That Huge Mediterranean Diet Study Was Flawed and Re-analysed

Gina Kolata wrote . . . . . . .

The study was a landmark, one of the few attempts to rigorously evaluate a particular diet. And the results were striking: A Mediterranean diet, with abundant vegetables and fruit, can slash the risk of heart attacks and strokes.

But now that trial, published in the New England Journal of Medicine in 2013, has come under fire. The authors retracted their original paper on Wednesday and published an unusual “re-analysis” of their data in the same journal.

Despite serious problems in the way the study was conducted, their conclusions are the same: A Mediterranean diet can cut the risk of heart attacks and strokes by about 30 percent in those at high risk.

Not everyone is convinced. “Nothing they have done in this re-analyzed paper makes me more confident,” said Dr. Barnett Kramer, director of the division of cancer prevention at the National Cancer Institute.

For decades, researchers have noted that people living in some Mediterranean countries have lower rates of heart disease and cancer. Scientists have long suspected that the regional diet — rich in fruits, vegetables, nuts and olive oil, with moderate levels of fat — played a protective role.

But the idea has been hard to prove. It is very difficult to test any diet in a clinical trial. Participants may be reluctant to stick to the prescribed meal plan, for instance, and it can be difficult to monitor them over months or years.

The original study was conducted in Spain by Dr. Miguel A. Martínez-González of the University of Navarra and his colleagues. The trial enrolled 7,447 participants aged 55 to 80 who were assigned one of three diets: a Mediterranean diet with at least four tablespoons a day of extra virgin olive oil; the same diet with an ounce of mixed nuts; or a traditional low-fat diet.

The participants were followed for a median of nearly five years. Dr. Martínez-González and his colleagues reported that there were fewer cardiovascular events in the groups consuming olive oil and nuts.

But last year Dr. Martínez-González found his study on a list of clinical trials whose data seemed suspect, compiled by Dr. John Carlisle of Torbay Hospital in England.

“That was the first hint that there could have been some imperfection,” Dr. Martínez-González said in an interview.

A statistician at the New England Journal of Medicine suggested the researchers look at the methods at each center that recruited participants.

The idea of a randomized trial is to assign treatments — in this case, diets — to participants with the statistical equivalent of a coin toss. That way, the groups being compared should be equivalent, with no group healthier or sicker, or older or younger, than another on average.

If subjects are not assigned at random, the investigators cannot be sure that the effects they see result from the treatment. And attempts to correct statistically after the fact are fraught with difficulty.

On re-evaluating their data, the scientists running the Mediterranean diet study soon found what Dr. Martínez-González said were “small problems affecting 10 percent of participants.”

Some investigators would assign one person in a household — the wife, for example — to one arm of the study — say, to the group consuming olive oil. Then they would ask other members of the household to share that diet, including them as though they had been randomly assigned to it.

“We realized we had never reported that,” Dr. Martínez-González said.

An omission like that erodes the randomized nature of the trial. Family members are likely to share more than just a diet: If a husband and wife both dodge heart disease, it’s difficult to say that their diet is the only reason.

In their re-analysis, the investigators statistically adjusted data on 390 people who happened to be household members but whose diets were not randomly assigned.

Then the investigators discovered another problem.

A researcher at one of the 11 clinical centers in the trial worked in small villages. Participants there complained that some neighbors were receiving free olive oil, while they got only nuts or inexpensive gifts.

So the investigator decided to give everyone in each village the same diet. He never told the leaders of the study what he had done.

“He did not think it was important,” Dr. Martínez-González said.

But the decision meant that participants were not truly randomized and forced Dr. Martínez-González and his colleagues to make another statistical adjustment to data on 652 people in the trial.

The investigators spent a year working on the re-analysis in collaboration with Dr. Miguel Hernan of the Harvard T.H. Chan School of Public Health.

In the end, they concluded that the original findings were still accurate.

“You cannot imagine what it has been like,” Dr. Martínez-González said, adding that he and his team worked through vacations and weekends — and swallowed considerable professional embarrassment.

Randomized trials are difficult, other experts agreed, and randomized diet studies so perilous they are seldom attempted.

