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More than a year after California revised its flame retardant standards so that new furniture (the polyurethane foam in upholstered sofas, sofa beds, and chairs) does not have to use flame retardants, it is still hard to find out whether the furniture is flame retardant free. This is what I have experienced in the last few months - the store doesn't know and the manufacturer won't respond to emails.

The new furniture label should say TB 117-2013 , and then you still need to ask the retailer if there are flame retardants in the upholstered furniture. The new label means that the manufacturer does NOT have to use flame retardant chemicals anymore, but it does NOT mean they are chemical free. And flame retardants are still found in many baby products (car seats, bumpers, crib mattresses, strollers, nursing pillows, etc), some personal care products, and electronics. It's a buyer beware situation.

More and more research is finding health problems with flame retardants because they are "not chemically bound" to the products in which they are used - thus they escape over time, and get into us via the skin (dermal), inhalation (from dust), and ingestion (from certain foods and dust on our fingers). And because flame retardants are persistant, they bioaccumulate (they build up over time). They can be measured in our urine and blood.

Evidence suggests that flame retardants may be endocrine disruptors, carcinogenic, alter hormone levels, decrease semen quality in men, thyoid disruptors, and act as developmental neurotoxicants (when developing fetus is exposed during pregnancy)  so that children have lowered IQ and more hyperactivity behaviors.

How does one know if the foam in your furniture has flame retardants in it? Duke University will test it for free if you send them a small piece of the furniture's foam. http://sites.nicholas.duke.edu/superfund/whats-in-my-foam/ I originally read about this service a few months ago in The Atlantic,

From The Atlantic: How to Test a Couch for Toxins

It began with a smell. Kerri Duntley had just bought a pair of large, cream-colored couches....As the scent continued to fill her living room, Duntley asked herself a troubling question: What was causing the couches to smell like industrial chemicals? The answers weren’t easy to find. Duntley searched in web forums and even tried contacting the couches’ manufacturer. “I called and called and called,” she said. “They just would not give me the information.” She grew frustrated and began looking for new couches. It was then that she discovered an unusual service run by a Duke University lab.

The lab’s offer was simple. First, the lab instructed, wield a pair of scissors. Grab something made with polyurethane foam—say, a mattress or the innards of a couch cushion. Cut a small chunk from the foam. Wrap the surgical work in tinfoil, ziplock seal it and mail the crime-scene-looking evidence off to Durham, North Carolina. Wait up to 45 days, the lab said, and it’ll arrive: a report detailing toxic flame retardants embedded in the foam.

Duntley complied. When the results came back, she learned that her couch sample had tested positive for two flame retardants, including one that has proven harmful in animal studies, a finding that she called heartbreaking. Her experience points to a vast gap in safety information about consumer goods. With the U.S. government’s limited power to regulate chemicals, many consumers, like Duntley, are left to piece together their own crude health-risk assessments. That fabric softener? It may smell like the Elysian Fields, but what if its unlisted ingredients cause cancer? 

Government officials , academic researchers, the chemical industry and environmentalists agree: The U.S. system of chemical regulation is broken. But while the fight over reform continues in Washington, consumers remain blind to many of the chemicals that enter their homes.

Duke’s service is looking in its small way to change that. The lab—which offers anyone a free chemical analysis of polyurethane foam—has informed hundreds of Americans about their furniture’s toxicity. At the same time, the foam samples have given Duke’s team a large bank of crowdsourced research. By offering a free service to an anxious public, Duke’s scientists are gaining a clearer view of chemical manufacturing. And they’re learning just how much we don’t know about the chemicals that enter our homes.

Stapleton was part of a scientific cohort that found ingesting dust—say, getting our dusty hands on a burger—is by far our largest source of exposure to flame retardants; flame retardants aren’t chemically bound to their products, and so they attach themselves to airborne dust.

But what began in California soon became a de facto national standard, since furniture companies didn’t want to manufacture separate lines. Stapleton was interested to see how chemically saturated our furniture really is. So she and her colleagues asked families for samples of their baby products’ foam. After reviewing 101 samples from across thirteen states, Stapleton’s 2011 study reached a startling conclusion: Flame retardants accounted for about 5 percent of the products’ weight, and the chemicals were found in 80 percent of the samples.

