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29 April 2011

Popular Drink Increases Stroke Risk

In a study of 2564 people of varying ethnic backgrounds, researchers at Columbia University in New York and the Miller School of Medicine in Miami found a significant correlation between diet soda consumption and the risk of stroke.

Begun in 1993, the Northern Manhattan Study known as NOMAS has been ongoing and still continues. Researchers divided people into seven groups: those who drank less than one soda of any type per month, those with moderate soda consumption (up to six per week), daily regular soda consumption (one or more daily), moderate diet soda only, daily diet soda only, moderate diet soda and sometimes regular soda, and daily diet soda with any regular soda consumption.

Scientists factored in the age, ethnicity, gender, exercise habits, smoking status, alcohol consumption, and caloric intake. During the test period participants had 559 strokes combined.

After considering all the other factors studied, researchers concluded that regular diet soda drinkers had a 48% increased chance of having a stroke, while those who drank diet soda every day had a 61% increased risk of stroke over those who drank other types of soda.

Concurrently, it is important to note that Diet Coke recently moved into the number two position of most popular beverage among Americans–a scary proposition considering the recent study findings.

The stroke culprit is likely aspartame, an artificial sweetener that has been linked to dozens of other health conditions. According to Lynne Melcombe, author of Health Hazards of White Sugar, research links aspartame to the following health conditions: anxiety attacks; appetite problems such as binge-eating and sugar cravings; birth defects; blindness and vision problems such as blurred vision, bright flashes, and tunnel vision; brain tumors; chest pain; depression and emotional problems; dizziness and vertigo; edema; epilepsy and seizures; fatigue; headaches and migraines; hearing loss and tinnitus; heart palpitations and arrhythmia; hyperactivity; insomnia; joint pain; learning disabilities; memory loss; menstrual irregularities and PMS (premenstrual syndrome); muscle cramps; nausea; numbness of extremities; psychiatric disorders; reproductive problems; skin lesions; slurred speech; and uterine tumors. Research even links aspartame to death. Aspartame’s effects can be mistaken for Alzheimer’s disease, chronic fatigue syndrome, epilepsy, Epstein-Barr virus, Huntington’s chorea, hypothyroidism, Lou Gehrig’s disease; Lyme disease, Ménière’s disease, multiple sclerosis, and postpolio syndrome.

According to Randall Fitzgerald, author of The Hundred-Year Lie, some of the cancers linked to aspartame include: brain, liver, lung, kidney, and lymphoreticular cancer.

26 April 2011

Bacterial Ecosystems Divide People Into 3 Groups, Scientists Say

Correction Appended
In the early 1900s, scientists discovered that each person belonged to one of four blood types. Now they have discovered a new way to classify humanity: by bacteria. Each human being is host to thousands of different species of microbes. Yet a group of scientists now report just three distinct ecosystems in the guts of people they have studied.

Blood type, meet bug type.

“It’s an important advance,” said Rob Knight, a biologist at the University of Colorado, who was not involved in the research. “It’s the first indication that human gut ecosystems may fall into distinct types.”

The researchers, led by Peer Bork of the European Molecular Biology Laboratory in Heidelberg, Germany, found no link between what they called enterotypes and the ethnic background of the European, American and Japanese subjects they studied.

Nor could they find a connection to sex, weight, health or age. They are now exploring other explanations. One possibility is that the guts, or intestines, of infants are randomly colonized by different pioneering species of microbes.

The microbes alter the gut so that only certain species can follow them.

Whatever the cause of the different enterotypes, they may end up having discrete effects on people’s health. Gut microbes aid in food digestion and synthesize vitamins, using enzymes our own cells cannot make.

Dr. Bork and his colleagues have found that each of the types makes a unique balance of these enzymes. Enterotype 1 produces more enzymes for making vitamin B7 (also known as biotin), for example, and Enterotype 2 more enzymes for vitamin B1 (thiamine).

The discovery of the blood types A, B, AB and O had a major effect on how doctors practice medicine. They could limit the chances that a patient’s body would reject a blood transfusion by making sure the donated blood was of a matching type. The discovery of enterotypes could someday lead to medical applications of its own, but they would be far down the road.

“Some things are pretty obvious already,” Dr. Bork said. Doctors might be able to tailor diets or drug prescriptions to suit people’s enterotypes, for example.

Or, he speculated, doctors might be able to use enterotypes to find alternatives to antibiotics, which are becoming increasingly ineffective. Instead of trying to wipe out disease-causing bacteria that have disrupted the ecological balance of the gut, they could try to provide reinforcements for the good bacteria. “You’d try to restore the type you had before,” he said.