“These people were naïve,” said Donald Berry, a statistician at MD Anderson Cancer Center in Houston. “They were sloppy and didn’t know they were being sloppy.”

Dr. Berry said he wants to believe the results. He loves nuts and has taken to cooking with extra virgin olive oil.

But he remains unconvinced, because the re-analysis did not solve the study’s problems, he said.

Dr. Bradley Efron, a statistics professor at Stanford University, also was skeptical. The revamped results “wouldn’t convince me to be on a Mediterranean diet,” he said.

But Dr. Steven Nissen, a cardiologist at the Cleveland Clinic, is persuaded and plans to continue advising patients to go on the Mediterranean diet.

When the initial paper was published, he said, “I was thrilled to see what seemed to be an impeccable trial.”

Although it was “sobering” to learn of the errors, “I was reassured that the conclusions are correct,” he said.

Source: The New York Times

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Scientist Says Salt Won’t Give You a Heart Attack If You are Healthy

Dr. James Dinicolantono wrote . . . . . . . . .

For more than 40 years, we’ve been told eating too much salt is killing us. Doctors say it’s as bad for our health as smoking or not exercising, and government guidelines limit us to just under a teaspoon a day.

We’re told not to cook with it and not to sprinkle it on our meals. The white stuff is not just addictive, goes the message — it’s deadly. Too much of it causes high blood pressure, which in turn damages our hearts. We must learn to live — joylessly, flavourlessly but healthily — without it.

Well, I’m here to tell you that all of that is wrong. As a leading cardiovascular research scientist — based at Saint Luke’s Mid-America Heart Institute, Missouri — I’ve contributed extensively to health policy and medical literature.

I am associate editor of the British Medical Journal’s Open Heart, published in partnership with the British Cardiovascular Society, and I sit on the editorial advisory board of several other medical journals.

In my work, I’ve examined data from more than 500 medical papers and studies about salt. And this is what I’ve learned: there was never any sound scientific evidence to support this low salt idea. What’s more, as I explain in my new book, eating too little of it can cause insulin resistance, increased fat storage and may even increase the risk of diabetes — not to mention decreasing our sex drive.

Current daily guidelines limit you to 2.4 g of sodium, which translates to 6 g of salt (or sodium chloride) or slightly less than a teaspoonful.

If you have high blood pressure, or belong to a group considered to be at greater risk of developing it — such as being over 60 or Afro-Caribbean — doctors even advise you to cut your intake to two-thirds of a teaspoon of salt per day.

Yet salt is an essential nutrient that our bodies depend on to live. And those limits go against all our natural instincts. When people are allowed as much salt as they fancy, they tend to settle at about a teaspoon-and-a-half a day. This is true all over the world, across all cultures, climates and social backgrounds.

If you’ve been struggling to cut your intake, it may come as a relief to learn your salt cravings are normal, a biological need akin to our thirst for water.

We are essentially salty people. We cry salt, we sweat salt and the cells in our bodies are bathed in salty fluids. Without salt we’d not be able to live. And it’s not only our bodies that work this way.

A yen for salt drives the elephants of Kenya to walk into the pitch-black caves of Mount Elgon to lick sodium sulphate salt crystals off the walls. Gorillas have been known to follow elephants to eat the salt-rich droppings, while monkeys that groom one another don’t do so to eat fleas, but to enjoy their salty skin secretions.

Salt is so fundamental to life that a deficiency of it acts as a natural contraceptive in all sorts of animals, including us.

A diet low in salt reduces the sex-drive, inhibits the chances of getting pregnant and affects the birth weight of infants. Clinical studies show that low-salt diets can increase the risk of erectile dysfunction, fatigue and the age at which females become fertile.

Salt helps the body withstand accidents and other traumas. Besides excessive bleeding, we experience a loss of other fluids in states of shock — for example, from burns. As the injured areas soak up fluids to speed healing, the body needs its salt reserves to keep the blood circulating and fend off vascular collapse.

So why do almost all doctors tell us that salt is bad for us?

The orthodox medical view on salt is based on a straightforward hypothesis, which says eating higher levels of salt leads to higher levels of blood pressure — end of story.

