What does long-term sleep deprivation do to your heart?
Prolonged sleep deprivation raises your risk of high blood pressure, coronary artery disease and diabetes through multiple biological pathways. Seven to nine hours of sleep per night is not a luxury but a serious heart-protective factor.
Chronically sleeping too little raises the risk of coronary artery disease and high blood pressure. This emerges from multiple epidemiological studies that accounted for other risk factors such as poverty or pre-existing illness. A link with cardiac arrhythmias has also been found, but is less well supported.
One important intermediate mechanism is your body's stress response. Sleep deprivation increases the production of the stress hormone cortisol and revs up the sympathetic nervous system: the branch of your nervous system that puts your body into 'alert mode'. Over the long term, that sustained activation contributes to atherosclerosis, inflammation and disruptions in blood clotting. These are precisely the processes that drive heart attacks and strokes.
On top of that, sleep deprivation increases the risk of type 2 diabetes and obesity. Both short sleep duration and chronic insomnia are, independently of each other, linked to these conditions. And diabetes and excess weight in turn raise cardiovascular risk further.
An animal study shows that chronically disrupted sleep worsens glucose metabolism and reduces insulin sensitivity. Whether this works in exactly the same way in humans has not yet been well studied, but it does provide biological insight into how sleep fragmentation can indirectly harm the heart.
The overall picture is this: persistent sleep deprivation wears down the body through multiple pathways simultaneously. Researchers call this cumulative wear: stress hormones that are useful in the short term cause damage under chronic exposure that can ultimately result in cardiovascular disease. The precise magnitude of all these risks has not been quantified exactly in the available studies, but the association with heart problems is consistent across multiple studies.
Findings come predominantly from epidemiological and observational studies; causality is plausible but not always formally proven. Effect sizes have not been quantified in the available abstracts. The glucose mechanism was demonstrated in a mouse study.