Dr. Bork notes that more testing is necessary. Researchers will need to search for enterotypes in people from African, Chinese and other ethnic origins. He also notes that so far, all the subjects come from industrial nations, and thus eat similar foods. “This is a shortcoming,” he said. “We don’t have remote villages.”

The discovery of enterotypes follows on years of work mapping the diversity of microbes in the human body — the human microbiome, as it is known. The difficulty of the task has been staggering. Each person shelters about 100 trillion microbes.

(For comparison, the human body is made up of only around 10 trillion cells.) But scientists cannot rear a vast majority of these bacteria in their labs to identify them and learn their characteristics.

As genetics developed, scientists learned how to study the microbiome by analyzing its DNA. Scientists extracted DNA fragments from people’s skin, saliva and stool. They learned how to recognize and discard human DNA, so that they were left with genes from the microbiome. They searched through the remaining DNA for all the variants of a specific gene and compared them with known species. In some cases, the variants proved to be from familiar bacteria, like E. coli. In other cases, the gene belonged to a species new to science.

These studies offered glimpses of a diversity akin to a rain forest’s. Different regions of the body were home to different combinations of species. From one person to another, scientists found more tremendous variety. Many of the species that lived in one person’s mouth, for example, were missing from another’s.

Scientists wondered if deeper studies would reveal a unity to human microbiomes. Over the past few years, researchers have identified the genomes — the complete catalog of genes — of hundreds of microbe species that live in humans. Now they can compare any gene they find with these reference genomes.

They can identify the gene’s function, and identify which genus of bacteria the microbe belongs to. And by tallying all the genes they find, the scientists can estimate how abundant each type of bacteria is.

In the recent work, Dr. Bork and his team carried out an analysis of the gut microbes in 22 people from Denmark, France, Italy and Spain. Some of their subjects were healthy, while others were obese or suffered from intestinal disorders like Crohn’s disease. Dr. Bork and his colleagues searched for fragments of DNA corresponding to the genomes of 1,511 different species of bacteria. The researchers combined their results with previous studies of 13 Japanese individuals and 4 Americans.

The scientists then searched for patterns. “We didn’t have any hypothesis,” Dr. Bork said. “Anything that came out would be new.”

Still, Dr. Bork was startled by the result of the study: all the microbiomes fell neatly into three distinct groups.

And, as Dr. Bork and his colleagues reported on Wednesday in the journal Nature, each of the three enterotypes was composed of a different balance of species. People with type 1, for example, had high levels of bacteria called Bacteroides. In type 2, on the other hand, Bacteroides were relatively rare, while the genus Prevotella was unusually common.

“You can cut the data in lots of different ways, and you still get these three clusters,” Dr. Bork said.

Dr. Bork and his colleagues found confirmation of the three enterotypes when they turned to other microbiome surveys, and the groups continue to hold up now that they have expanded their own study to 400 people.

25 April 2011

Consumption of polyunsaturated fatty acids, fish, and nuts and risk of inflammatory disease mortality

Background: n–3 (omega-3) Polyunsaturated fatty acids (PUFAs), fish, and nuts can regulate inflammatory processes and responses.

Objective: We investigated whether dietary intakes of PUFAs [n−3, n–6 (omega-6), and α-linolenic acid], fish, and nuts were associated with 15-y mortality attributed to noncardiovascular, noncancer inflammatory diseases.

Design: The analyses involved 2514 participants aged ≥49 y at baseline. Dietary data were collected by using a semiquantitative food-frequency questionnaire, and PUFA, fish, and nut intakes were calculated. Inflammatory disease mortality was confirmed from the Australian National Death Index.

Results: Over 15 y, 214 subjects died of inflammatory diseases. Women in the highest tertiles of total n−3 PUFA intake, compared with those in the lowest tertile of intake at baseline, had a 44% reduced risk of inflammatory disease mortality (P for trend = 0.03). This association was not observed in men. In both men and women, each 1-SD increase in energy-adjusted intake of α-linolenic acid was inversely associated with inflammatory mortality (hazard ratio: 0.83; 95% CI: 0.71, 0.98). Subjects in the second and third tertiles of nut consumption had a 51% and 32% reduced risk of inflammatory disease mortality, respectively, compared with those in the first tertile (reference). Dietary intakes of long-chain n−3 and n−6 PUFAs and fish were not associated with inflammatory disease mortality.