Some of the chemicals were carcinogens. Others were from a chemical class known as polybrominated diphenyl ethers, or PBDEs, which have been linked to lower IQ scores, attention deficit hyperactivity disorder, and thyroid disorders. The most common flame retardant among the samples was tris (1,3-dichloroisopropyl)phosphate, or TDCPP, which researchers say is likely to harm the neurological development of infants. TDCPP, in fact, was used throughout the 1970s in children’s pajamas, until critical health research led manufacturers in 1977 to stop using it. Yet the chemical had reemerged in products like strollers and baby mattresses.

The lab offered to test some of these strangers’ furniture for free. But the requests kept coming. That’s when Stapleton and her colleagues decided to expand the scope of the testing and conceived of a free service for the public. They’d test anyone’s polyurethane foam for a suite of seven common flame retardants as something of a public service, since it would be funded by a federal grant (itself funded by taxpayer dollars). The service would also aid Stapleton’s research, offering a valuable stream of crowdsourced data about the chemicals used in furniture.

By crowdsourcing her research, Stapleton has also uncovered a flame retardant that academic literature has yet to identify. The flame retardant is a chlorinated organophosphate, like TDCPP, and its health effects are unknown, she said. Stapleton said that this recent discovery-by-accident followed the same pattern as her research on Firemaster 550, a popular flame retardant that replaced two widespread PBDEs after they were withdrawn from the market... But emerging research has raised concerns about Firemaster 550, too. One study from Boston University and Duke researchers found that the chemical mixture may cause obesity in humans. Stapleton found the same effect in rats.

Here is an article to what I referred to in my recent Feb. 27 Feast and Famine Diet post about intermittent fasting being beneficial to health and resulting in weight loss. This definitely seems easier than sticking to very low calorie diets weeks on end. From NPR:

Minifasting: How Occasionally Skipping Meals May Boost Health

If you've ever gone to sleep hungry and then dreamed of chocolate croissants, the idea of fasting may seem completely unappealing. But what if the payoff for a 16-hour fast — which might involve skipping dinner, save a bowl of broth — is a boost in energy and a decreased appetite?

This is what we've experienced as we've tried out the so-called 5:2 diet. It's an intermittent fasting approach that, as we've reported, has been popularized by books by British physician and television broadcaster Michael Mosley. The diet calls for two days per week of minifasting where the aim is to go a long stretch, say 14 to 18 hours, without eating. During these two fasting days, you also eat only about 600 calories, give or take. But here's the easy part: The other five days of the week you forget about dieting and return to your normal pattern of eating.

The fascination is what researchers say may be the broader benefits. Scientists are looking into how fasting may help control blood sugar, improve memory and energy and perhaps boost immunity. A study by researchers at the University of Manchester found that when overweight women followed a 5:2 approach, they lost more weight and body fat and improved their insulin resistance compared with women who followed a more traditional diet of limiting calories seven days per week.

One explanation for the success of the 5-2 dieters could be that a day of minifasting can lead to a diminished appetite. As Allison reports on All Things Considered, she found that she's just less hungry the day after a fast.

Mark Mattson, a researcher at the National Institute of Aging, says when we go without food, the body uses up its stored glucose, the basic fuel for the body, and starts burning fat....During fasting, he says, fat can convert to compounds called ketones, "which have beneficial effects in making neurons more resistant to injury and disease.

There may be an evolutionary explanation for this because humans (and other animals) have fasted intermittently for much of our time on Earth, after all. As a recent paper in the Proceedings of the National Academy of Sciences notes, "The most common eating pattern in modern societies, three meals plus snacks every day, is abnormal from an evolutionary perspective."

Longo and other experts gave Eliza some of their other tips on how to do it right: - Fasting is easier with a buddy. - On a minifast, choose the food you do eat carefully. Researchers recommend high-protein, high-fiber foods. Avoid refined carbs and sugar, which will spike blood sugar and may leave you hungry late in the day. - To minimize temptation, stay out of the kitchen and away from food establishments. - Try a pattern of weekly intermittent fasting for at least a month. Studies have shown that a long-term lifestyle change (and the benefits associated with it) is more likely for people who can stick with the diet for at least a month. And tolerating some hunger gets easier the longer you do it. - Don't be surprised if there are some side effects, like trouble sleeping or gastrointestinal issues.