But as with so many simplistic health theories, this is based on a fundamental misunderstanding, compounded by faulty science.

The faulty hypothesis goes like this: when we eat salt, we get thirsty, so we drink more water.

The dangerous myth that salt raises blood pressure began more than 100 years ago

The excess salt causes the body to hold on to that water to dilute the saltiness of the blood.

That water retention increases blood volume, which leads to higher blood pressure, and thus to heart disease, strokes and other serious conditions.

Although this makes sense in theory, there’s a problem: the facts don’t back it up.

Evidence in medical literature suggests approximately 80 per cent of people with normal blood pressure (that is, a reading of below 120 over 80) do not suffer any signs of raised blood pressure — none at all — when they increase their salt intake.

Among those with prehypertension, or higher blood pressure, three quarters are not sensitive to salt. And even among those with full-blown high blood pressure, more than half — about 55 per cent — are totally immune to salt’s effects.

The dangerous myth that salt raises blood pressure began more than 100 years ago, with French scientists Ambard and Beauchard. They based their findings on studies of just six patients.

Successive researchers misinterpreted and misused their data, building on a theory that earned media attention without any solid foundation in fact.

In the early Fifties, at Brookhaven National Laboratory in New York, Dr Lewis Dahl was determined to make science fit his own preconceptions.

A man of ‘strong convictions’, he was a proponent of racial theories that claimed Japanese people had high levels of hypertension while Inuit tribes did not — and that this was due to the amount of salt in their diets.

He proposed to prove this with experiments on rodents. However, as even Dr Dahl was obliged to concede, normal rats are not sensitive to salt. It does nothing to their blood pressure.

So he decided to selectively modify them through in-breeding over several generations to create what are now known as ‘Dahl salt-sensitive rats’.

That’s right: Dahl created salt-sensitive rats in a lab and then used them to prove his hypothesis that salt affected blood pressure.

Dahl popularised the notion that salt is nothing but a flavouring we add to food. He cited medical studies that, he claimed, were proof humans could survive on a quarter of the recommended levels.

But a closer look at the papers he promoted is alarming: one 1945 experiment into a low-salt diet may have killed people.

One patient placed on a restricted salt regime died soon afterwards, and another sustained circulatory collapse, due to inadequate supplies of oxygen and nutrients to the tissues — a classic symptom of salt deprivation.

One of Dahl’s most dramatic experiments involved giving human baby food with high salt content to his special salt-sensitive rats. It killed them, which Dahl proclaimed as proof that baby food could be lethal for human infants, too.

Of course, human babies are much larger than rats, and the salt-sensitive rats had been genetically engineered to suffer from hypertension.

But based partly on this research, the Committee on Nutrition at the American Academy of Paediatrics concluded that infants were consuming too much sodium, and manufacturers began to lower the salt content in all kinds of food.

The link between high blood pressure and salt was established in the public mind, on the most spurious of pretexts.

But this misinformation did not take hold worldwide. The average Korean, for instance, eats over 4g of sodium a day. They feast on tteokguk, a broth-based soup full of salt, and bulgogi, grilled meat marinated in a sea of sodium-packed soy sauce. They eat kimchi — cabbage preserved in salt — with every meal.

Yet Koreans have some of the world’s lowest rates for hypertension, coronary heart disease and death due to cardiovascular disease. This is known as the ‘Korean Paradox’. South Korea also has one of the lowest death rates from coronaries in the world, along with Japan and France.

What do people from these three countries have in common? They all eat a very high-salt diet.

The Mediterranean diet, too, widely recommended as heart-healthy, is not exactly low in salt — think of all those anchovies and sardines. Even where blood pressure does increase, the benefits of a higher salt intake — a lower heart rate, reduced insulin levels, more balanced adrenal hormones and better kidney function — are likely to outweigh any risks.

Low salt intake has several side-effects that magnify our risk of heart disease, such as increased heart rate, compromised kidney function, underactive thyroid glands, heightened insulin levels — a risk factor for diabetes — as well as heightened cholesterol.

All through lack of salt. This white crystal that has been unfairly demonised for many decades is diverting blame from the real culprit of these illnesses.