Conclusions: We report on a novel link between dietary intake of total n−3 PUFA and risk of inflammatory disease mortality in older women. Furthermore, our data indicate a protective role of nuts, but not fish, against inflammatory disease mortality.

21 April 2011

Is Sugar Toxic?

On May 26, 2009, Robert Lustig gave a lecture called “Sugar: The Bitter Truth,” which was posted on YouTube the following July. Since then, it has been viewed well over 800,000 times, gaining new viewers at a rate of about 50,000 per month, fairly remarkable numbers for a 90-minute discussion of the nuances of fructose biochemistry and human physiology.

Lustig is a specialist on pediatric hormone disorders and the leading expert in childhood obesity at the University of California, San Francisco, School of Medicine, which is one of the best medical schools in the country. He published his first paper on childhood obesity a dozen years ago, and he has been treating patients and doing research on the disorder ever since.

The viral success of his lecture, though, has little to do with Lustig’s impressive credentials and far more with the persuasive case he makes that sugar is a “toxin” or a “poison,” terms he uses together 13 times through the course of the lecture, in addition to the five references to sugar as merely “evil.” And by “sugar,” Lustig means not only the white granulated stuff that we put in coffee and sprinkle on cereal — technically known as sucrose — but also high-fructose corn syrup, which has already become without Lustig’s help what he calls “the most demonized additive known to man.”

It doesn’t hurt Lustig’s cause that he is a compelling public speaker. His critics argue that what makes him compelling is his practice of taking suggestive evidence and insisting that it’s incontrovertible. Lustig certainly doesn’t dabble in shades of gray. Sugar is not just an empty calorie, he says; its effect on us is much more insidious. “It’s not about the calories,” he says. “It has nothing to do with the calories. It’s a poison by itself.”

If Lustig is right, then our excessive consumption of sugar is the primary reason that the numbers of obese and diabetic Americans have skyrocketed in the past 30 years. But his argument implies more than that. If Lustig is right, it would mean that sugar is also the likely dietary cause of several other chronic ailments widely considered to be diseases of Western lifestyles — heart disease, hypertension and many common cancers among them.

The number of viewers Lustig has attracted suggests that people are paying attention to his argument. When I set out to interview public health authorities and researchers for this article, they would often initiate the interview with some variation of the comment “surely you’ve spoken to Robert Lustig,” not because Lustig has done any of the key research on sugar himself, which he hasn’t, but because he’s willing to insist publicly and unambiguously, when most researchers are not, that sugar is a toxic substance that people abuse. In Lustig’s view, sugar should be thought of, like cigarettes and alcohol, as something that’s killing us.

This brings us to the salient question: Can sugar possibly be as bad as Lustig says it is?

It’s one thing to suggest, as most nutritionists will, that a healthful diet includes more fruits and vegetables, and maybe less fat, red meat and salt, or less of everything. It’s entirely different to claim that one particularly cherished aspect of our diet might not just be an unhealthful indulgence but actually be toxic, that when you bake your children a birthday cake or give them lemonade on a hot summer day, you may be doing them more harm than good, despite all the love that goes with it. Suggesting that sugar might kill us is what zealots do. But Lustig, who has genuine expertise, has accumulated and synthesized a mass of evidence, which he finds compelling enough to convict sugar. His critics consider that evidence insufficient, but there’s no way to know who might be right, or what must be done to find out, without discussing it.

If I didn’t buy this argument myself, I wouldn’t be writing about it here. And I also have a disclaimer to acknowledge. I’ve spent much of the last decade doing journalistic research on diet and chronic disease — some of the more contrarian findings, on dietary fat, appeared in this magazine —– and I have come to conclusions similar to Lustig’s.

High blood pressure? Maybe not

High blood pressure is a serious problem. It raises your risk for heart trouble… and it can raise your insurance rates, too. Once you’ve been labeled with this problem, it stays on your medical records for good. And it can haunt you like the infamous “Scarlet Letter.”

That’s why it’s so important to get an accurate blood pressure reading – and a true one. But a common problem has left untold thousands – possibly millions – thinking they have high blood pressure when they actually don’t.

The problem is called “white coat syndrome.”

White coat syndrome is simply feeling tense and nervous at the doctor’s office… which raises your blood pressure to a level that’s above normal. When the doctor or nurse takes your blood pressure, this abnormally high reading is what goes into your record.

You could even wind up taking medications you don’t need… for a problem you don’t really have.

A recent Spanish study points out just how widespread this problem is.