Of course some foods are addictive. Anyone who tries to eat just one french fry or one piece of chocolate or one potato chip knows that it's very, very hard to do that. Do people have raw carrot cravings? Nah... Chocolate cravings? Yup..Does this research really tell us anything new? From Science Daily:

Want pizza, chocolate, French fries? Highly processed foods linked to addictive eating

A new University of Michigan study confirms what has long been suspected: highly processed foods like chocolate, pizza and French fries are among the most addictive.

This is one of the first studies to examine specifically which foods may be implicated in "food addiction," which has become of growing interest to scientists and consumers in light of the obesity epidemic.Previous studies in animals conclude that highly processed foods, or foods with added fat or refined carbohydrates (like white flour and sugar), may be capable of triggering addictive-like eating behavior. Clinical studies in humans have observed that some individuals meet the criteria for substance dependence when the substance is food.

Unprocessed foods, with no added fat or refined carbohydrates like brown rice and salmon, were not associated with addictive-like eating behavior.

Individuals with symptoms of food addiction or with higher body mass indexes reported greater problems with highly processed foods, suggesting some may be particularly sensitive to the possible "rewarding" properties of these foods, said Erica Schulte, a U-M psychology doctoral student and the study's lead author...."This is a first step towards identifying specific foods, and properties of foods, which can trigger this addictive response," she said. "This could help change the way we approach obesity treatment. It may not be a simple matter of 'cutting back' on certain foods, but rather, adopting methods used to curtail smoking, drinking and drug use.

A variation of this study - intermittent fasting (one day eat normally, then have a low-calorie day, repeat) has shown to result in health benefits and weight loss. But both versions show that having some low calorie days are beneficial to health. And once again, antioxidants do not have any health benefits. From Science Daily:

Feast-and-famine diet could help extend life, study suggests

University of Florida Health researchers have found that putting people on a feast-or-famine diet may mimic some of the benefits of fasting, and that adding antioxidant supplements may counteract those benefits.

Fasting has been shown in mice to extend lifespan and to improve age-related diseases. But fasting every day, which could entail skipping meals or simply reducing overall caloric intake, can be hard to maintain..."We started thinking about the concept of intermittent fasting.

Michael Guo, a UF M.D.-Ph.D. student who is pursuing the Ph.D. portion of the program in genetics at Harvard Medical School, said the group measured the participants’ changes in weight, blood pressure, heart rate, glucose levels, cholesterol, markers of inflammation and genes involved in protective cell responses over 10 weeks.“We found that intermittent fasting caused a slight increase to SIRT 3, a well-known gene that promotes longevity and is involved in protective cell responses,” Guo said.

The SIRT3 gene encodes a protein also called SIRT3. The protein SIRT3 belongs to a class of proteins called sirtuins. Sirtuins, if increased in mice, can extend their lifespans, Guo said. Researchers think proteins such as SIRT3 are activated by oxidative stress, which is triggered when there are more free radicals produced in the body than the body can neutralize with antioxidants. However, small levels of free radicals can be beneficial: When the body undergoes stress -- which happens during fasting -- small levels of oxidative stress can trigger protective pathways, Guo said. “The hypothesis is that if the body is intermittently exposed to low levels of oxidative stress, it can build a better response to it,” Wegman said.

The researchers found that the intermittent fasting decreased insulin levels in the participants, which means the diet could have an anti-diabetic effect as well.

The group recruited 24 study participants in the double-blinded, randomized clinical trial. During a three-week period, the participants alternated one day of eating 25 percent of their daily caloric intake with one day of eating 175 percent of their daily caloric intake. For the average man’s diet, a male participant would have eaten 650 calories on the fasting days and 4,550 calories on the feasting days. To test antioxidant supplements, the participants repeated the diet but also included vitamin C and vitamin E.

