In the past, mothers encouraged their daughters to get their “beauty sleep,” but the effects of a good night’s rest are more than skin deep. Suboptimal quantity and quality of sleep have health consequences that far eclipse shadowy bags under the eyes. A new study in the Journal of the American College of Cardiology revealed an association between short sleep duration, poor sleep quality, and increased risk for subclinical atherosclerosis. We’ve known for a while that diet plays a driving role in heart health, and it appears that getting some quality shut-eye is something else we can do to protect the cardiovascular system. We can’t change our genetics or our family histories, but fortunately, we do have control over what we eat and when we go to sleep.
Previous research has shown associations between inadequate sleep and greater risk for insulin resistance and type 2 diabetes, and obesity and insulin resistance in teenagers. Inadequate duration of sleep (short sleep) and poor quality sleep have also been associated with increased risk for ulcerative colitis and Crohn’s disease and even Alzheimer’s disease (a.k.a. “type 3 diabetes”). Considering insulin resistance may be a major driver of cardiovascular disease, it’s not a surprise that increased atherosclerosis could indirectly result from inadequate or fragmented sleep.
The study, conducted in Spain, measured noncoronary atherosclerosis and coronary calcification in nearly 4000 middle-aged participants who were asymptomatic for atherosclerosis (mean age 45.8 ± 4.3 years; 62.6% men). Noncoronary atherosclerosis and coronary calcification were assessed via carotid and femoral 3-dimensional vascular ultrasound and cardiac computed tomography. Sleep duration and quality was measured objectively by each participant wearing an actigraph for seven days.
Researchers found that participants who slept less than six hours a night were 27 percent more likely to have atherosclerosis throughout the body compared to those who slept seven to eight hours (the reference sleep duration). Regarding sleep quality, those with poor quality sleep were 34 percent more likely to have atherosclerosis than those with good quality sleep.
These findings corroborated earlier findings from a study that looked at coronary, carotid, and femoral subclinical atherosclerosis in nearly 2000 healthy middle-aged men (age 40-60). The study found that participants reporting 7 hours of sleep a night had the lowest prevalence of subclinical coronary atherosclerosis (assessed by coronary artery calcification [CAC]). Those with very short (<5-6 hours) or very long (>9 hours) sleep duration were shown to have increased risk for atherosclerosis.
In a systematic review that looked at associations between subjective and objective measures of sleep duration and quality with non-invasive markers of subclinical CVD, objective measurements of short sleep and poor sleep quality were positively correlated with increased carotid intima media thickness (CIMT). Subjective assessments of short sleep duration were associated with increased CIMT and CAC, while poor subjective sleep quality was significantly associated with endothelial dysfunction and increased arterial stiffness, but variably with CAC and CIMT.
A study that assessed the effects of inadequate sleep on blood pressure and endothelial inflammation in women participating in the American Heart Association’s Go Red for Women Strategically Focused Research Network found that even when sleep duration was adequate, poor sleep quality and prolonged time to fall asleep was associated with higher blood pressure and increased vascular inflammation.
These findings don’t mean that more sleep is automatically better. Participants in the Spanish study who slept more than 8 hours had increased noncoronary plaque burden, with this effect being particularly pronounced in women. Other research has shown that individuals who sleep more than 9 hours a night have higher fasting glucose and HOMA-IR and lower insulin sensitivity compared to those who sleep 6-9 hours a night. It’s unlikely that long sleep would cause these issues, though; it’s more likely that compromised health—even in people unaware of just how compromised they are—causes people to sleep longer.
Short sleep and fragmented sleep have multiple serious adverse consequences for gluco-regulation, insulin sensitivity, nervous system function, and overall metabolic health. These include reduced beta cell function, insulin resistance, increased sympathetic nervous system activation, altered cortisol rhythms, increased systemic inflammation, lower leptin and higher ghrelin (driving increased appetite without concomitant increase in energy expenditure), and even a decrease in brain glucose utilization, which is a key feature of Alzheimer’s disease and its precursor, mild cognitive impairment.
The relationship between short and/or fragmented sleep and compromised metabolic health may be the unifying factor between suboptimal sleep and increased atherosclerotic plaque. Metabolic syndrome—driven by chronic hyperinsulinemia—is associated with increased oxidized LDL, which, in turn, is associated with greater risk for heart attack, even after adjusting for other risk factors. The authors of a paper exploring the vascular effects of diabetes couldn’t have stated it more clearly: “Hyperglycemia and insulin resistance are key players in the development of atherosclerosis and its complications.” By way of contributing to both hyperglycemia and elevated insulin, short and/or fragmented sleep sets off a cascade of adverse effects that may ultimately end in increased plaque deposition.
Changing one’s sleep habits may not be easy and it can take time to establish new routines, but as is true for dietary changes, the benefits are worth it.