Check out this article by Leah Zerbe for Yahoo! Health:

The 4 Best and 3 Worst Sweeteners to Have in Your Kitchen

At this point, it’s common knowledge that high-fructose corn syrup and refined sugar are bad for us. But given all the marketing hype behind different “natural” alternatives, it’s hard to know which ones really are the best sweeteners. Complicating matters, new studies, like one just published in the journal Cancer Research, are finding that fructose, a sugar found in high-fructose corn syrup, agave, honey, and, in small amounts, even in fruit, actually feeds some cancers. But don’t give up apples and oranges, or even honey, based on a single study. “Natural sugars found in fruits and vegetables—things like berries, green apples, grapefruit, kiwi—are needed to feed beneficial microflora in the gut for a healthy immune system,” explains Donna Gates, who led the movement to bring stevia, a natural sweetener, into this country more than a decade ago. “That’s why nature put a little bit of sugar in fruits and vegetables. It keeps the ecosystem alive in us,” she says, adding that the small amounts of fructose in fruits and vegetables are balanced with minerals, vitamins, and other vital nutrients. “Our body reads it differently,” she notes.Fruits and vegetables provide a perfect sugar fix, but when you’re in need of a sweetener to add to iced tea, baked goods, or anything else, make sure you know the difference between the good guys and bad guys of the sweetener world. (Some of the not-so-sweet details could leave you gagging.)

Bad Guy #1: Aspartame

There’s conflicting evidence regarding the safety of aspartame, a common chemical sweetener used in diet soda and other low-cal or low-sugar goods, but some people report headaches or generally feeling unwell after ingesting anything containing the chemical. To make life easier for everyone, this is one instance where you may want to follow the “better safe than sorry” principle. That’s because a University of Liverpool test-tube study found that when mixed with a common food color ingredient, aspartame actually became toxic to brain cells. Making matters worse, aspartame is used in many diet sodas, and studies have found drinking diet soda may increase your risk of developing diabetes and metabolic syndrome. Also of concern with aspartame, researchers have found that one harmful breakdown product is formaldehyde. Sweet? We don’t think so.

Bad Guy #2: Agave

While your health food store likely stocks agave sweeteners, it may be best to keep them out of your cart. Many agave nectars consist of 70 to 80 percent fructose—that’s more than what’s found in high-fructose corn syrup! If you don’t want to give up agave, look for types that contain no more than 30 to 40 percent fructose, recommends Christine Gerbstadt, MD, PhD, RD, spokeswoman for the American Dietetic Association. Agave is also very heavily processed in an extremely energy-intensive manner that’s similar to the way corn is converted into high-fructose corn syrup.

Bad Guy #3: Sucralose

While sucralose, better known by its brand name, Splenda, may originate with sugar, the end product is anything but natural. It’s processed using chlorine, and researchers are finding that the artificial sweetener is passing through our bodies and winding up in wastewater treatment plants, where it can’t be broken down. Tests in Norway and Sweden found sucralose in surface water released downstream from treatment discharge sites. Scientists worry it could change organisms’ feeding habits and interfere with photosynthesis, putting the entire food chain at risk. The chemically derived artificial sweetener acesulfame K (sold under the brand name Sunett) was also detected in treated wastewater and tap water.

Good Guy #1: Stevia

“We need to be off of sugar, but we need good alternatives, and stevia is the safest sweetener there is, period,” says Gates, who coauthored The Stevia Cookbook: Cooking with Nature’s Calorie-Free Sweetener (Avery Trade, 2004). All types of stevia are extracted from the leaves of the stevia plant, but some forms taste better than others, says Gates. People tend to overuse powders, in which the sweetness is really concentrated, so if you’ve tried powders in the past and didn’t like them, try liquid forms, explains Gates, who helped develop a liquid stevia sweetener product. Stevia contains zero calories, but its one downfall is that it doesn’t work well for baking. Expect to see more stevia on store shelves, as Coke and Pepsi got the green light to use Truvia (a sweetener made in part from stevia) starting later this year.

