Tag: risk

  • The Stroke Risk of Vegetarians 

    The Stroke Risk of Vegetarians 

    The first study in history on the incidence of stroke in vegetarians and vegans suggests they may be at higher risk.

    “When ranked in order of importance, among the interventions available to prevent stroke, the three most important are probably diet, smoking cessation, and blood pressure control.” Most of us these days are doing pretty good about not smoking, but less than half of us exercise enough. And, according to the American Heart Association, only 1 in 1,000 Americans is eating a healthy diet and less than 1 in 10 is even eating a moderately healthy diet, as you can see in the graph below and at 0:41 in my video Do Vegetarians Really Have Higher Stroke Risk?. Why does it matter? It matters because “diet is an important part of stroke prevention. Reducing sodium intake, avoiding egg yolks, limiting the intake of animal flesh (particularly red meat), and increasing the intake of whole grains, fruits, vegetables, and lentils….Like the sugar industry, the meat and egg industries spend hundreds of millions of dollars on propaganda, unfortunately with great success.” 

    The paper goes on to say, “Box 1 provides links to information about the issue.” I was excited to click on the hyperlink for “Box 1” and was so honored to see four links to my videos on egg industry propaganda, as you can see below and at 1:08 in my video

    The strongest evidence for stroke protection lies in increasing fruit and vegetable intake, with more uncertainty regarding “the role of whole grains, animal products, and dietary patterns,” such as vegetarian diets. One would expect meat-free diets would do great. Meta-analyses have found that vegetarian diets lower cholesterol and blood pressure, as well as enhance weight loss and blood sugar control, and vegan diets may work even better. All the key biomarkers are going in the right direction. Given this, you may be surprised to learn that there hadn’t been any studies on the incidence of stroke in vegetarians and vegans until now. And if you think that is surprising, wait until you hear the results. 

    “Risks of Ischaemic Heart Disease and Stroke in Meat Eaters, Fish Eaters, and Vegetarians Over 18 Years of Follow-Up: Results from the Prospective EPIC-Oxford Study”: There was less heart disease among vegetarians (by which the researchers meant vegetarians and vegans combined). No surprise. Been there, done that. But there was more stroke, as you can see below, and at 2:14 in my video

    An understandable knee-jerk reaction might be: Wait a second, who did this study? Was there a conflict of interest? This is EPIC-Oxford, world-class researchers whose conflicts of interest may be more likely to read: “I am a member of the Vegan Society.”

    What about overadjustment? When the numbers over ten years were crunched, the researchers found 15 strokes for every 1,000 meat eaters, compared to only 9 strokes for every 1,000 vegetarians and vegans, as you can see below and at 2:41 in my video. In that case, how can they say there were more strokes in the vegetarians? This was after adjusting for a variety of factors. The vegetarians were less likely to smoke, for example, so you’d want to cancel that out by adjusting for smoking to effectively compare the stroke risk of nonsmoking vegetarians to nonsmoking meat eaters. If you want to know how a vegetarian diet itself affects stroke rates, you want to cancel out these non-diet-related factors. Sometimes, though, you can overadjust

    The sugar industry does this all the time. This is how it works: Imagine you just got a grant from the soda industry to study the effect of soda on the childhood obesity epidemic. What could you possibly do after putting all the studies together to conclude that there was a “near zero” effect of sugary beverage consumption on body weight? Well, since you know that drinking liquid candy can lead to excess calories that can lead to obesity, if you control for calories, if you control for a factor that’s in the causal chain, effectively only comparing soda drinkers who take in the same number of calories as non-soda-drinkers, then you could undermine the soda-to-obesity effect, and that’s exactly what they did. That introduces “over adjustment bias.” Instead of just controlling for some unrelated factor, you control for an intermediate variable on the cause-and-effect pathway between exposure and outcome.