High blood pressure, cardiovascular disease and chronic kidney disease can all be caused by the real health hazard, excessive consumption of sugar.

We all need salt to live. But you could go the rest of your life, and probably extend its span, if you never ingested another gram of added sugar.

It is extraordinary that no food advertisement or leaflet in your GP’s surgery ever tells you that a low-salt diet doesn’t just increase your risk of an elevated heart rate, it practically guarantees it. This harmful effect occurs in nearly everyone who restricts salt intake.

The damage done by an average increase of four heartbeats a minute is compounded by other salt-related stresses inflicted on our bodies by modern life.

We lose salt by following fashionable diets such as low-carb regimes. Some medications cause salt loss. Intestinal problems including Crohn’s disease, ulcerative colitis, irritable bowel syndrome and leaky gut also decrease salt absorption.

And kidney damage from refined carbs and sugar will reduce those organs’ capacity to retain salt.

We may discover that low-salt guidelines have created more heart disease than they ever prevented.

They may even have been a contributing factor in the greatest public health challenge of our time: the rising epidemic of diabetes, caused in part by an increasingly common, yet little-known, phenomenon called ‘internal starvation’.

To understand this, we need to begin by looking at the obesity epidemic. The conventional explanation for this is an imbalance between the consumption of calories and our expenditure of energy — in other words, we eat more than we burn off. We’re told to eat less and move more, though it’s obvious this strategy isn’t working for everyone.

Consuming too little salt can set into motion an unfortunate cascade of changes that result in insulin resistance, an increase in sugar cravings, an out-of-control appetite and ultimately internal starvation, sometimes known as hidden cellular semi-starvation, which promotes weight gain.

Someone who appears massively overweight on the outside may be literally starving on the inside.

When you start restricting your salt intake, your body will do anything to try to hold on to it.

Unfortunately, one of its main defence mechanisms is to increase insulin levels, which it does by becoming more resistant to insulin itself. The body is then less able to shuttle glucose into cells.

That means more and more insulin is secreted to control blood glucose. This keeps the body’s stored fat and protein reserves locked away. The fat cannot be converted into energy. To make matters worse, salt restriction also stimulates hormones such as renin, angiotensin and aldosterone. They help retain the ebbing salt levels, but they also increase the absorption of fat.

So a low-salt diet doesn’t just force the body to pile on fat, but prevents it from being burned off. No wonder ‘Eat Less Move More’ can make no difference for some.

It gets worse. If you slash salt intake dramatically, you could also develop an iodine deficiency, since salt is our best source of iodine. We need iodine for proper thyroid function, without which the metabolic rate may slow down.

A slower metabolic rate results in the body storing more fat, particularly in the organs, which in turn promotes insulin resistance. Once again, weight gain results.

Plus, low-salt diets increase the risk of overall dehydration. That’s a problem because well-hydrated cells consume less energy.

Dehydrated cells leave you feeling exhausted, which encourages you to consume more calories — which are immediately translated into weight gain.

Exercise now seems unappealing. Your body cannot access its stored energy and so the brain switches into conservation mode, trying to hang on to every calorie.

Even though weight is piling on, every function in the body is behaving as though it’s fighting to survive a full-scale famine.

So how much salt should you be eating? Many healthy people needn’t worry about overloading. The body takes care of any excess. Research suggests the optimal range for healthy adults is between 3g and 6g of sodium a day — about one-and-a-third to two-and-two-thirds of a teaspoon of salt.

Listen to your body. It has a built-in ‘salt thermostat’, an interconnected set of brain sensors that monitor sodium supplies in an effort to avoid activating those starvation hormones.

And your brain would much prefer that you simply eat salt rather than having to scavenge it from vulnerable parts of the body.

So next time you feel a craving for salt, do yourself a favour and give in to it. Your body says these things for a reason.

Drop the guilt — not the salt.

Source: The Daily Mail


Read also:

Nutrient Reference Values for Australia and New Zealand – Sodium . . . . .

World Health Organization – Salt Reduction . . . . .

Sodium and Heart Health

Bridget M. Kuehn wrote . . . . . . .