Good Guy #2: Sugar alcohols

Popular sugar alcohol sweeteners include xylitol, sorbitol, and erythritol, natural sweeteners made through a fermentation process of corn or sugar cane. They contain fewer calories than sweeteners like pure sugar and honey, but more than stevia. They also leave a cooling sensation in the mouth, and have been found to prevent cavities, explains Dr. Gerbstadt. Just don’t overdo it—too much can cause GI distress.

Good Guy #3: Organic, raw local honey

While honey does boast higher fructose levels, it also contains a bounty of cancer-defending antioxidants, and local honey has been said to help alleviate allergy symptoms. Don’t limit raw honey’s use to your tea, either. Use it to speed healing on burns, and as a natural antiseptic on cuts and scrapes. Honey also has a low glycemic index, so adding it to your tea or yogurt won’t lead to energy-busting blood sugar drops later in the day.

Good Guy #4: Blackstrap molasses

Although heavy on the calorie content, blackstrap is rich in iron, potassium, and calcium, making it a healthier choice than nutritionally defunct artificial sweeteners or even regular refined sugar, despite the fact that blackstrap and refined sugar both come from sugar cane. (Dr. Gerbstadt says calorie-containing sweeteners are not recommended for people with diabetes.) We like the organic, Fair Trade Certified version of blackstrap molasses from Wholesome Sweeteners.

However, my “guilty pleasure” was indulging my sweet tooth. (I’m not talking about a little bit now and then. I mean going overboard–e.g. eating a whole package of Oreos within a short period of time.) I couldn’t find much to back up my suspicion that sugar was the culprit, but in just being honest with myself, it was the only thing that really stood out to me as being a possible cause of my cancer. I don’t believe cancer happens randomly and I don’t believe it happens as God’s judgement. I see it simply as cause-and-effect.

So why is so much money being spent on “research” and so little said about not just how much, but what we Westerners (and increasingly the rest of the world, as well) were putting into our bodies??? My conclusion has been that the big pharmaceuticals have, naturally, directed their R & D budget to developing drugs that they can sell to those who have become cancer victims. Surprise, surprise.

Since my cancer diagnosis, I’ve been going to a traditional herbal medicine doctor here in Vietnam. From the beginning, he told me my liver and kidneys were not healthy and that was what he began treating. Interestingly, when I went ahead and had the tumor removed, it was measurably smaller than when I was first diagnosed, about 3 weeks earlier! In that short time, I also eliminated all sugars from my diet except from vegetables and certain less-sweet fruit.

If I had not had surgery so quickly, I wonder how small the tumor would have become. I’ll never know, but I suspect it would have continued to shrink.

Since diagnosis in September 2008, I avoided sugar entirely for about 18 months. After that, I’ve been careful to limit sweets to (mostly) once a week. It’s harder when I travel and don’t have much control over the food I eat, but when I have a choice, I believe the smart choice is to avoid sugar like the plague!!!

Here’s the full article:

Is Sugar Toxic?

By Gary Taubes, NY Times Magazine, April 13, 2011
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, 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.”

Below is the article taken from the Australian newspaper The Age, but the information and results certainly apply to all. So, on to the article!

In the meantime, I couldn’t resist the temptation to post the article I just read in the New York Times called, “Mammograms’ Value in Cancer Fight at Issue”. As I’ve written before, I discovered the tumor in my breast myself and wish I’d never done the mammogram as other means of examining the tissue had already raised enough suspicion that a biopsy was done confirming cancer. So much pressure is applied that it’s excruciating and something I now testify that I’ll never repeat the procedure if I can possibly avoid it. (Perhaps the discomfort is less if your breasts are bigger???)  I’d also read that the results of the application of such force on a cancerous tumor could also spread the cancer to the surrounding tissue or blood–not a good thing. So I’m glad to read in this article that mammograms aren’t necessarily all that valuable and may even be considered just an option.

