an important event central to the pathogenesis
of atherosclerosis. Continued endothelial dysfunction con-
tributes to plaque initiation and progression [].
Endothelial function can be measured in coronary arter-
ies and in the periphery by measuring vasomotor function
aer intra-arterial infusion of pharmacologic substances that
these methods is their invasive nature, which generally makes
them unsuitable for studies involving asymptomatic subjects.
For this reason, noninvasivetests of endothelial function have
been developed and are more commonly used. Flow mediated
dilation (FMD) is an ultrasound-based method that measures
arterial diameter in response to an increase in shear stress,
which causes endothelium-dependent dilatation []. is
method can be applied more widely for the evaluation of
endothelial dysfunction and has been applied to patients with
sleep disorders.
3.2. Insomnia. One major study, the HUNT  (Nord-
Trøndelag Health Study) tness study, has explored the
connection between insomnia and endothelial function. e
study produced negative results, providing no association
between endothelial dysfunction and insomnia. ere were
no consistent associations between the cumulative number
of insomnia symptoms and FMD. However, when the study
analyzed individual insomnia symptoms, it found that certain
symptoms might be related to endothelial dysfunction and,
interestingly, those symptoms diered by gender. Among
women, there was an inverse association of early awakenings
with endothelial function, but there was an opposite asso-
ciation for men. In addition, women who reported daytime
e HUNT  study had followed earlier health studies
in Norway including the HUNT study which researched the
association between insomnia and ill health and showed that
insomnia is a signicant risk factor for myocardial infarction
[]. e negative results of the HUNT  tness study were
not expected. It should be noted that the study had several
limitations that may have led to such results, such as a self-
selection bias and the fact that the study restricted itself to
stratication bias excluding a signicant population who may
exhibit endothelial dysfunction.
3.3. Total Sleep Deprivation. In contrast to insomnia, there is
more literature on the eects of TSD on endothelial function.
One particular study which examined cardiologists on call
for  hours showed that, aer being on call, along with an
physicians had a brachial artery dilatation that did not reach
.%, and ve of them did not have any dilation at all [].
is analysis attributes the dierence in endothelial function
to stress since it is traditionally accepted that mental stress
is linked to activation of the sympathetic nervous system. In
this case apparently there was a double stress: stress induced
by a lack of sleep and stress secondary to high level medical
decision making. e dierentiation between the results that
were caused due to a lack of sleep and those due to the
mental stress of being on call for a long period of time
is not clear however. Ghiadoni et al. conducted a study
investigating the link between mental stress and endothelial
function and found that brief episodes of mental stress, like
those encountered in everyday life, may cause transient (up to
a period of  hours) endothelial dysfunction in healthy young
individuals [].
Another study by Sauvet et al., exploring the eect
of acute sleep deprivation on vascular function in twelve
healthy males, found that the endothelium-dependent and
the endothelium-independent cutaneous vascular reactivity
indices were signicantly decreased aer  hours of TSD.
By contrast, heart rate, systolic blood pressure, and the nor-
malized low-frequency component of heart rate variability
(.–. Hz), a marker of sympathetic activity, increased
signicantly within  hours of TSD []. is same group
of researchers then conducted a follow-up study in rats.
ey found that TSD induced a reduction in endothelial-
dependent vasodilation [].
3.4. Partial Sleep Deprivation. e relationship between PSD
and endothelial dysfunction has received more attention than
TSD and insomnia. In the several studies performed in the
literature, PSD has consistently been linked to decreased
vasodilation. Covassin et al. conducted a study on  healthy
subjects who underwent a -day inpatient protocol consist-
ing of a three-day acclimation period, eight days of either
sleep deprivation or normal sleep, and four days of recovery.
sleep occurred, FMD decreased during the experimental
phase in the sleep deprived group (. ±.% versus . ±
.%, 𝑃 = 0.008), while it remained unchanged in controls
(. ±% versus . ±.%, 𝑃 = 0.109)[]. A study
International Journal of Hypertension
conducted by Pugh et al. demonstrated that, compared to
the control group who received three nights of full sleep and
did not exhibit any changes in their endothelial function, the
participants who received three nights of PSD ( hours of
aer the second night of sleep restriction but, interestingly,
recovered aer the third night of PSD []. Dettoni et al.
males. ey found a reduction in the maximum endothelial-
dependent venodilation ( ± versus  ±%) [].
