Healthy sleep patterns were associated with about a one third reduced risk for heart disease and stroke, even among those with high genetic risk, a new study shows. 

During a median follow-up of 8.5 years and with 7280 documented heart disease and stroke events, individuals who scored 5 out of 5 for healthy sleep behaviors — early chronotype, sleeping 7–8 hours per day, never or rarely experiencing insomnia, not snoring, and not experiencing frequent excessive daytime sleepiness — had a 35% lower risk for incident cardiovascular disease (CVD), a 34% lower risk for coronary heart disease (CHD), and a 34% lower risk for stroke, as compared to those who reported none or only one of these healthy sleep behaviors. 

"Since we know that sleep behaviors are complex and interact with each other, we wanted to consider them all together," said Lu Qi, MD, PhD, in an interview with theheart.org | Medscape Cardiology. "For example, if you look at sleep duration, you have to also consider insomnia; otherwise, the relationship is kind of spurious." 

Indeed, when all five sleep behaviors were considered in combination, the association with cardiovascular risk was stronger as compared to any individual sleep behavior, Qi reported. 

Qi, director of the Tulane University Obesity Research Center in New Orleans, and colleagues' findings were published December 18 in the European Heart Journal. 

Given the known relationship between genetic and behavioral factors in the development of CVD, Qi and colleagues went a step further and investigated whether healthy sleep patterns might modify the effect of genetic predisposition to disease. 

The researchers used data from the UK Biobank for 385,292 participants who were initially free of CVD. The UK Biobank is a large, prospective study of individuals aged 37 to 73 years who have provided blood samples for genotyping and have self-reported through online questionnaires information regarding sleep and other health-related behaviors. For the current study, participants with established CVD were excluded. 

The researchers analyzed single-nucleotide polymorphisms known to be associated with CHD and stroke. Participant were stratified as being at high, intermediate, or low genetic risk for each outcome. 

"We know that things like dietary factors and physical activity can modify genetic risk, so we assumed we'd see something similar with sleep behavior, but in fact we didn't find any statistical interaction between the healthy sleep score and genetic CV risk," Qi said. 

"What we did find, however, was a so-called additive effect with sleep behavior and genetic risk, such that those with the higher genetic risk and the fewest healthy sleep behaviors had the highest risk of heart disease and stroke, even though there was no interaction between healthy sleep score and genetic susceptibility to coronary heart disease." 

To clarify, Qi explained that an additive effect might be thought of as "one plus one equals two," whereas an interaction implies that one plus one is greater than two. 

Indeed, a clear, stepwise pattern of increased risk for CHD was seen as genetic risk increased and healthy sleep pattern decreased. At the extreme, participants at high genetic risk who had a poor sleep pattern were at more than 2.5-fold increased risk for CHD compared to those with low genetic risk and a healthy sleep pattern (hazard ratio, 2.54; 95% confidence interval, 1.80 – 3.57). 

On the flip side, those at low genetic risk appeared to lose some of their inherent protection if they had poor sleep behaviors. 

This study was observational in nature, and the association between sleep pattern and cardiovascular events cannot be considered causal. Nevertheless, the researchers assessed the population attributable risk and suggested that if the associations are indeed causal, "more than 10% of CVD, CHD, and stroke events would not have occurred if all participants had been in the low-risk group for all five sleep factors." 

Encouraging healthy sleep pattern and treating sleep disorders "may play an important role in the primary prevention of CVD...regardless of the individuals' genetic risk profile," conclude Qi and coauthors.