Here’s the full article:

A new study suggests that increased awareness and improved treatments rather than mammograms are the main force in reducing the breast cancer death rate. MultimediaGraphicA Small Benefit
RelatedHealth Guides: Breast Cancer | MammographyReaders’ CommentsReaders shared their thoughts on this article.Read All Comments (75) »
Starting in their 40s or 50s, most women in this country faithfully get a mammogram every year, as recommended by health officials. But the study suggests that the decision about whether to have the screening test may now be a close call.
The study, medical experts say, is the first to assess the benefit of mammography in the context of the modern era of breast cancer treatment. While it is unlikely to settle the debate over mammograms — and experts continue to disagree about the value of the test — it indicates that improved treatments with hormonal therapy and other targeted drugs may have, in a way, washed out most of mammography’s benefits by making it less important to find cancers when they are too small to feel.
Previous studies of mammograms, done decades ago, found they reduced the breast cancer death rate by 15 to 25 percent, a meaningful amount. But that was when treatment was much less effective.
In the new study, mammograms, combined with modern treatment, reduced the death rate by 10 percent, but the study data indicated that the effect of mammograms alone could be as low as 2 percent or even zero. A 10 percent reduction would mean that if 1,000 50-year-old women were screened over a decade, 996 women rather than 995.6 would not die from the cancer — an effect so tiny it may have occurred by chance.
The study, published Thursday in The New England Journal of Medicine, looked at what happened in Norway before and after 1996, when the country began rolling out mammograms for women ages 50 to 69 along with special breast cancer teams to treat all women with breast cancer.
The study is not perfect. The ideal study would randomly assign women to have mammograms or not. But, cancer experts said, no one would do such a study today when mammograms are generally agreed to prevent breast cancer deaths. In the study, which is continuing, women were followed for a maximum of 8.9 years. It is possible that benefits may emerge later.
Nonetheless, the new study is “very credible,” said Dr. Barnett Kramer, associate director for disease prevention at the National Institutes of Health.
“This is the first time researchers used real populations to compare the effects of treatment and mammography in the modern era of treatment,” Dr. Kramer said. “It shows the relative impacts of screening versus therapy in an era in which therapy has been improving.”
Dr. Otis Brawley of the American Cancer Society said in a statement that the investigators used “careful methodology.” The society, Dr. Brawley said, “believes that the total body of the science supports the fact that regular mammography is an important part of a woman’s preventive health care.”
Dr. Carol Lee, a radiologist at Memorial Sloan-Kettering Cancer Center and chairwoman of the breast imaging commission of the American College of Radiology, said the new study affirmed that mammography saves lives.
“Mortality from breast cancer is decreasing, and I have to believe that screening mammography has played a part,” Dr. Lee said.
In their study, the investigators analyzed data from all 40,075 Norwegian women who had received a diagnosis of breast cancer from 1986 to 2005, a time when treatment was changing markedly.
In that period, 4,791 women died. And, starting in 1996, Norway began offering mammograms to women ages 50 to 69 and assigning multidisciplinary treatment teams to all women with breast cancer, similar to the teams at many major medical centers in the United States. The question was, Did the program of mammograms and optimal new treatment with coordinated teams of surgeons, pathologists, oncologists, radiologists and nurses lower the breast cancer death rate?
The investigators found that women 50 to 69 who had mammograms and were treated by the special teams had a 10 percent lower breast cancer death rate than similar women who had had neither.
They also found, though, that the death rate fell by 8 percent in women over 70 who had the new treatment teams but had not been invited to have mammograms. And Dr. Kramer said he knew of no evidence that breast cancer was more easily treated in women over 70 than in women ages 50 to 69.
That means, Dr. H. Gilbert Welch of Dartmouth wrote in an additional analysis in an accompanying editorial, that mammography could have reduced the breast cancer death rate by as little as 2 percent, an amount so small that it is not really different from zero.
Two percent is an estimate, Dr. Welch said. But, he said, whatever the effect of mammograms is, “all the signals here are that it is much smaller than we believed.”
Dr. Laura Esserman, a professor of surgery and radiology at the University of California in San Francisco, said it tells her that “if you get the same treatment and the outcome is the same if you find it earlier or later, then you don’t make a difference when you find it early.”
And screening has a cost, Dr. Welch said. Screening 2,500 50-year-olds for a decade would identify 1,000 women with at least one suspicious mammogram resulting in follow-up tests. Five hundred would have biopsies. And 5 to 15 of those women would be treated for cancers that, if left alone, would have grown so slowly they would never have been noticed.
When the study was planned, the scientists expected that screening would be even more effective than it was in studies from decades ago. After all, mammography had improved and, in Norway, each mammogram was independently read by two radiologists, which should make it less likely that cancers would be missed. The researchers expected mammograms to reduce the breast cancer death rate by a third.
“We were surprised,” said Dr. Mette Kalager, the lead author of the paper who is a breast surgeon at Oslo University and a visiting scientist at the Harvard School of Public Health.
Marvin Zelen, a statistician at the Harvard School of Public Health and the Dana-Farber Cancer Institute, who was a member of the research team said even though the mammography benefit is small, if he were a woman he would get screened.
“It all depends on how you approach risk,” Dr. Zelen said. His approach, he says, is “minimax” — he wants to minimize the maximum risk — which, in this case, is dying of a cancer.
Dr. Kalager came to the opposite conclusion. She worries about the small chance of benefit in light of the larger chance of finding and treating a cancer that did not need to be treated.
“Since I’m a breast cancer surgeon, I know what being treated is like,” she says. The decision to be screened, she says, “is a matter of personal preference. Is it worth it to risk becoming a patient without it being necessary?”
Many women may still want mammograms, she says, and that is fine.
“I think we have to respect what women want to do.”