3.5. Shi Work. Compared to the other sleep habits that
were mentioned, shi work has received the most attention
when considering its eects on endothelial function. One
showed that aer they worked  sequential night shis the
FMD was signicantly decreased from baseline FMD taken
aer one regular workday []
pared  male shi workers with  male nonshi workers
from a glass manufacturer using the EndoPAT technique
to determine peripheral arterial tone (PAT). ey found
that, despite a greater percentage of regular physical activity
among the shi workers (. versus .%), shi work was
associated with a reduced PAT index compared to working
only on the day shi (PAT index . ±. versus . ±.)
[]. While physical activity has been associated with better
endothelial function [], this study suggested that the eects
of sleep deprivation override the benets of physical activity
on vascular health. Wehrens et al. studied the long term
eects of shi work. eir study compared the dierence in
FMD aer two groups (shi workers compared to nonshi
workers) were put through sleep deprivation and recovery
sleep in identical laboratory settings. Aer correcting for the
dierence in body mass index (BMI), there was a trend for
lower %FMD (𝑃 = 0.08) observed among shi workers
compared to nonshi workers []. Amir et al. conducted
a study that had results consistent with this trend. irty
healthy physicians who had worked night shis for an average
of  ± years had their endothelial function examined aer
a regular workday as the baseline and aer a continuous
a signicant decrease in FMD aer shi work compared with
baseline measurements (. ±.% versus . ±.%). e
authors more importantly also noted that FMD decreased
signicantly in all subsets except in physicians with a shorter
(< years) history of night shis. In these physicians with
the shorter history, the change in FMD aer the shi was
independently related to the length of shi work history [].
ese results were consistent with those found in the previous
be long term implications of shi work on vascular function.
4. Mechanisms of Endothelial Dysfunction
Caused by Sleep Deprivation (Figure 1)
4.1. Sympathetic Activation. Sympathetic overactivity has
been a proposed explanation to the link that is seen between
sleep deprivation and endothelial dysfunction. Dettoni et
dependent venodilation found in healthy males aer PSD to
an increase in sympathetic activity as the participants also
experienced an increase in percent low-frequency ( ±
versus  ±) and a decrease in percent high-frequency ( ±
 versus  ±) components of heart rate variability, increase
in low-frequency band of blood pressure variability, and an
increase in their serum norepinephrine (119 ± 46 versus
162 ± 58 ng/mL) [].
Other studies, however, have rejected the association of
sleep deprivation and sympathetic activation. Of the nine
studies that link sleep deciency and endothelial function
mentioned in our review, three studies had a signicant
change in blood pressure, four studies did not investigate
blood pressure, and two studies saw no dierence in blood
pressure. Studies that did not show a change in blood
pressure, or did show a change but the change came aer
evidence of endothelial dysfunction, argue that endothelial
dysfunction may not be due to increased sympathetic activity
of being awake for a prolonged period of time but rather due
to another factor. In a study on rats by Sauvet et al., they
concluded that while sleep deprivation did decrease endothe-
lial vasodilation, it was not due to changes in blood pres-
sure and was independent of sympathetic activity because
it was still evident aer pharmacological sympathectomy.
Rather, it appears to be associated with NO synthase and
cyclooxygenase pathway alterations, specically, a decrease
in the activity of those pathways []. e authors, however,
mentioned that a persistent increase in sympathetic activity
could lead to endothelial dysfunction. is was supported by
studies that have shown that subjects with a greater history
of night shi work are more likely to have more endothelial
dysfunction than subjects who rarely took the night shi
and therefore argue the direct causal eect of sympathetic
activation [,].
