Is Sugar Toxic?

Paul — Mon, 16 May 2011 00:54:05 +0000

Kenji Aoki for The New York Times

Thanks To a client of mine, Ryan Gray, we have been brought aware of this great article. Thanks Ryan! I hope you all get as much out of it as Ryan and I did!!

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.

What the average American consumes in added sugars:

High-Fructose Corn Syrup Consumption

Sugar Consumption

Kenji Aoki for The New York Times

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.

The history of the debate over the health effects of sugar has gone on far longer than you might imagine. It is littered with erroneous statements and conclusions because even the supposed authorities had no true understanding of what they were talking about. They didn’t know, quite literally, what they meant by the word “sugar” and therefore what the implications were.

So let’s start by clarifying a few issues, beginning with Lustig’s use of the word “sugar” to mean both sucrose — beet and cane sugar, whether white or brown — and high-fructose corn syrup. This is a critical point, particularly because high-fructose corn syrup has indeed become “the flashpoint for everybody’s distrust of processed foods,” says Marion Nestle, a New York University nutritionist and the author of “Food Politics.”

This development is recent and borders on humorous. In the early 1980s, high-fructose corn syrup replaced sugar in sodas and other products in part because refined sugar then had the reputation as a generally noxious nutrient. (“Villain in Disguise?” asked a headline in this paper in 1977, before answering in the affirmative.) High-fructose corn syrup was portrayed by the food industry as a healthful alternative, and that’s how the public perceived it. It was also cheaper than sugar, which didn’t hurt its commercial prospects. Now the tide is rolling the other way, and refined sugar is making a commercial comeback as the supposedly healthful alternative to this noxious corn-syrup stuff. “Industry after industry is replacing their product with sucrose and advertising it as such — ‘No High-Fructose Corn Syrup,’ ” Nestle notes.

But marketing aside, the two sweeteners are effectively identical in their biological effects. “High-fructose corn syrup, sugar — no difference,” is how Lustig put it in a lecture that I attended in San Francisco last December. “The point is they’re each bad — equally bad, equally poisonous.”

Refined sugar (that is, sucrose) is made up of a molecule of the carbohydrate glucose, bonded to a molecule of the carbohydrate fructose — a 50-50 mixture of the two. The fructose, which is almost twice as sweet as glucose, is what distinguishes sugar from other carbohydrate-rich foods like bread or potatoes that break down upon digestion to glucose alone. The more fructose in a substance, the sweeter it will be. High-fructose corn syrup, as it is most commonly consumed, is 55 percent fructose, and the remaining 45 percent is nearly all glucose. It was first marketed in the late 1970s and was created to be indistinguishable from refined sugar when used in soft drinks. Because each of these sugars ends up as glucose and fructose in our guts, our bodies react the same way to both, and the physiological effects are identical. In a 2010 review of the relevant science, Luc Tappy, a researcher at the University of Lausanne in Switzerland who is considered by biochemists who study fructose to be the world’s foremost authority on the subject, said there was “not the single hint” that H.F.C.S. was more deleterious than other sources of sugar.

The question, then, isn’t whether high-fructose corn syrup is worse than sugar; it’s what do they do to us, and how do they do it? The conventional wisdom has long been that the worst that can be said about sugars of any kind is that they cause tooth decay and represent “empty calories” that we eat in excess because they taste so good.

By this logic, sugar-sweetened beverages (or H.F.C.S.-sweetened beverages, as the Sugar Association prefers they are called) are bad for us not because there’s anything particularly toxic about the sugar they contain but just because people consume too many of them.

Those organizations that now advise us to cut down on our sugar consumption — the Department of Agriculture, for instance, in its recent Dietary Guidelines for Americans, or the American Heart Association in guidelines released in September 2009 (of which Lustig was a co-author) — do so for this reason. Refined sugar and H.F.C.S. don’t come with any protein, vitamins, minerals, antioxidants or fiber, and so they either displace other more nutritious elements of our diet or are eaten over and above what we need to sustain our weight, and this is why we get fatter.

Whether the empty-calories argument is true, it’s certainly convenient. It allows everyone to assign blame for obesity and, by extension, diabetes — two conditions so intimately linked that some authorities have taken to calling them “diabesity” — to overeating of all foods, or underexercising, because a calorie is a calorie. “This isn’t about demonizing any industry,” as Michelle Obama said about her Let’s Move program to combat the epidemic of childhood obesity. Instead it’s about getting us — or our children — to move more and eat less, reduce our portion sizes, cut back on snacks.

Lustig’s argument, however, is not about the consumption of empty calories — and biochemists have made the same case previously, though not so publicly. It is that sugar has unique characteristics, specifically in the way the human body metabolizes the fructose in it, that may make it singularly harmful, at least if consumed in sufficient quantities.

The phrase Lustig uses when he describes this concept is “isocaloric but not isometabolic.” This means we can eat 100 calories of glucose (from a potato or bread or other starch) or 100 calories of sugar (half glucose and half fructose), and they will be metabolized differently and have a different effect on the body. The calories are the same, but the metabolic consequences are quite different.

The fructose component of sugar and H.F.C.S. is metabolized primarily by the liver, while the glucose from sugar and starches is metabolized by every cell in the body. Consuming sugar (fructose and glucose) means more work for the liver than if you consumed the same number of calories of starch (glucose). And if you take that sugar in liquid form — soda or fruit juices — the fructose and glucose will hit the liver more quickly than if you consume them, say, in an apple (or several apples, to get what researchers would call the equivalent dose of sugar). The speed with which the liver has to do its work will also affect how it metabolizes the fructose and glucose.

In animals, or at least in laboratory rats and mice, it’s clear that if the fructose hits the liver in sufficient quantity and with sufficient speed, the liver will convert much of it to fat. This apparently induces a condition known as insulin resistance, which is now considered the fundamental problem in obesity, and the underlying defect in heart disease and in the type of diabetes, type 2, that is common to obese and overweight individuals. It might also be the underlying defect in many cancers.

If what happens in laboratory rodents also happens in humans, and if we are eating enough sugar to make it happen, then we are in trouble.

The last time an agency of the federal government looked into the question of sugar and health in any detail was in 2005, in a report by the Institute of Medicine, a branch of the National Academies. The authors of the report acknowledged that plenty of evidence suggested that sugar could increase the risk of heart disease and diabetes — even raising LDL cholesterol, known as the “bad cholesterol”—– but did not consider the research to be definitive. There was enough ambiguity, they concluded, that they couldn’t even set an upper limit on how much sugar constitutes too much. Referring back to the 2005 report, an Institute of Medicine report released last fall reiterated, “There is a lack of scientific agreement about the amount of sugars that can be consumed in a healthy diet.” This was the same conclusion that the Food and Drug Administration came to when it last assessed the sugar question, back in 1986. The F.D.A. report was perceived as an exoneration of sugar, and that perception influenced the treatment of sugar in the landmark reports on diet and health that came after.

The Sugar Association and the Corn Refiners Association have also portrayed the 1986 F.D.A. report as clearing sugar of nutritional crimes, but what it concluded was actually something else entirely. To be precise, the F.D.A. reviewers said that other than its contribution to calories, “no conclusive evidence on sugars demonstrates a hazard to the general public when sugars are consumed at the levels that are now current.” This is another way of saying that the evidence by no means refuted the kinds of claims that Lustig is making now and other researchers were making then, just that it wasn’t definitive or unambiguous.

What we have to keep in mind, says Walter Glinsmann, the F.D.A. administrator who was the primary author on the 1986 report and who now is an adviser to the Corn Refiners Association, is that sugar and high-fructose corn syrup might be toxic, as Lustig argues, but so might any substance if it’s consumed in ways or in quantities that are unnatural for humans. The question is always at what dose does a substance go from being harmless to harmful? How much do we have to consume before this happens?

When Glinsmann and his F.D.A. co-authors decided no conclusive evidence demonstrated harm at the levels of sugar then being consumed, they estimated those levels at 40 pounds per person per year beyond what we might get naturally in fruits and vegetables — 40 pounds per person per year of “added sugars” as nutritionists now call them. This is 200 calories per day of sugar, which is less than the amount in a can and a half of Coca-Cola or two cups of apple juice. If that’s indeed all we consume, most nutritionists today would be delighted, including Lustig.

But 40 pounds per year happened to be 35 pounds less than what Department of Agriculture analysts said we were consuming at the time — 75 pounds per person per year — and the U.S.D.A. estimates are typically considered to be the most reliable. By the early 2000s, according to the U.S.D.A., we had increased our consumption to more than 90 pounds per person per year.

