Eating a vegetarian diet rich in nuts, vegetables, soy linked to lower stroke risk

People who eat a vegetarian diet rich in nuts, vegetables and soy may have a lower risk of stroke than people who eat a diet that includes meat and fish, according to a study published in the February 26, 2020, online issue of Neurology®, the medical journal of the American Academy of Neurology.

“Stroke is the second most common cause of death worldwide and a leading cause of disability,” said study author Chin-Lon Lin, M.D., of Tzu Chi University in Hualien, Taiwan. “Stroke can also contribute to dementia. If we could reduce the number of strokes by people making changes to their diets, that would have a major impact on overall public health.”

The study involved two groups of people from Buddhist communities in Taiwan where a vegetarian diet is encouraged, and smoking and drinking alcohol are discouraged. Approximately 30% of participants in both groups were vegetarians. Of the vegetarians, 25% were men. Researchers defined vegetarians as people who did not eat any meat or fish.

At the start of the study, the average age of all participants was 50 and none had experienced stroke. The first group of 5,050 people was followed for an average of six years. The second group of 8,302 people was followed for an average of nine years. Participants were given medical exams at the start of the study and asked about their diet.

Vegetarians ate more nuts, vegetables and soy than non-vegetarians and consumed less dairy. Both groups consumed the same amount of eggs and fruit. Vegetarians ate more fiber and plant protein. They also ate less animal protein and fat.

Researchers then looked at a national database to determine the numbers of strokes participants had during the course of the study.

In the first group of 5,050 people, there were 54 strokes. For ischemic strokes, which are strokes when blood flow to part of the brain is blocked, there were three strokes among 1,424 vegetarians, or 0.21%, compared to 28 strokes among 3,626 non-vegetarians, or 0.77%. After adjusting for age, sex, smoking and health conditions like high blood pressure and diabetes, researchers found vegetarians in this group had a 74% lower risk of ischemic stroke than non-vegetarians.

In the second group of 8,302 people, there were 121 strokes. For both ischemic and hemorrhagic strokes, also called bleeding strokes, there were 24 strokes among 2,719 vegetarians, or 0.88%, compared to 97 strokes among 5,583 non-vegetarians, or 1.73%. After adjusting for other factors, researchers found vegetarians in this group had a 48% lower risk of overall stroke than non-vegetarians, a 60% lower risk of ischemic stroke and a 65% lower risk of hemorrhagic stroke.

“Overall, our study found that a vegetarian diet was beneficial and reduced the risk of ischemic stroke even after adjusting for known risk factors like blood pressure, blood glucose levels and fats in the blood,” said Lin. “This could mean that perhaps there is some other protective mechanism that may protecting those who eat a vegetarian diet from stroke.”

One limitation of the study was that the diet of participants was only assessed at the start of the study, so it is not known if participants’ diets changed over time. Another limitation was that study participants did not drink or smoke, so results may not reflect the general population. Also, results from the study population in Taiwan may not be generalizable worldwide. Finally, there could be other factors, not accounted for, that might affect stroke risk.

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The effects of obesity mirror those of aging

Globally, an estimated 1.9 billion adults and 380 million children are overweight or obese. According to the World Health Organization, more people are dying from being overweight than underweight. Researchers at Concordia are urging health authorities to rethink their approach to obesity.

In their paper published in the journal Obesity Reviews, the researchers argue that obesity should be considered premature aging. They look at how obesity predisposes people to acquiring the kinds of potentially life-altering or life-threatening diseases normally seen in older individuals: compromised genomes, weakened immune systems, decreased cognition, increased chances of developing type 2 diabetes, Alzheimer’s disease, cardiovascular disease, cancer and other illnesses.

The study was led by Sylvia Santosa, associate professor of health, kinesiology and applied physiology in the Faculty of Arts and Science. She and her colleagues reviewed more than 200 papers that looked at obesity’s effects, from the level of the cell to tissue to the entire body. The study was co-authored by Bjorn Tam, Horizon postdoctoral fellow, and José Morais, an associate professor in the Department of Medicine at McGill University.