At the end of the three weeks, the researchers tested the same health parameters. They found that the beneficial sirtuin proteins such as SIRT 3 and another, SIRT1, tended to increase as a result of the diet. However, when antioxidants were supplemented on top of the diet, some of these increases disappeared. This is in line with some research that indicates flooding the system with supplemental antioxidants may counteract the effects of fasting or exercise, said Christiaan Leeuwenburgh, Ph.D., co-author of the paper and chief of the division of biology of aging in the department of aging and geriatric research.“You need some pain, some inflammation, some oxidative stress for some regeneration or repair,” Leeuwenburgh said. 

On the study participants’ fasting days, they ate foods such as roast beef and gravy, mashed potatoes, Oreo cookies and orange sherbet -- but they ate only one meal. On the feasting days, the participants ate bagels with cream cheese, oatmeal sweetened with honey and raisins, turkey sandwiches, apple sauce, spaghetti with chicken, yogurt and soda -- and lemon pound cake, Snickers bars and vanilla ice cream.

Anecdotal evidence has been saying this for years.From Science Daily:

Keep calm, anger can trigger a heart attack!

The risk of a heart attack is 8.5 times higher in the two hours following a burst of intense anger, researchers have found after investigating the link between acute emotional triggers and high risk of severe cardiac episodes. High levels of anxiety were associated with a 9.5 fold increased risk of triggering a heart attack in the two hours after an anxiety episode.

"The data shows that the higher risk of a heart attack isn't necessarily just while you're angry -- it lasts for two hours after the outburst. In the study, 'anger' was qualified as 5 and above on a 1-7 scale, referring to 'very angry, body tense, clenching fists or teeth, ready to burst', up to 'enraged, out of control, throwing objects'. Anger below this level was not associated with increased risk. "The triggers for these burst of intense anger were associated with arguments with family members (29 per cent), argument with others (42 per cent), work anger (14 per cent) and driving anger (14 per cent)," said Dr Buckley.

"Increased risk following intense anger or anxiety is most likely due to increased heart rate, blood pressure, tightening of blood vessels and increased clotting, all associated with triggering heart attacks," he said.

The study was an investigation of consecutive patients suspected of heart attack and confirmed by angiography reports at Royal North Shore hospital. Patients confirmed with acute coronary blockage were admitted, interviewed about their activities in the 48 hours before the onset of symptoms, and usual frequencies of activities were recorded for comparison.

"Although the incidence of anger-triggered heart attacks is around 2%, of the sample, those people were 8.5 times more likely to have a heart attack within two hours of the emotional episode. So while the absolute risk of any one episode triggering a heart attack is low, this data demonstrates that the danger is very present.

Another study finding a benefit of coffee consumption - this time linked to a lower rate of MS. Keep in mind that numerous studies have shown a strong association of higher sunlight exposure (especially in childhood), and living at lower latitudes (more sunlight exposure) with lower rates of multiple sclerosis. From Science Daily:

Can coffee reduce your risk of MS?

Drinking coffee may be associated with a lower risk of developing multiple sclerosis (MS), according to a study released today that will be presented at the American Academy of Neurology's 67th Annual Meeting in Washington, DC, April 18 to 25, 2015."Caffeine intake has been associated with a reduced risk of Parkinson's and Alzheimer's diseases, and our study shows that coffee intake may also protect against MS, supporting the idea that the drug may have protective effects for the brain," said study author Ellen Mowry, MD, MCR, with Johns Hopkins University School of Medicine in Baltimore and a member of the American Academy of Neurology.

For the study, researchers looked at a Swedish study of 1,629 people with MS and 2,807 healthy people, and a U.S. study of 1,159 people with MS and 1,172 healthy people. The studies characterized coffee consumption among persons with MS one and five years before MS symptoms began (as well as 10 years before MS symptoms began in the Swedish study) and compared it to coffee consumption of people who did not have MS at similar time periods. The study also accounted for other factors such as age, sex, smoking, body mass index, and sun exposure habits.

The Swedish study found that compared to people who drank at least six cups of coffee per day during the year before symptoms appeared, those who did not drink coffee had about a one and a half times increased risk of developing MS. Drinking large amounts of coffee five or 10 years before symptoms started was similarly protective.