That this increase happened to coincide with the current epidemics of obesity and diabetes is one reason that it’s tempting to blame sugars — sucrose and high-fructose corn syrup — for the problem. In 1980, roughly one in seven Americans was obese, and almost six million were diabetic, and the obesity rates, at least, hadn’t changed significantly in the 20 years previously. By the early 2000s, when sugar consumption peaked, one in every three Americans was obese, and 14 million were diabetic.

This correlation between sugar consumption and diabetes is what defense attorneys call circumstantial evidence. It’s more compelling than it otherwise might be, though, because the last time sugar consumption jumped markedly in this country, it was also associated with a diabetes epidemic.

In the early 20th century, many of the leading authorities on diabetes in North America and Europe (including Frederick Banting, who shared the 1923 Nobel Prize for the discovery of insulin) suspected that sugar causes diabetes based on the observation that the disease was rare in populations that didn’t consume refined sugar and widespread in those that did. In 1924, Haven Emerson, director of the institute of public health at Columbia University, reported that diabetes deaths in New York City had increased as much as 15-fold since the Civil War years, and that deaths increased as much as fourfold in some U.S. cities between 1900 and 1920 alone. This coincided, he noted, with an equally significant increase in sugar consumption — almost doubling from 1890 to the early 1920s — with the birth and subsequent growth of the candy and soft-drink industries.

Emerson’s argument was countered by Elliott Joslin, a leading authority on diabetes, and Joslin won out. But his argument was fundamentally flawed. Simply put, it went like this: The Japanese eat lots of rice, and Japanese diabetics are few and far between; rice is mostly carbohydrate, which suggests that sugar, also a carbohydrate, does not cause diabetes. But sugar and rice are not identical merely because they’re both carbohydrates. Joslin could not know at the time that the fructose content of sugar affects how we metabolize it.

Joslin was also unaware that the Japanese ate little sugar. In the early 1960s, the Japanese were eating as little sugar as Americans were a century earlier, maybe less, which means that the Japanese experience could have been used to support the idea that sugar causes diabetes. Still, with Joslin arguing in edition after edition of his seminal textbook that sugar played no role in diabetes, it eventually took on the aura of undisputed truth.

Until Lustig came along, the last time an academic forcefully put forward the sugar-as-toxin thesis was in the 1970s, when John Yudkin, a leading authority on nutrition in the United Kingdom, published a polemic on sugar called “Sweet and Dangerous.” Through the 1960s Yudkin did a series of experiments feeding sugar and starch to rodents, chickens, rabbits, pigs and college students. He found that the sugar invariably raised blood levels of triglycerides (a technical term for fat), which was then, as now, considered a risk factor for heart disease. Sugar also raised insulin levels in Yudkin’s experiments, which linked sugar directly to type 2 diabetes. Few in the medical community took Yudkin’s ideas seriously, largely because he was also arguing that dietary fat and saturated fat were harmless. This set Yudkin’s sugar hypothesis directly against the growing acceptance of the idea, prominent to this day, that dietary fat was the cause of heart disease, a notion championed by the University of Minnesota nutritionist Ancel Keys.

A common assumption at the time was that if one hypothesis was right, then the other was most likely wrong. Either fat caused heart disease by raising cholesterol, or sugar did by raising triglycerides. “The theory that diets high in sugar are an important cause of atherosclerosis and heart disease does not have wide support among experts in the field, who say that fats and cholesterol are the more likely culprits,” as Jane E. Brody wrote in The Times in 1977.

At the time, many of the key observations cited to argue that dietary fat caused heart disease actually support the sugar theory as well. During the Korean War, pathologists doing autopsies on American soldiers killed in battle noticed that many had significant plaques in their arteries, even those who were still teenagers, while the Koreans killed in battle did not. The atherosclerotic plaques in the Americans were attributed to the fact that they ate high-fat diets and the Koreans ate low-fat. But the Americans were also eating high-sugar diets, while the Koreans, like the Japanese, were not.

In 1970, Keys published the results of a landmark study in nutrition known as the Seven Countries Study. Its results were perceived by the medical community and the wider public as compelling evidence that saturated-fat consumption is the best dietary predictor of heart disease. But sugar consumption in the seven countries studied was almost equally predictive. So it was possible that Yudkin was right, and Keys was wrong, or that they could both be right. The evidence has always been able to go either way.

European clinicians tended to side with Yudkin; Americans with Keys. The situation wasn’t helped, as one of Yudkin’s colleagues later told me, by the fact that “there was quite a bit of loathing” between the two nutritionists themselves. In 1971, Keys published an article attacking Yudkin and describing his evidence against sugar as “flimsy indeed.” He treated Yudkin as a figure of scorn, and Yudkin never managed to shake the portrayal.

By the end of the 1970s, any scientist who studied the potentially deleterious effects of sugar in the diet, according to Sheldon Reiser, who did just that at the U.S.D.A.’s Carbohydrate Nutrition Laboratory in Beltsville, Md., and talked about it publicly, was endangering his reputation. “Yudkin was so discredited,” Reiser said to me. “He was ridiculed in a way. And anybody else who said something bad about sucrose, they’d say, ‘He’s just like Yudkin.’ ”

What has changed since then, other than Americans getting fatter and more diabetic? It wasn’t so much that researchers learned anything particularly new about the effects of sugar or high-fructose corn syrup in the human body. Rather the context of the science changed: physicians and medical authorities came to accept the idea that a condition known as metabolic syndrome is a major, if not the major, risk factor for heart disease and diabetes. The Centers for Disease Control and Prevention now estimate that some 75 million Americans have metabolic syndrome. For those who have heart attacks, metabolic syndrome will very likely be the reason.

The first symptom doctors are told to look for in diagnosing metabolic syndrome is an expanding waistline. This means that if you’re overweight, there’s a good chance you have metabolic syndrome, and this is why you’re more likely to have a heart attack or become diabetic (or both) than someone who’s not. Although lean individuals, too, can have metabolic syndrome, and they are at greater risk of heart disease and diabetes than lean individuals without it.

Having metabolic syndrome is another way of saying that the cells in your body are actively ignoring the action of the hormone insulin — a condition known technically as being insulin-resistant. Because insulin resistance and metabolic syndrome still get remarkably little attention in the press (certainly compared with cholesterol), let me explain the basics.

You secrete insulin in response to the foods you eat — particularly the carbohydrates — to keep blood sugar in control after a meal. When your cells are resistant to insulin, your body (your pancreas, to be precise) responds to rising blood sugar by pumping out more and more insulin. Eventually the pancreas can no longer keep up with the demand or it gives in to what diabetologists call “pancreatic exhaustion.” Now your blood sugar will rise out of control, and you’ve got diabetes.

Not everyone with insulin resistance becomes diabetic; some continue to secrete enough insulin to overcome their cells’ resistance to the hormone. But having chronically elevated insulin levels has harmful effects of its own — heart disease, for one. A result is higher triglyceride levels and blood pressure, lower levels of HDL cholesterol (the “good cholesterol”), further worsening the insulin resistance — this is metabolic syndrome.

When physicians assess your risk of heart disease these days, they will take into consideration your LDL cholesterol (the bad kind), but also these symptoms of metabolic syndrome. The idea, according to Scott Grundy, a University of Texas Southwestern Medical Center nutritionist and the chairman of the panel that produced the last edition of the National Cholesterol Education Program guidelines, is that heart attacks 50 years ago might have been caused by high cholesterol — particularly high LDL cholesterol — but since then we’ve all gotten fatter and more diabetic, and now it’s metabolic syndrome that’s the more conspicuous problem.

This raises two obvious questions. The first is what sets off metabolic syndrome to begin with, which is another way of asking, What causes the initial insulin resistance? There are several hypotheses, but researchers who study the mechanisms of insulin resistance now think that a likely cause is the accumulation of fat in the liver. When studies have been done trying to answer this question in humans, says Varman Samuel, who studies insulin resistance at Yale School of Medicine, the correlation between liver fat and insulin resistance in patients, lean or obese, is “remarkably strong.” What it looks like, Samuel says, is that “when you deposit fat in the liver, that’s when you become insulin-resistant.”

That raises the other obvious question: What causes the liver to accumulate fat in humans? A common assumption is that simply getting fatter leads to a fatty liver, but this does not explain fatty liver in lean people. Some of it could be attributed to genetic predisposition. But harking back to Lustig, there’s also the very real possibility that it is caused by sugar.