Low-salt diets have been a mainstay of treatment for patients with heart conditions and hypertension, but emerging evidence suggests potential harms to this approach.

A growing body of observational data has suggested there may be potential harms to salt restriction. As a result, some groups such at the World Heart Federation have recommended moderate rather than low levels of salt intake. But the data are complex, and many questions remain that only randomized trials can answer definitively.

This is particularly true for patients with heart failure. Some studies have found increased mortality or poor nutritional status for patients with heart failure consuming a low-salt diet. Gold standard clinical trial data are lacking to verify this correlation, although some trials are underway.

“What we know is a lot less than we think we know,” said Scott Hummel, MD, MS, an assistant professor of cardiovascular medicine at the University of Michigan and director of the heart failure program at the Ann Arbor Veterans Affairs Health System.

Some observational studies have suggested that low-salt intake may be associated with a poor health outcome for patients with heart failure. Now, some randomized trials have been launched to provide more definitive answers.

The Skinny on Salt

Much of the evidence supporting a low-salt diet stems from studies that demonstrate that lowering sodium intake can help reduce hypertension, explained Andrew Mente, PhD, associate professor in Health Research Methods, Evidence, and Impact at McMaster University in Ontario, Canada. But more recent data from studies in the general population have not found a benefit to lowering sodium for people without elevated blood pressure.

“We believed that lower was better,” Mente explained. “It doesn’t quite work that way. For people without hypertension who are generally healthy, eating a normal amount of salt has a minimal effect on blood pressure.”

Data from the Framingham Study published in the Journal of the Federation of American Societies for Experimental Biology in April that analyzed the blood pressure and dietary intakes of 2632 people aged 30 to 64 with normal blood pressures found that individuals with the lowest blood pressures actually had higher intakes of both sodium and potassium, whereas those with low sodium and potassium intakes tended to have higher blood pressure.

“These long-term data from the Framingham Study provide no support for lowering sodium intake among healthy adults to 5 g/d reduce their intake, according to a January report in the European Heart Journal.

Data from observational studies find that both very high sodium consumption >5 g/d and very low sodium intake are associated with an elevated risk of heart attack, stroke, and death, Mente noted. Those individuals who fall in the middle, consuming 3 to 5 g of sodium per day, a fairly typical amount for a Western diet, seem to fare best, he said.

“We find that there is actually a sweet spot for sodium, where being in the middle tends to be optimal,” Mente said.

One reason lowering salt too much may be harmful is that it activates the renin-angiotensin system triggering the production of hormones that could have harmful cardiovascular effects, Mente explained.

Although the observational data are concerning, there is wide agreement that randomized trials are needed to provide definitive data. There is always a possibility that factors associated with salt intake and not salt itself might be responsible for the trends seen in the observational studies. For example, people who are very ill and at risk for poor outcomes may have poor nutritional status overall, including less intake of salt and many other nutrients, as well. This may give the impression in observational data that low-salt intake is associated with worse outcomes.

“To settle the debate, what we need is a large, long-term randomized trial comparing low sodium (<2 g/d) with the usual intake (of ≈3.5 g/d) in the general population,” Mente suggested.

Until more randomized trial data are available, Mente suggested clinicians recommend moderate sodium levels in the 3- to 3.5-g/d range. “Right now, a more cautious approach would be appropriate,” he said.

Salt and Heart Failure

There is an urgent need for clinical trials of salt restriction in patients with heart conditions, in particular, studies that can help clinicians better understand the risks and benefits of this intervention for patients with heart failure.

“It’s hard for people to follow a low-salt diet, but it is thought it might be physiologically helpful for (patients with heart failure),” explained Hummel.

The aim of sodium restriction in this population is to reduce fluid retention, and the current target recommended by the Heart Failure Society of America falls into the low-to-moderate range of 2 to 3 g/d.

But several studies have identified potential harms of low sodium consumption among patients with heart failure, including higher mortality, longer hospitalizations, and higher rates of readmission.

One potential reason for harm is activation of the renin-angiotensin and sympathetic nervous systems, noted Hummel. However, contemporary treatment regimens for patients with heart failure include drugs that would block these effects. He noted that some of the studies that found harm used older treatment regimens and prolonged high diuretic doses.

