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How the Right Foods May Lead to a Healthier Gut, and Better Health

How the Right Foods May Lead to a Healthier Gut, and Better Health

A diet full of highly processed foods with added sugars and salt promoted gut microbes linked to obesity, heart disease and diabetes.

Credit…Getty Images
Anahad O’Connor

  • Jan. 11, 2021, 11:00 a.m. ET

Scientists know that the trillions of bacteria and other microbes that live in our guts play an important role in health, influencing our risk of developing obesity, heart disease, Type 2 diabetes and a wide range of other conditions. But now a large new international study has found that the composition of these microorganisms, collectively known as our microbiomes, is largely shaped by what we eat.

By analyzing the diets, health and microbiomes of more than a thousand people, researchers found that a diet rich in nutrient-dense, whole foods supported the growth of beneficial microbes that promoted good health. But eating a diet full of highly processed foods with added sugars, salt and other additives had the opposite effect, promoting gut microbes that were linked to worse cardiovascular and metabolic health.

The researchers found that what people ate had a more powerful impact on the makeup of their microbiomes than their genes. They also discovered that a variety of plant and animal foods were linked to a more favorable microbiome.

One critical factor was whether people ate foods that were highly processed or not. People who tended to eat minimally processed foods like vegetables, nuts, eggs and seafood were more likely to harbor beneficial gut bacteria. Consuming large amounts of juices, sweetened beverages, white bread, refined grains, and processed meats, on the other hand, was associated with microbes linked to poor metabolic health.

“It goes back to the age-old message of eating as many whole and unprocessed foods as possible,” said Dr. Sarah E. Berry, a nutrition scientist at King’s College London and a co-author of the new study, which was published Monday in Nature Medicine. “What this research shows for the first time is the link between the quality of the food we’re eating, the quality of our microbiomes and ultimately our health outcomes.”

The findings could one day help doctors and nutritionists prevent or perhaps even treat some diet-related diseases, allowing them to prescribe personalized diets to people based on the unique makeup of their microbiomes and other factors.

Many studies suggest that there is no one-size-fits-all diet that works for everyone. The new study, for example, found that while some foods were generally better for health than others, different people could have wildly different metabolic responses to the same foods, mediated in part by the kinds of microbes residing in their guts.

“What we found in our study was that the same diet in two different individuals does not lead to the same microbiome, and it does not lead to the same metabolic response,” said Dr. Andrew T. Chan, a co-author of the study and a professor of medicine at Harvard Medical School and Massachusetts General Hospital. “There is a lot of variation.”

The new findings stem from an international study of personalized nutrition called Predict, which is the world’s largest research project designed to look at individual responses to food. Started in 2018 by the British epidemiologist Tim Spector, the study has followed over 1,100 mostly healthy adults in the United States and Britain, including hundreds of identical and nonidentical twins.

The researchers collected data on a wide range of factors that influence metabolism and disease risk. They analyzed the participants’ diets, microbiomes and body fat. They took blood samples before and after meals to look at their blood sugar, hormones, cholesterol and inflammation levels. They monitored their sleep and physical activity. And for two weeks they had them wear continuous glucose monitors that tracked their blood sugar responses to different meals.

The researchers were surprised to discover that genetics played only a minor role in shaping a person’s microbiome. Identical twins were found to share just 34 percent of the same gut microbes, while people who were unrelated shared about 30 percent of the same microbes. The composition of each person’s microbiome appeared instead to be driven more by what they ate, and the types of microbes in their guts played a strong role in their metabolic health.

The researchers identified clusters of so-called good gut bugs, which were more common in people who ate a diverse diet rich in high-fiber plants — like spinach, broccoli, tomatoes, nuts and seeds — as well as minimally processed animal foods such as fish and full-fat yogurt. They also found clusters of “bad” gut bugs that were common in people who regularly consumed foods that were highly processed. One common denominator among heavily processed foods is that they tend to contain very little fiber, a macronutrient that helps to nourish good microbes in the gut, the researchers said.

Among the “good” strains of gut microbes were Prevotella copri and Blastocystis, both of which were associated with lower levels of visceral fat, the kind that accumulates around internal organs and that increases the risk of heart disease. These microbes also appeared to improve blood sugar control, an indicator of diabetes risk. Other beneficial microbes were associated with reduced inflammation and lower spikes in blood fat and cholesterol levels after meals, all of which play a role in cardiovascular health.

The new study was funded and supported by Zoe Global, a health science company, as well as by the Wellcome Trust, a British nonprofit, and several public health groups.