BARCELONA, Spain (AP)–Up to a third of breast cancer cases in Western countries could be avoided if women ate less and exercised more, researchers at a breast cancer conference said Thursday, renewing debate on a sensitive topic.

While better treatments, early diagnosis and mammogram screenings have dramatically slowed the disease, experts said the focus should now shift to changing behaviors like diet and physical activity. The comments added to a series of findings that lifestyle changes in areas such as smoking, eating, exercise and sun exposure can have a significant effect on all sorts of cancer rates.

“What can be achieved with screening has been achieved. We can’t do much more,” Carlo La Vecchia, head of epidemiology at the University of Milan, told The Associated Press. “It’s time to move onto other things.”

La Vecchia spoke Thursday on the influence of lifestyle factors at a European breast cancer conference in Barcelona.

Michelle Holmes, a cancer expert at Harvard University, said people might wrongly think their chances of getting cancer are more dependent on their genes than their lifestyle.

“The genes have been there for thousands of years, but if cancer rates are changing in a lifetime, that doesn’t have much to do with genes,” she told The Associated Press in a phone interview from Cambridge, Massachusetts.

Breast cancer is the most common cancer in women. In Europe, there were about 421,000 new cases and nearly 90,000 deaths in 2008, the latest available figures. The United States last year saw more than 190,000 new cases and 40,000 deaths.

Karen Benn, a spokeswoman for Europa Donna, a patient-focused breast cancer group, said it was impossible to ignore the increasingly stronger links between lifestyle and breast cancer.

“If we know there are healthier choices, we can’t not recommend them just because people might misinterpret the advice and feel guilty,” she said.

“If we are going to prevent breast cancer, then this message needs to get out, particularly to younger women.”

Other patient advocates agreed.

“We hope that no one comes away from these studies with the idea that they’re an attempt to ‘blame’ anyone for breast cancer,” said Diana Rowden, a vice president at Susan G. Komen for the Cure, a breast cancer group in Dallas. Rowden said the research was essential to warn people of their potential risks for developing breast cancer.

Other lifestyle factors like smoking and spending time in the sun have long been implicated in lung cancer and melanoma. Experts say there is now increasing evidence that what people eat and how much they weigh can contribute significantly to whether or not they develop cancers including those of the colon, stomach, and esophagus.

La Vecchia cited figures from the International Agency for Research on Cancer, which estimated that 25 to 30 percent of breast cancer cases could be avoided if women were thinner and exercised more.

The recommendation to stay slim applies only to breast cancer in post-menopausal women, as there isn’t enough evidence to know whether this applies to younger women.