    Overadjustment is how meat and dairy industry-funded researchers have been accused of “obscuring true associations” between saturated fat and cardiovascular disease. We know that saturated fat increases cholesterol, which increases heart disease risk. Therefore, if you control for cholesterol, effectively only comparing saturated fat eaters with the same cholesterol levels as non-saturated-fat eaters, that could undermine the saturated fat-to-heart disease effect.

    Let’s get back to the EPIC-Oxford study. Since vegetarian eating lowers blood pressure and a lowered blood pressure leads to less stroke, controlling for blood pressure would be an overadjustment, effectively only comparing vegetarians to meat eaters with the same low blood pressure. That’s not fair, since lower blood pressure is one of the benefits of vegetarian eating, not some unrelated factor like smoking. So, that would undermine the afforded protection. Did the researchers do that? No. They only adjusted for unrelated factors, like education, socioeconomic class, smoking, exercise, and alcohol. That’s what you want. You want to tease out the effects of a vegetarian diet on stroke risk. You want to try to equalize everything else to tease out the effects of just the dietary choice. And, since the meat eaters in the study were an average of ten years older than the vegetarians, you can see how vegetarians could come out worse after adjusting for that. Since stroke risk can increase exponentially with age, you can see how 9 strokes among 1,000 vegetarians in their 40s could be worse than 15 strokes among 1,000 meat-eaters in their 50s. 

    The fact that vegetarians had greater stroke risk despite their lower blood pressure suggests there’s something about meat-free diets that so increases stroke risk it’s enough to cancel out the blood pressure benefits. But, even if that’s true, you would still want to eat that way. As you can see in the graph below and at 6:16 in my video, stroke is our fifth leading cause of death, whereas heart disease is number one. 

    So, yes, in the study, there were more cases of stroke in vegetarians, but there were fewer cases of heart disease, as you can see below and at 6:29. If there is something increasing stroke risk in vegetarians, it would be nice to know what it is in hopes of figuring out how to get the best of both worlds. This is the question we will turn to next. 

    I called it 21 years ago. There’s an old video of me on YouTube where I air my concerns about stroke risk in vegetarians and vegans. (You can tell it’s from 2003 by my cutting-edge use of advanced whiteboard technology and the fact that I still had hair.) The good news is that I think there’s an easy fix.

    This is the third in a 12-video series on stroke risk. Links to the others are in the related posts below.



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  • Study Says Reducing Red Meat Could Lower Risk

    Study Says Reducing Red Meat Could Lower Risk

    Iron is beneficial for health, but the source of iron can affect your diabetes risk, according to a study. Researchers found that heme iron, which is present in red meat and other animal products, could increase the risk of type 2 diabetes. In contrast, non-heme iron in plant-based food does not pose a similar risk.

    The latest study conducted by researchers at Harvard T.H. Chan School of Public Health adds more evidence to previous studies that have identified diabetes risks associated with red meat.

    The research evaluated 206,615 adults enrolled in the Nurses’ Health Studies I and II and the Health Professionals Follow-up Study for their dietary details over 36 years. The iron intake of the participants including the total, heme, non-heme, dietary, and supplemental was noted along with their type 2 diabetes status. The results were published in Nature Metabolism.

    “The study found a significant association between higher heme iron intake and T2D risk. Participants in the highest intake group had a 26% higher risk of developing T2D than those in the lowest intake group,” the news release stated.

    The results also showed that heme iron accounted for more than half of the type 2 diabetes risk associated with unprocessed red meat and also contributed moderately to the risk from various dietary patterns related to type 2 diabetes. However, there was no significant association between intakes of non-heme iron from diet or supplements with diabetes risk.

    “Compared to prior studies that relied solely on epidemiological data, we integrated multiple layers of information, including epidemiological data, conventional metabolic biomarkers, and cutting-edge metabolomics. This allowed us to achieve a more comprehensive understanding of the association between iron intake and T2D risk, as well as potential metabolic pathways underlying this association,” said lead author Fenglei Wang, research associate in the Department of Nutrition.

