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Tag: atherosclerosis

  • Ideal vs. Normal Cholesterol Levels  | NutritionFacts.org

    Having a “normal” cholesterol level in a society where it’s normal to die from a heart attack isn’t necessarily a good thing.

    “Consistent evidence” from a variety of sources “unequivocally establishes” that so-called bad LDL cholesterol causes atherosclerotic cardiovascular disease—strokes and heart attacks, our leading cause of death. This evidence base includes hundreds of studies involving millions of people. “Cholesterol is the cause of atherosclerosis,” the hardening of the arteries, and “the message is loud and clear.” “It’s the Cholesterol, Stupid!” noted the editor of the American Journal of Cardiology, William Clifford Roberts, whose CV is more than 100 pages long as he has published about 1,700 articles in peer-reviewed medical literature. Yes, there are at least ten traditional risk factors for atherosclerosis, as seen below and at 1:11 in my video How Low Should You Go for Ideal LDL Cholesterol?, but, as Dr. Roberts noted, only one is required for the progression of the disease: elevated cholesterol.

    Your doctor may have just told you that your cholesterol is normal, so you’re relieved. Thank goodness! But, having a “normal” cholesterol level in a society where it’s normal to have a fatal heart attack isn’t necessarily good. With heart disease, the number one killer of men and women, we definitely don’t want to have normal cholesterol levels; we want to have optimal levels—and not optimal by current laboratory standards, but optimal for human health.

    Normal LDL cholesterol levels are associated with the hidden buildup of atherosclerotic plaques in our arteries, even in those who have so-called “optimal risk factors by current standards”: blood pressure under 120/80, normal blood sugars, and total cholesterol under 200 mg/dL. If you went to your doctor with those kinds of numbers, you’d likely get a gold star and a lollipop. But, if your doctor used ultrasound and CT scans to actually peek inside your body, atherosclerotic plaques would be detected in about 38% of individuals with those kinds of “optimal” numbers.

    Maybe we should define an LDL cholesterol level as optimal only when it no longer causes disease. What a concept! When more than a thousand men and women in their 40s were scanned, having an LDL level under 130 mg/dL left them with atherosclerosis throughout their body, and that’s a cholesterol level at which most lab tests would consider normal.

    In fact, atherosclerotic plaques were not found with LDL levels down around 50 or 60, which just so happens to be the levels most people had “before the introduction of western lifestyles.” Indeed, before we started eating a typical American diet, “the majority of the adult population of the world had LDLs of around 50 mg per deciliter (mg/dL)”—so that’s the true normal. “Present average values…should not be regarded as ‘normal.’” We don’t want to have a normal cholesterol based on a sick society; we want a cholesterol that is normal for the human species, which may be down around 30 to 70 mg/dL or 0.8 to 1.8 mmol/L.

    “Although an LDL level of 50 to 70 mg/dl seems excessively low by modern American standards, it is precisely the normal range for individuals living the lifestyle and eating the diet for which we are genetically adapted.” Over millions of years, “through the evolution of the ancestors of man,” we’ve consumed a diet centered around whole plant foods. No wonder we have a killer epidemic of atherosclerosis, given the LDL level “we were ‘genetically designed for’ is less than half of what is presently considered ‘normal.’”

    In medicine, “there is an inappropriate tendency to accept small changes in reversible risk factors,” but “the goal is not to decrease risk but to prevent atherosclerotic plaques!” So, how low should you go? “In light of the latest evidence from trials exploring the benefits and risks of profound LDLc lowering, the answer to the question ‘How low do you go?’ is, arguably, a straightforward ‘As low as you can!’” “‘Lower’ may indeed be better,” but if you’re going to do it with drugs, then you have to balance that with the risk of the drug’s side effects.

    Why don’t we just drug everyone with statins, by putting them in the water supply, for instance? Although it would be great if everyone’s cholesterol were lower, there are the countervailing risks of the drugs. So, doctors aim to use statin drugs at the highest dose possible, achieving the largest LDL cholesterol reduction possible without increasing risk of the muscle damage the drugs may cause. But when you’re using lifestyle changes to bring down your cholesterol, all you get are the benefits.