Dr. Berry said the findings suggest that by looking at microbiome profiles they can identify people at high risk of developing metabolic diseases and intervene early on. She and her colleagues are now planning a clinical trial that will test whether telling people to change specific foods in their diets can alter levels of good and bad microbes in their guts and subsequently improve their health.

“We think there are lots of small changes that people can make that can have a big impact on their health that might be mediated through the microbiome,” she said.

Weekly Health Quiz: Coconut Oil, Coronavirus and Exercise Goals

1 of 7

Which statement about coconut oil is not true?

A tablespoon of coconut oil contains more calories than a tablespoon of butter

Coconut oil is primarily an unsaturated fat, similar to the fats in avocado

Coconut oil raises blood levels of LDL (“bad”) cholesterol

Coconut oil raises levels of HDL (“good”) cholesterol

2 of 7

People who walked about 5,000 steps a day were most likely to stick with a ramped-up exercise routine when they set an exercise target of about:

5,500 steps

7,500 steps

10,000 steps

15,000 steps

3 of 7

This state became the fifth to surpass a million coronavirus cases, after California, Texas, Florida and New York:

Illinois

Pennsylvania

Ohio

Georgia

4 of 7

Total Covid-related deaths have been highest in this state, with more than 38,000:

California

New York

Texas

Florida

5 of 7

A difference in blood pressure readings taken from the right and left arms may signal an increased risk of:

Heart attack

Stroke

Early death

All of the above

6 of 7

Women who have used oral contraceptives may be at lower risk of this form of cancer:

Thyroid cancer

Breast cancer

Ovarian or endometrial cancer

Cervical cancer

7 of 7

Julius Schachter, a microbiologist, died in December from Covid-19. He is perhaps best known for his reserach into this eye disease caused by the Chlamydia bacterium:

Keratitis

Blepharitis

Trachoma

Stye

Does Coconut Oil Deserve Its Health Halo?

Personal Health

Does Coconut Oil Deserve Its Health Halo?

“It’s been known for a long time that coconut oil raises blood levels of artery-damaging LDL cholesterol,” one expert said.

Credit…Gracia Lam
Jane E. Brody

  • Jan. 4, 2021, 5:00 a.m. ET

Coconut oil continues to be widely touted as a miracle food. Proponents, including a slew of celebrities, claim it promotes weight loss, lowers blood pressure and blood glucose, protects against heart disease, increases energy, reduces inflammation, erases wrinkles and even counters Alzheimer’s disease. Plus it tastes great, so what could be bad? And if you believe all that, I’ll offer to sell you the Brooklyn Bridge.

“When I see a product with a long list of things it’s supposed to fix, I know it can’t possibly be true,” said Marion Nestle, a New York University specialist on nutrition and food policy. “Coconut oil has acquired a healthful aura as a superfood and lots of people believe it’s true. They’re guilty of magical thinking and need to stop and think, ‘They’re trying to sell me something.’” Nonetheless, a survey conducted in 2016 found that 72 percent of Americans viewed coconut oil as a healthy food.

The time is long overdue to relieve coconut oil of a halo that scientific evidence shows it doesn’t deserve and instead give consumers a chance to use the $40 they may spend on a 32-ounce jar of coconut oil to invest in foods that can actually enhance their health.

I hope the science-based evidence that follows will convince you to relegate coconut oil to the status of, say, ice cream — an occasional treat best used in modest amounts because you enjoy its flavor and texture.

First, let’s examine exactly what it is. Coconut oil is not really an oil, at least not at room temperatures for most people living in the Northern Hemisphere. It’s more like butter or beef fat, solid when cold. That’s the first clue to the fact that, unlike most other oils derived from plants that primarily contain unsaturated fatty acids, coconut oil is a highly saturated fat, 87 percent saturated, in fact, far higher than butter (63 percent) or beef fat (40 percent). Most experts recommend limiting saturated fats, which can drive up cholesterol levels and lead to clogged arteries.

Nor is coconut oil a diet food. Like other vegetable oils, a tablespoon of coconut oil supplies 117 calories, 15 more than a tablespoon of butter.

Perhaps you’ve heard the claim that the primary fatty acid in coconut oil, called lauric acid, doesn’t act like a saturated fat in the body. Not true. Its action most closely mimics that of beef tallow and butter, both of which can promote atherosclerotic heart disease, the nation’s leading killer.

To better understand how coconut oil behaves when ingested, I consulted two experts, Dr. Frank M. Sacks, nutrition and cardiovascular disease specialist at Harvard’s T.H. Chan School of Public Health, and Dr. Philip Greenland, professor of cardiology at the Feinberg School of Medicine in Chicago.