The researchers looked at 8,295 people with high blood pressure that didn’t seem to respond to blood pressure pills. Because they didn’t seem to respond to medications, they were all taking at least three different drugs to lower their blood pressure.
In the doctor’s office, their blood pressure read at least 140/90… even with all the drugs. The average reading was 161/88.

Then researchers tested the subjects’ blood pressure periodically over 24 hours – as they went about a normal day. Their average blood pressure reading was significantly lower – 134/75. In fact, more than a third – 37% – actually had normal blood pressure readings.(1)

In other words, almost 4 out of every 10 of these people were receiving aggressive treatments they really didn’t need. They were just tense or nervous at the doctor’s office. (And who isn’t?)

So how do you avoid white coat syndrome? Here are a few tips…

Don’t let the nurse or doctor take your blood pressure immediately after bringing you into the examining room. You should be able to sit quietly for a few minutes before they take a reading. And be sure to sit in a chair – not on the examining table.

Sit comfortably, leaning against the backrest. Both your feet should be flat on the floor. Your arm shouldn’t be hanging limply at your side when the nurse takes a reading. It should be supported – on a table or armrest – at heart level.

The cuff is also important. When it comes to blood pressure cuffs, one size does not fit all. The cuff should be fitted to the size of your arm. And it should be on bare skin, not wrapped around your shirtsleeve.

If the first reading is high, ask to have a second reading taken after a few minutes of quiet. Your blood pressure may also measure differently in your other arm.

All of these steps can help lower your readings to more normal levels. But there’s one other step that’s even better.

Monitor your blood pressure at home.

Modern home blood pressure monitors are easy to use, reasonably priced… and the best way to be sure you don’t fall victim to white coat syndrome. If you check your own blood pressure regularly, you’ll know immediately if your doctor’s reading is out of line.

Is Your Peanut Butter Full of Carcinogens?

we’re learning more about our foods—ingredient by ingredient—and sometimes what we discover isn’t pretty. Sometimes it isn’t even clear. Such is the case with peanut butter and the carcinogen aflatoxin. This cancer-causing chemical is produced by naturally-occurring fungus in the soil, where foods like peanuts are grown. Peanuts, unlike hard-shelled nuts, are encased in a rather soft, porous shell, which allows for contaminants like the fungus to take hold. Is peanut butter carcinogenic? Read on.

The chemical aflatoxin has been shown to cause liver cancer in developing countries where there is a large consumption of corn, peanuts and grains grown without strict regulation of the quality of soil—yet it hasn’t been proven to be a cancer-causing agent in the United States... as far as we know. Yet for individuals who are susceptible to cancer or already have compromised liver function, the issue of peanuts may be one to get familiar with.

Interestingly enough, natural peanut butters may contain more aflatoxins than commercially-processed brands like Skippy. And the “grind-your-own” peanut butter machines you see in health food stores may be the most likely culprit for containing the carcinogen, since they “sit around” the longest without refrigeration, allowing any fungus present to multiply—and these machines aren’t tested for their aflatoxin levels. One shouldn’t be discouraged from buying organic peanut butters—rather, always refrigerate your peanut butter, especially if organic, and even when not, to ensure any undetectable mold doesn’t grow inside your jar.

Currently, all commercially-produced peanut butters, whether organic or not, must be tested for levels of aflatoxin. Some claim that conventional peanut butters contain lower levels of aflatoxin, whereas companies like Whole Foods Market advertise their products to be far below national standards. Yet proponents of commercial, conventional peanut butters like Skippy are missing something—these non-organic brands still have a contamination issue of a different name: pesticides. As stated earlier, peanuts have a very light, porous shell that allows for easy leaching of outside materials into the peanut. And conventionally-grown peanuts have an alarmingly high rate of pesticides and other chemical contamination.

The bottom line when it comes to peanut butter and your health: Buy organic to prevent pesticide contamination. Refrigerate your jar to prevent fungal growth. And if you’re particularly concerned about aflatoxins, buy from top-notch natural brands like Arrowhead Mills, which claim to be completely aflatoxin-free.

For an Exercise Afterburn, Intensity May Be the Key

Depending on whom you ask, the answer to this question is either one of the great myths of exercise or one of the great unappreciated truths: Is there an afterburn effect from a workout?

Whether the metabolism speeds up for hours after exercise an old question, first studied a century ago, and over the years, study after study has been carried out, with decidedly mixed results. Some investigators found no post-exercise effect. Others reported effects so small they were almost unnoticeable — one found male triathletes burned just 12 to 30 extra calories after a workout. Others found as many as 700 additional calories were burned after a long and exhausting exercise session.