    Can we get our LDL low enough with diet alone? Ask some of the country’s top cholesterol experts what they shoot for, “and the odds are good that many will say 70 or so.” So, yes, we should try to avoid the saturated fats and trans fats found in junk foods and meat, and the dietary cholesterol found mostly in eggs, but “it is unlikely anyone can achieve an LDL cholesterol level of 70 mg/dL with a low-fat, low-cholesterol diet alone.” Really? Many doctors have this mistaken impression. An LDL of 70 isn’t only possible on a healthy enough diet, but it may be normal. Those eating strictly plant-based diets can average an LDL that low, as you can see here and at 5:28 in my video.

    No wonder plant-based diets are the only dietary patterns ever proven to reverse coronary heart disease in a majority of patients. And their side effects? You get to feel better, too! Several randomized clinical trials have demonstrated that more plant-based dietary patterns significantly improve psychological well-being and quality of life, with improvements in depression, anxiety, emotional well-being, physical well-being, and general health.

    For more on cholesterol, see the related posts below.

    Michael Greger M.D. FACLM

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  • What About Homocysteine, Vitamin B12, and Vegetarians’ Stroke Risk?  | NutritionFacts.org

    What About Homocysteine, Vitamin B12, and Vegetarians’ Stroke Risk?  | NutritionFacts.org

    Not taking vitamin B12 supplements or regularly eating B12-fortified foods may explain the higher stroke risk found among vegetarians.

    Leonardo da Vinci had a stroke. Might his vegetarian diet have been to blame? “His stroke…may have been related to an increase in homocysteine level because of the long duration of his vegetarian diet.” A suboptimal intake of vitamin B12 is common in those eating plant-based diets (unless they take B12 supplements or regularly eat B12-fortified foods) and can lead to an increased level of homocysteine in the blood, which “is accepted as an important risk factor for stroke.”

    “Accepted” may be overstating it as there is still “a great controversy” surrounding the connection between homocysteine and stroke risk. But, as you can see in the graph below and at 0:57 in my video Vegetarians and Stroke Risk Factors: Vitamin B12 and Homocysteine?, those with higher homocysteine levels do seem to have more atherosclerosis in the carotid arteries that lead up to the brain, compared to those with single-digit homocysteine levels, and they also seem to be at higher risk for clotting ischemic strokes in observational studies and, more recently, bleeding hemorrhagic strokes, as well as increased risk of dying from cardiovascular disease and all causes put together. 

    Even more convincing are the genetic data. About 10 percent of the population has a gene that increases homocysteine levels by about 2 points, and they appear to have significantly higher odds of having a stroke. Most convincing would be randomized, double-blind, placebo-controlled trials to prove that lowering homocysteine with B vitamins can lower strokes, and, indeed, that appears to be the case for clotting strokes: Strokes with homocysteine-lowering interventions were more than five times as likely to reduce stroke compared with placebo.

    Ironically, one of the arguments against the role of homocysteine in strokes is that, “assuming that vegetarians have lower vitamin B12 concentrations than meat-eaters and that low vitamin B12 concentrations cause ischaemic stroke, then the incidence of stroke should be increased among vegetarians…but this is not the case.” However, it has never been studied until now.

    As you can see in the graph below and at 2:16 in my video, the EPIC-Oxford study researchers found that vegetarians do appear to be at higher risk.

    And no wonder, as about a quarter of the vegetarians and nearly three-quarters of the vegans studied were vitamin B12-depleted or B12-deficient, as you can see below and at 2:23, and that resulted in extraordinarily high homocysteine levels.

    Why was there so much B12 deficiency? Because only a small minority were taking a dedicated B12 supplement. And, unlike in the United States, B12 fortification of organic foods isn’t allowed in the United Kingdom. So, while U.S. soymilk and other products may be fortified with B12, UK products may not. We don’t see the same problem among U.S. vegans in the Adventist study, presumably because of the B12 fortification of commonly eaten foods in the United States. It may be no coincidence that the only study I was able to find that showed a significantly lower stroke mortality risk among vegetarians was an Adventist study.

    Start eating strictly plant-based without B12-fortified foods or supplements, and B12 deficiency can develop. However, that was only for those not eating sufficient foods fortified with B12. Those eating plant-based who weren’t careful about getting a regular reliable source of B12 had lower B12 levels and, consequently, higher homocysteine levels, as you can see below and at 3:27 in my video.