“It’s been known for a long time that coconut oil raises blood levels of artery-damaging LDL cholesterol, and the newest research has strengthened that early understanding,” Dr. Sacks told me. In preparing an editorial published last March in the journal Circulation, he said, “I could find nothing in the scientific literature to support advertising claims that coconut oil has some beneficial effects.”

Dr. Greenland echoed that assessment, stating that “the marketing of coconut oil is confusing. It’s trying to sell it as a healthy fat, but those who know its composition don’t think that at all.”

These and other experts part company with advertisers and advocates for coconut oil based on its chemical makeup and the well-established biological activity of different kinds of fatty acids.

“Fat can’t circulate by itself,” Dr. Greenland said, explaining that long-chain fatty acids like those prominent in beef tallow are absorbed into the bloodstream by fat-carrying particles called chylomicrons that deliver the fat to tissues throughout the body. Chylomicrons keep LDL cholesterol in circulation, giving it ample opportunity to get stuck in arteries. Fats that are mainly medium-chain fatty acids, on the other hand, are more water-soluble; they can be absorbed into the bloodstream without the assistance of chylomicrons and transported directly to the liver, where they are used for energy.

Although lauric acid is usually referred to as a medium-chain fatty acid, Dr. Sacks said, this label is really arbitrary. “Classifying lauric acid as a medium-chain fatty acid is a misnomer,” he wrote. “Rather than the number of carbon atoms in a fat,” he said, “what counts is how the fat is metabolized in the body. Lauric acid behaves like a long-chain fatty acid,” the kind that promotes atherosclerosis. In addition, coconut oil has two other long-chain fatty acids — myristic and palmitic — and all three have an artery-damaging effect on cholesterol levels in the blood.

One claim made for coconut oil is undisputed: It can raise blood levels of HDL cholesterol, which has long been thought to protect against heart disease. However, a clear-cut health benefit of HDL cholesterol has yet to be demonstrated in people. As Dr. Sacks reported, “Genetic studies and HDL-raising drugs have not so far supported a causal relationship between HDL cholesterol and cardiovascular disease. HDL is composed of a huge array of subparticles that may have adverse or beneficial actions. It is unknown which, if any, foods or nutrients that raise HDL cholesterol do so in a way that reduces atherosclerosis and coronary events.”

Ditto, said Dr. Greenland. “Efforts to raise HDL have not led to beneficial clinical improvements.”

Proponents are also fond of citing the fact that a number of Indigenous populations — including Polynesians, Melanesians, Sri Lankans and Indians — consume rather large amounts of coconut products without suffering high rates of cardiovascular disease. However, most of these people have traditionally eaten coconut flesh or squeezed coconut cream as part of a diet that is low in processed foods and rich in fruits and vegetables, with fish as the main source of protein. They are also far more active physically than typical Westerners.

But even that is now changing, a New Zealand research team reported, with the “imports of unhealthy foods such as corned beef, fast food and processed ingredients, leading to huge increases in obesity and poor health.”

The team’s review of 21 studies of coconut oil consumption prompted the conclusion that consuming coconut products that contain fiber, such as coconut flesh and flour, in a diet rich in polyunsaturated fats and absent in excessive calories from refined carbohydrates would not pose a risk for heart disease. But the researchers found no evidence that could justify substituting coconut oil for other unsaturated plant oils.

Or as Dr. Nestle put it, “If you like the way it tastes, in limited amounts it’s fine, but it’s by no means a superfood.” However, she added, if you want to use coconut oil on your hair or skin, no problem.

How Exercise Changes Our Blood

While we exercise, we raise and lower the levels of hundreds of molecules in our bloodstreams that are related to our metabolic health, even if we work out for only a few minutes, according to a complex and encouraging new study of the molecular effects of being active. The study, which involved more than 1,000 men and women, adds to growing evidence that exercise improves our health in large part by transforming the numbers and types of cells inside of us.

There is at this point, of course, no reasonable debate about whether exercise is good for us. It is. Countless studies show that people who are active are less likely than more-sedentary people to develop or die from a host of health problems, including heart disease, diabetes, dementia, cancer, obesity and many others. Active people also tend to live longer and feel happier.

But we still know surprisingly little about just how exercise changes us for the better. What are the many, interconnected biological steps and transmutations that allow a walk today to add to our life span decades from now?

That question has been driving considerable interest recently in research looking at exercise “omics” — the study of all of the molecules in our blood or other tissues that are part of a particular biological process. Genomics, for instance, quantifies the many, many molecules involved in genetic activities. Proteomics does the same for proteins, microbiomics for the multiple contents of our microbiomes and metabolomics for molecules related to metabolic processes. (There can be overlap between various ’omics, obviously.)