As it happens, metabolic syndrome and insulin resistance are the reasons that many of the researchers today studying fructose became interested in the subject to begin with. If you want to cause insulin resistance in laboratory rats, says Gerald Reaven, the Stanford University diabetologist who did much of the pioneering work on the subject, feeding them diets that are mostly fructose is an easy way to do it. It’s a “very obvious, very dramatic” effect, Reaven says.

By the early 2000s, researchers studying fructose metabolism had established certain findings unambiguously and had well-established biochemical explanations for what was happening. Feed animals enough pure fructose or enough sugar, and their livers convert the fructose into fat — the saturated fatty acid, palmitate, to be precise, that supposedly gives us heart disease when we eat it, by raising LDL cholesterol. The fat accumulates in the liver, and insulin resistance and metabolic syndrome follow.

Michael Pagliassotti, a Colorado State University biochemist who did many of the relevant animal studies in the late 1990s, says these changes can happen in as little as a week if the animals are fed sugar or fructose in huge amounts — 60 or 70 percent of the calories in their diets. They can take several months if the animals are fed something closer to what humans (in America) actually consume — around 20 percent of the calories in their diet. Stop feeding them the sugar, in either case, and the fatty liver promptly goes away, and with it the insulin resistance.

Similar effects can be shown in humans, although the researchers doing this work typically did the studies with only fructose — as Luc Tappy did in Switzerland or Peter Havel and Kimber Stanhope did at the University of California, Davis — and pure fructose is not the same thing as sugar or high-fructose corn syrup. When Tappy fed his human subjects the equivalent of the fructose in 8 to 10 cans of Coke or Pepsi a day — a “pretty high dose,” he says —– their livers would start to become insulin-resistant, and their triglycerides would go up in just a few days. With lower doses, Tappy says, just as in the animal research, the same effects would appear, but it would take longer, a month or more.

Despite the steady accumulation of research, the evidence can still be criticized as falling far short of conclusive. The studies in rodents aren’t necessarily applicable to humans. And the kinds of studies that Tappy, Havel and Stanhope did — having real people drink beverages sweetened with fructose and comparing the effect with what happens when the same people or others drink beverages sweetened with glucose — aren’t applicable to real human experience, because we never naturally consume pure fructose. We always take it with glucose, in the nearly 50-50 combinations of sugar or high-fructose corn syrup. And then the amount of fructose or sucrose being fed in these studies, to the rodents or the human subjects, has typically been enormous.

This is why the research reviews on the subject invariably conclude that more research is necessary to establish at what dose sugar and high-fructose corn syrup start becoming what Lustig calls toxic. “There is clearly a need for intervention studies,” as Tappy recently phrased it in the technical jargon of the field, “in which the fructose intake of high-fructose consumers is reduced to better delineate the possible pathogenic role of fructose. At present, short-term-intervention studies, however, suggest that a high-fructose intake consisting of soft drinks, sweetened juices or bakery products can increase the risk of metabolic and cardiovascular diseases.”

In simpler language, how much of this stuff do we have to eat or drink, and for how long, before it does to us what it does to laboratory rats? And is that amount more than we’re already consuming?

Unfortunately, we’re unlikely to learn anything conclusive in the near future. As Lustig points out, sugar and high-fructose corn syrup are certainly not “acute toxins” of the kind the F.D.A. typically regulates and the effects of which can be studied over the course of days or months. The question is whether they’re “chronic toxins,” which means “not toxic after one meal, but after 1,000 meals.” This means that what Tappy calls “intervention studies” have to go on for significantly longer than 1,000 meals to be meaningful.

At the moment, the National Institutes of Health are supporting surprisingly few clinical trials related to sugar and high-fructose corn syrup in the U.S. All are small, and none will last more than a few months. Lustig and his colleagues at U.C.S.F. — including Jean-Marc Schwarz, whom Tappy describes as one of the three best fructose biochemists in the world — are doing one of these studies. It will look at what happens when obese teenagers consume no sugar other than what they might get in fruits and vegetables. Another study will do the same with pregnant women to see if their babies are born healthier and leaner.

Only one study in this country, by Havel and Stanhope at the University of California, Davis, is directly addressing the question of how much sugar is required to trigger the symptoms of insulin resistance and metabolic syndrome. Havel and Stanhope are having healthy people drink three sugar- or H.F.C.S.-sweetened beverages a day and then seeing what happens. The catch is that their study subjects go through this three-beverage-a-day routine for only two weeks. That doesn’t seem like a very long time — only 42 meals, not 1,000 — but Havel and Stanhope have been studying fructose since the mid-1990s, and they seem confident that two weeks is sufficient to see if these sugars cause at least some of the symptoms of metabolic syndrome.

So the answer to the question of whether sugar is as bad as Lustig claims is that it certainly could be. It very well may be true that sugar and high-fructose corn syrup, because of the unique way in which we metabolize fructose and at the levels we now consume it, cause fat to accumulate in our livers followed by insulin resistance and metabolic syndrome, and so trigger the process that leads to heart disease, diabetes and obesity. They could indeed be toxic, but they take years to do their damage. It doesn’t happen overnight. Until long-term studies are done, we won’t know for sure.

One more question still needs to be asked, and this is what my wife, who has had to live with my journalistic obsession on this subject, calls the Grinch-trying-to-steal-Christmas problem. What are the chances that sugar is actually worse than Lustig says it is?

One of the diseases that increases in incidence with obesity, diabetes and metabolic syndrome is cancer. This is why I said earlier that insulin resistance may be a fundamental underlying defect in many cancers, as it is in type 2 diabetes and heart disease. The connection between obesity, diabetes and cancer was first reported in 2004 in large population studies by researchers from the World Health Organization’s International Agency for Research on Cancer. It is not controversial. What it means is that you are more likely to get cancer if you’re obese or diabetic than if you’re not, and you’re more likely to get cancer if you have metabolic syndrome than if you don’t.

This goes along with two other observations that have led to the well-accepted idea that some large percentage of cancers are caused by our Western diets and lifestyles. This means they could actually be prevented if we could pinpoint exactly what the problem is and prevent or avoid that.

One observation is that death rates from cancer, like those from diabetes, increased significantly in the second half of the 19th century and the early decades of the 20th. As with diabetes, this observation was accompanied by a vigorous debate about whether those increases could be explained solely by the aging of the population and the use of new diagnostic techniques or whether it was really the incidence of cancer itself that was increasing. “By the 1930s,” as a 1997 report by the World Cancer Research Fund International and the American Institute for Cancer Research explained, “it was apparent that age-adjusted death rates from cancer were rising in the U.S.A.,” which meant that the likelihood of any particular 60-year-old, for instance, dying from cancer was increasing, even if there were indeed more 60-years-olds with each passing year.

The second observation was that malignant cancer, like diabetes, was a relatively rare disease in populations that didn’t eat Western diets, and in some of these populations it appeared to be virtually nonexistent. In the 1950s, malignant cancer among the Inuit, for instance, was still deemed sufficiently rare that physicians working in northern Canada would publish case reports in medical journals when they did diagnose a case.

In 1984, Canadian physicians published an analysis of 30 years of cancer incidence among Inuit in the western and central Arctic. While there had been a “striking increase in the incidence of cancers of modern societies” including lung and cervical cancer, they reported, there were still “conspicuous deficits” in breast-cancer rates. They could not find a single case in an Inuit patient before 1966; they could find only two cases between 1967 and 1980. Since then, as their diet became more like ours, breast cancer incidence has steadily increased among the Inuit, although it’s still significantly lower than it is in other North American ethnic groups. Diabetes rates in the Inuit have also gone from vanishingly low in the mid-20th century to high today.

Now most researchers will agree that the link between Western diet or lifestyle and cancer manifests itself through this association with obesity, diabetes and metabolic syndrome — i.e., insulin resistance. This was the conclusion, for instance, of a 2007 report published by the World Cancer Research Fund and the American Institute for Cancer Research — “Food, Nutrition, Physical Activity and the Prevention of Cancer.”

So how does it work? Cancer researchers now consider that the problem with insulin resistance is that it leads us to secrete more insulin, and insulin (as well as a related hormone known as insulin-like growth factor) actually promotes tumor growth.