    The only way to prove vitamin B12 deficiency is a risk factor for cardiovascular disease in vegetarians is to put it to the test. When researchers measured the amount of atherosclerosis in the carotid arteries, the main arteries supplying the brain, “no significant difference” was found between vegetarians and nonvegetarians. They both looked just as bad even though vegetarians tend to have better risk factors, such as lower cholesterol and blood pressure. The researchers suggest that B12 deficiency plays a role, but how do they know? Some measures of artery function weren’t any better either. Again, they surmised that vitamin B12 deficiency was overwhelming the natural plant-based benefits. “The beneficial effects of vegetarian diets on lipids and blood glucose [cholesterol and blood sugars] need to be advocated, and efforts to correct vitamin B12 deficiency in vegetarian diets can never be overestimated.”

    Sometimes vegetarians did even worse. Worse artery wall thickness and worse artery wall function, “raising concern, for the first time, about the vascular health of vegetarians”—more than a decade before the new stroke study. Yes, their B12 was low, and, yes, their homocysteine was high, “suggest[ing] that vitamin B12 deficiency in vegetarians might have adverse effects on their vascular health.” What we need, though, is an interventional study, where participants are given B12 to see if that fixes it, and here we go. The title of this double-blind, placebo-controlled, randomized crossover study gives it away: “Vitamin B-12 Supplementation Improves Arterial Function in Vegetarians with Subnormal Vitamin B-12 Status.” So, compromised vitamin B12 status among those eating more plant-based diets due to not taking B12 supplements or regularly eating vitamin B12-fortified foods may explain the higher stroke risk found among vegetarians.

    Unfortunately, many vegetarians resist taking vitamin B12 supplements due to “misconceptions,” like “hold[ing] on to the old myth that deficiency of this vitamin is rare and occurs only in a small proportion of vegans.” “A common mistake is to think that the presence of dairy products and eggs in the diet, as in LOV [a lacto-ovo vegetarian diet], can still ensure a proper intake [of B12]…despite excluding animal flesh.”

    Now that we may have nailed the cause, maybe “future studies with vegetarians should focus on identifying ways to convince vegetarians to take vitamin B12 supplements to prevent a deficiency routinely.” 

    I have updated my recommendation for B12 supplementation. I now suggest at least 2,000 mcg (µg) of cyanocobalamin once weekly, ideally as a chewable, sublingual, or liquid supplement taken on an empty stomach, or at least 50 mcg daily of supplemental cyanocobalamin. (You needn’t worry about taking too much.) You can also have servings of B12-fortified foods three times a day (at each meal), each containing at least 190% of the Daily Value listed on the nutrition facts label. (Based on the new labeling mandate that started on January 1, 2020, the target is 4.5 mcg three times a day.) Please note, though, that those older than the age of 65 have only one option: to take 1,000 micrograms a day. 

    We started this series on what to eat and not eat for stroke prevention, and whether vegetarians really have a higher stroke risk. Check related posts for the last few videos that looked at specific factors.

    Stay tuned for: 

    Michael Greger M.D. FACLM

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  • What About Animal Protein and Vegetarians’ Stroke Risk?  | NutritionFacts.org

    What About Animal Protein and Vegetarians’ Stroke Risk?  | NutritionFacts.org

    Might animal protein-induced increases in the cancer-promoting growth hormone IGF-1 help promote brain artery integrity? 

    In 2014, a study on stroke risk and dietary protein found that greater intake was associated with lower stroke risk and, further, that the animal protein appeared particularly protective. Might that help explain why, as shown in the graph below and at 0:31 in my video Vegetarians and Stroke Risk Factors: Animal Protein?, vegetarians were recently found to have a higher stroke rate than meat eaters?

    Animal protein consumption increases the levels of a cancer-promoting growth hormone in the body known as IGF-1, insulin-like growth factor 1, which “accelerates the progression of precancerous changes to invasive lesions.” High blood concentrations are associated with increased risks of breast, colorectal, lung, and prostate cancers, potentially explaining the association between dairy milk intake and prostate cancer risk, for example. However, there are also IGF-1 receptors on blood vessels, so perhaps IGF-1 promotes cancer and brain artery integrity.