“You have to adjust the treatments patients are receiving to their physiological state,” Hummel explained. He noted that preliminary results from the pilot phase of a trial called SODIUM HF (Study of Dietary Intervention Under 100 mmol in Heart Failure) that adjusted diuretics and other patient medications found beneficial effects of sodium restriction on patient quality of life and B-type natriuretic peptide levels.

Hummel and his colleagues identified another potential explanation for sodium restriction–related harms in a study they presented at the American College of Cardiology Meeting in March. When they assessed the diets of 37 elderly patients with heart failure on hospital admission, they found that patients who reported low-sodium intake ate fewer calories overall and had micronutrient deficiencies, confirming the results previous studies.

“It doesn’t necessarily mean people shouldn’t eat a low-sodium diet,” Hummel said. “But when you recommend a low-sodium diet, some people take that as I should eat less of everything.”

The results suggest that clinicians may need to pay closer attention to their patient’s overall nutritional status.

“We’ve been focused on dietary sodium for so long, and that may be important, but there are probably a lot of other important aspects of diet we are not paying attention to.”

To better understand the role of diet and salt in heart failure, he and his colleagues are wrapping up their GOURMET-HF study (Geriatric Out of Hospital Randomized Meal Trial in Heart Failure). The trial randomly assigned 66 patients discharged from the hospital after treatment for heart failure to either home-delivered meals that are low sodium and compliant with the DASH (Dietary Approaches to Stop Hypertension) diet or to usual dietary advice. They hope the trial will yield more information on how to boost patients’ quality of life, and will analyze biomarker data to look for potential signs of harm.

Until more data are available, Hummel says he typically recommends a lower sodium intake between 2 and 3 g/d to his patients with appropriate medication adjustments and monitors their overall nutrition status. He expects that even with these recommendations most will end up at ≈3 to 3.5 g/d. He also often refers patients to a dietician who can help them to develop a nutritious lower-sodium diet that takes into account their own food preferences.

“What we know is that one size does not fit all,” Hummel said. “What makes sense for a treatment plan 1 day may not be the same the next day. You have to keep assessing your patients and deciding what is appropriate.”

Source: Circulation

Mediterranean-style Diet with Lean, Unprocessed Red Meat Reduces Cardiovascular Disease Risks

Adopting a Mediterranean-style eating pattern improves heart health, with or without reducing red meat intake, if the red meat consumed is lean and unprocessed, according to a Purdue University nutrition study.

“This study is important because it shows that red meat can be part of a heart-healthy eating pattern like a Mediterranean-style eating pattern,” said Wayne W. Campbell, professor of nutrition science. “This study was not designed to promote red meat intake, and we are not encouraging people who otherwise consume a vegetarian-style eating pattern to begin consuming red meat.”

The study is published online at the American Journal of Clinical Nutrition. It was funded by the Beef Checkoff and the Pork Checkoff, with support from the National Institutes of Health’s Indiana Clinical and Translational Sciences Institute and a National Institutes of Health pre-doctoral training grant through the Ingestive Behavior Research Center at Purdue.

“Most healthy eating pattern recommendations include a broad statement to reduce red meat intake,’” said Lauren E. O’Connor, lead author and recent doctoral degree recipient. “Our study compared Mediterranean-style eating patterns with red meat intake that is typical in the United States, about 3 ounces per day, versus a commonly recommended intake amount that is 3 ounces twice per week. Overall, heart health indicators improved with both Mediterranean-style eating patterns. Interestingly, though, participants’ LDL cholesterol, which is one of the strongest predictors we have to predict the development of cardiovascular disease, improved with typical but not lower red meat intake.”

The study assessed the health-promoting effects of a Mediterranean-style eating pattern, without intended weight loss, for adults who are overweight and at risk for developing heart disease. All 41 study participants – 28 females and 13 males – completed three study phases. The phases included a five-week period of consuming a Mediterranean-style eating pattern containing three ounces per day of lean, unprocessed red meat, an amount of red meat the typical United States resident consumes; a five-week return to their regular eating pattern; and a five-week period of consuming a Mediterranean-style eating pattern with less red meat, three ounces twice weekly, which is commonly recommended for heart health. The order of the typical and lower red meat interventions were randomly assigned among participants.