The latest sally comes in a recent paper in the journal Medicine & Science in Sports & Exercise. Its lead author, Amy A. Knab of Appalachian State University, says it trumps studies that preceded it because of its careful design. And its results are good news — sort of.

Dr. Knab and her colleagues recruited 10 men, ages 22 to 33, who agreed to spend two periods of 24 hours each in a metabolic chamber, a small room that measures the calories people burn while they are inside. The men were not all athletes, but they did have to be able to ride a bike vigorously.

On the first visit to the chamber, the subjects had to stay perfectly still, sitting in a chair and moving only to eat meals, which were sent in through an air lock. In the afternoon, they were permitted a two-minute stretch every hour. Bedtime was 10:30 p.m. At 6:30 the next morning, the subjects were awakened and allowed to leave. They burned, on average, 2,400 calories on this totally sedentary day.

The second visit to the chamber came two days later. Everything was the same, with one exception. At 11 a.m., the subjects rode a stationary bicycle at a high intensity for 45 minutes.

The exercise itself burned about 420 calories, Dr. Knab and her colleagues reported. But what was most interesting was the calories burned afterward. Over the next 14 hours, the men burned an extra 190 calories, increasing the total calories burned by 37 percent.

“We were surprised,” Dr. Knab said. She thought there might be extra calories burned, but she did not expect so many, nor did she expect the effect to last so long.

She suspects one reason she saw such a pronounced effect was that the exercise was so intense. The subjects had had to cycle at 70 percent of their so-called VO2 max, the maximum amount of oxygen a person’s body can take in during exercise — an effort that made them breathe too heavily to carry on a conversation. And they had to keep it up for 45 minutes.

A different study, also using a metabolic chamber, tested the effects of moderate exercise and found no afterburn. Those subjects exercised at 50 percent of their VO2 max, a level that still allows conversation.

Claude Bouchard, a scientist at the Pennington Biomedical Research Center in Baton Rouge, La., along with other researchers, investigated the exercise effect with conventional methods using a mouthpiece and nose clip or a ventilated hood to determine oxygen used and carbon dioxide exhaled. From those measures, researchers can calculate calories burned.

They find, he says, that when studies are done properly (many are not), extra calories are burned in the hours after exercise — but only if subjects exercise at least as hard and long as Dr. Knab’s subjects. And if they exercise even harder, they burn even more calories afterward.

A recent book that Dr. Bouchard and a colleague edited notes two studies that found this effect. The researchers found that if subjects ran at 70 percent of their VO2 max or cycled at 75 percent of it, they could burn 300 to 700 extra calories after the exercise was over, though 700 calories was unusual.

It is not clear why extra calories should be burned after a bout of intense exercise, Dr. Bouchard says. Part of the effect may be due to post-exercise energy metabolism: the body starts using more fat and less carbohydrate after a hard exercise session. Several hormones that are released during exercise remain elevated in the blood afterward, increasing metabolism. And extra calories may be burned when the body replenishes glycogen, the sugar stored in muscles. But for the most part, the effect remains a mystery.

Whatever the cause, researchers say, the extra calories burned after exercise can help people lose weight. Unfortunately, those who may have the most to lose may have the hardest time doing the sort of exercise that gives them a calorie-burning bonus.

The usual guideline for general health is 30 minutes of moderate exercise most days of the week. That’s doable for most people and should increase heart health, even if it provides no calorie bonus.

But that sort of moderate exercise, Dr. Bouchard said, “is what we recommend — that’s the target.”

Coming Soon? Whey Protein Soft Drinks

The beverage industry, for those of you who aren’t aware, is a multi-billion dollar business. Whether it’s fruit juice, soda pop, or bottled water, consumers spend a lot of money on hydration every day. Beverage marketers spend gazillions advertising their products. It’s competitive as hell too. What’s amazing is that there are continually new innovations in the field.

We covered one such splashy (pun intended) product launch a few days ago. If you’ve been following Fooducate for a while, you know we are not fans of this industry. Tap water is where we’d like to see more people turn to. It’s healthier for you and the planet.

So each time we hear about new beverage trends and products, we shudder a bit.

What’s the upcoming buzz? Drinks “fortified” with whey protein. From the Beverage Industry website:

In 2010, performance beverages, juices, beverage mixes, enhanced waters, meal replacement drinks and even teas launched with whey protein included. Innovations such as Kellogg’s Special K2O Protein Water Mixes and Bolthouse Farms Protein Plus All Natural Protein Shakes have taken whey protein out of just the performance arena and beverage-makers continue to expand its use.