    People who have strokes appear to have lower blood levels of IGF-1, but it could just be a consequence of the stroke rather than the cause. There weren’t any prospective studies over time until 2017 when researchers found that, indeed, higher IGF-1 levels were linked to a lower risk of stroke—but is it cause and effect? In mice, the answer seems to be yes, and in a petri dish, IGF-1 appears to boost the production of elastin, a stretchy protein that helps keep our arteries elastic. As you can see in the graph below and at 1:41 in my video, higher IGF-1 levels are associated with less artery stiffness, but people with acromegaly, like Andre the Giant, those with excessive levels of growth hormones like IGF-1, do not appear to have lower stroke rates, and a more recent study of dietary protein intake and risk of stroke that looked at a dozen studies of more than half a million people (compared to only seven studies with a quarter million in the previous analysis), found no association between dietary protein intake and the risk of stroke. If anything, dietary plant protein intake may decrease the risk of stroke. 

    However, those with high blood pressure who have low IGF-1 levels do appear to be at increased risk of developing atherosclerosis, which is the thickening of the artery walls leading up to the brain, but no such association was found in people with normal blood pressure. So, there may be “a cautionary lesson for vegans” here. Yes, a whole food, plant-based diet “can down-regulate IGF-1 activity” and may slow the human aging process, not to mention reduce the risk of some of the common cancers that plague the Western world. But, “perhaps the ‘take-home’ lesson should be that people who undertake to down-regulate IGF-1 activity [by cutting down on animal protein intake] as a pro-longevity measure should take particular care to control their blood pressure and preserve their cerebrovascular health [the health of the arteries in their brain] – in particular, they should keep salt intake relatively low while insuring an ample intake of potassium” to keep their blood pressures down. So, that means avoiding processed foods and avoiding added salt, and, in terms of potassium-rich foods, eating beans, sweet potatoes, and dark-green leafy vegetables. 

    Might this explain the higher stroke risk found among vegetarians? No—because dairy and egg whites are animal proteins, too. Only vegans have lower IGF-1 levels in both men and women, so low levels of IGF-1 can’t explain why higher rates of stroke were found in vegetarians. Then what is it? I think the best explanation for the mystery is something called homocysteine, which I cover next. 

    If you aren’t familiar with IGF-1, my videos Flashback Friday: Animal Protein Compared to Cigarette Smoking and How Not to Die from Cancer are good primers. 

    Beyond eating a plant-based diet, how else can we lower our blood pressure? Check out the chapter of hypertension in my book How Not to Die at your local public library. 

    This is the eighth video in a 12-part series on vegetarians’ stroke risk. If you missed any of the previous ones, check out the related posts below.

    Coming up, we turn to what I think is actually going on:

    Michael Greger M.D. FACLM

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  • How to Treat High Lp(a), an Atherosclerosis Risk Factor  | NutritionFacts.org

    How to Treat High Lp(a), an Atherosclerosis Risk Factor  | NutritionFacts.org

    What could help explain severe coronary disease in someone with a healthy lifestyle who is considered to be at low cardiovascular disease risk? A young man ended up in the ER after a heart attack and was ultimately found to have severe coronary artery disease. Given his age, blood pressure, and cholesterol, his ten-year risk of a heart attack should have only been about 2 percent, but he had a high lipoprotein(a), also known as Lp(a). In fact, it was markedly high at 80 mg/dL, which may help explain it. You can see the same in women: a 27-year-old with a heart attack with a high Lp(a). What is Lp(a), and what can we do about it? 

    As I discuss in my video Treating High Lp(a): A Risk Factor for Atherosclerosis, Lp(a) is an “underestimated cardiovascular risk factor.” It causes coronary artery disease, heart attacks, strokes, peripheral arterial disease, calcified aortic valve disease, and heart failure. And these can occur in people who don’t even have high cholesterol—because Lp(a) is cholesterol, as you can see below and at 1:15 in my video. It’s an LDL cholesterol molecule linked to another protein, which, like LDL, transfers cholesterol into the lining of our arteries, contributing to the inflammation in atherosclerotic plaques. But “this increased risk caused by Lp(a) has not yet gained recognition by practicing physicians.” 

    “The main reason for the limited clinical use of Lp(a) is the lack of effective and specific therapies to lower Lp(a) plasma levels.” Because “Lp(a) concentrations are approximately 90% genetically determined,” the conventional thinking has been you’re just kind of born with higher or lower levels and there isn’t much you can do about it. Even if that were the case, though, you might still want to know about it. If it were high, for instance, that would be all the more reason to make sure all the other risk factors that you do have more control over are as good as possible. It may help you quit smoking, for example, and motivate you to do everything you can to lower your LDL cholesterol as much as possible.  