4.2.eRoleofNitricOxide.Endothelial dysfunction is
lead to disruption of vascular homeostasis. NO is responsible
for the modulation of vascular dilator tone, regulation of local
cell growth, and protection of blood vessels from injurious
consequences of platelets and cells circulating in blood. NO
therefore plays a crucial role in normal endothelial function
[]. In the study conducted by Suessenbacher et al. on
female nurses, in addition to the fact that aer working
sequential night shis endothelial function was impaired,
the results also showed that mono-nitrogen oxides (NO𝑥)
were also signicantly decreased aer  sequential night shis
compared with the baseline measurements (from . ±
. mmol/dL to . ±. mmol/dL, 𝑃 = 0.033), although,
in the end, there was no correlation between changes in NO𝑥
and FMD before and aer  sequential night shis (𝑟=
−0.218,𝑃 = 0.356)[]. In rats, TSD was found to lead to
It is possible that the reduction in the bioavailability
of NO in these sleep deprivation cases may be due to the
decreased expression of NO synthase (eNOS) by endothelial
[,]. Altered signaling is also a possibility. However, when
International Journal of Hypertension
Sleep deciency/deprivation
Insomnia Shi work
Total sleep deprivation Partial sleep deprivation
Endothelial dysfunction
Increased level of coagulability
Increased Cytokine/growth
Cardiovascular complications
vasoconstrictor and
decreased levels of
vasodilator mediators
F 
considering sleep deciency, oxidative damage seems to be
the mechanism. Oxidative stress occurs when there is an
imbalance between oxidizing free radicals and antioxidant
defenses. Free radicals or reactive oxygen species (ROS) such
as O2are quick to react with and inactivate NO. us, vas-
cular oxidative stress can lead to a decrease in NO bioavail-
ability. Under normal physiological conditions, endogenous
antioxidant defenses minimize this interaction, thus allowing
tion has been linked to increased uncompensated oxidative
stress in peripheral tissues; however, a positive nding shows
that recovery sleep can actually restore antioxidant activities
[]. A more recent study found that sleep deprivation does
aect antioxidant activity by producing and imbalance in the
oxidizing of the spleen cells. While the mechanisms of the
cytoxic-like eects of sleep deprivation are likely “related to
dysfunction in mitochondrial metabolism and vulnerability
in cell signaling pathways,” the exact mechanisms are not
understood and require further study [].
5. Conclusion
While there is evidence of an association between endothelial
dysfunction and sleep deprivation, it still remains to be
evaluated if sleep deprivation is a cause of or is associated with
increased risk of CVD. However, endothelial dysfunction
is an established independent risk factor for cardiovascular
disease. erefore, many of the factors that link endothelial
dysfunction to cardiovascular disease are likely a result of the
negative eects of sleep deciency and deprivation. Further
research in the area of sleep deprivation/deciency is needed
especially its relation to cardiovascular disease.
Conflict of Interests
e authors declare that there is no conict of interests
regarding the publication of this paper.
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, pp. –, .
Sleep Deficiency and Deprivation Leading to Cardiovascular Disease.pdf
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  • Article
    There is extensive data supporting a high prevalence of both overweight and obesity status in people with multiple sclerosis, and increases in body mass index has been associated with an increased risk of multiple sclerosis. Body composition may influence the course, treatment and management of multiple sclerosis. One proposed strategy for managing overweight and obesity status and associated secondary effects in people with multiple sclerosis involves increasing the levels of physical activity. In fact, increased levels of physical activity affect various physiological (endurance capacity, strength, balance) and biological processes (fat oxidation, insulin sensitivity, anti-inflammation, neurotrophic factors) which are known to be dysfunctional in multiple sclerosis and which may worsen with increases in obesity. When designing personalized exercise programs it should be kept in mind that current exercise recommendations for people with multiple sclerosis should exceed energy expenditure recommendations to efficiently counteract weight gain. Therefore, it is necessary to consider body composition as a primary endpoint in experimental studies. In addition, designing guidelines for weight control or weight loss in people MS is needed. The most comprehensive weight management guidelines are outlined in the American College of Sports Medicine Position Statement, which recommends between 150–250 minutes per week of moderate-intensity physical activity for preventing weight gain, and between 225–420 minutes per week of moderate-intensity physical activity for weight loss. These recommendations seem applicable for people with multiple sclerosis.
  • Article
    Previous studies have reported the effects of obstructive sleep apnea (OSA) and cardiometabolic disorders on cardiovascular disease (CVD), but associations between cardiometabolic biomarkers and two cardinal features of OSA (chronic intermittent hypoxia and sleep fragmentation) and their interactions on CVD in OSA populations remain unclear. A total of 1727 subjects were included in this observational study. Data on overnight polysomnography parameters, biochemical biomarkers, and anthropometric measurements were collected. Metabolic syndrome (MS), including blood pressure, waist circumference (WC), fasting glucose, triglycerides (TG), and high‐density lipoprotein cholesterol (HDL‐C), was diagnosed based on modified criteria of the Adult Treatment Panel III. WC, mean arterial pressure, TG and low‐density lipoprotein cholesterol (LDL‐C) were independently associated with apnea‐hypopnea index (AHI) after adjustment for confounding factors (β = 0.578, P = 0.000; β = 0.157, P = 0.001; β = 1.003, P = 0.019; and β = 4.067, P = 0.0005, respectively). Furthermore, the interaction analysis revealed joint effects between hypertension, obesity, hyperglycemia, and LDL‐C dyslipidemia and AHI on CVD. The relative excess risks of CVD due to the interactions with OSA were 2.06, 1.02, 0.48, and 1.42, respectively (all P < 0.05). In contrast, we found no independent effect of the microarousal index (MAI) on CVD. However, LDL‐C level and some MS components (WC, TG) were associated with MAI. Our findings indicate that hypoxemia and cardiometabolic disorders in OSA may potentiate their unfavorable effects on CVD. Sleep fragmentation may indirectly predispose patients with OSA to an increased risk of CVD. Thus, cardiometabolic disorders and OSA synergistically influence cardiometabolic risk patterns.