As it was explained to me by Craig Thompson, who has done much of this research and is now president of Memorial Sloan-Kettering Cancer Center in New York, the cells of many human cancers come to depend on insulin to provide the fuel (blood sugar) and materials they need to grow and multiply. Insulin and insulin-like growth factor (and related growth factors) also provide the signal, in effect, to do it. The more insulin, the better they do. Some cancers develop mutations that serve the purpose of increasing the influence of insulin on the cell; others take advantage of the elevated insulin levels that are common to metabolic syndrome, obesity and type 2 diabetes. Some do both. Thompson believes that many pre-cancerous cells would never acquire the mutations that turn them into malignant tumors if they weren’t being driven by insulin to take up more and more blood sugar and metabolize it.

What these researchers call elevated insulin (or insulin-like growth factor) signaling appears to be a necessary step in many human cancers, particularly cancers like breast and colon cancer. Lewis Cantley, director of the Cancer Center at Beth Israel Deaconess Medical Center at Harvard Medical School, says that up to 80 percent of all human cancers are driven by either mutations or environmental factors that work to enhance or mimic the effect of insulin on the incipient tumor cells. Cantley is now the leader of one of five scientific “dream teams,” financed by a national coalition called Stand Up to Cancer, to study, in the case of Cantley’s team, precisely this link between a specific insulin-signaling gene (known technically as PI3K) and tumor development in breast and other cancers common to women.

Most of the researchers studying this insulin/cancer link seem concerned primarily with finding a drug that might work to suppress insulin signaling in incipient cancer cells and so, they hope, inhibit or prevent their growth entirely. Many of the experts writing about the insulin/cancer link from a public health perspective — as in the 2007 report from the World Cancer Research Fund and the American Institute for Cancer Research — work from the assumption that chronically elevated insulin levels and insulin resistance are both caused by being fat or by getting fatter. They recommend, as the 2007 report did, that we should all work to be lean and more physically active, and that in turn will help us prevent cancer.

But some researchers will make the case, as Cantley and Thompson do, that if something other than just being fatter is causing insulin resistance to begin with, that’s quite likely the dietary cause of many cancers. If it’s sugar that causes insulin resistance, they say, then the conclusion is hard to avoid that sugar causes cancer — some cancers, at least — radical as this may seem and despite the fact that this suggestion has rarely if ever been voiced before publicly. For just this reason, neither of these men will eat sugar or high-fructose corn syrup, if they can avoid it.

“I have eliminated refined sugar from my diet and eat as little as I possibly can,” Thompson told me, “because I believe ultimately it’s something I can do to decrease my risk of cancer.” Cantley put it this way: “Sugar scares me.”

Sugar scares me too, obviously. I’d like to eat it in moderation. I’d certainly like my two sons to be able to eat it in moderation, to not overconsume it, but I don’t actually know what that means, and I’ve been reporting on this subject and studying it for more than a decade. If sugar just makes us fatter, that’s one thing. We start gaining weight, we eat less of it. But we are also talking about things we can’t see — fatty liver, insulin resistance and all that follows. Officially I’m not supposed to worry because the evidence isn’t conclusive, but I do.

Gary Taubes (gataubes@gmail.com) is a Robert Wood Johnson Foundation independent investigator in health policy and the author of “Why We Get Fat.” Editor: Vera Titunik (v.titunik-MagGroup@nytimes.com).

Just Because It’s A “Supplement”, Doesn’t Mean It’s Good For You

Paul — Fri, 08 Apr 2011 09:26:31 +0000

Energy Drinks Pose Serious Health Risks for Young People

Emma Hitt, PhD

February 14, 2011 — A lack of research and regulation associated with energy drinks, combined with reports of toxicity and high consumption, may result in potentially dangerous health consequences in children, adolescents, and young adults, according to a review of scientific literature and Internet sources.

Sara M. Seifert, BS, and colleagues from the Department of Pediatrics and the Pediatric Integrative Medicine Program at the University of Miami, Leonard M. Miller School of Medicine in Florida, reported their findings in a report published online February 14 and in the March print issue of Pediatrics.

According to the review, self-report surveys indicate that energy drinks are regularly consumed by 30% to 50% of children, adolescents, and young adults. The current trial questions the use of energy drinks in these young populations, as they provide no therapeutic benefit and are associated with risks for serious adverse health effects.

The authors note that because energy drinks are categorized as nutritional supplements, they avoid the limit of 71 mg caffeine per 12 fluid ounces that the US Food and Drug Administration has set for soda, as well as the safety testing and labeling that is required of pharmaceuticals. As a consequence, energy drinks can contain as much as 75 to 400 mg caffeine per container, with additional caffeine not included in the listed total often coming from additives such as guarana, kola nut, yerba mate, and cocoa.

"Of the 5448 US caffeine overdoses reported in 2007, 46% occurred in those younger than 19 years," the authors note.

One study included in the review, conducted in New Zealand, found that on average, all children, teenagers, and young men would exceed an adverse effect level of 3 mg/kg per day of caffeine after consuming a single retail unit of energy drink or energy shot in addition to baseline dietary exposure.

Advertising, Risky Behavior Compound Overdose Potential

The authors suggest that youth-aimed advertising of energy drinks and a tendency for risky behavior help compound the potential for caffeine overdose in young people. The authors recommend a maximum caffeine intake of 2.5 mg/kg per day for children and 100 mg/day for adolescents, although safe levels of consumption of other energy drink ingredients have not been established.

Although US poison centers have only recently begun tracking toxicity of energy drinks, Germany, Australia, and New Zealand have reported numerous adverse outcomes associated with energy drink consumption. These include liver damage, kidney failure, respiratory disorders, agitation, confusion, seizures, psychotic conditions, nausea, vomiting, abdominal pain, rhabdomyolysis, tachycardia, cardiac dysrhythmias, hypertension, myocardial infarction, heart failure, and death.

Despite these reports, there has been a lack of research into the physiological effects of individual energy drink ingredients. Drug interactions and dose-dependent effects remain largely unknown, although the current study reports that the ingredients 5-hydroxy tryptophan, vinpocetine, yohimbine, and ginseng have the potential for drug interactions that could result in adverse effects.

Seifert and colleagues also describe populations at highest risk for adverse health effects from energy drink consumption; these include children, adolescents, and young adults with cardiac conditions, attention-deficit hyperactivity disorder, eating disorders, and diabetes, and those taking other medications or consuming alcohol. The researchers also note that the caffeine in energy drinks may interfere with bone mineralization during a critical period of skeletal development.

"In the short-term, pediatric health care providers need to be aware of energy-drink consumption by children, adolescents, and young adults and the potentially dangerous consequences of inappropriate use," the authors conclude.

They add that more research is required to determine maximum safe doses, establish effects of long-term use, and better understand adverse health effects of energy drinks. In addition, pediatric healthcare providers should screen for consumption, especially in high-risk populations, and educate families about potential adverse outcomes. Furthermore, until the safety of energy drinks is ensured, appropriate regulation of sales and consumption should be put in place to protect minors, they suggest.

In a telephone interview with Medscape Medical News, the paper’s senior author Steven E. Lipshultz, MD, from the University of Miami, noted that child healthcare providers, as well as teachers and coaches, should have information on this so that they can guide conversations, at least on the available data.

"We were really surprised," said Dr. Lipshultz. "The [FDA] considers regular soft drinks to be foods, and tightly regulates the content and the labeling, but energy drinks are classified as dietary supplements and as such, are not subject to the same regulation or postmarketing surveillance," he said.

"Questions about consumption of these energy drinks should become a regular part of the questions pediatricians ask so that they can get into informed discussions with parents and their children," he added.

Dangers Go Beyond Excess Caffeine Consumption

According to independent commentator Dana M. Vieselmeyer, RD, LD, MPH, the special interest group chair of diabetes, wellness and weight management with the Pediatric Nutrition Practice Group of the American Dietetic Association, "this review highlights that consumption of energy drinks goes beyond the dangers of excess caffeine consumption, especially for children and adolescents, due to the supplemental additives these drinks contain and the unknown dangers of those in combination with caffeine and other medications. The fact that there is no known safe dose of any of those additives, or of caffeine, poses a risk."

"The long-term health consequences of regular energy drink consumption in children and adolescents is unknown, but what information we do have tells us that these drinks can have many harmful and potentially fatal effects," she told Medscape Medical News.

"Until further research is conducted, clinicians should make it standard practice to assess energy drink consumption when seeing their young patients, and also to educate the patient and families on the dangers of energy drink use, advising against its consumption," Vieselmeyer said.

