Sleep deficit and cardiometabolic risk

Sleeping less than 7 hours a night is associated with increased morbidity and mortality, especially due to cardiovascular diseases.

Three specialized institutions (US National Sleep Foundation, American Academy of Sleep Medicine, and Sleep Research Society) report that the appropriate duration of sleep for adults is from 7 – 9 hours per night. However, this indication does not correspond to real life, since approximately 35% of the general population sleeps ≤6 hours per night and 29.5% sleeps 7 hours per night.

Insufficient sleep is a prevalent health problem in developed countries. In addition, the term “acute” is usually used with reference to short-term sleep for 1-2 days, while “chronic” refers to longer periods.
Short-term sleep has a considerable influence on health. This short duration of sleep can be a consequence of lifestyle habits, environmental factors or a sleep disorder, such as insomnia or a respiratory sleep disorder.
Some evidence suggests that short-term sleep and decreased sleep quality are associated with a higher incidence of cardiovascular diseases and metabolic disorders.

Several biological mechanisms have been proposed as a possible link between the short duration of sleep and these diseases, such as the participation of the neurovegetative nervous system (SNNV), endothelial function, metabolic regulation, inflammation and the coagulation system.

Inflammation is one of the most important intermediate mechanisms involved in the onset of cardiovascular diseases. Currently it is known that it is a complex process involving the overexpression of several adhesion molecules, chemokines, cytokines and growth factors, which are central to the appearance of atherosclerosis. Increased mRNA values and IL-6 and tumor necrosis factor production were found in monocytes after a single night of partial sleep deprivation (sleep limited to 4 h).

Oxidative stress is another presumed mechanism underlying the increased risk of cardiovascular disease associated with short-term sleep. Several vasoactive factors, including endothelin.

  • nitric oxide and prostacyclin, are involved in the maintenance of vascular homeostasis. The increase in endothelin.
  • values was reported in adults with short duration sleep In addition, decreased vascular reactivity dependent on the endothelium and independent of it after acute total sleep deprivation was observed, associated with increased values of the intercellular adhesion molecule.
  • which is a marker of endothelial activation and IL-6, that inhibits the endothelium-dependent relaxation in which nitric oxide intervenes.

The increase in the values of prothrombotic markers could reflect an inflammatory state that causes endothelial dysfunction and atherosclerosis, making the causal relationship between CE and prothrombotic markers less clear.

SNNV has been highly investigated as a possible mechanism for increased risk of cardiovascular disease after sleep deprivation. Almost all data indicate an increase in sympathetic activity after partial or total acute sleep deprivation or fragmentation thereof.

Regarding the Metabolic and Endocrine Functions, several epidemiological studies suggested an association between short-term sleep and the increased risk of suffering from type 2 diabetes mellitus (T2DM) and obesity. Sleep and circadian rhythms are fundamental to regulate metabolic and endocrine functions.

The hormones leptin and ghrelin, which are involved in the control of satiety and hunger, were studied in relation to the duration of sleep.

Short-term sleep seems to be associated with decreased leptin values and increased ghrelin values, generating increased hunger, which can lead to increased consumption of junk food and an increasing incidence of obesity of those who sleep little in relation to those who sleep as necessary. In addition, sleep deprivation can reduce sensitivity to endogenous stimuli that increase energy expenditure and therefore cause weight gain.

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