  • Article
    Full-text available
    Fatigue and workplace sleepiness are consequences of modern industrial society. Fatigue is a complex biological phenomenon that occurs as a function of time awake, time-of-day, workload, health, and off-duty lifestyle. Fatigue is a function of two major biological factors – the homeostatic drive for sleep and circadian rhythm of sleepiness. The greatest cause of fatigue is insufficient or disrupted sleep. Excessive sleepiness in the workplace and on highways is a serious safety hazard, and insufficient or disrupted sleep results in numerous accidents and adverse mental and physical health outcomes. Evidence-based strategies that promote better sleep and optimize work/rest schedules can mitigate the impact of fatigue and sleep loss. Proper nap and sleep scheduling, work breaks, modeling and monitoring tools, fatigue detection technologies, and pharmacological countermeasures can be implemented at home and/or in the workplace to reduce performance and safety hazards. Education about obtaining adequate sleep, the dangers of fatigue in terms of both health and cognitive consequences, and the availability of scientifically-proven sleep-enhancement and alertness-management strategies is essential.
  • Article
    Sleep deficiency is a major public health concern. Since epidemiological studies play an important role in public health evaluations, this theoretical paper pursues answers to the question: ‘How can we compute sleep deficiency as informative measures of exposures or doses in observational research?’ Starting from the social jetlag concept and based on the chronodisruption rationale, we illustrate and discuss five approaches (one established and four untested, each with unique strengths and limitations) to quantify sleep deficiency by focusing on the timing and duration of sleep. Hitherto, social jetlag and chronodisruption rationale were neither explicitly proposed nor developed as assessments of sleep deficiency but, as we suggest, could potentially be utilized to this end. This first foray into computing sleep deficiency in epidemiological studies makes clear that laboratory, field and epidemiological collaboration is pre-requisite to elucidating potential (co-)causal roles of sleep deficiency in disease endpoints.
  • Article
    The purpose of this study was to investigate the effects of chronic rapid eye movement sleep deprivation on cardiovascular system using blood levels of lipocalin-2, nitric oxide synthase-3, interleukin-6, and cardiotrophin-1. We included sixteen Wistar Albino rats of 300–350 g weight in the study. To create a chronic rapid eye movement sleep deprivation, we used water tanks with platform including modified multiple sleep deprivation platforms, and we used water tanks with grid to grab for control group. We left 8 rats in water tanks with platform (study group) and 8 rats in water tanks with grid to grab (control group) for 21 days. Finally, we drew blood from the hearts of the rats, just before scarifying all the rats. We performed statistical comparisons of lipocalin-2, nitric oxide synthase-3, interleukin-6 and cardiotrophin-1 levels between the study group and the control group. The lipocalin-2, nitric oxide synthase-3, interleukin-6 and cardiotrophin-1 levels were 29.8 ng/mL, 116.99 ng/mL, 4.32 ng/L and 33.26 ng/L in the study group, respectively; and 122.74 ng/mL, 85.74 ng/mL, 3.23 ng/L and 23.02 ng/L in the control group, respectively. In the study group, mean lipocalin-2 levels were significantly lower (p = 0.003) but mean cardiotrophin-1 levels were significantly higher compared with the control group (p = 0.001). Mean interleukin-6 and nitric oxide synthase-3 levels did not significantly differ between the groups (p = 0.135 and p = 0.157). Our study showed that chronic rapid eye movement sleep deprivation might be associated with cardiovascular diseases owing to higher blood cardiotropin-1 levels in the study group, a novel biomarker that has been shown to indicate endothelial dysfunction, atherosclerosis and fibrosis in the cardiovascular system.