"This review provides a good summation of the current body of knowledge regarding energy beverages," said John P. Higgins, MD, from the University of Texas Medical School at Houston, whose group also conducted a similar literature query on this topic.

"The marketing of energy beverages is targeting towards males in the preadolescent, adolescent, and young adult ages," Dr. Higgins told Medscape Medical News. "The fact that a child can walk into a grocery store or supermarket and buy these and consume [them] is frightening."

According to Dr. Higgins, as clinicians, it is "our daily duty to promote the health and well being of our patients while minimizing risk. The medical profession, in a global manner, needs to alert our patients to the dangers of these seemingly innocuous drinks and continue to advocate for strict control or overall removal."

This work was funded by the National Institutes of Health, the Health Resources and Services Administration, the Children’s Cardiomyopathy Foundation, and the Women’s Cancer Association. The authors and commentators have disclosed no relevant financial relationships.

Lentil Burgers

Paul — Thu, 10 Mar 2011 10:12:01 +0000

Something for the vegetarians. As most of you know the vegetarian path isn’t my preferred way to go, however those of you who have made that choice need options too, so I want to be able add things in that don’t alienate you all. I hope you enjoy this one!!

Fiber-packed lentils lend this meatless burger nutritional pizzazz. They also hold their own next to meatier varieties in taste. Keep in mind lentils form a complete protein when paired with a whole grain (in this case, brown rice) but as you’ll see in the nutritional facts at the end of this blog there is not enough in each burger for this to be the only protein source in your meal.

Serves: 6
Hands-on time: 45 minutes max
Total time: 65 minutes

INGREDIENTS:

1 cup dried green lentils, rinsed
6 cloves garlic, minced
3/4 cup diced yellow onion
2 celery stalks, minced
1/4 cup leeks, finely diced
2 tbsp ground flaxseed
5 tsp Dijon mustard
3 tbsp unsalted tomato paste
1 tsp chile powder
1 tsp ground turmeric
2 tsp ground cumin
1 cup cooked long-grain brown rice
2 tbsp extra-virgin olive oil

INSTRUCTIONS:

Preheat oven to 375°F. Line a baking sheet with parchment paper. Cook lentils according to package directions.
In a large bowl, mix garlic, onion, celery, leeks, flaxseed, Dijon, tomato paste and spices. When lentils are cooked, mash them with the back of a fork, leaving some whole. Add mashed lentils and rice to bowl. Mix all ingredients together.
Heat oil in a medium saucepan on medium-high. While oil is heating, form lentil-rice mixture into 6 lentil patties. Add them to pan and cook for 2 to 3 minutes per side, until light brown. Transfer patties to prepared baking sheet and cook in oven for 15 minutes to warm through. Serve with a side salad and topped with diced tomatoes and avocado, if desired. Add two egg whites on the side or on top to complete the protein needed for a single meal.

NOTE: There is no need to sandwich these burgers between a bun since you’ll be consuming a healthy amount of fiber thanks to the brown rice and lentils.

Nutrients per 5-oz patty: Calories: 220, Total Fat: 6 g, Sat. Fat: 1 g, Carbs: 34 g, Fiber: 8 g, Sugars: 3 g, Protein: 9 g, Sodium: 135 mg, Cholesterol: 0 mg

A Sore Subject for Me

Paul — Sat, 05 Mar 2011 09:57:47 +0000

Childhood obesity is running rampant in our country, and increasing by the month. We, as the adults in this community we call America, need to band together to fight this monster. Of course the only way to combat something like this is the acquisition of knowledge. The following study can REALLY help us on the way to protecting our children. Read on…..Let me know what you think.

Early Introduction of Solid Foods Linked to Risk for Early Childhood Obesity

Laurie Barclay, MD

February 7, 2011 — Early introduction of solid foods is linked to a risk for early childhood obesity, according to the results of a prospective prebirth cohort study reported online February 7 in Pediatrics.

"Parental feeding practices during early infancy, such as the timing of solid food introduction, may be 1 key modifiable determinant of childhood obesity," write Susanna Y. Huh, MD, MPH, from the Division of Gastroenterology and Nutrition, Children’s Hospital Boston in Boston, Massachusetts, and colleagues. "Data suggest that the introduction of solid foods earlier than 4 months of age is associated with increased body fat or weight in childhood or with greater weight gain during infancy, which itself predicts later adiposity. Other studies have found no association between the timing of solid food introduction and body fat or an association between delayed introduction of solid foods after 6 months and greater adiposity."

The goal of the study was to evaluate the association between timing of introduction of solid foods during infancy and obesity at age 3 years, defined as a body mass index for age and sex at the 95th percentile or above, using a cohort of 847 children enrolled in Project Viva. Timing of introduction of solid foods was categorized as younger than 4 months, ages 4 to 5 months, and 6 months or older. Logistic regression models were applied separately for infants who were breast-fed for at least 4 months ("breast-fed"; n = 568; 67%) and for infants who were never breast-fed or in whom breast-feeding was stopped before age 4 months ("formula-fed"; n = 279; 32%). These models were adjusted for child and maternal factors, including change in weight-for-age z score from 0 to 4 months as a marker of early infant growth.

Obesity was present in 75 children (9%) at age 3 years. The timing of solid food introduction was not associated with odds of obesity in breast-fed infants, (odds ratio, 1.1; 95% confidence interval [CI], 0.3 – 4.4). However, introducing formula-fed infants to solid foods before age 4 months was associated with a 6-fold increase in odds of obesity at age 3 years, which was not explained by rapid early growth (odds ratio after adjustment, 6.3; 95% CI, 2.3 – 6.9).

"Among infants who were never breastfed or those who stopped breastfeeding before the age of 4 months, the introduction of solids before the age of 4 months was associated with a sixfold increase in the odds of obesity at the age of 3 years," the study authors write.

Limitations of this study include possible residual confounding; some loss of the cohort to follow-up; limited generalizability to more socioeconomically disadvantaged populations; and small numbers in some cells, leading to possible chance results.

"Among infants breastfed for 4 months or longer, the timing of the introduction of solid foods was not associated with the odds of obesity," the study authors conclude. "Increased adherence to guidelines regarding the timing of solid food introduction may reduce the risk of obesity in childhood."

The National Institutes of Health supported this study. The study authors have disclosed no relevant financial relationships.

Pediatrics. Published online February 7, 2011. Abstract

Sugar-Sweetened Drinks Linked to Elevations in Blood Pressure

Paul — Fri, 04 Mar 2011 10:10:36 +0000

This may seem a little redundant, but the horse ain’t dead yet, soooo here it is….

Michael O’Riordan

February 28, 2011 (London, United Kingdom) — There is yet another reason to stay away from soft drinks, sweetened fruit juices, and sugar-loaded sports drinks: a new study has shown that there is a direct association between fructose and glucose intake and increases in blood pressure and that these sugar-sweetened beverages are associated with significant increases in systolic and diastolic blood pressures [1].

Each beverage consumed, report investigators, is associated with a 1.1-mm-Hg increase in systolic and 0.4-mm-Hg increase in diastolic blood pressure after adjustment for weight and height.

"Sugar-sweetened beverages have been linked to high blood pressure, obesity, type 2 diabetes, and heart-disease risk, and this is one more piece of evidence showing that if individuals want to drink these drinks, they should do so in moderation," lead investigator Dr Ian Brown (Imperial College London, UK) told heartwire . "Also, one of our interesting findings was that the association between sugar-sweetened beverage consumption and blood pressure was stronger in people who are consuming more sodium. We already know that salt is bad for blood pressure, but what we’re finding is that if you’re consuming more sodium, you appear to be, at least in this study, exacerbating the effects of these sugar-sweetened beverages."

The INTERMAP Study

The study, published online February 28, 2011 in Hypertension, is an analysis of patients included in the International Study of Macro/Micronutrients and Blood Pressure (INTERMAP). In the study, the researchers assessed the consumption of sugar-sweetened drinks, sugars, and diet beverages in 2696 healthy individuals aged 40 to 59 years old in the US and UK. Over the course of four days, participants recorded what they ate and drank and underwent two 24-hour urine collections and eight blood-pressure recordings, as well as answered questions about their lifestyle and medical history.

The mean systolic and diastolic blood pressure was 119/73 mm Hg among the US participants and 120/77 mm Hg among the participants from the UK. On average, US residents drank more sugar-sweetened and diet beverages than those from the UK, with Americans drinking nearly a full serving per day compared with 0.2 servings per day in the UK.