“We are trying to comprehensively make the argument that obesity parallels aging,” explains Santosa, a Tier II Canada Research Chair in Clinical Nutrition. “Indeed, the mechanisms by which the comorbidities of obesity and aging develop are very similar.”

From cells to systems

The paper looks at ways obesity ages the body from several different perspectives. Many previous studies have already linked obesity to premature death. But the researchers note that at the lowest levels inside the human body, obesity is a factor that directly accelerates the mechanisms of aging.

For instance, Santosa and her colleagues look at the processes of cell death and the maintenance of healthy cells — apoptosis and autophagy, respectively — that are usually associated with aging.

Studies have shown that obesity-induced apoptosis has been seen in mice hearts, livers, kidneys, neurons, inner ears and retinas. Obesity also inhibits autophagy, which can lead to cancer, cardiovascular disease, type 2 diabetes and Alzheimer’s.

At the genetic level, the researchers write that obesity influences a number of alterations associated with aging. These include the shortening of protective caps found on the ends of chromosomes, called telomeres. Telomeres in patients with obesity can be more than 25 per cent shorter than those seen in control patients, for instance.

Santosa and her colleagues further point out that obesity’s effects on cognitive decline, mobility, hypertension and stress are all similar to those of aging.

Pulling out from the cellular level, the researchers say obesity plays a significant role in the body’s fight against age-related diseases. Obesity, they write, speeds up the aging of the immune system by targeting different immune cells, and that later weight reduction will not always reverse the process.

The effects of obesity on the immune system, in turn, affect susceptibility to diseases like influenza, which often affects patients with obesity at a higher rate than normal-weight individuals. They are also at higher risk of sarcopenia, a disease usually associated with aging that features a progressive decline in muscle mass and strength.

Finally, the paper spells out how individuals with obesity are more susceptible to diseases closely associated with later-life onset, such as type 2 diabetes, Alzheimer’s and various forms of cancer.

Similarities too big to ignore

Santosa says the inspiration for this study came to her when she realized how many children with obesity were developing adult-onset conditions of diseases, such as hypertension, high cholesterol and type 2 diabetes. She also realized that the comorbidities of obesity were similar to that of aging.

“I ask people to list as many comorbidities of obesity as they can,” Santosa says. “Then I ask how many of those comorbidities are associated with aging. Most people will say, all of them. There is certainly something that is happening in obesity that is accelerating our aging process.'”

She thinks this research will help people better understand how obesity works and stimulate ideas on how to treat it.

“I’m hoping that these observations will focus our approach to understanding obesity a little more, and at the same time allow us to think of obesity in different ways. We’re asking different types of questions than that which have traditionally been asked.”

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Study of 418,000 Europeans finds different foods linked to different types of stroke

Different types of food are linked to risks of different types of stroke, according to the largest study to investigate this, published in the European Heart Journal today (Monday).

Until now, most studies have looked at the association between food and total stroke (all types of stroke combined), or focused on ischaemic stroke only. However, the current study of more than 418,000 people in nine European countries investigated ischaemic stroke and haemorrhagic stroke separately.

The study found that while higher intakes of fruit, vegetables, fibre, milk, cheese or yoghurt were each linked to a lower risk of ischaemic stroke, there was no significant association with a lower risk of haemorrhagic stroke. However, greater consumption of eggs was associated with a higher risk of haemorrhagic stroke, but not with ischaemic stroke.

Ischaemic stroke occurs when a blood clot blocks an artery supplying blood to the brain or forms somewhere else in the body and travels to the brain where it blocks blood flow. Haemorrhagic stroke occurs when there is bleeding in the brain that damages nearby cells. About 85% of strokes are ischaemic and 15% are haemorrhagic. Stroke is the second leading cause of deaths worldwide.