  • Chapter
    This chapter discusses about tablet computers, which are being increasingly used by the general public and in households, and the effect of their use on the onset of sleep. Recently, it has been suggested that devices containing light-emitting diode (LED)-backlit liquid crystal displays (LCDs), like tablet computers, should not be used in the evening because continuous exposure to strong light causes melatonin suppression and thus contributes to circadian rhythm disturbances (increase in the degree of awareness). Previous related studies have reported inconsistent findings on the relationship between melatonin suppression and increase in the degree of awareness. We assumed the existence of a physiological factor capable of interrupting the onset of sleep regardless of suppressing melatonin. In particular, we focused on cerebral activity. Our hypothesis was that using devices with LED-backlit LCDs changes cerebral activity required for the onset of sleep. This chapter describes our comparative study on cerebral activity using near-infrared spectroscopy (NIRS) for functional brain imaging in order to demonstrate the above hypothesis; participants read from either a printed book or a tablet computer. From this study, we concluded that reading a book on a tablet computer before sleep onset leads to the potential inhibition of comfortable sleep through mechanisms other than the suppression of melatonin secretion.
  • Article
    Study objectives: Many studies suggest an association of both short and long sleep duration with all-cause mortality, but the effect of co-occurrence of sleep duration and other lifestyle risk factors or health status remains unclear. Methods: A total of 17,184 participants aged 18 years or older from rural areas of China were examined at baseline from 2007 to 2008 and followed up from 2013 to 2014. Cox proportional hazard models were used to estimate the hazard ratio (HR) and 95% confidence interval (CI). Results: During 6-year follow-up, we identified 1,101 deaths. The multivariable-adjusted mortality risk was significantly higher with short-duration sleepers (< 6.5 hours) (HR = 1.37, 95% CI 1.01-1.86) and long-duration sleepers (≥ 9.5 hours) (HR = 1.35, 95% CI 1.05-1.74) versus 6.5-7.5 hours. The multiplicative interaction of long sleep duration with some lifestyle risk factors and health statuses increased the mortality risk in men (low level of physical activity: HR = 1.03, 95% CI 1.02-1.04; hypertension: HR = 1.06, 95% CI 1.04-1.09; type 2 diabetes mellitus [T2DM]: HR = 1.07, 95% CI 1.04-1.11). Similar results were found in women (low level of physical activity: HR = 1.03, 95% CI 1.02-1.05; T2DM: HR = 1.07, 95% CI 1.05-1.10). Conclusions: Sleep duration could be a predictor of all-cause mortality and its interaction with physical activity, hypertension, and T2DM may increase the risk of mortality.
  • Article
    Objectives: By measuring cerebral blood flow in the prefrontal cortex, we aimed to determine how reading a book on a tablet computer affects sleep. Methods: Seven students (7 men age range, 21-32 years) participated in this study. In a controlled illuminance environment, the subjects read a novel in printed form or on a tablet computer from any distance. As the subjects were reading, the cerebral blood flow in their prefrontal cortex was measured by near-infrared spectroscopy. The study protocol was as follows. 1) Subjects mentally counted a sequence of numbers for 30 s as a pretest to standardized thinking and then 2) read the novel for 10 min, using the printed book or tablet computer. In step 2), the use of the book or tablet computer was in a random sequence. Subjects rested between the two tasks. Results: Significantly increased brain activity (increase in regional cerebral blood flow) was observed following reading a novel on a tablet computer compared with that after reading a printed book. Furthermore, the region around Broca's area was more active when reading on a tablet computer than when reading a printed book. Conclusions: Considering the results of this study and previous studies on physiological characteristics during nonrapid eye movement sleep, we concluded that reading a book on a tablet computer before the onset of sleep leads to the potential inhibition of sound sleep through mechanisms other than the suppression of melatonin secretion.