Promising scientific research is being conducted as well with whey protein focusing on several of its bioactive components that can offer protection against infections and viruses, enhance immunity, protect against some cancers and positively affect cardiovascular health and muscle tone, says Gwen Bargetzi, Hilmar Ingredients’ director of marketing.

What you need to know:

Whey protein comes from whey. Whey is the liquid part of milk that is left over when it coagulates into a cheese. The liquid whey is not very appetizing, but when dried, and after fats have been removed, the remaining powder is what we know as whey protein.

Bodybuilders have been adding whey protein to shakes for ages. The proteins in whey are quickly made available to muscles. The use of whey protein has trickled over to other fitness enthusiasts, and you can find whey protein in many energy bars.

But the big breakthrough comes when products and ingredients that make it to the big leagues – mainstream consumers.

So, will we be seeing a “Whey fortified Tropicana OJ” anytime soon? How about a “Pepsi Whey-back” ?

Broccoli helps clear damaged lungs

Here's another reason to eat your greens. As well as helping to prevent cancer, broccoli may also help the immune system to clean harmful bacteria from the lungs. A compound found in the vegetable is now being trialled as a treatment for people with lung disease.

To ensure that the lungs function correctly, white blood cells called macrophages remove debris and bacteria that can build up in the lungs and cause infection.

This cleaning system is defective in smokers and people with chronic obstructive pulmonary disease (COPD) – a combination of emphysema and bronchitis – who suffer from frequent infections.

Now, researchers have figured out that a chemical pathway in the lungs called NRF2, involved in macrophage activation, is wiped out by smoking. They also found that sulphoraphane, a plant chemical that is made by broccoli, cauliflower and other cruciferous vegetables when damaged, such as when chewed, can restore this pathway.

Service restored
Shyam Biswal at Johns Hopkins University in Baltimore, Maryland, and colleagues, exposed defective macrophages from the lungs of 43 people with COPD to two bacterial strains that are common causes of COPD-associated infections.

In the presence of sulphoraphane, the NRF2 pathway was boosted and the macrophages' ability to recognise and engulf bacteria was restored.

The researchers then exposed mice to smoke for one week or six months. Both groups were found to have increased bacterial colonisation of the lungs, similar to that seen in COPD. After treating the mice with sulphoraphane, they found that bacterial clearance increased. Rather than activate more macrophages, sulphoraphane appeared to improve the functionality of the cells already present.

Good greens
Sulphoraphane is present in broccoli in its precursor form and is converted to the active compound by enzymes present in saliva and intestinal bacteria, says Christopher Harvey, co-author of the research.

The levels of enzyme vary between people, and it would therefore be expected that the dose of sulphoraphane obtained by dietary consumption would vary between people too. Further human studies are required to establish beneficial effects of a sulforaphane-rich diet on immune defenses, he says.

Biswal's team has started phase 2 clinical trials to test the compound in people with COPD to see if it improves their lung function, but says it will be three years before they have results. "There are many diseases that have defective lung function as a result of increased bacterial function in the lungs," he says, "so this study can be extrapolated to those diseases too."

The Claim: To Reduce Snoring, Try Sleeping on Your Side

Chronic snoring can be more than a noisy nuisance. Up to three-quarters of nightly snorers also have sleep apnea, which causes breathing interruptions throughout the night. Sleep apnea raises the risk of heart disease, stroke and high blood pressure.

Snorers looking for a cure are often told to sleep on their sides, not on their backs, so that the base of the tongue will not collapse into the back of the throat, narrowing the airway and obstructing breathing. But for some snorers, changing sleep position may not make much of a difference.

Scientists say there are two types of snorers: those who snore only when they sleep on their backs, and those who do it regardless of their position. After sleep researchers in Israel examined more than 2,000 sleep apnea patients, for example, they found that 54 percent were “positional,” meaning they snored only when asleep on their backs. The rest were “nonpositional.”

Other studies have shown that weight plays a major role. In one large study, published in 1997, patients who snored or had breathing abnormalities only while sleeping on their backs were typically thinner, while their nonpositional counterparts usually were heavier. The latter group, wrote the authors, consequently suffered worse sleep and more daytime fatigue.

But that study also found that patients who were overweight saw reductions in the severity of their apnea when they lost weight. According to the National Sleep Foundation, in people who are overweight, slimming down is generally the best way to cure sleep apnea and end snoring for good.

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