In a multiple linear regression analysis, there was a direct association with systolic and diastolic blood pressure. In a model that adjusted for energy intake, urinary sodium, potassium, dietary alcohol, cholesterol, and fatty-acid intake, consuming one sugar-sweetened beverage was associated with a systolic blood pressure increase of 1.6 mm Hg and a diastolic blood pressure increase of 0.8 mm Hg, adjusted down to 1.1/0.4 mm Hg when height and weight were included in the model. Diet beverage intake, on the other hand, was inversely associated with blood-pressure levels.

"If you imagine, there are probably people who are consuming two or three cans of soda a day," said Brown. "It’s possible that their blood pressure could be higher by several mm Hg, and as we know, it can be difficult even with multiple drug therapies to reduce an individual’s blood pressure by more than 10 mm Hg."

The American Heart Association (AHA) has published recommendations for maximum dietary intake of "added sugars," such as those found in sodas and fruit drinks. These upper limits vary by sex, age, and activity level, but the AHA puts them at 140 kcal for most American men and 100 kcal for most American women. As Brown noted, however, those who drank the sugary drinks in INTERMAP consumed approximately 400 kcal more than those who did not, and these people also had a higher body-mass index (BMI).

Interaction With Sodium

The researchers also observed a direct association with glucose and fructose consumption and blood pressure as well as a strong interaction with glucose, fructose, and sodium. In a stratified analysis, fructose- and glucose-related differences in blood pressure were observed only for participants who had higher levels of urinary sodium excretion. For example, for individuals with above-the-median 24-hour urinary sodium excretion, an increase in fructose consumption (2 standard deviations) was associated with an increase of 2.5/1.7 mm Hg systolic and diastolic blood pressure after adjustment for height and weight.

Right now, investigators aren’t sure what underlying mechanism is causing the increase in blood pressure with sugar-sweetened beverages. They suspect, however, that the drinks increase serum uric-acid levels, and this in turn inhibits nitric oxide in the blood, thereby decreasing vasodilation. Although the mechanisms might not yet be clear, Brown said the data are more evidence clinicians can use in communicating to their patients the importance of following a healthy diet.

"As I look at it, this is an additional nutritional intervention that we have in our toolbox," Brown told heartwire . "The DASH trial showed that if you consume a high-vegetable, lean-meat, low-fat-dairy, no-sugar-added diet, and if you also reduce sodium, hypertensive individuals can lower their blood pressure by 8 to 10 mm Hg, which is as effective as multiple drug therapies. This is just another tool to help us reduce blood-pressure levels at the population level."

The authors report no conflicts of interest.

Resistance Tubing Workout

Paul — Tue, 08 Feb 2011 10:06:00 +0000

Here’s a good one from our friends at ACE fitness. Check it out…..and implement!

For those times when you just can’t make it to the gym, resistance tubing offers an inexpensive and portable way to get a full-body strength-training workout at home or on the road.

As with all exercise, it is important to warm up for five to 10 minutes and gently stretch the muscles you will be working. For beginners, it is best to do one set of 12 to 15 repetitions of each exercise. Intermediate exercisers (those that have been lifting weights for up to three months) can perform one to two sets of each exercise. More advanced strength trainers (those who have been lifting weights or using tubing for more than three months) should try to complete two or three sets of 12 to 15 repetitions. Stretch each muscle group after each set and at the end of the entire workout to improve flexibility.

Perform the following exercises for a quick full-body workout:

Seated row (lats)—Sit on the floor and grasp one handle. Wrap the tubing around a bedpost or some type of anchor close to the ground and grab the other handle. Sit back so that there is tension on the elastic when your arms are extended forward. Extend your legs in front of you with your knees slightly bent. Pull the handles so that your elbows form right angles as you squeeze your shoulder blades together.
Bring your elbows back as far as you can, keeping your spine neutral. Slowly let your arms extend back to the starting position and begin your second repetition. Be sure not to slouch.

Bench press (pecs)—Secure the center of the tubing at chest level and face away from the anchor, grabbing the handles in each hand. Begin with your thumbs at your armpits and step far enough away from the anchor that the tube is not gapping at this starting position. Fully extend your arms in front of your body. Slowly release to the starting position and repeat.

Military press (deltoids)—Stand on the center of the band with your feet shoulder-width apart. With your palms facing forward and hands by your shoulders, extend your arms straight up while keeping your back straight (do not arch your back) and abdominal muscles tight. Slowly lower and repeat.

Triceps extension (triceps)—Step on the tubing and pull one handle up behind your head. Bring your elbow up close to your ear and, beginning with your arm bent behind you, extend straight up until your arm is straight. You may use your other arm to hold your elbow in close to your head. Slowly lower back to the starting position and switch arms.

Biceps curl (biceps)—Step on one end of the exercise band and grab the handle with the same hand. Be sure that there is some tension on the tubing when your arm is extended down by your side. With your palm facing forward, bend your elbow, bringing your hand up toward your shoulder. Keep your wrist straight and bend only at the elbow. Slowly release and repeat. If you are using light resistance, you may be able to stand on the center of the tube and work both arms simultaneously.

Squats (quadriceps, hamstrings, glutes)—Stand on the tubing so that you are centered. Grab the handles with both hands and stand with your feet about shoulder-width apart. Hold the handles up by your shoulders and bend as if you are going to sit in a chair. Return to standing and repeat. Be sure to keep a flat back and contract your abdominal muscles.

Kneeling crunches (abdominals)—Anchor the tubing above your head and let the handles drop down. Kneel on the floor with the anchor behind you. Hold the handles with your hands up by your ears and elbows in. Bending from the waist, curl down, bringing your head toward your knees and keeping the handles locked by your ears. Slowly return to the starting position and repeat.

Additional Resources

Page, P. Ellenbecker, T.S. (2003). The Scientific and Clinical Application of Elastic Resistance. Champaign, Ill.: Human Kinetics.
About.com: www.exercise.about.com/cs/exerciseworkouts/l/blbandworkout.htm

Tubing Safety Tips

Pulling on exercise tubing isn’t exactly a risky activity. Still, to keep the tube from snapping into your face—and to give your muscles the best challenge—follow these important guidelines.
Check for holes or worn spots in the tubing. Replace the tube if you see
any tears.
Do your workout on carpeting, wood floors or grass—anywhere but asphalt or cement. Abrasive surfaces can tear your tube.
Wear comfortable, supportive athletic shoes, not sandals or dress shoes.
Make sure the tubing is secured underfoot or on an anchor before you begin each exercise.
Maintain good posture throughout each exercise: Keep your knees slightly bent, your abdominal muscles pulled in and your chest expanded.
Perform the exercises in a slow and controlled manner, to work against resistance both when you pull on the tube and when your return to the
starting position.

Excerpted from Fitness for Travelers: The Ultimate Workout Guide for the Road, by Suzanne Schlosberg (Houghton Mifflin, 2002), available at www.acefitness.org.

Great and Emotional

Paul — Sat, 05 Feb 2011 10:27:20 +0000

I have the privilege of sharing with you another great testimonial from a recent client. My thanks to you Amy, for the kind words, the heart felt emotion, the hard work and dedication to your health. It really paid off and you deserve all the results you were able to achieve.

See her story here (or open the rest of this post) You can read more about Amy at her BlogSpot here. Show her some love!