Dr Tammy Tong, the first author of the paper and a nutritional epidemiologist at the Nuffield Department of Population Health, University of Oxford (UK), said: “The most important finding is that higher consumption of both dietary fibre and fruit and vegetables was strongly associated with lower risks of ischaemic stroke, which supports current European guidelines. The general public should be recommended to increase their fibre and fruit and vegetable consumption, if they are not already meeting these guidelines.

“Our study also highlights the importance of examining stroke subtypes separately, as the dietary associations differ for ischaemic and haemorrhagic stroke, and is consistent with other evidence, which shows that other risk factors, such as cholesterol levels or obesity, also influence the two stroke subtypes differently.”

The total amount of fibre (including fibre from fruit, vegetables, cereal, legumes, nuts and seeds) that people ate was associated with the greatest potential reduction in the risk of ischaemic stroke. Every 10g more intake of fibre a day was associated with a 23% lower risk, which is equivalent to around two fewer cases per 1000 of the population over ten years.

Fruit and vegetables alone were associated with a 13% lower risk for every 200g eaten a day, which is equivalent to one less case per 1000 of the population over ten years. No foods were linked to a statistically significant higher risk of ischaemic stroke.

Based on UK estimates, two thick slices of wholemeal toast provide 6.6g of fibre, a portion of broccoli (around eight florets) provides about 3g, and a medium raw, unpeeled apple provides about 1.2g of fibre. The European Society of Cardiology (ESC) and the World Health Organization Regional Office for Europe recommend consuming at least 400g of fruit and vegetables a day; the ESC also suggests people should consume 30-45g of fibre a day.

The researchers found that for every extra 20g of eggs consumed a day there was a 25% higher risk of haemorrhagic stroke, equivalent to 0.66 extra cases per 1000 (or around two cases per 3000) of the population over ten years. An average large-sized egg weighs approximately 60g. Egg consumption in the EPIC study was low overall, with an average of less than 20g eaten a day.

The researchers say the associations they found between different foods and ischaemic and haemorrhagic stroke might be explained partly by the effects on blood pressure and cholesterol.

Dr Tong and her colleagues analysed data from 418,329 men and women in nine countries (Denmark, Germany, Greece, Italy, The Netherlands, Norway, Spain, Sweden and the United Kingdom) who were recruited to the European Prospective Investigation into Cancer and Nutrition (EPIC) study between 1992 and 2000. The participants completed questionnaires asking about diet, lifestyle, medical history and socio-demographic factors, and were followed up for an average of 12.7 years. During this time, there were 4281 cases of ischaemic stroke and 1430 cases of haemorrhagic stroke.

Food groups studied included meat and meat products (red meat, processed meat and poultry), fish and fish products (white fish and fatty fish), dairy products (including milk, yogurt, cheese), eggs, cereals and cereal products, fruit and vegetables (combined and separately), legumes, nuts and seeds, and dietary fibre (total fibre and cereal, fruit and vegetable fibre).

Major strengths of the study include the large numbers of people studied in several different countries and long follow-up period. Most types of food were included in the study, although information on diet was collected at only one point in time, when the participants joined the study. As the study is observational it cannot show that the foods studied cause an increase or decrease in risk of ischaemic or haemorrhagic stroke, only that they are associated with different risks. Information on medication use (including statins) was not available.

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Brain cells protect muscles from wasting away

While many of us worry about proteins aggregating in our brains as we age and potentially causing Alzheimer’s disease or other types of neurodegeneration, we may not realize that some of the same proteins are aggregating in our muscles, setting us up for muscle atrophy in old age.

University of California, Berkeley, scientists have now found brain cells that help clean up these tangles and prolong life — at least in worms (Caenorhabditis elegans) and possibly mice. This could lead to drugs that improve muscle health or extend a healthy human lifespan.