Understanding how exercise affects the levels of the various molecules within us is important, because these changes are likely to be the preliminary step in a complex cascade of further biological actions that contribute to better health. Increase some molecules, decrease others, and you jump-start inter-organ messaging, gene expression and other processes that subsequently alter how we make and use insulin, burn or store fat, respond to cholesterol and so on.

A number of important recent studies have delved into the ’omics of exercise, including a fascinating experiment showing that a short workout rapidly changes the levels of 9,815 molecules in people’s bloodstreams. But that study, like most other examinations of exercise and ’omics, involved relatively few volunteers — 36, in that case — and did not link molecular changes with subsequent health outcomes.

So, for the new study, which was published in September in Circulation, researchers at Massachusetts General Hospital in Boston and other institutions decided to up the number of exercisers whose ’omics would be parsed and also try to find connections between the ’omics data and later health.

Conveniently, they had access to a large group of potential volunteers among men and women already enrolled in the long-term Framingham Heart Study, which is overseen primarily by researchers at Massachusetts General Hospital. The scientists now asked 411 middle-aged volunteers enrolled in the study to visit the lab and exercise, by pedaling to exhaustion on a stationary bicycle. Most riders’ efforts lasted for a little less than 12 minutes. The researchers drew blood before the ride and afterward, within about a minute of when, worn out, the cyclists quit.

The scientists then ran the blood samples through a mass spectrometer, a machine that counts and quantifies molecules. The researchers focused on metabolites, which are molecules related to metabolic processes. The label “metabolite” is somewhat arbitrary, but for this study, the researchers focused mostly on molecules that could affect people’s insulin, fat burning, cholesterol, blood sugar and other aspects of cellular fueling.

They found plenty. Of 588 metabolites checked, the levels of more than 80 percent generally grew or dropped during the short rides. To reinforce those findings, the scientists repeated the experiment with another 783 Framingham volunteers, checking their blood before and after exercise for changes in about 200 of the molecules that had been most altered in the first group. Again, these metabolites changed in the same ways as before.

Last and perhaps most intriguing, the researchers created what they called molecular “signatures” of the levels of a few, representative metabolites that changed with exercise. They then looked for these same patterns of metabolites in stored blood samples gathered decades before from past Framingham participants, while also checking to see if and when any of these volunteers had passed away.

The relevant signatures popped up in some of the blood samples, the researchers found, and these samples tended to be from people who had not died prematurely, suggesting that the kinds of metabolite changes that occur with exercise might influence and improve health well into the future.

That idea is “speculative,” though, says Dr. Gregory Lewis, the section head of the heart failure program and director of the cardiopulmonary exercise laboratory at Massachusetts General Hospital, who oversaw the new study. The decades-old blood samples were drawn during standard medical testing, not after exercise, he says, so some people with desirable metabolite signatures might have been born that way and not needed workouts to remodel their metabolites.

Even among the current volunteers, he points out, different people’s molecules responded somewhat differently to their exercise. Over all, people with obesity developed fewer changes than leaner riders, suggesting they might somehow resist some of the benefits of exercise. Men and women, as groups, also showed slightly discordant molecular signatures, but age did not influence people’s molecular responses.

Larger future ’omics studies should help scientists tease out how and why we each react as we do to exercise, Dr. Lewis says, and enable researchers to define more-precise molecular signatures that might indicate, with a blood test, how fit someone is or how their bodies may respond to different types of exercise.

But for now, the current study underscores just how pervasive and immediate the effects of exercise can be. “This was barely 10 minutes of exercise,” Dr. Lewis says, “but it shifted so much” inside people.

Being Unfit May Be Almost as Bad for You as Smoking

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Credit Getty Images

Being out of shape could be more harmful to health and longevity than most people expect, according to a new, long-term study of middle-aged men. The study finds that poor physical fitness may be second only to smoking as a risk factor for premature death.

It is not news that aerobic capacity can influence lifespan. Many past epidemiological studies have found that people with low physical fitness tend to be at high risk of premature death. Conversely, people with robust aerobic capacity are likely to have long lives.

But most of those studies followed people for about 10 to 20 years, which is a lengthy period of time for science but nowhere near most of our actual lifespans. Some of those studies also enrolled people who already were elderly or infirm, making it difficult to extrapolate the findings to younger, healthier people.

So for the new study, which was published this week in the European Journal of Preventive Cardiology, researchers from the University of Gothenburg in Sweden and other institutions turned to an impressively large and long-term database of information about Swedish men.

The data set, prosaically named the Study of Men Born in 1913, involved exactly that. In 1963, almost 1,000 healthy 50-year-old men in Gothenburg who had been born in 1913 agreed to be studied for the rest of their lives, in order to help scientists better understand lifetime risks for disease, especially heart disease.

