Daylight Saving Time (DST) is often a contentious subject. While we're luckily "falling back" an hour (and hopefully soaking up the extra hour of sleep!), the adverse effects of the bi-annual time change are often commonly shared. In particular, the "spring forward" shift may actually increases the chance of experiencing a myocardium infarction, or heart attack.
In 2018, responding to Finland's EU representation's call for the abolition of DST, researchers at the University of Ferrara in Ferrara, Italy conducted a review on the relationships between DST, circadian rhythms, and cardiovascular health. In this, they found that the available evidence suggests an association between DST and a decent increase in the occurrence of acute myocardial infarction, particularly in the first week after the time change.
We're all fairly familiar with our individual circadian rhythms (especially after the sleep challenge). However, the physiology of this concept is a little more complex than it just being a 24-hour cycle. Circadian rhythms are driven by the central and peripheral clocks. Circadian clocks consist of proteins that generate positive and negative transcriptional feedback loops with a free-running period of ~24 hours. The central circadian clock, or master clock, is located within superchiasmatic nucleus (SCN) of the hypothalamus. Peripheral circadian clocks also exist and are often found within most mammalian cells and tissues. Central and peripheral circadian clocks can influence numerous functions, including sleep/rest, either directly or indirectly. The cardiovascular system has biological clocks as well, often found in the cardiomyocytes of the heart, in blood vessels, and in the vascular endothelial cells. The circadian clock within cardiomyocytes directly regulates myocardial metabolic gene expression, most likely in anticipation of the sleep/wake and feeding/fasting cycle. As such, results obtained on murine models show that the circadian clock within the cardiomyocytes allows for the rapid adaptation of the heart to the prolongation of fasting. Thus, a desynchronization of an organism with its environment, through circadian clock derangements, may also contribute to the development of CV diseases.
Commonly, regular disruption of the circadian rhythm cycle can lead to chronic heart disease. Activities such as shift work, a circadian misalignment resulting from a 12-h inversion of the behavioral cycle (including sleep/wake and fasting/feeding cycles), is a typical example of rhythm disruption. Often, shift workers are exposed to a misalignment of their behavioral and environmental cycles, which is a risk factor for hypertension, inflammation, and CV disease. It's been observed that when compared with circadian alignment, circadian misalignment can (a) increase both systolic and diastolic blood pressure (BP); (b) decrease heart rate (HR) during wake periods and increase HR during sleep time; (c) reduce the sleep opportunity-associated dip in BP and HR; (d) affect the 24-h urinary epinephrine and norepinephrine excretion rates; (e) decrease markers of cardiac vagal modulation; (f) increase inflammatory markers, particularly 24-h interleukin-6 (IL-6), 24-h C-reactive protein (CRP), resistin, and tumor necrosis factor (TNF); and (g) decrease plasminogen activator inhibitor-1 (PAI-1) levels. Taken together, all these effects can explain the increased prevalence of CV disease in night workers versus day workers.
By extension, circadian differences in the physiological status of the CV system give rise to rhythmic—and predictable-in-time—variations either in the susceptibility of human beings to morbid and mortal events, or in the ability to precipitate the overt expression of disease. It is known that the occurrence of CV events exhibits varies across the 24 hours of the day. These patterns coincide with the timing variation in the (a) pathophysiological mechanisms that trigger CV events and (b) physiological changes in the body rhythms. A series of factors, though not harmful if considered alone, are capable of triggering unfavorable events when they all occur within the same general temporal window.
Over the last two to three decades, an evident circadian (morning) rhythm for acute myocardial infarction (AMI) has been understood. It's been estimated that the incidence rate of AMI onset is 40% higher in the morning than throughout the rest of the day, and nearly 28% of morning AMIs (accounting for approximately 9% of all AMIs) are attributable to the morning excess. Moreover, rupture or dissection of aortic aneurysms shows a circadian variation, with an evident morning preference as well. The similarity of these timing patterns of such different acute CV and cerebrovascular events suggests that they share common underlying mechanisms. Several pathophysiologic phenomena, such as increased BP, HR, sympathetic activity, basal vascular tone, vasoconstrictive hormones, increased viscosity, fibrinogen, platelet aggregability, and reduced fibrinolytic activity, exhibit prominent circadian rhythms with phases positively correlated with the timing of excess in CV events. Moreover, the effect of stress on human cardiac, vascular, and hemostatic status appears to be circadian rhythmic, with the effects being greater in the morning. An exaggerated CV response to behavioral challenges has been suggested as a potential factor that enhances the risk of hypertension and CV disease. As such, individuals who exhibit large increases in BP during acute psychological stress are at risk of atherosclerosis, probably secondary to endothelial damage by a BP surge, via increased flow turbulence, and a subsequent release of inflammatory and pro-atherogenic cytokines.
The fact of sleep depravation may also be a factor, as the central master clock is primarily entrained by light, and reduced exposure to light during the day and over exposure to light at night due to artificial lighting may impair the circadian organization of sleep. Changes in sleep architecture during sleep disruption may lead to increased energy intake, reduced energy expenditure, and insulin resistance. Short (< 6 h) sleep has been associated with negative health outcomes including hypertension, diabetes mellitus, obesity, and even mortality. Short sleep, compared with normal sleep, is associated with a significant increase in the relative risk of mortality due to all causes. Moreover, short sleepers have increased rates of obesity (38%), diabetes mellitus (37%), coronary heart disease (26%), and hypertension (17%).
TL;DR - While we're easily soaking up the extra hour of sleep now, come springtime, make sure you're healthily managing your stress levels and taking care of yourself! While the risk increase is slight, it still exists! Keep prioritizing your sleep and maintaining good sleep hygiene, too!
- Via
Source: Manfredini, R., Fabbian, F., Cappadona, R., & Modesti, P. A. (2018). Daylight saving time, circadian rhythms, and cardiovascular health. Internal and emergency medicine, 13(5), 641–646. https://doi.org/10.1007/s11739-018-1900-4
Hi Via! This was such an interesting read. I think it is very interesting how the time of day matters to when acute myocardial infarctions occur. It makes sense that our inner clock would be influenced by the light in our environments, and why people are so likely to fall into a depression during the winter with the loss of daylight. 24% increase in occurrence of a cardiovascular event is not a small percentage at all!! I wonder why it is so much more likely to get a heart attack in the morning? Thank you for sharing all of this insightful information!
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