“I can’t remember a darker or more terrifying time in my life then when I struggled with an eating disorder (please note the past tense feel of that sentence… no worried emails or phone calls please) and when the process of my divorce commenced it came back with a serious vengeance … it was like the year of therapy I went through never happened. I started to see signs of those old and nasty habits. I started to see a distorted reflection. I started to see everything that was wrong with me. I stopped eating. The hunger pangs in a strange way were comforting – they distracted me from the real hurt and pain that I was facing and I soon found myself at the top of a very slippery slope. I knew that if I continued to humor these thoughts and behaviors that a relapse was inevitable and I was not about to subject myself again to that kind of torture.
I decided that finding a personal trainer was a good idea. I searched around and finally settled on one that seemed comfortable. As part of my initial consultation I was to receive a free fitness assessment and a complimentary training session… a "try before you buy" sort of thing.
That trainer’s name is Paul Van Slambrouck and I owe so much of where I am now because of him. …honestly he helped keep me from losing my mind.
The first time I met him in person was on the morning of my fitness assessment. He was super warm and friendly … which looking back now, his friendly smile almost feels like false advertising because he is crazy tough. I mean really crazy tough… I walked into it completely unsuspecting to any potential threats to my comfort zone. I was under the impression that a fitness assessment was like one of those gym tests in middle school (you know like running around the track a couple of times and climbing a rope etc.) Instead I was lead into a small room with a computer and a scale. He asked a variety of questions about my lifestyle and when he asked me what I ate on any given day, I felt defensive. I started to second guess my decision to be there. What was I supposed to say, "I feel incredibly fat and have decided that food is my arch nemesis." ????
I think the defensiveness surfaced because a large part of me didn’t want help and was attracted to that old way of life- which is a weird way of saying that because ‘living’ with an eating disorder is no way to live at all. So you can imagine my horror when he asked me to get on the scale and when he measured my body fat percentage. I heavily considered bolting out of the door and never coming back but I decided to stay because a larger part of me knew that I needed… wanted… his help. I was however not prepared to deal with all of the sudden emotions that resurfaced and spent the rest of our appointment trying to keep myself from coming completely unsoldered.
My first training session with him didn’t go very well either. I hadn’t eaten anything since lunchtime the day before and only 5 or 10 minutes in I felt severely nauseous. I couldn’t stand upright. I couldn’t bring myself to do the exercises that he was asking me to do. I felt weak. I felt defeated. I felt like a failure…. or in other words I felt like total crap- rock bottom.
When he sat down with me after, we talked about the benefits that training would offer me and I was sold. Up until a few days ago I trained with Paul three times a week and that was one of the best strategic moves I have made … ever. I wonder and have been meaning to ask him what it was like to see me from the sidelines because I started to train with Paul right after I moved out of my house up until just a few days ago. If anyone saw the progression of my recent "learning experience", it would have been him.
It is a major understatement to say that my life during that time was high stress and having tough workouts helped me cope. You know it’s bad when you cry yourself to sleep but it is even worse when you consistently wake up in the morning in tears. I can’t tell you how many times I drove to the gym crying, upset, overwhelmed, and ready to just throw in the towel. Then when I would get to the parking lot, I would wipe away my tears and walk through those gym doors pretending that I was tough and unbreakable… all the while feeling totally shattered and fragile inside and completely afraid that I would fail myself.
I remember asking him why he chose to be a personal trainer and his response was that he wanted to help people. And help people he does. I would almost always leave the gym feeling strong and confident. Capable. Which is a stark difference to when I would arrive. More than that I could talk to him and trust him… he always seemed to know exactly what to say.

Paul was a rock for me… a stabling and grounding force amidst the chaos of my life. He showed me that I have way more strength than I ever dared to believe. He helped me develop a more healthy relationship with food and to have a better body image. He taught me to have confidence and to not quit because of difficulty. He taught me to deliberately trust in myself and my ability to succeed. He inspired me to live with tenacity.

…And when I couldn’t find that strength in me, when I let myself quit, he was there.
He was always there to pick me back up both figuratively and literally (there were many times that I would lay down on the gym floor or crouch up in the fetal position… and I am not exaggerating.) Paul really witnessed me at my worst, but then again he brought out the best in me too. I am so grateful to him. I could not have survived without him and without his torturous workouts. I will miss training with Paul like crazy because who else is going to pick me back up from my fetal position when the going gets tough??
But I guess maybe it is time for me to start doing that on my own. I certainly have the tools. Now it is up to me to put in the effort.
I am also grateful for my family who offered to pay for my last semester of school. Because of their generosity I was able to take the money I had saved up for tuition and use it to fund this endeavor… it truly was an essential component to surviving last year and getting me to where I am today.
If you are in the Ann Arbor/Ypsi area and are interested in working with a trainer, I highly recommend Paul Van Slambrouk. He is the absolute best and worth every penny.”

-Amy Cromar, 26 years old

Does there need to be any other reason than living longer?

Paul — Wed, 05 Jan 2011 14:09:36 +0000

Higher Exercise Capacity Equals Improved Survival in Older Adults

Michael O’Riordan

August 17, 2010 (Washington, DC) — Exercise capacity is inversely associated with all-cause mortality in older men, according to the results of a new study [1]. The survival benefit was observed among individuals able to participate in moderate daily exercise, such as brisk walking, report investigators.

"Most health benefits are evident at fitness levels of greater than 5 [metabolic equivalents] METs," lead investigator Dr Peter Kokkinos (Georgetown University School of Medicine, Washington, DC) told heartwire. "Now, those benefits are graded, so that the more exercise you do, the greater the survival benefit."

The results, published online August 9, 2010 in Circulation, are in line with other studies linking higher exercise capacity with reductions in mortality. Unique to this analysis, said Kokkinos, is the patient population, showing that it is never too late to receive some survival benefit from moderate physical activity.

Patients Aged 65 to 92 Years Old

In the study, researchers assessed the association between exercise capacity and all-cause mortality in 5314 males aged 65 to 92 years old who completed exercise testing at Veterans Affairs hospitals between 1986 and 2008. Individuals were tested on a treadmill, and peak exercise workload was estimated in METs, allowing researchers to gauge exercise capacity on the basis of exercise time.

After an average of eight years of follow-up, 2137 individuals died. Among those who died, baseline exercise capacity was 5.3 METs, whereas exercise capacity at baseline was 6.3 among those who survived. For each MET increase in exercise capacity, there was a statistically significant 12% reduction in the risk of all-cause mortality. In terms of the graded survival benefit, those able to achieve a MET level >5.0 had a 38% lower risk of death compared with the least fit individuals, whereas the fittest individuals, those able to achieve a MET level >9.0, had a 61% lower mortality risk.

Mortality Risk Hazard Ratios Based on Exercise Capacity

Variable	Hazard ratio (95% CI)
Exercise capacity (based on each 1-MET increment)*	0.88 (0.86–0.90)

*Adjusted for age, body-mass index, resting blood pressure, cardiovascular risk factors, medications, and disease

Adjusted Hazard Ratios for Mortality Risk of Entire Cohort

MET level achieved	Number of deaths (%)	Hazard ratio (95% CI)
<4	615 (57)	1.0
4.1–5.0	622 (51)	0.93 (0.83–1.04)
5.1–6.0	298 (34)	0.62 (0.54–0.71)
6.1–7.0	260 (31)	0.53 (0.46–0.62)
7.1–8.0	148 (30)	0.53 (0.44–0.64)
8.1–9.0	95 (27)	0.48 (0.38–0.60)
>9.0	101 (22)	0.39 (0.28–0.49)

Speaking with heartwire , Kokkinos also noted that there were no differences in the effect of exercise capacity on mortality in older patients, such as those older than 70 years old, when compared with the younger patients. The results also showed that unfit individuals who improved their exercise capacity, as shown with serial testing, had a 35% lower risk of death compared with those who remained physically unfit.

In one last analysis, the group also attempted to show that the higher mortality rates in the low-fitness categories were not influenced by preexisting disease. To do so, they excluded patients who died within two years, those unable to achieve 85% of their peak maximal heart rate, and those in the lowest fitness categories who also had a very low body-mass index. Very skinny patients, as well as those unable to increase their heart rate, might have some sort of underlying disease, such as previous stroke or the possibility of cancer in skinny older adults, but even when these were excluded, the results of the study did not change.

Kokkinos said the results are of clinical importance given the aging of the US population, stressing that such fitness levels, >5 METs, can be achieved with 20 to 40 minutes of brisk daily exercise. He noted that he has one patient, a 90-year-old man, who returns for follow-up who has an exercise capacity of 12 METs, all garnered through daily walking.

Start Early If You Can But It’s NEVER Too Late

Paul — Fri, 17 Dec 2010 13:14:13 +0000

Staying Active Lessens Age-Related Weight Gain, Especially in Women

December 14, 2010 (Chicago, Illinois) — Staying active in young adulthood appears to help individuals lessen the fattening effects of time, with results of a new study showing that physically active young adults do not put on as much weight as their less active counterparts [1]. While some weight gain appears inevitable–even the most active individuals had increases in weight and waist circumference over a 20-year period–maintaining high activity levels lessens the weight gain as people move into middle age, report investigators.

"Preventing weight gain can be something that is appropriate for people who are overweight, normal weight, or obese, so it crosses weight classes," lead investigator Dr Arlene Hankinson (Northwestern University, Chicago, IL) told heartwire . "And like many prevention strategies, it’s usually easier to prevent something from happening than to treat it after you’ve already developed the problem."

The study is published in the December 15, 2010 issue of the Journal of the American Medical Association.