The men completed baseline health testing in 1963, including measures of their blood pressure, weight and cholesterol, and whether they exercised and smoked. Four years later, when the volunteers were 54, some underwent more extensive testing, including an exercise stress test designed to precisely determine their maximum aerobic capacity, or VO2 max. Using the results, the scientists developed a mathematical formula that allowed them to estimate the aerobic capacity of the rest of the participants.

Aerobic capacity is an interesting measure for scientists to study, because it is affected by both genetics and lifestyle. Some portion of our VO2 max is innate; we inherit it from our parents. But much of our endurance capacity is determined by our lifestyle. Being sedentary lowers VO2 max, as does being overweight. Exercise raises it.

Among this group of middle-aged men, aerobic capacities ranged from slight to impressively high, and generally reflected the men’s self-reported exercise habits. Men who said that they seldom worked out tended to have a low VO2 max. (Because VO2 max is more objective than self-reports about exercise, the researchers focused on it.)

To determine what impact fitness might have on lifespan, the scientists grouped the men into three categories: those with low, medium or high aerobic capacity at age 54.

Then they followed the men for almost 50 years. During that time, the surviving volunteers completed follow-up health testing about once each decade. The scientists also tracked deaths among the men, based on a national registry.

Then they compared the risk of relatively early death to a variety of health parameters, particularly each man’s VO2 max, blood pressure, cholesterol profile and history of smoking. (They did not include body weight as a separate measure, because it was indirectly reflected by VO2 max.)

Not surprisingly, smoking had the greatest impact on lifespan. It substantially shortened lives.

But low aerobic capacity wasn’t far behind. The men in the group with the lowest VO2 max had a 21 percent higher risk of dying prematurely than those with middling aerobic capacity, and about a 42 percent higher risk of early death than the men who were the most fit.

Poor fitness turned out to be unhealthier even than high blood pressure or poor cholesterol profiles, the researchers found. Highly fit men with elevated blood pressure or relatively unhealthy cholesterol profiles tended to live longer than out-of-shape men with good blood pressure and cholesterol levels.

Of course, this study found links between poor fitness and shortened lifespans. It cannot prove that one caused the other, or explain how VO2 max might affect lifespan. However, the findings raise the possibility, as the scientists speculate, that by strengthening the body, better fitness may lower the risk of a variety of chronic diseases.

This study also involved men — and Swedish men at that. So whether the findings are applicable to other people, particularly women, is uncertain.

But “there is no reason not to think” that the rest of us would also share any beneficial associations between fitness and longevity, said Per Ladenvall, a researcher at the Sahlgrenska Academy at the University of Gothenburg, who led the study. Past studies involving women have found such links, he said.

Encouragingly, if you now are concerned about the state of your particular aerobic capacity, you most likely can increase it just by getting up and moving. “Even small amounts of physical activity,” Dr. Ladenvall said, “may have positive effects on fitness.”

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Cutting Sugar Rapidly Improves Heart Health Markers

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Obese children who cut sugar from their diets saw improvements in markers of heart disease after just nine days, a study in Atherosclerosis found.

For the study, researchers evaluated 37 children ages 9 to 18 who were obese and at high risk for heart disease and Type 2 diabetes. The children were given food and drinks totaling the same number of calories, fat, protein and carbohydrates as their typical diets.

The only change was their sugar intake: The researchers swapped foods high in added sugars, like pastries and sweetened yogurts, for options like bagels and pizza. This lowered dietary sugar from 28 percent to 10 percent, and fructose from 12 percent to 4 percent of total calories.

After nine days, the researchers found a 33 percent drop in triglycerides, a type of fat tied to heart disease; a 49 percent reduction in a protein called apoC-III that is tied to high triglyceride levels; and dramatic reductions in small, dense LDL cholesterol, a risk factor for heart disease.

Though this study is small and short-term, it builds on this group’s previous research implicating added sugars as a contributor to metabolic disorders and heart disease.

“Sugar calories are not like other carbohydrate calories,” said Dr. Robert Lustig, a co-author of the study and professor of pediatrics at Benioff Children’s Hospital at the University of California, San Francisco. “Without changing total carbohydrate, or fat, or protein, we were able to accomplish this enormous improvement in their cardiovascular risk factors,” unrelated to weight loss, he said.

A Decades-Old Study, Rediscovered, Challenges Advice on Saturated Fat

A four-decades-old study — recently discovered in a dusty basement — has raised new questions about longstanding dietary advice and the perils of saturated fat in the American diet.

The research, known as the Minnesota Coronary Experiment, was a major controlled clinical trial conducted from 1968 to 1973, which studied the diets of more than 9,000 people at state mental hospitals and a nursing home.

