Numerous studies strongly suggest that sleep is a central pillar of health and wellbeing. Sleep duration is associated with a host of health outcomes, with short sleep – that is, shorter than about seven hours – being predictive of obesity, Type 2 diabetes, cardiovascular disease, and general all-cause mortality (Buxton & Marcelli, 2010; Cappuccio, et al., 2010; Cappuccio, et al, 2010b; Buxton, Broussard, Zahl, & Hall, 2014; Garndner, Hale, Moore, & Patel, 2010).
“The leading causes of disease and death in developed nations - diseases that are crippling health-care systems, such as heart disease, obesity, dementia, diabetes, and cancer - all have recognised causal links to a lack of sleep.” - Matthew Walker
Beyond just sleep duration, sleep disorders such as insomnia or obstructive sleep apnoea are strongly associated with a risk of developing cardiovascular disease, myocardial infarction, hypertension, as well as increased risk of stroke coronary heart disease and heart failure (St-Onge, Garndner, et al., 2016; Laugsand, Vatten, Platou, & Janszky, 2011; Siversten, et al., 2014; Somers, et al., 2008; Jean-Louis, et al., 2008).
This becomes all the more important in light of the fact that cardiovascular disease and related complications are still the most prevalent cause of mortality globally (Ritchie, 2018).
So how does sleep affect our health to such a degree? As it turns out, there are diverse ways in which sleep impacts health, and in particular cardiometabolic health.
"Sleep restriction leads to hormonal and cognitive effects that cause us to eat more, and more of the bad stuff with high caloric density and sugar content, while also making our bodies less effective at dealing with such food through decreased insulin sensitivity."
Lifestyle Factors and Metabolic Function
Sleep deprivation can affect cardiometabolic health through affecting lifestyle choices as well as increasing various risk factors.
Sleep has been found to impact lifestyle choices and decision making, as well as adiposity, insulin sensitivity, glucose control, blood pressure and inflammation (St-onge, et al., 2016). Sleep restriction has been associated with the risk of developing metabolic syndrome, which is itself a major predictor of cardiovascular issues and mortality (Hall, et al., 2008).
Experimental studies have demonstrated that sleep restriction leads to hormonal and cognitive effects that cause us to eat more, and more of the bad stuff with high caloric density and sugar content, while also making our bodies less effective at dealing with such food through decreased insulin sensitivity. More specifically, studies have found that sleep deprivation, even for a single night, leads to increases in the release of hormones – such as ghrelin – that make us feel hungry, while decreasing the release of other hormones – such as leptin – that promote satiation (Taheri, et al., 2004; Schmid, et al., 2008). This has been found to lead to increased feelings of hunger in waking hours, and consequently, increased weight gain and adiposity.
This is important because shorter sleep duration when combined with excess weight and a sedentary lifestyle has been found to contribute to increased likelihood of cardiovascular issues and mortality (Garndner, et al., 2010; St-Onge, et al., 2016). In addition, disrupted or restricted sleep leads to decreased effectiveness in management of glucose - or blood sugar - increasing blood glucose and blood insulin levels, which are significant risk-markers of hyperinsulinemia and Type 2 diabetes (St-Onge, et al., 2016).
Systemic Inflammation
Sleep deprivation or disruption can also exert negative effects on cardiometabolic health directly, through increasing systemic inflammation that can lead to hardening or thickening of blood vessels.
Sleep restriction has been linked to an increase in a range of pro-inflammatory markers, and a decrease in anti-inflammatory factors (St-Onge, et al., 2016; Kanagsabai & Ardern, 2015). For example, moderate sleep restriction - 4 hours of sleep per night for 5 consecutive nights - in otherwise healthy adults leads to an increase in pro-inflammatory cytokines, which represent a significant marker of elevated risk for developing metabolic syndrome and cardiovascular complications (van Leeuwen, et al., 2009).
Furthermore, recent investigations have found that disrupted sleep quality, through sleep deprivation or fragmentation, leads to a significant increase of inflammatory-related white blood cells – neutrophils and monocytes – which increase the severity of atherosclerosis, or the thickening and hardening of arterial walls through the build-up of lipid and cortisol based plaque (Vallat, Shah, Redline, Attia, & Walker, 2020).
Given the prevalence of cardiometabolic issues and the disease burden of cardiovascular disease11, there is a good chance that any one of us, or someone close to us, experiences this first hand. And while genetic, biological and lifestyle factors are hugely important in this process, the central role of sleep cannot be understated.
As they say, the popular mindset of “I’ll sleep when I am dead” will only serve to get you there faster. So, sleep on it.
REFERENCES
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Buxton, O. M., Broussard, J. L., Zahl, A. K. and Hall, M. in (2014). Impact of Sleep and Sleep Disturbances on Obesity and Cancer (eds. Redline, S. & Berger, N. A.) 25–50, Springer New York.
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Taheri, Shahrad et al. (2004). Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index. PLoS medicine vol. 1,3 (2004): e62. doi:10.1371/journal.pmed.0010062
Vallat R., Shah VD., Redline S., Attia P. and Walker MP. (2020). Broken sleep predicts hardened blood vessels. Plos Biol, 18(6): e300726.
van Leeuwen WM, Lehto M, Karisola P, Lindholm H, Luukkonen R, Sallinen M, Härmä M, Porkka-Heiskanen T, and Alenius H. (2009). Sleep restriction increases the risk of developing cardiovascular diseases by augmenting proinflammatory responses through IL-17 and CRP. PLoS One.; 4:e4589. doi: 10.1371/journal.pone.0004589.