Getting too little sleep causes changes in the metabolism of cholesterol, demonstrates a study conducted at the University of Helsinki. According to the results, long-term sleep loss may contribute to the development of cardiovascular disease.
Lack of sleep has previously been found to impact the activation of the immune system, inflammation, carbohydrate metabolism and the hormones that regulate appetite. Now University of Helsinki researchers have found that sleep loss also influences cholesterol metabolism.
The study examined the impact of cumulative sleep deprivation on cholesterol metabolism in terms of both gene expression and blood lipoprotein levels. With state-of-the-art methods, a small blood sample can simultaneously yield information about the activation of all genes as well as the amounts of hundreds of different metabolites. This means it is possible to seek new regulating factors and metabolic pathways which participate in a particular function of the body.
“In this case, we examined what changes sleep loss caused to the functions of the body and which of these changes could be partially responsible for the elevated risk for illness,” explains Vilma Aho, researcher from the Sleep Team Helsinki research group.
The study established that the genes which participate in the regulation of cholesterol transport are less active in persons suffering from sleep loss than with those getting sufficient sleep. This was found both in the laboratory-induced sleep loss experiment and on the population level.
While analysing the different metabolites, the researchers found that in the population-level data, persons suffering from sleep loss had fewer high-density HDL lipoproteins, commonly known as the good cholesterol transport proteins, than persons who slept sufficiently.
Together with other risk factors, these results help explain the higher risk of cardiovascular disease observed in sleep-deprived people and help understand the mechanisms through which lack of sleep increases this risk.
“It is particularly interesting that these factors contributing to the onset of atherosclerosis, that is to say, inflammatory reactions and changes to cholesterol metabolism, were found both in the experimental study and in the epidemiological data,” Aho says.
The results highlight the health impact of good sleep. The researchers emphasise that health education should focus on the significance of good, sufficient sleep in preventing common diseases, in addition to healthy food and exercise. Even a small reduction in illnesses, or even postponing the onset of an illness, would result in significant cost savings for society at large.
“The experimental study proved that just one week of insufficient sleep begins to change the body’s immune response and metabolism. Our next goal is to determine how minor the sleep deficiency can be while still causing such changes,” Aho states.
Sleep loss and insufficient sleep are risk factors for cardiometabolic diseases, but data on how insufficient sleep contributes to these diseases are scarce. These questions were addressed using two approaches: an experimental, partial sleep restriction study (14 cases and 7 control subjects) with objective verification of sleep amount, and two independent epidemiological cohorts (altogether 2739 individuals) with questions of sleep insufficiency. In both approaches, blood transcriptome and serum metabolome were analysed. Sleep loss decreased the expression of genes encoding cholesterol transporters and increased expression in pathways involved in inflammatory responses in both paradigms. Metabolomic analyses revealed lower circulating large HDL in the population cohorts among subjects reporting insufficient sleep, while circulating LDL decreased in the experimental sleep restriction study. These findings suggest that prolonged sleep deprivation modifies inflammatory and cholesterol pathways at the level of gene expression and serum lipoproteins, inducing changes toward potentially higher risk for cardiometabolic diseases.