During the study, which was paid for by the National Heart, Lung and Blood Institute and led by Dr. Ivan Frantz Jr. of the University of Minnesota Medical School, researchers were able to tightly regulate the diets of the institutionalized study subjects. Half of those subjects were fed meals rich in saturated fats from milk, cheese and beef. The remaining group ate a diet in which much of the saturated fat was removed and replaced with corn oil, an unsaturated fat that is common in many processed foods today. The study was intended to show that removing saturated fat from people’s diets and replacing it with polyunsaturated fat from vegetable oils would protect them against heart disease and lower their mortality.

So what was the result? Despite being one of the largest controlled clinical dietary trials of its kind ever conducted, the data were never fully analyzed.

Several years ago, Christopher E. Ramsden, a medical investigator at the National Institutes of Health, learned about the long-overlooked study. Intrigued, he contacted the University of Minnesota in hopes of reviewing the unpublished data. Dr. Frantz, who died in 2009, had been a prominent scientist at the university, where he studied the link between saturated fat and heart disease. One of his closest colleagues was Ancel Keys, an influential scientist whose research in the 1950s helped establish saturated fat as public health enemy No. 1, prompting the federal government to recommend low-fat diets to the entire nation.

“My father definitely believed in reducing saturated fats, and I grew up that way,” said Dr. Robert Frantz, the lead researcher’s son and a cardiologist at the Mayo Clinic. “We followed a relatively low-fat diet at home, and on Sundays or special occasions, we’d have bacon and eggs.”

The younger Dr. Frantz made three trips to the family home, finally discovering the dusty box marked “Minnesota Coronary Survey,” in his father’s basement. He turned it over to Dr. Ramsden for analysis.

The results were a surprise. Participants who ate a diet low in saturated fat and enriched with corn oil reduced their cholesterol by an average of 14 percent, compared with a change of just 1 percent in the control group. But the low-saturated fat diet did not reduce mortality. In fact, the study found that the greater the drop in cholesterol, the higher the risk of death during the trial.

The findings run counter to conventional dietary recommendations that advise a diet low in saturated fat to decrease heart risk. Current dietary guidelines call for Americans to replace saturated fat, which tends to raise cholesterol, with vegetable oils and other polyunsaturated fats, which lower cholesterol.

While it is unclear why the trial data had not previously been fully analyzed, one possibility is that Dr. Frantz and his colleagues faced resistance from medical journals at a time when questioning the link between saturated fat and disease was deeply unpopular.

“It could be that they tried to publish all of their results but had a hard time getting them published,” said Daisy Zamora, an author of the new study and a research scientist at the University of North Carolina at Chapel Hill.

The younger Dr. Frantz said his father was probably startled by what seemed to be no benefit in replacing saturated fat with vegetable oil.

“When it turned out that it didn’t reduce risk, it was quite puzzling,” he said. “And since it was effective in lowering cholesterol, it was weird.”

The new analysis, published on Tuesday in the journal BMJ, elicited a sharp response from top nutrition experts, who said the study was flawed. Walter Willett, the chairman of the nutrition department at the Harvard T.H. Chan School of Public Health, called the research “irrelevant to current dietary recommendations” that emphasize replacing saturated fat with polyunsaturated fat.

Frank Hu, a nutrition expert who served on the government’s 2015 dietary guidelines committee, said the Minnesota trial was not long enough to show the cardiovascular benefits of consuming vegetable oil because the patients on average were followed for only about 15 months. He pointed to a major 2010 meta-analysis that found that people had fewer heart attacks when they increased their intake of vegetable oils and other polyunsaturated fats over at least four years.

“I don’t think the authors’ strong conclusions are supported by the data,” he said.

To investigate whether the new findings were a fluke, Dr. Zamora and her colleagues analyzed four similar, rigorous trials that tested the effects of replacing saturated fat with vegetable oils rich in linoleic acid. Those, too, failed to show any reduction in mortality from heart disease.

“One would expect that the more you lowered cholesterol, the better the outcome,” Dr. Ramsden said. “But in this case the opposite association was found. The greater degree of cholesterol-lowering was associated with a higher, rather than a lower, risk of death.”

One explanation for the surprise finding may be omega-6 fatty acids, which are found in high levels in corn, soybean, cottonseed and sunflower oils. While leading nutrition experts point to ample evidence that cooking with these vegetable oils instead of butter improves cholesterol and prevents heart disease, others argue that high levels of omega-6 can simultaneously promote inflammation. This inflammation could outweigh the benefits of cholesterol reduction, they say.