The research team’s most recent discovery, published Jan. 24 in the journal Science, is that a mere four glial cells in the worm’s brain control the stress response in cells throughout its body and increase the worm’s lifespan by 75%. That was a surprise, since glial cells are often dismissed as mere support cells for the neurons that do the brain’s real work, like learning and memory.

This finding follows a 2013 study in which the UC Berkeley group reported that neurons help regulate the stress response in peripheral cells, though in a different way than glial cells, and lengthen a worm’s life by about 25%. In mice, boosting neuronal regulation increases lifespan by about 10%.

Together, these results paint a picture of the brain’s two-pronged approach to keeping the body’s cells healthy. When the brain senses a stressful environment — invading bacteria or viruses, for example — a subset of neurons sends electrical signals to peripheral cells to get them mobilized to respond to the stress, such as through breaking up tangles, boosting protein production and mobilizing stored fat. But because electrical signals produce only a short-lived response, the glial cells kick in to send out a long-lasting hormone, so far unidentified, that maintains a long-term, anti-stress response.

“We have been discovering that if we turn on these responses in the brain, they communicate to the periphery to protect the whole organism from the age onset decline that naturally happens. It rewires their metabolism, it also protects against protein aggregation,” said Andrew Dillin, UC Berkeley professor of molecular and cell biology and Howard Hughes Medical Institute (HHMI) investigator. As a result of the new study, “We think that glia are going to be more important than neurons.”

While the roundworm C. elegans is a long way evolutionarily from humans, the fact that glial cells seem to have a similar effect in mice suggests that the same may be true of humans. If so, it may lead to drugs that combat muscle wasting and obesity and perhaps increase a healthy lifespan.

“If you look at humans with sarcopenia or at older mice and humans, they have protein aggregates in their muscle,” Dillin said. “If we can find this hormone, perhaps it can keep muscle mass higher in older people. There is a huge opportunity here.”

In a commentary in the same Jan. 24 issue of Science, two Stanford University scientists, Jason Wayne Miklas and Anne Brunet, echoed that potential. “Understanding how glial cells respond to stress and what neuropeptides they secrete may help identify specific therapeutic interventions to maintain or rebalance these pathways during aging and age-related diseases,” they wrote.

How to extend lifespan

Dillin studies the seemingly simultaneous deterioration of cells throughout the body as it ages into death. He has shown in worms and mice that hormones and neurotransmitters released by the brain keep this breakdown in check by activating a stress response in the body’s cells and tuning up their metabolism. The response likely originated to fight infection, with the side effect of keeping tissues healthy and extending lifespan. Why our cells stop responding to these signals as we age is the big question.

Over the past decade, he and his colleagues have identified three techniques used by worms to keep their cells healthy and, consequently, longer-lived. Activating the body’s heat shock response, for example, protects the cytoplasm of the cell. Stimulating the unfolded protein response protects the cells’ energy producing structures, the mitochondria. The unfolded protein response is the cell’s way of making sure proteins assume their proper 3D structure, which is crucial for proper functioning inside the cell.

His latest discovery is that glia, as well as neurons, stimulate the unfolded protein response in the endoplasmic reticulum (ER). The ER is the cellular structure that hosts the ribosomes that make proteins — the ER is estimated to be responsible for the folding and maturation of as many as 13 million proteins per minute.

“A lot of the work we have done has uncovered that certain parts of the brain control the aging of the rest of the animal, in organisms from worms to mice and probably humans,” Dillin said.

Two other interventions also increase lifespan in worms: diet restriction, which may call into play other anti-aging mechanisms, and reducing the production of a hormone called insulin-like growth factor (IGF-1).

Dillin’s discoveries have already led to new treatments for diseases. He cofounded a company, Mitobridge Inc. (recently acquired by Astellas Pharma Inc.), based on the finding that certain proteins help tune up mitochondria. A drug the company developed is now in phase II clinical trials for treating the damage that occurs when kidneys restart after sudden failure, such as during an operation.