  • Article
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    Background: Health coaching is potentially a practical method to assist patients in achieving and maintaining healthy lifestyles. In health coaching, the coach partners with the patient, helping patients discover their own strengths, challenges, and solutions. Methods: Two medical assistants were provided with brief training. The 12-week program consisted of telephone coaching with in-person visits at the beginning and end of the program. Coaching targeted improvements in diet, physical activity, and/or sleep habits using a self-care planning form. Results: A total of 82 subjects enrolled in the program, 72% completed 8 weeks and 49% completed 12 weeks. Subjects who completed assessments at 12 weeks had significant weight loss despite the fact that weight loss was not a study goal. There also were improvements in diet and physical activity. Subject who completed the study were highly satisfied with the program and felt that health coaching should be available in all family medicine clinics. The main barrier providers voiced was remembering to refer patients. The medical providers indicated high satisfaction with the study and valued having coaching available for their patients. Conclusions: Medical assistants can be trained to assist patients with lifestyle changes that are associated with improved health and weight control.
Literature Review
  • Article
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    Sleep loss is suspected to induce endothelial dysfunction, a key factor in cardiovascular risk. We examined whether sympathetic activity is involved in the endothelial dysfunction caused by total sleep deprivation (TSD). TWO GROUPS: TSD (24-h wakefulness), using slowly rotating wheels, and wheel control (WC). Seven-month-old male Wistar rats. Pharmacological sympathectomy (reserpine, 5 mg/kg, intraperitoneal), nitric oxide synthase (NOS) inhibition (N (G)-nitro-L-arginine, 20 mg/kg, intraperitoneally 30 min before experiment) and cyclooxygenase (COX) inhibition (indomethacin, 5 mg/kg, intraperitoneally 30 min before experiment). In protocol 1, changes in heart rate (HR) and blood pressure were continuously recorded in the sympathectomized and non-sympathectomized rats. Blood pressure and HR increased during TSD in non-sympathectomized rats. In protocol 2, changes in skin blood flow (vasodilation) were assessed in the sympathectomized and non-sympathectomized rats using laser-Doppler flowmetry coupled with iontophoretic delivery of acetylcholine (ACh), sodium nitroprusside (SNP), and anodal and cathodal currents. ACh- and cathodal current-induced vasodilations were significantly attenuated after TSD in non-sympathectomized and sympathectomized rats (51% and 60%, respectively). In protocol 3, ACh-induced vasodilation was attenuated after NOS and COX inhibition (66% and 49%, respectively). Cathodal current-induced vasodilation decreased by 40% after COX inhibition. In TSD compared to WC a decrease in ACh-induced vasodilation was still observed after COX inhibition. No changes in SNP- and anodal current-induced vasodilation were detected. These results demonstrate that total sleep deprivation induces a reduction in endothelial-dependent vasodilation. This endothelial dysfunction is independent of blood pressure and sympathetic activity but associated with nitric oxide synthase and cyclooxygenase pathway alterations. Sauvet F; Florence G; Van Beers P; Drogou C; Lagrume C; Chaumes C; Ciret S; Leftheriotis G; Chennaoui M. Total sleep deprivation alters endothelial function in rats: a nonsympathetic mechanism. SLEEP 2014;37(3):465-473.
  • Article
    Insomnia co-occurs with many health problems, but less is known about the prospective associations. The aim of the current study was to investigate if insomnia predicts cumulative incidence of mental and physical conditions. Prospective population-based data from the two last Nord-Trøndelag Health Studies (HUNT2 in 1995–97 and HUNT3 in 2006–08), comprising 24 715 people in the working population, were used to study insomnia as a risk factor for incidence of physical and mental conditions. Insomnia was defined according to the 4th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). Insomnia at HUNT2 was a significant risk factor for incidence of a range of both mental and physical conditions at HUNT3 11 years later. Most effects were only slightly attenuated when adjusting for confounding factors, and insomnia remained a significant risk factor for the following conditions in the adjusted analyses: depression [odds ratio (OR): 2.38, 95% confidence interval (CI): 1.91–2.98], anxiety (OR: 2.08, 95% CI: 1.63–2.64), fibromyalgia (OR: 2.05, 95% CI: 1.51–2.79), rheumatoid arthritis (OR: 1.87, 95% CI: 1.29–2.52), whiplash (OR: 1.71, 95% CI: 1.21–2.41), arthrosis (OR: 1.68, 95% CI: 1.43–1.98), osteoporosis (OR: 1.52, 95% CI: 1.14–2.01, headache (OR: 1.50, 95% CI: 1.16–1.95, asthma (OR: 1.47, 95% CI: 1.16–1.86 and myocardial infarction (OR: 1.46, 95% CI: 1.06–2.00). Insomnia was also associated significantly with incidence of angina, hypertension, obesity and stroke in the crude analyses, but not after adjusting for confounders. We conclude that insomnia predicts cumulative incidence of several physical and mental conditions. These results may have important clinical implications, and whether or not treatment of insomnia would have a preventive value for both physical and mental conditions should be studied further.