In 2013, Dr. Ramsden and his colleagues published a controversial paper about a large clinical trial that had been carried out in Australia in the 1960s but had never been fully analyzed. The trial found that men who replaced saturated fat with omega-6-rich polyunsaturated fats lowered their cholesterol. But they were also more likely to die from a heart attack than a control group of men who ate more saturated fat.

Ron Krauss, the former chairman of the American Heart Association’s dietary guidelines committee, said the new research was intriguing. But he said there was a vast body of research supporting polyunsaturated fats for heart health, and that the relationship between cholesterol-lowering and mortality could be deceiving.

People who have high LDL cholesterol, the so-called bad kind, typically experience greater drops in cholesterol in response to dietary changes than people with lower LDL. Perhaps people in the new study who had the greatest drop in cholesterol also had higher mortality rates because they had more underlying disease.

“It’s possible that the greater cholesterol response was in people who had more vascular risk related to their higher cholesterol levels,” he said.

Dr. Ramsden stressed that the findings by he and his colleagues should be interpreted cautiously. The research does not show that saturated fats are beneficial, he said: “But maybe they’re not as bad as people thought.”

The research underscores that the science behind dietary fat may be more complex than nutrition recommendations suggest. The body requires omega-6 fats like linoleic acid in small amounts. But emerging research suggests that in excess linoleic acid may play a role in a variety of disorders including liver disease and chronic pain.

A century ago, it was common for Americans to get about 2 percent of their daily calories from linoleic acid. Today, Americans on average consume more than triple that amount, much of it from processed foods like lunch meats, salad dressings, desserts, pizza, french fries and packaged snacks like potato chips. More natural sources of fat such as olive oil, butter and egg yolks contain linoleic acid as well but in smaller quantities.

Eating whole, unprocessed foods and plants may be one way to get all the linoleic acid your body needs, Dr. Ramsden said.

Making a Case for Eating Fat

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Credit Mark Hyman

For years Dr. Mark Hyman was a vegetarian who kept his intake of dietary fat to a minimum. Whole-wheat bread, grains, beans, pasta and fruits and vegetables made up the bulk of his diet, just as the federal government’s dietary guidelines had long recommended. But as he got older, Dr. Hyman noticed something that bothered him: Despite plenty of exercise and a seemingly healthy diet, he was gaining weight and getting flabby.

At first he wrote it off as a normal part of aging. But then he made a shift in his diet, deciding to eat more fat, not less – and the changes he saw surprised him.

He lost weight, his love handles disappeared, and he had more energy. He encouraged his patients to consume more fat as well, and many of them lost weight and improved their cholesterol. Some even reversed their Type 2 diabetes.

Today, as the director of the Cleveland Clinic’s Center for Functional Medicine, Dr. Hyman has become an outspoken advocate about the health benefits of eating fat. He promotes it on talk shows, educates other doctors, and has even managed to wean his close friend Bill Clinton off of his previously prescribed low-fat vegan diet.

Now in a new book called “Eat Fat, Get Thin,” Dr. Hyman takes a deep dive into the science behind dietary fat, making sense of decades of confusing health recommendations and building a case for why even saturated fats, which have long been vilified, belong in a healthy diet. Dr. Hyman argues that Americans have been misled about the benefits of fat because of a disconnect between nutrition science and food policy. In the book he challenges the nutrition orthodoxy while also exploring the food industry’s outsize influence on official health recommendations.

Recently, we sat down with Dr. Hyman to discuss his thoughts on the gap between nutrition science and health recommendations, the reason you should always plan your meals, and why he never leaves home without a stash of “emergency foods” in his backpack. Here are edited excerpts from our conversation:

Q.

Why did you write “Eat Fat, Get Thin”?

A.

I wrote it because we’ve been suffering from 40 years of bad advice about fat that’s led to the biggest obesity and diabetes epidemic in history. The myth that fat makes you fat and causes heart disease has led to a total breakdown in our nutritional framework. I felt it was important to tell the story of how fat makes you thin and how it prevents heart disease and can reverse diabetes. I think people are still very confused about fat.

Q.

In the book you argue that nutrition recommendations are often contradictory. How so?

A.

This year, for example, the U.S. Dietary Guidelines for the first time removed their longstanding restrictions on dietary fat. But they still have recommendations to eat low-fat foods. They say total fat is not an issue, but you should drink low-fat milk and eat low-fat dairy and other low-fat foods. It’s a schizophrenic recommendation from the government, and it’s the same with other professional organizations such as the American College of Cardiology and the American Heart Association. There’s a mismatch between the science and the government and professional recommendations.

Q.

What’s driving this disconnect?

A.