    Lp(a) levels in the blood can vary a thousand-fold between individuals, “from less than 0.1 mg/dL to as high as 387 mg/dL.” You can see a graph of the odds of heart disease at different levels in the graph below and at 2:20 in my video. Less than 20 mg/dL is probably optimal, with greater than 30 to 50 mg/dL considered to be elevated. Even when the more conservative threshold of greater than 50 mg/dL is used, that describes about 10 to 30 percent of the global population, an estimated 1.4 billion people. So, if we’re in the one in five people with elevated levels, what can we do about it? 

    The way we know that Lp(a) causes atherosclerosis is that we can put it to the ultimate test. There is something called apheresis, which is essentially like a dialysis machine where they can take out your blood, wash out some of the Lp(a), and give your blood back to you. And when you do that, you can reverse the progression of the disease. As you can see in the graph below and at 3:06 in my video, atherosclerosis continues to get worse in the control group, but it gets better in the apheresis group. This is great for proving the role of Lp(a), but it has limited clinical application, given the “cost, limited access to centers, and the time commitment required for biweekly sessions of 2 to 4 h each.” 

    It causes a big drop in blood levels, but they quickly creep back up, so you have to keep going in, as you can see in the graph below and at 3:26 in my video, costing more than $50,000 a year. 

    There has to be a better way. We’ll explore the role diet can play, next.  

    I’ve been wanting to do videos about Lp(a), but there just wasn’t much we could do about it until now. So, how do we lower Lp(a) with diet? Stay tuned for the exciting conclusion in my next video.

    What can we do to minimize heart disease risk? My video How Not to Die from Heart Disease is a good starting point. 

    Michael Greger M.D. FACLM

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  • Similar Processes Could Link MS With Heart Disease

    Similar Processes Could Link MS With Heart Disease

    By Cara Murez 

    HealthDay Reporter

    WEDNESDAY, March 22, 2023 (HealthDay News) — Multiple sclerosis (MS) and atherosclerosis both involve an abnormal hardening of body tissue, and recent research suggests they may be linked.

    MS is a neurodegenerative disease that attacks the brain and spinal cord. Atherosclerosis is hardening of the arteries.

    Studies show connections between the two, according to Ochsner Health System in New Orleans. In 2018, a team of Romanian researchers led by Dr. Raluca Ileana Mincu of the University of Medicine and Pharmacy Carol Davila, Bucharest, used state-of-the-art echocardiography to conduct heart and vascular assessments in patients with MS.

    The exams, which show how blood flows through the heart and valves, found that MS patients had more impairments on both sides of the heart compared to healthy people.

    A more recent study followed more than 84,000 people for 10 years, comparing heart health in participants with and without MS. People with MS were 50% more likely to die from heart disease, researchers found. They were 28% more likely to have a heart attack and 59% more likely to have a stroke. Raffaele Palladino of Imperial College London led the study.

    The findings highlight the importance of comprehensive heart exams for people with MS. Advanced techniques can help prevent life-threatening heart disease in patients who are at high risk.

    This preliminary research doesn’t show that MS causes atherosclerosis, but a strong association between the two diseases is emerging, according to Ochsner Health.

    More studies are needed to understand the underlying processes that link these two conditions.

    In atherosclerosis, fatty deposits build up in the arteries, causing a thickening of the blood vessel wall, curtailing blood flow. As a result, lower levels of oxygen and important nutrients are able to reach various parts of the body.

    A chronic condition, it can lead to coronary artery disease, angina, peripheral artery disease and kidney problems.

    Causes aren’t fully known, according to the American Heart Association, but elevated cholesterol and triglycerides in the blood, high blood pressure, cigarette smoking and diabetes are risk factors.

    In MS, the body’s immune system mistakenly attacks its own central nervous system. This interrupts nerve signals between the brain and spinal cord and other parts of the body, leading to hardened scar tissue after each attack.

    About 1 million U.S. adults live with MS. Symptoms can include impaired vision, sensory changes, cognitive changes, weakness, pain, fatigue, bowel and bladder incontinence, impaired coordination and walking difficulties, according to the National MS Society.

    The U.S. National Institutes of Health has more on atherosclerosis, and the National Multiple Sclerosis Society has more on MS.