    The researchers also raised concern about the addition of heme to plant-based meat alternatives to enhance their meaty flavor and appearance. As these alternatives gain popularity, they suggest that further investigation into the health effects is needed.

    “This study underscores the importance of healthy dietary choices in diabetes prevention. Reducing heme iron intake, particularly from red meat, and adopting a more plant-based diet can be effective strategies in lowering diabetes risk,” said corresponding author Frank Hu, Fredrick J., Stare Professor of Nutrition and Epidemiology.

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  • Sugar Substitute Erythritol Raises Risk Of Heart Attacks, Stroke: Study

    Sugar Substitute Erythritol Raises Risk Of Heart Attacks, Stroke: Study

    Sugar is a known health risk for several metabolic diseases, including diabetes, obesity, and cardiovascular diseases. But are sugar substitutes risk-free?

    Adding more evidence to the increased risk associated with sugar substitutes, researchers of a recent study have identified that erythritol, a common low-calorie sweetener, could raise the risk of heart attacks and strokes.

    A team of Cleveland Clinic researchers came across startling findings while they were investigating the physiological effects of common sugar substitutes. Based on the study results published in the journal Arteriosclerosis, Thrombosis, and Vascular Biology, the researchers now caution that erythritol might not be as safe as food regulatory agencies currently classify it, calling for a reevaluation of its use.

    Erythritol is a naturally occurring sugar alcohol found in fruits and vegetables and is a byproduct of glucose metabolism in human tissue. Since it is a low-carbohydrate sweetener, it is used in many “keto” products. Both the U.S. Food and Drug Administration (FDA) and the European Food Safety Authority classify erythritol as GRAS, (generally recognized as safe). This classification allows its unrestricted use in food products.

    The new study points to the cardiovascular risk associated with erythritol, suggesting that even a standard serving size of the sweetener could raise blood clot risk.

    “Many professional societies and clinicians routinely recommend that people at high cardiovascular risk – those with obesity, diabetes or metabolic syndrome – consume foods that contain sugar substitutes rather than sugar. These findings underscore the importance of further long-term clinical studies to assess the cardiovascular safety of erythritol and other sugar substitutes,” senior and corresponding author Dr. Stanley Hazen said in a news release.

    In a study conducted last year, it was found that cardiac patients with high erythritol levels were twice as likely to experience a major cardiac event within the next three years compared to those with lower levels. Additionally, the study revealed that adding erythritol to patients’ blood or platelets increased clot formation.

    To further investigate the effects of erythritol on blood platelets, researchers used a human intervention study that tested its use on 20 healthy individuals. The participants ingested erythritol in the form of a standard “sugarless” soda or muffin and compared the results with glucose consumption.

    The researchers then noted that after consumption of erythritol products, the level of erythritol in the blood increased by over 1,000 times compared to before. Additionally, the study showed that blood clotting increased after consuming erythritol, but this effect was not seen after consuming glucose.

    “This research raises some concerns that a standard serving of an erythritol-sweetened food or beverage may acutely stimulate a direct clot-forming effect. Erythritol and other sugar alcohols that are commonly used as sugar substitutes should be evaluated for potential long-term health effects, especially when such effects are not seen with glucose itself,” said study co-author Dr. W. H. Wilson Tang.

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  • Friend’s Genetic Traits Can Influence Your Mental Health Risk: Study

    Friend’s Genetic Traits Can Influence Your Mental Health Risk: Study

    Friendships during teen years can make or break mental health. It’s not just about the support they provide during tough times that the researchers are talking about, but how their genetic traits can affect you. The traits of your friends, particularly their genetic predisposition to mental health issues, can influence your mental health risks, a recent study revealed.

    Socio-genomics is a topic of growing interest that investigates the influence of a person’s genotype on the observable traits of another. The study published in the American Journal of Psychiatry investigated the peer’s social genetic effects and found that a person’s genetic predisposition to addiction, anxiety, and depression can have long-term consequences for their adolescent peers, affecting their risk of developing similar mental health issues later in life.