  • Article
    The objective was to determine if the stress caused by 24 hours on call in a cardiology emergency room alters endothelial function assessed by high-resolution ultrasonography in the brachial artery. Fifteen young physicians were studied in a crossover design: a) after a normal night of sleep at home, and b) after 24 hours on call without sleeping in an emergency room. Both studies were made at rest, 5 minutes after forearm occlusion and 3 minutes after administration of sublingual nitroglycerin. High-resolution ultrasonography and a 7.5-MHz linear array transducer were used to measure the brachial artery lumen. After 24 hours on call, physicians had significantly higher resting systolic and diastolic blood pressure. They also had a non-significant increase in heart rate and a lower brachial artery diameter. Brachial artery dilatation caused by hyperemia was only 3.35%, while it increased to 11.34% after normal sleep (p < 0.001). Only 2 physicians showed more than 4.4% dilatation, which was considered a normal response, while 13 had more than 4.4% after a normal night of sleep at home (p < 0.01). The response to nitroglycerin was similar under control conditions and after 24 hours of duty oncall. In conclusion, stress caused by 24 hours on call in a cardiology emergency room depresses or abolishes endothelial function.
  • Article
    Cellular defense against the formation of reactive oxygen species involves a number of mechanisms in which antioxidant enzymes such as catalase (CAT) and superoxide dismutase (SOD) play an important role. The relation between sleep deprivation and oxidative stress has not yet been completely elucidated. Although some authors did not find evidence of this relationship, others found alterations in some oxidative stress markers in response to sleep deprivation. Thus, the objective of this study was to identify changes induced by sleep deprivation in the activity and gene expression of antioxidant enzymes in mice splenocytes, ideally corroborating a better understanding of the observed effects related to sleep deprivation, which could be triggered by oxidative imbalance. Splenocytes from mice sleep deprived for 72 h showed no significant difference in CAT and CuZnSOD gene expression compared to normal sleep mice. However, sleep-deprived mice did show higher MnSOD gene expression than the control group. Concerning enzymatic activity, CuZnSOD and MnSOD significantly increased after sleep deprivation, despite the expression in CuZnSOD remained unchanged. Moreover, CAT activity was significantly lower after sleep deprivation. The data suggest that the antioxidant system is triggered by sleep deprivation, which in turn could influence the splenocytes homeostasis, thus interfering in physiological responses.
  • Article
    Full-text available
    Insomnia is associated with increased risk of coronary heart disease (CHD), but the underlying mechanisms are not understood. To our knowledge, no previous studies have examined insomnia in relation to endothelial function, an indicator of preclinical atherosclerosis. Our aim was to assess the association of insomnia with endothelial function in a large population based study of healthy individuals. A total of 4 739 participants free from known cardiovascular or pulmonary diseases, cancer, and sarcoidosis, and who were not using antihypertensive medication were included in the study. They reported how often they had experienced difficulties falling asleep at night, repeated awakenings during the night, early awakenings without being able to go back to sleep, and daytime sleepiness. Endothelial function was measured by flow mediated dilation (FMD) derived from the brachial artery. We found no consistent association between the insomnia symptoms and endothelial function in multiadjusted models, but individual insomnia symptoms may be related to endothelial function. Among women who reported early awakenings, endothelial function may be lower than in women without this symptom (p = 0.03). This study provided no evidence that endothelial function, an early indicator of atherosclerosis, is an important linking factor between insomnia and CHD. Further studies are needed to explore the complex interrelation between sleep and cardiovascular pathology.
  • Article
    Full-text available
    Hypertension and insomnia are very common and often coexist. There is evidence to suggest that the increasing prevalence of arterial hypertension in the past decade might be related both to an increased prevalence of insomnia and to the decline of sleep duration due to modern lifestyle. The aim of this paper is to reconsider both the clinical evidence of the relationship between conditions of sleep loss and of perceived impairment in sleep quality with hypertension and the potential pathophysiological mechanisms underlying the biological plausibility of their relationship. Through a systematic search from MEDLINE, EMBASE, PsychINFO we selected articles, which reported experimental sleep deprivation designs, or studied sleep duration or insomnia and their relationship with blood pressure or hypertension in participants over 18 years. This analysis shows that experimental sleep deprivation, short sleep duration, and persistent insomnia are associated with increased blood pressure and increased risk of hypertension, even after controlling for others risk factors. Pathophysiological mechanisms underlying this association might be related to inappropriate arousal ("hyperarousal") due to an overactivation of stress system functions. According this hypothesis, prolonged sleep loss or alterations of sleep quality might act as a neurobiological and physiologic stressor that impair brain functions and contribute to allostatic load, compromising stress resilience and somatic health.