Analysis From the CARDIA Trial

To heartwire , Hankinson said there has been a lot of work looking at the association between physical activity and weight loss, with clinical trials testing different types of physical activity and their effects on helping obese individuals lose weight. Less is known, however, about what is required to prevent weight gain in the future.

Currently, public-health guidelines recommend regular physical exercise to prevent age-related weight gain. While this implies that higher physical-activity levels can prevent weight gain, said Hankinson, the data supporting the recommendation are based largely on cross-sectional observational and short-term clinical trials. Short-term studies, she noted, can’t account for the changing risk of gaining weight with age. The purpose of this study was to evaluate the relationship between habitual physical-activity levels and changes in body-mass index (BMI) and waist circumference over a 20-year period.

In this analysis, the researchers analyzed data from the Coronary Artery Risk Development in Young Adults (CARDIA) trial, a prospective, longitudinal study with 20 years of follow-up. The group used an algorithm to compute a total activity score that factored in the intensity, frequency, and duration of the physical activity over the previous 12 months. As a reference, a score of 300 exercise units corresponded to at least 150 minutes of moderate to vigorous intensity exercise per week, the approximate amount recommended by the US Department of Health and Human Services (HHS).

Men and women who had high physical-activity levels in young adulthood (ages 18 to 30 years) gained less weight than individuals with low measures of physical activity. Based on BMI, men who maintained high physical-activity levels in young adulthood gained 2.6 kg less than their less active peers over the 20 years of the study, while women who were most active gained 6.1 fewer kg than those with low physical-activity scores.

Similarly, over the 20 years, the most active men and women gained 3.1 and 3.8 fewer cm in waist circumference than individuals with the lowest physical-activity scores in young adulthood.

Average Annual Changes in BMI And Waist Circumference in Men

Long-term physical-activity category	BMI, mean changes/y (95% CI)	BMI, mean change/y relative to lower activity level (95% CI)	Waist circumference, mean changes/y (95% CI)	Waist circumference, mean change/y relative to lower activity level (95% CI)
Lower	0.20 (0.17–0.23)	1.0 (reference)	0.67 (0.60–0.75)	1.0 (reference)
Moderate	0.14 (0.09–0.19)	-0.06 (-0.11 to 0.00)	0.50 (0.36–0.64)	-0.17 (-0.33 to -0.02)
Higher	0.15 (0.11–0.18)	-0.05 (-10 to -0.01)	0.52 (0.43–0.61)	-0.15 (-0.27 to -0.03)

Average Annual Changes in BMI and Waist Circumference in Women

Long-term physical-activity category	BMI, mean changes/y (95% CI)	BMI, mean change/y relative to lower activity level (95% CI)	Waist circumference, mean changes/y (95% CI)	Waist circumference, mean change/y relative to lower activity level (95% CI)
Lower	0.30 (0.25–0.34)	1.0 (reference)	0.67 (0.60–0.75)	1.0 (reference)
Moderate	0.25 (0.15–0.34)	-0.05 (-0.16 to 0.05)	0.59 (0.40–0.79)	0.59 (0.40–0.79)
Higher	0.17 (0.12–0.21)	-0.13 (-0.19 to -0.07)	0.49 (0.39–0.58)	-0.19 (-0.31 to -0.06)

Overall, men and women who engaged in a high level of physical activity, exceeding the recommended HHS guidelines for duration, frequency, and intensity, gained approximately 9 kg, or roughly 20 lbs over 20 years. On the other hand, men who did not participate regularly in physical activity, those with a "low" physical-activity score, gained nearly 13 kg (28 lbs), while women with a low score gained 15 kg (33 lbs) over 20 years.

"It’s very possible that there are physiologic differences between men and women–the chief among them being pregnancy and menopause–that might account for the differences in weight gain, but there could be other reasons," said Hankinson. "However, I think there are different ways that women behave compared with men, and we are not able to capture all of those behaviors and account for them in a way that explains the gender differences."

The overall data showing weight gain in even the most active adults support previous studies suggesting that individuals might need to exercise more as they age to prevent incremental gains in weight over time, Hankinson told heartwire .

Of the 1338 individuals included in the analysis, more than one-third met the daily physical-activity requirements outlined by the HHS. These individuals experienced smaller annual increases in mean BMI and waist circumference than those who did not meet the recommended activity levels. Overall, men and women who exercised for more than 150 minutes per week at moderate to vigorous intensity gained 1.8 and 4.7 fewer kgs, respectively, that those who did not meet the HHS physical-activity requirements.

"The federal guidelines are a great starting point," said Hankinson. "We used it as an alternative definition to high activity in our study, and we found really similar results. The benefit of those guidelines is to prevent weight gain, and not just weight loss for cardiovascular benefit."

Michael O’Riordan

There are no conflicts of interest to report. The study is funded by grants from the National Heart, Lung, and Blood Institute.

We Are Finally Getting Somewhere

Paul — Mon, 13 Dec 2010 01:39:16 +0000

It looks like the the medical community is finally starting to catch up to us forward thinkers. Let’s start to act, not re-act, everyone. If everything is treated symptomatically rather than with proactive measures we should just call it sick care, not health care. You’ll see below that they’re finally getting it.

From Medscape Medical News

New Guidelines for Exercise in Type 2 Diabetes

Fran Lowry

December 10, 2010 — New guidelines issued jointly by the American Diabetes Association and the American College of Sports Medicine stress the crucial role that physical activity plays in the management of type 2 diabetes.

They replace recommendations made in the American College of Sports Medicine Position Stand "Exercise and Type 2 Diabetes" that were issued in 2000.

Developed by a panel of 9 experts, the new guidelines are published concurrently in the December issue of Medicine & Science in Sports & Exercise and Diabetes Care.

"High-quality studies establishing the importance of exercise and fitness in diabetes were lacking until recently," the expert panel writes, "but it is now well established that participation in regular physical activity improves blood glucose control and can prevent or delay type 2 diabetes mellitus, along with positively affecting lipids, blood pressure, cardiovascular events, mortality, and quality of life."

Most of the benefits of exercise are realized through acute and long-term improvements in insulin action, accomplished with both aerobic and resistance training, the experts write.

For people who already have type 2 diabetes, the new guidelines recommend at least 150 minutes per week of moderate to vigorous aerobic exercise spread out at least 3 days during the week, with no more than 2 consecutive days between bouts of aerobic activity. These recommendations take into account the needs of those whose diabetes may limit vigorous exercise.

"Most people with type 2 diabetes do not have sufficient aerobic capacity to undertake sustained vigorous activity for that weekly duration, and they may have orthopaedic or other health limitations," said writing chair Sheri R. Colberg, PhD, professor of exercise science at Old Dominion University and adjunct professor of internal medicine at Eastern Virginia Medical School, Norfolk, Virginia, in a statement. "For this reason, the ADA [American Diabetes Association] and ACSM [American College of Sports Medicine] call for a regimen of moderate-to-vigorous activity and make no recommendation for a lesser amount of vigorous activity."

The panel specifically recommends that such moderate exercise correspond to approximately 40% to 60% of maximal aerobic capacity and states that for most people with type 2 diabetes, brisk walking is a moderate-intensity exercise.

The expert panel also recommends that resistance training be part of the exercise regimen. This should be done at least twice a week — ideally 3 times a week — on nonconsecutive days. The panel also recommends that people just beginning to do weight training be supervised by a qualified exercise trainer "to ensure optimal benefits to blood glucose control, blood pressure, lipids, and cardiovascular risk and to minimize injury risk."

Regular use of a pedometer is also encouraged. In a meta-analysis of 8 randomized controlled trials and 18 observational studies, people who used pedometers increased their physical activity by 27% over baseline. Having a goal, such as taking 10,000 steps per day, was an important predictor of increased physical activity, according to the expert panel.

Finally, the new guidelines emphasise that exercise must be done regularly to have continued benefits and should include regular training of varying types.

Physicians should prescribe exercise, Dr. Colberg said in a statement. "Many physicians appear unwilling or cautious about prescribing exercise to individuals with type 2 diabetes for a variety of reasons, such as excessive body weight or the presence of health-related complications. However, the majority of people with type 2 diabetes can exercise safely, as long as certain precautions are taken. The presence of diabetes complications should not be used as an excuse to avoid participation in physical activity."

Dr. Colberg and the other authors have disclosed no relevant financial relationships.

Med Sci Sports Exerc. 2010;2282-2303.