In the US study, people who didn't drink coffee were also about one and a half times more likely to develop the disease than those who drank four or more cups of coffee per day in the year before symptoms started to develop the disease.

This research suggests that emulsifiers (which are added to most processed foods to aid texture and extend shelf life) can alter the gut microbiota (the community of microbes that live in our gut) in such a way as to cause intestinal inflammation. Even though the study was done on mice, it is thought it also applies to humans. From Medical Daily:

You Are What You Eat: Food Additive Emulsifier Inflames Mouse Gut And Causes Obesity

Processed foods have changed the way we eat. Food can sit longer on shelves, but what does that mean for the stomach? In a new study published in the journal Nature, researchers from Georgia State University investigated how the widely used processed food additive emulsifiers played a role in the gut.

Emulsifiers are added to most processed foods in order to extend shelf life and add texture to the foods. The research team decided to feed mice a couple of the most common emulsifiers on the market — polysorbate 80 and carboxymethylcelluloseat doses comparable to a human’s consumption of processed foods. They watched the emulsifier change the mice’s gut microbiota, which is an individual’s personal 100 trillion bacteria inside the intestinal tract. Not only did this increase their chance of developing obesity-related disorders, but also inflammatory bowel disease. It’s no coincidence both conditions have been increasing since the 1950s.

"The dramatic increase in these diseases has occurred despite consistent human genetics, suggesting a pivotal role for an environmental factor," the study’s coauthor Benoit Chassaing, a researcher from GSU’s Institute for Biomedical Sciences, said in a press release. "Food interacts intimately with the microbiota, so we considered what modern additions to the food supply might possibly make gut bacteria more pro-inflammatory."

The emulsifiers, which are groups of oil-and water-friendly molecules, help to hold food together. Mayonnaise without emulsifiers, for example, will separate from an oily top layer to a thicker white layer that rests on the bottom of the jar. Once the emulsifiers were digested by the mice, their blood-glucose levels went awry, inflamed their intestinal mucus layer, which left them with weight gain, specifically concentrated in the abdomen. The bacterial changed triggered chronic colitis from causing intestinal inflammation and metabolic syndrome, which includes obesity, hyperglycemia, and insulin resistance.

Ultimately, microbiologists say you are what you eat. If your diet is smeared with margarine, mayonnaise, creamy sauces, candy, ice cream, and most other packaged and processed baked goods, you and your gut may be at risk. "We do not disagree with the commonly held assumption that over-eating is a central cause of obesity and metabolic syndrome," the study’s coauthor Andrew T. Gewirtz, a researcher from GSU’s Institute for Biomedical Sciences, said in a press release. "Rather, our findings reinforce the concept suggested by earlier work that low-grade inflammation resulting from an altered microbiota can be an underlying cause of excess eating."

It is surprising how beneficial short 30 minute naps are after sleep deprivation. From Medscape:

Napping Restores Immune System After Sleep Deprivation

Simply taking a couple of naps may counteract the impact of a sleep-restricted night on stress and immune markers, a finding that could potentially benefit night and shift workers or other chronically sleep-deprived populations, the results of a French study indicate.

Brice Faraut, PhD, from the Université Paris Descartes-Sorbonne Paris Cité, France, and colleagues found that, after a night with only 2 hours of sleep, taking two naps of just 30 minutes each appeared to normalize levels of cytokines and catecholamines.

"Napping as a countermeasure to sleep restriction could, in addition to benefits on alertness, improve neuroendocrine stress and immune recovery, with a potential prophylactic long-term effect on cardiovascular health," the researchers write.

They conducted their crossover, randomized study in which 11 healthy men aged between 25 and 32 years underwent two sessions of laboratory sleep testing in which their sleep–wake status, light environment, and caloric intake were strictly controlled.

In a "sleep-restriction" session, the participants slept for just 2 hours for one night after a baseline night of 8 hours of sleep, followed by a recovery night of sleeping. In the "sleep-restriction/nap" session, they repeated the protocol, but with two 30-minute naps after the sleep-restricted night. Salivary samples were taken every 2 hours and analyzed for interleukin (IL)-6 levels, an inflammatory cytokine known to have diurnal variations in concentration. In addition, urine samples were taken every 3 hours to measure levels of epinephrine, norepinephrine, and dopamine.