“It’s also very encouraging that the improvements these people experienced – which included improvements in blood pressure, blood lipids and lipoproteins – were noticeable in five weeks,” Campbell said.

The Mediterranean-style eating pattern, which was ranked No. 1 by Consumer Reports, is recommended by the Dietary Guidelines for Americans. A Mediterranean-style eating pattern has clinically proven effects on health especially related to heart health and risks for heart disease such as heart attack or stroke.

“The composition of a Mediterranean-style eating pattern varies across countries and cultures,” Campbell said. “What is common across most Mediterranean regions is consumption of olive oil, fruit, vegetables and legumes, but protein sources depend on what country and geographic region. If they live on the coast, they will eat more seafood, but if they live inland they will eat more red meat.”

Source: Purdue University


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Study: Millions of Americans May be Getting the Wrong Treatment to Prevent Heart Attack or Stroke

Serena Gordon wrote . . . . . . . .

Prescriptions for blood-thinning aspirin, cholesterol-lowering statins and blood pressure medications might be incorrect because a tool that estimates risk appears to be off by as much as 20 percent, Stanford University researchers reported.

That means almost 12 million Americans could have the wrong medication, according to the team led by Dr. Sanjay Basu, an assistant professor of medicine.

It appears medications are overprescribed in many cases. But for black patients, outdated risk calculations may actually underestimate risk, the study authors said.

Risk estimate tools predict the likelihood of a future heart attack or stroke in the next 10 years. Doctors use these tools to help them decide what treatment a patient needs, if any at all.

But these tools are only helpful if they’re accurate. There’s been concern that some of the statistical methods used to develop a commonly used risk estimate tool in 2013 may be prone to miscalculating risk.

“What initially prompted us to do this study was a patient I had, an African-American gentleman who I thought was at pretty high risk for a heart attack or stroke. But when I put his information into the web calculator, it returned a bizarrely low-risk estimate,” explained Basu.

When he looked into this issue, Basu said he saw other doctors commenting on the problem. And it seemed as if the risk estimates were both over- and underestimated.

The study authors cited the example of a 46-year-old white male smoker with normal blood pressure and abnormal cholesterol levels. The risk estimate tool said this man would have about an 11 percent risk of a heart attack or stroke resulting from plaque buildup in the arteries in the next 10 years.

When the researchers used the same information but changed his race to black, the tool dropped the risk to less than 7 percent. That would mean that being black lowered the man’s risk of a heart attack or stroke by 40 percent. Yet past research suggests that being black raises — not reduces — the risk of heart attack and stroke.

Basu said the risk calculator assesses age, gender, race, whether or not people have diabetes, high blood pressure or abnormal cholesterol, and if they smoke tobacco.

Dr. Andrew DeFilippis, who wrote an editorial accompanying the study, said the 2013 risk tool uses information from research studies done decades ago.

DeFilippis is an associate professor of medicine at the University of Louisville.

Basu said using more recent data is one way to boost accuracy. When he and his colleagues updated the statistical modeling, they produced what they feel is a more accurate estimation.

However, Basu said this new risk estimation calculator needs to be validated by other researchers to ensure its accuracy. To that end, the researchers have made their statistical models and calculations available to anyone on the internet.

But if those initial calculations were off by 20 percent, potentially affecting 11.8 million people, where does that leave patients?

“If you’re concerned, the most important thing to do is to talk to your doctor. Risk calculation is one of many factors that go into the decision about treatment. I’m more concerned about people who may have been given false assurances,” Basu said.

DeFilippis concurred. “No one is saying this is a recipe you have to follow. For most clinicians it’s a starting point. This is one tool we use to try to balance the risks of therapy with the potential benefit,” he said.

“People who are at very low risk or very high risk are unlikely to get a different answer, but people who were borderline are the ones who may get a different answer,” DeFilippis said.

Findings from the study were released online in the Annals of Internal Medicine.

Source: HealthDay


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