I think the government based its recommendations on some very flawed science, which took hold. It became policy that was turned into the dietary guidelines and the food pyramid that told us to eat six to 11 servings of bread, rice, cereal and pasta a day and to eat fats and oils sparingly. It’s very hard to overturn dogma like that. It’s embedded in our culture now. It’s embedded in food products. The food industry jumped on the low-fat bandwagon, and the professional associations kept driving the message. Unfortunately the science takes decades to catch up into policy and into practice. And I’m trying to close that gap by bringing awareness to the latest science on how fats and carbs work in your body.

Q.

You reviewed hundreds of studies while writing this book. What is your conclusion on saturated fat?

A.

It’s a huge area of controversy. But large reviews of randomized trials, observational research and blood-level data have all found no link between saturated fat or total fat and heart disease. Yet there are still recommendations to limit saturated fat because it raises total cholesterol and LDL cholesterol. But it also raises HDL, and it increases cholesterol particle size, so you actually get a net benefit.

Q.

What do you say to scientists who argue that saturated fat does in fact cause heart disease?

A.

I think the challenge with the research is that a lot of the data combines saturated fat in the context of a high-carbohydrate diet. The real danger is sweet fat. If you eat fat with sweets – so sugar and fat, or refined carbohydrates and fat – then insulin will rise and it’ll make you fat. But if you eliminate the refined carbs and sugar, that doesn’t happen. I think saturated fats can be bad in the context of a high-carbohydrate diet. But in the absence of that, they’re not.

Q.

What foods do you eat and recommend to your patients?

A.

What I eat is a cross between paleo and vegan diets. It combines elements of the two, so I call it a “pegan” diet. It’s low in sugars and refined carbs, and it’s very high in plant foods. About 70 to 80 percent of your diet should be plant foods. It should also include good-quality fats like nuts and seeds, olive oil, avocado, coconut oil and fatty fish. It should basically include whole, fresh food that’s unprocessed and high in fiber and phytonutrients. I always say that vegetables should make up 50 to 75 percent of your plate.

Q.

In a world where fast food is everywhere, wouldn’t that be fairly difficult for most people?

A.

It’s actually very easy to eat well if you just know what to do. The reason most people don’t succeed is they don’t plan their food. They plan their vacations, they plan their kitchen redesign, but they don’t plan out what they’re eating, and that’s a recipe for failure. I always think through how and where I’m going to get my food every day of every week. I also carry with me a set of emergency food so that I’m never in a food emergency.

Q.

What are the “emergency foods” that you carry?

A.

I have to protect myself from myself because I’ll eat whatever if I’m hungry in an airport. So I always carry packets of almond butter, cashew butter, an Evolution bar, a Bulletproof bar, a Tanka bar and a KIND bar. I basically have fat and protein as my snacks, and I have enough food in my bag to last an entire day so I don’t make bad choices.

Q.

We talked a lot about fat. But what is one overarching message you would most like people to understand?

A.

I think we have to get rid of the prevailing dogma that all calories are the same, and that we just need to exercise more and eat less, which is what the food industry and the government promote. The truth is that you can’t exercise your way out of a bad diet. Metabolism is not a math problem. It’s a hormonal problem. Food is not just energy. It’s information. It’s instructions that turn on or off different switches in your body that regulate hunger and metabolism. Obesity is not about how much you eat. It’s about what you eat. If you just focus on quality, not calories, then the quantity takes care of itself.

Foods High in Cholesterol Don’t Raise Heart Risks

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A new study provides more evidence that eating high-cholesterol food does not increase the risk for heart disease.

The Finnish study, in The American Journal of Clinical Nutrition, followed 1,032 initially healthy men ages 42 to 60. About a third were carriers of ApoE4, a gene variant known to increase the risk for heart disease (and Alzheimer’s). The researchers assessed their diets with questionnaires and followed them for an average of 21 years, during which 230 men developed coronary artery disease.

The men consumed an average of about 2,800 milligrams of cholesterol a week, more than a quarter of it from eating an average of four eggs weekly. (An egg contains about 180 milligrams of cholesterol.)

After controlling for age, education, smoking, B.M.I., diabetes, hypertension and other characteristics, the researchers found no association between cardiovascular disease and total cholesterol or egg consumption in either carriers or noncarriers of ApoE4.

The researchers also examined carotid artery thickness, a measure of atherosclerosis. They found no association between cholesterol consumption and artery thickness, either.

The lead author, Jyrki K. Virtanen, an adjunct professor of epidemiology at the University of Eastern Finland, said that for healthy people, “Moderate intake of cholesterol,” including up to one egg a day, “doesn’t seem to increase the risk of heart disease, even among those people at higher risk.”