In the sleep-restricted session, there was a significant 2.5-fold increase in norepinephrine levels in the afternoon compared with the control day (P = .003). However, those differences were not seen when participants were able to take two 30-minute naps. No significant differences were seen either for epinephrine or dopamine, the researchers report.

After a sleep-restricted night, IL-6 levels were significantly lower at 10:00 am and 7:00 pm than levels measured at the same times after the control night's sleep (P = .01 and P = .05, respectively). Again, those differences were not observed when participants were able to take the two 30-minute naps.

Interestingly, daytime napping was associated with a significantly reduced amount of slow-wave sleep during the recovery night compared with sleep restriction alone (P = .01) and a trend toward decreased total sleep time."Our data suggest that napping has stress-releasing and immune effects," the researchers conclude.

Very exciting research. And it's the exact opposite advice that doctors used to tell parents - which was if there was a high risk for a specific allergy that ran in the family (peanuts, dogs, etc.) to have the young child try to avoid exposure to that item (or in the case of peanuts - until the age of 3). From NPR:

Feeding Babies Foods With Peanuts Appears To Prevent Allergies

Babies at high risk for becoming allergic to peanuts are much less likely to develop the allergy if they are regularly fed foods containing the legumes starting in their first year of life. That's according to a big new study released Monday involving hundreds of British babies. The researchers found that those who consumed the equivalent of about 4 heaping teaspoons of peanut butter each week, starting when they were between 4 and 11 months old, were about 80 percent less likely to develop a peanut allergy by their fifth birthday.

"This is certainly good news," says Gideon Lack of King's College London, who led the study. He presented the research at the annual meeting of the American Academy of Allergy, Asthma and Immunology. It was also published in The New England Journal of Medicine.

As many as 2 million U.S. children are estimated to be allergic to peanuts — an allergy that has been increasing rapidly in the United States, Britain and other countries in recent years. While most children who are allergic to peanuts only experience relatively mild symptoms, such as hives, some have life-threatening reactions that can include trouble breathing and heart problems.

Lack's study was launched after he noticed that Israeli kids are much less likely to have peanut allergies than are Jewish kids in Britain and the United States."My Israeli colleagues and friends and young parents were telling me, 'Look, we give peanuts to these children very early. Not whole peanuts, but peanut snacks,' " Lack says. Peanut snacks called Bamba, which are made of peanut butter and corn, are wildly popular in Israel, where parents give them to their kids when they're very young. That's very different from what parents do in Britain and the United States, where fears about food allergies have prompted many parents to keep their children away from peanuts, even though the American Academy of Pediatrics revised a recommendation to do so in 2008.

"That raised the question whether early exposure would prevent these allergies" by training babies' immune systems not to overreact to peanuts, Lack says. "It's really a very fundamental change in the way we're approaching these children." To try to find out, Lack and his colleagues got funding from the U.S. National Institutes of Health to launch a study. They found 640 babies who were at high risk for developing peanut allergies because they already had eczema or egg allergy. They asked half of the infants' parents to start feeding them Bamba, peanut butter, peanut soup or peanut in some other form before their first birthday and followed them for about five years.

"What we found was a very great reduction in the rate of peanut allergy," Lack says. About 17 percent of the kids who avoided peanuts developed peanut allergies, compared with only 3.2 percent of the kids who ate peanuts, the researchers reported.

Based on the findings, Lack thinks most parents should start feeding their babies peanut products as early as possible — not whole peanuts or globs of peanut butter, but peanut mixed in some other food to avoid any possible choking hazard."We've moved, really, 180 degrees from complete avoidance to we should give peanuts to young children actively," Lack says. Other allergy experts hailed the results as an important advance. "This is a major study — really what we would call a landmark study," says Scott Sicherer, who advises the American Academy of Pediatrics on allergies. 