    “Peers’ genetic predispositions for psychiatric and substance use disorders are associated with an individual’s own risk of developing the same disorders in young adulthood,” said Jessica E. Salvatore, lead author of the study in a news release.

    “What our data exemplifies is the long reach of social genetic effects,” Salvatore said.

    The study was based on a database of more than 1.5 million people born in Sweden between 1980 and 1998. The researchers first mapped individuals by location and school during their teenage years. They then examined medical, pharmacy, and legal records to track substance use and mental health disorders into adulthood. Using models they tested if peers’ genetic risks predicted an individual’s risk of experiencing substance abuse, major depression, or anxiety. Peer genetic risks were assessed using family genetic risk scores for the same conditions.

    “Even when controlling for factors such as the target individuals’ own genetic predispositions and family socioeconomic factors, the researchers found a clear association between peers’ genetic predispositions and target individuals’ likelihood of developing a substance use or psychiatric disorder. The effects were stronger among school-based peers than geographically defined peers,” the news release stated.

    The researchers noted that these links were most noticeable among upper secondary school classmates, particularly those in the same vocational or college-preparatory track between ages 16 and 19. The peer’s genetic impact was greater for issues such as drug and alcohol use disorders compared to major depression and anxiety disorders.

    “The most obvious explanation for why peers’ genetic predispositions might be associated with our own well-being is the idea our peers’ genetic predispositions influence their phenotype, or the likelihood that peers are also affected by the disorder. But in our analysis, we found that peers’ genetic predispositions were associated with target individuals’ likelihood of disorder even after we statistically controlled for whether peers were affected or unaffected,” Salvatore said, adding that more research is needed to understand the mechanism.

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  • How to Treat High Lp(a), an Atherosclerosis Risk Factor 

    How to Treat High Lp(a), an Atherosclerosis Risk Factor 

    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. 



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  • Pesticide Use In Farms Poses Cancer Risk Similar To Smoking: Study

    Pesticide Use In Farms Poses Cancer Risk Similar To Smoking: Study

    Pesticides are vital for achieving high crop yields and ensuring food security, but what is the cost to human health? A study adds to the growing concern, revealing that the cancer risk associated with pesticide use in agriculture is similar to that of smoking.

    The cancer risk from smoking is well-known, but researchers are now drawing a stark comparison with the dangers posed by agricultural use of pesticides. Their findings reveal significant links between pesticide exposure and several forms of cancer, including leukemia, non-Hodgkin’s lymphoma, as well as bladder, lung, and pancreatic cancers.

    “In our study, we found that for some cancers, the effect of agricultural pesticide usage is comparable in magnitude to the effect of smoking,” Dr. Isain Zapata, the study’s senior author from the College of Osteopathic Medicine, Colorado, said in a news release.

    “It is difficult to explain the magnitude of an issue without presenting any context, so we incorporated smoking data. We were surprised to see estimates in similar ranges,” Zapata said.

    To explore potential connections between pesticide exposure and cancer rates, the researchers analyzed data on 69 different pesticides from the United States Geological Survey. In a population-based, nationwide study, they examined county-wide agricultural pesticide use alongside cancer incidence and found that the impact of pesticides on cancer rates might rival that of smoking. The results of the study were published in the journal Frontiers.

    Since pesticides are rarely used in isolation, pinpointing a single culprit is difficult. Although some pesticides may be more frequently discussed in connection with cancer, it is the combination of several pesticides that often makes the impact, the researchers explained.

    “In the real world, it is not likely that people are exposed to a single pesticide, but more to a cocktail of pesticides within their region,” Zapata said.

    “Geographic trends showed that counties with higher agricultural productivity, such as the leading corn-producing states of the Midwest, also have increased cancer risk due to pesticide exposure. Our results highlight the relevance of comprehensive assessments for the development of policy considerations and the implementation of preventive measures to mitigate the risks for vulnerable communities. Our study pioneers and lays a holistic vision foundation for future pesticide-related cancer risk assessments,” the researchers wrote.

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