Proper Sleep Patterns Can Offset Inherited Or Genetically Linked Risk Of Heart Disease And Stroke
Source: Thailand Medical News Dec 18, 2019 4 years, 11 months, 5 days, 21 hours, 14 minutes ago
Researchers from Tulane University, New Orleans have for the first time assessed the impact on the risk of
heart or blood vessel problems from the combination of
sleep patterns and genetic susceptibility to cardiovascular disease. The study, which is published in the
European Heart Journal, found that even if people had a high
genetic risk of
heart disease or
stroke, this appeared to be offset to some extent by good sleep patterns.
The medical researchers, led by Professor Dr Lu Qi, Director of Tulane University Obesity Research Center at Tulane University, New Orleans, USA, looked at genetic variations known as SNPs (single nucleotide polymorphisms) that were already known to be
genetically linked to the development of
heart disease and
stroke. They analysed the SNPs from blood samples taken from 385 292 healthy participants in the UK Biobank project and used them to create a genetic risk score to determine whether the participants were at high, intermediate or low risk of cardiovascular problems.
Dr Qi and his colleagues also created a new, "
healthy sleep score" by asking the participants whether they were a "morning" or an "evening" person, how long they slept for, and whether or not they suffered from insomnia, snoring or frequent, excessive daytime sleepiness. The
healthy sleep score ranged from 0 to 5, with 5 being the healthiest
sleep pattern, representing a 'morning" person, who slept between 7-8 hours a night, without insomnia, snoring or daytime sleepiness.
However, it should be noted that excessive
sleep ie more than 8 hours could lead to a higher risk of getting a
stroke as shown by other studies.
The medical researchers followed the participants for an average of 8.5 years, during which time there were 7280 cases of
heart disease or
stroke.
Dr Qi told
Thailand Medical News, "We wanted to test whether the relation between sleep scores and cardiovascular outcomes was different according to the genetic risk. This is the first time this has been done. We also wanted to estimate the proportion of cardiovascular problems that would not have occurred if all participants had a
healthy sleep pattern, if we assume there is a causal relationship."
The team found that compared to those with a
sleep score of 0-1 (unhealthy sleep pattern), participants with a score of 5 had a 35% reduced risk of cardiovascular disease, and a 34% reduced risk of both
heart disease and
stroke.
Dr Qi said: "If the link between sleep and cardiovascular disease proves to be causal, then more than a tenth of all heart disease and strokes would not have occurred if all the participants had a
healthy sleep score of 5.
Among people with a
healthy sleep score of 5, there were nearly seven fewer cases of cardiovascular disease per 1000 people per year compared to those with a
sleep score of less than 5."
Looking at the combined effect of sleep score and genetic susceptibility on cardiovascular disease, the researchers found that participants with both a high
genetic risk and a poor
sleep pattern had a more than 2.5-fold greater risk o
f heart disease and a 1.5-fold greater risk of stroke compared to those with a low genetic risk and a healthy sleep pattern. This meant that there were 11 more cases of
heart disease and five more cases of
stroke per 1000 people a year among poor sleepers with a
high
genetic risk compared to good sleepers with a low
genetic risk. However, a healthy sleep pattern compensated slightly for a high genetic risk, with just over a two-fold increased risk for these people.
Dr Qi added, "We found that a high
genetic risk could be partly offset by a
healthy sleep pattern. In addition, we found that people with a low
genetic risk could lose this inherent protection if they had a poor
sleep pattern."
An individual with a high
genetic risk but a
healthy sleep pattern had a 2.1-fold greater risk of
heart disease and a 1.3-fold greater risk of
stroke compared to someone with a low
genetic risk and a good
sleep pattern. While someone with a low
genetic risk, but an unhealthy
sleep pattern had 1.7-fold greater risk of
heart disease and a 1.6-fold greater risk of
stroke.
The medical researchers cannot exclude the possibility that a poor
sleep pattern might be indicative of some underlying and undetected health problem that might play a role in the increased risk of cardiovascular disease. However, they tried to minimise this risk by excluding all patients with cardiovascular disease at the start of the study and they also took account of factors that could affect the results and were related to a person's health, such as age, sex, ethnicity, deprivation, physical activity, smoking, alcohol consumption, body mass index, other health problems and family history of
heart disease and
stroke.
Dr Qi concluded: "As with other findings from observational studies, our results indicate an association not a causal relation. However, these findings may motivate other investigations and, at least, suggest that it is essential to consider overall
sleep behaviours when considering a person's risk of
heart disease or
stroke."
Some limitations of the study include: the researchers relied on the participants reporting their sleep patterns, and this occurred only once at the beginning of the study; the healthy sleep score did not include all sleep problems such as restless legs syndrome; and the majority of UK Biobank participants are of European descent, which may affect the generalisation of the results to other populations.
The researchers are not clear what mechanisms may be responsible for the link between sleep and risk of cardiovascular disease. The researchers say disrupted sleep could upset the hormonal or metabolic regulation of the body, increase the body's 'fight or flight' responses, increase inflammation and disrupt the body's natural circadian rhythm.
Reference: "Sleep patterns, genetic susceptibility, and incident cardiovascular disease: a prospective study of 385 292 UK Biobank participants", European Heart Journal (2019). DOI: 10.1093/eurheartj/ehz849