  • Article
    Arterial endothelial dysfunction is one of the key early events in atherogenesis, preceding structural atherosclerotic changes. It is also important in the late stages of obstructive atherosclerosis, predisposing to constriction and/or thrombosis. Endothelial function can be measured in coronary arteries and in the periphery by measuring vasomotor function after intra-arterial infusion of pharmacologic substances which enhance the release of endothelial nitric oxide. The disadvantage of these methods is their invasive nature, which generally makes them unsuitable for studies involving asymptomatic subjects. For this reason, noninvasive tests of endothelial function have been developed. In the most widely used of these, an ultrasound-based method, arterial diameter is measured in response to an increase in shear stress, which causes endothelium-dependent dilatation. Endothelial function assessed by this method correlates with invasive testing of coronary endothelial function, as well as with the severity and extent of coronary atherosclerosis. This noninvasive endothelial function testing has provided valuable insights into early atherogenesis, as well as into the potential reversibility of endothelial dysfunction by various strategies, including pharmacological agents (lipid lowering, ACE inhibition), l-arginine, antioxidants and hormones.
  • Article
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    Sleep deprivation is common in Western societies and is associated with increased cardiovascular morbidity and mortality in epidemiological studies. However, the effects of partial sleep deprivation on the cardiovascular system are poorly understood. In the present study, we evaluated 13 healthy male volunteers (age: 31 ± 2 yr) monitoring sleep diary and wrist actigraphy during their daily routine for 12 nights. The subjects were randomized and crossover to 5 nights of control sleep (>7 h) or 5 nights of partial sleep deprivation (<5 h), interposed by 2 nights of unrestricted sleep. At the end of control and partial sleep deprivation periods, heart rate variability (HRV), blood pressure variability (BPV), serum norepinephrine, and venous endothelial function (dorsal hand vein technique) were measured at rest in a supine position. The subjects slept 8.0 ± 0.5 and 4.5 ± 0.3 h during control and partial sleep deprivation periods, respectively (P < 0.01). Compared with control, sleep deprivation caused significant increase in sympathetic activity as evidenced by increase in percent low-frequency (50 ± 15 vs. 59 ± 8) and a decrease in percent high-frequency (50 ± 10 vs. 41 ± 8) components of HRV, increase in low-frequency band of BPV, and increase in serum norepinephrine (119 ± 46 vs. 162 ± 58 ng/ml), as well as a reduction in maximum endothelial dependent venodilatation (100 ± 22 vs. 41 ± 20%; P < 0.05 for all comparisons). In conclusion, 5 nights of partial sleep deprivation is sufficient to cause significant increase in sympathetic activity and venous endothelial dysfunction. These results may help to explain the association between short sleep and increased cardiovascular risk in epidemiological studies.
  • Article
    The vascular endothelium is a monolayer of cells between the vessel lumen and the vascular smooth muscle cells. Nitric oxide (NO) is a soluble gas continuously synthesized from the amino acid L-arginine in endothelial cells by the constitutive calcium-calmodulin-dependent enzyme nitric oxide synthase (NOS). This substance has a wide range of biological properties that maintain vascular homeostasis, including modulation of vascular dilator tone, regulation of local cell growth, and protection of the vessel from injurious consequences of platelets and cells circulating in blood, playing in this way a crucial role in the normal endothelial function. A growing list of conditions, including those commonly associated as risk factors for atherosclerosis such as hypertension, hypercholesterolemia, smoking, diabetes mellitus and heart failure are associated with diminished release of nitric oxide into the arterial wall either because of impaired synthesis or excessive oxidative degradation. The decreased production of NO in these pathological states causes serious problems in endothelial equilibrium and that is the reason why numerous therapies have been investigated to assess the possibility of reversing endothelial dysfunction by enhancing the release of nitric oxide from the endothelium. In the present review we will discuss the important role of nitric oxide in physiological endothelium and we will pinpoint the significance of this molecule in pathological states altering the endothelial function.