This article raises serious questions about the recently published American College of Cardiology and American Heart Association calculators to predict future cardiovascular events (heart attack, strike, etc) which then give recommendations for who needs to take daily statins while they are still healthy. This calculator (ACC/AHA risk calculator) has sparked much debate because many experts believe it overestimates risk. Now a study that looked at untreated people (MESA) showed that the calculator (as well as 3 other calculators) seriously overpredict the chance of a future cardiovascular event. In other words, many, many healthy people told they "may" have a chance of an event in the future are actually not at risk and so statins would not help them, but may harm them. Remember, all medicines have side-effects. Written by cardiac electrophysiologist Dr. John Mandrola (who has his own blog-site www,drjohnm.org) . From Medscape:

Statins in Primary Prevention: Welcome to the Gray Zone

A new study published in the Annals of Internal Medicine confirmed something that ought to be obvious: predicting the future is hard—especially when it comes to cardiovascular events.

We know cardiovascular disease is the number-one killer of humans; we know its first manifestation is often heart attack, stroke, or death; and we know all medical therapy comes with trade-offs. Medical treatment of healthy people in the name of preventing something that may or may not happen in the future is dicey. Think do no harm. That is where risk prediction comes in. You have to know the odds of something (or nothing) happening without treatment. The gamble of statins and aspirin, for instance, looks most favorable in patients who are most likely to have an event.

 But where to draw that line, at what future risk is it worth taking a chemical, is the issue at hand. The extreme cases are easy. Most everyone agrees that statins and aspirin provide enough benefit in patients who have suffered a cardiovascular event. For secondary prevention, future risk is high, so benefits outweigh harms. It's the opposite in very low-risk patients. The middle ground is not so easy.

Here is where we have to consider the tools—calculators—to predict future risk. We know certain conditions, such as age, gender, blood pressure, diabetes, smoking, biomarkers, family history, and coronary calcium, contribute to future risk. Numerous expert panels, including the American College of Cardiology and American Heart Association, have compiled different calculators to predict the future. The ACC/AHA risk calculator for atherosclerotic CVD (ASCVD) has sparked debate because many experts believe it overestimates risk.

Dr Andrew DeFillippis (University of Louisville, KY) and a team of Multi-Ethnic Study of Atherosclerosis (MESA) coinvestigators used this community-based, sex-balanced, multiethnic cohort to compare the calibration and discrimination of the new ASCVD risk score with alternative risk scores.They compared the observed and expected events for the ASCVD score with three Framingham-based scores and the Reynolds risk score in 4227 MESA subjects aged 50 to 74 years over a 10-year follow-up. Using this real-world population, they found four of the five risk scores overestimated risk. Calibration was worse in men: overestimates ranged from 37% to 154%. In women, three of four scores overestimated risk by 46% to 67%, and the Reynolds Risk score underestimated risk by 21%. 

It's worth saying this another way: when the ACC/AHA ASCVD score predicted event rates of 7.5 to 10%—a range deemed above the statin-benefit cutoff—the actual events were just 3%.

Speaking by phone (we live in the same city), lead author Dr DeFillippis explained to me the important business of looking only at untreated patients. He described their sensitivity analysis, which excluded all patients who received aspirin or any lipid-lowering or antihypertensive drug. To lessen the chance of bias, they analyzed this drug-free group of 790 patients separately and found the same overprediction.The authors concluded that if these findings are validated, overestimation of ASCVD risk may have substantial implications for individual patients and the healthcare system.

On that modern theme, Dr DeFillippis made an interesting point to me about the overall best-performing Reynolds Risk score. He noted the Reynolds score uses genetics (family history) and CRP (inflammation) levels to predict the future. Bookmark that for the future—genetics and inflammation, that is.

These findings have major implications. Drugs are not free. Aspirin and statins come with side effects and dollar costs. The patient who takes these drugs in hopes of preventing future events makes the gamble that the costs are worth the benefit. Policy makers who recommend these drugs expose millions of people to a therapy that turns on delicate balance between future benefit and harm.

The final point to make is that the use of statins and other drugs for the prevention of future events is not a doctor's or professional society's decision. The human being who swallows a drug must ultimately decide whether the gamble is favorable.