He cofounded another company, Proteostatis Therapeutics, to develop a treatment for cystic fibrosis that is based on activating the unfolded protein response to repair ion channels in people with the disease.

The new discovery about how neurotransmitter and hormones impact the ER could have implications for diseases that involve muscle wasting, such as Huntington’s disease and forms of myocytis.

Glial cells

In 2013, Dillin and his colleagues discovered that boosting expression of a protein called xbp-1s in sensory nerve cells in the worm brain boosts the misfolded protein response throughout the worm’s body. Shortly afterward, postdoctoral fellow Ashley Frakes decided to see if the glial cells enshrouding these neurons were also involved. When she overexpressed the same protein, xbp-1s, in a subset of these glia (cephalic astrocyte-like sheath glia, or CEPsh), she discovered an even larger effect on peripheral cells, as measured by how they deal with a high-fat diet.

Frakes was able to pinpoint the four CEPsh glia responsible for triggering the ER response, because the C. elegans body is so well studied. There are only 959 cells in the entire worm, 302 of which are nerve cells, and 56 are glial cells.

The CEP neurons and CEPsh glia work differently, but additively, to improve metabolism and clean up protein aggregates as the worms slim down and live twice as long as worms without this protection from a high-fat diet.

“The fact that just a few cells control the entire organism’s future is mind-boggling,” Dillin said. “Glia work 10 times better than neurons in promoting this response and about twice as good in extending lifespan.”

Frakes is currently trying to identify the signaling hormone produced by these glial cells, a first step toward finding a way to activate the response in cells that are declining in function and perhaps to create a drug to tune up human cells and stave off the effects of aging, obesity or other types of stress.

Frakes also found that the worms slimmed down because their fat stores, in the form of lipid droplets, were turned into ER. Another research group in Texas has shown that activating xbp-1s in the neurons of mice also has the effect of reducing fat stores and slimming the mice, protecting them from the effects of a high-fat diet and extending their lifespan.

“When they activate it in the neurons, they see the liver getting rid of fat, redistributing metabolic demands,” Dillin said. “I think we would see the same thing in humans, as well.”

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Mediterranean diet ingredient may extend life

Researchers at the University of Minnesota Medical School discover a potential new way in which diet influences aging-related diseases.

Doug Mashek, PhD, a professor in the Departments of Medicine and Biochemistry, Molecular Biology and Biophysics, leads a team of researchers who discovered that olive oil in the Mediterranean diet may hold the key to improving lifespan and mitigating aging-related diseases. Over the last eight years, with the help of multiple grants from the National Institutes of Health, their research findings were recently published in Molecular Cell.

Early studies on the diet suggested red wine was a major contributor to the health benefits of the Mediterranean diet because it contains a compound called resveratrol, which activated a certain pathway in cells known to increase lifespan and prevent aging-related diseases. However, work in Mashek’s lab suggests that it is the fat in olive oil, another component of the Mediterranean diet, that is actually activating this pathway.

According to Mashek, merely consuming olive oil is not enough to elicit all of the health benefits. His team’s studies suggest that when coupled with fasting, limiting caloric intake and exercising, the effects of consuming olive oil will be most pronounced.

“We found that the way this fat works is it first has to get stored in microscopic things called lipid droplets, which is how our cells store fat. And then, when the fat is broken down during exercising or fasting, for example, is when the signaling and beneficial effects are realized,” Mashek said.

The next steps for their research are to translate it to humans with the goal of discovering new drugs or to further tailor dietary regimens that improve health, both short-term and long-term.

“We want to understand the biology, and then translate it to humans, hopefully changing the paradigm of healthcare from someone going to eight different doctors to treat his or her eight different disorders,” Mashek said. “These are all aging-related diseases, so let’s treat aging.”

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Materials provided by University of Minnesota Medical School. Original written by Angel Mendez. Note: Content may be edited for style and length.

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