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  • Irregular Sleep Tied to Increased Heart Disease Risk

    Irregular Sleep Tied to Increased Heart Disease Risk

    Feb. 24, 2023 — Irregular sleep, such as sleeping for an inconsistent number of hours each night or falling asleep at different times, may increase the risk of developing atherosclerosis, or the hardening of the arteries, among adults over age 45, a new study suggests.

    In particular, a variation in sleep duration of more than 2 hours per night in the same week was tied to the development of hardened arteries.

    “Poor sleep is linked with several cardiovascular conditions, including heart disease, hypertension, and type 2 diabetes,” says study author Kelsie Full, PhD, assistant professor of medicine at Vanderbilt University Medical Center.

    “Overall, we found that participants who slept varying amounts of hours throughout the week (meaning that one night they slept less, one night they slept more) were more likely to have atherosclerosis than participants who slept about the same amount of time each night,” she says. 

    The findings were published in theJournal of the American Heart Association.

    Atherosclerosis is the buildup of fatty deposits, known as plaque, on artery walls. This can lead to narrowed arteries and reduced blood flow and oxygen in the body. The plaque can also burst and create a blood clot that blocks the artery, which can lead to a heart attack or stroke.

    To examine the links to sleep, Full and colleagues examined observational data from more than 2,000 participants in the Multi-Ethnic Study of Atherosclerosis (MESA) Sleep Ancillary Study. The study included adults between ages 45 to 84 in six U.S. communities: St. Paul, MN; Baltimore City and Baltimore County, MD; Chicago; Forsyth County, NC; Los Angeles County, CA; and Northern Manhattan and the Bronx, NY. 

    Between 2010 to 2013, the people in the study wore a wrist device that detected when they were awake and asleep for 7  days in a row, and they completed a 7-day sleep diary. They also completed a one-night sleep study to measure sleep disorders that involve breathing, sleep stages, and heart rate. 

    The research team looked at sleep duration, or the total amount of time spent in bed fully asleep in a night, and sleep timing, which was defined as the time the person fell asleep each night. They measured the presence of plaque in the arteries by assessing for coronary artery calcium (or calcified plaque buildup in arteries), carotid plaque (or fatty plaque buildup in neck arteries), carotid intima-media thickness (or thickness of the inner two layers of the neck arteries), and the ankle-brachial index (or narrow peripheral arteries), all of which indicate the presence of atherosclerosis.

    Overall, the average age in the study was 69, and 54% were women. About 38% identified as white, 28% as Black or African American, 23% as Hispanic American, and 11% as Chinese American.

    Across the 7-day period, about 38% of participants had a sleep duration change of more than 90 minutes, and 18% had a sleep duration change of more than 120 minutes. Those who had irregular sleep were more likely to be non-white, current smokers, have lower average annual incomes, work shift schedules or not work, and have a higher average body mass index.

    Participants who had greater sleep duration irregularity, varying by more than 2 hours in a week, were 1.4-times more likely to have high coronary artery calcium scores than those who had more regular sleep durations that varied by 60 minutes or less. They were also more likely to have carotid plaque and an abnormal ankle-brachial index.

    Those who had irregular sleep timing (that varied by more than 90 minutes in a week) were also 1.43-times more likely to have high coronary artery calcium burden than those with more regular sleep timing (that varied by 30 minutes or less). 

    “The biggest surprise to me was that 30% of the participants in the study had total sleep times that varied by more than 90 minutes over the course of the week,” Full says. “This is consistent with prior studies that suggest that a large proportion of the general public have irregular sleep patterns, not just shift workers.”

    Additional studies are needed to understand the mechanisms, the study authors write. Night-to-night variability in sleep duration and sleep timing can cause desynchronization in the sleep-wake timing and circadian disruption.

    “Sleep is a naturally recurring phenomenon, and maintaining regularity helps provide stability and predictability to the body,” says Michael Grandner, PhD, associate professor of psychiatry and director of the Sleep and Health Research Program at the University of Arizona College of Medicine.

    “When people have very irregular sleep schedules, it may make it harder for the body to optimally make good use of the sleep it is getting since it such a moving target.”

    Grandner, who wasn’t involved with this study, has researched sleep irregularity and associations with cardiovascular disease, diabetes, obesity, and many other adverse outcomes.

    “Sleep health is more than just getting enough sleep,” he says. “It also means getting quality sleep, at the right time, regularly.”

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