Drinking less alcohol could also help. Experts estimate that having more than a couple of drinks a day can boost a woman’s risk of getting breast cancer by four to 10 percent.

The American Cancer Society recommends 45 to 60 minutes of physical activity five or more days a week to reduce a women’s risk of breast cancer.

In one study from the Women’s Health Initiative, as little as 1.25 to 2.5 hours per week of brisk walking reduced a woman’s risk by 18%. Walking 10 hours a week reduced the risk a little more.

La Vecchia said countries like Italy and France–where obesity rates have been stable for the past two decades–show that weight can be controlled at a population level.

“It’s hard to lose weight, but it’s not impossible,” he said. “The potential benefit of preventing cancer is worth it.”

It’s hard, but it’s not impossible to drastically reduce your sugar intake. I was really a sugar “junkie” even when I knew how bad it was–though I didn’t yet know the cancer connection. This great article, which I’ve shortened a bit, is quoting experts who know their stuff. Dr. David Servan-Schreiber, the fairly well-known cofounder of Doctors Without Borders, who also diagnosed his own brain cancer about 15 years ago is definitely someone worth listening to.

Here it is:

Is Eating Sugar Really That Bad for Us?

Is Eating Sugar Really That Bad for Us?
By Anneli Rufus, AlterNet, January 27, 2010
Excerpts of long article
Want to gross yourself out? Imagine eating eight teaspoons of sugar straight out of the bag. Yeek, right? That’s how much sugar is in a can of Coke. A Grande Vanilla Starbucks Frappuccino has 11. A McDonald’s Strawberry Triple Thick Shake has 27.
The American Heart Association’s latest guidelines stipulate that a moderately active woman should eat no more than six teaspoons of sugar per day; her male counterpart no more than nine. Yet according to the AHA’s latest statistics, the average American devours 22, and the average teenager devours 34.
Sugar is being blamed far and wide for the catastrophic rise in obesity, diabetes and cardiovascular disease—not to mention acne and tooth decay. In his bestselling book Anticancer: A New Way of Life (Viking, 2009), Doctors Without Borders cofounder David Servan-Schreiber avows that refined sugars “directly fuel the growth of cancer.” Killjoy. I gave up sweet drinks years ago, but I would live on ice cream if it wasn’t so embarrassing.
It’s a biblical-sounding question: Can something that tastes like heaven really be so bad? But this begs further questions: Good for whom? Bad for whom? Precisely how? Well, we know it’s good for business. Soft drinks represent a $115 billion industry in this country. Candy represents a $32 billion industry. (Americans spend $2 billion on Halloween candy alone.) According to the Centers for Disease Control, the annual cost of treating obesity-related medical conditions topped $140 billion in 2008, having nearly doubled in the previous decade. Diabetes isn’t simply a matter of insulin injections. Blindness and amputations, anyone?
Like any territory where our bodies and other people’s profits intersect, sugar is a battlefield. We enter that fray within hours of being born.
“When a brand-new baby is struggling to make sense of this scary world,” says nutrition therapist Elyse Resch, coauthor of Intuitive Eating (St. Martin’s, 2003), “the first thing it tastes is breast milk or formula.” Both fluids are rich in lactose, a disaccharide containing glucose, which the human body requires for survival; it’s our cells’ chief energy source. “Tasting that sweetness,” Resch says, “what’s the baby going to think? ‘Hey, every time I eat this, I’m going to get really calm and my tummy’s going to feel better and I’ll be happy.’”
But somewhere between the nipple and the artisanal chocolate, we transfer our affection from lactose to other sweet-tasting chemical compounds derived from other sources; mainly sugarcane, corn, beets and fruit. Although each of these sweeteners—too often collectively called “sugar” or “sugars,” which has traditionally landed sucrose, aka white sugar, with most of the bad rap—possesses a different chemical makeup, all of them contain a certain percentage of glucose.
When sugar enters the bloodstream during digestion, the pancreas releases insulin, a hormone that regulates the blood-sugar level by allowing cells throughout the body to absorb and use the glucose. Frequent deluges of glucose wreak havoc on blood-sugar levels. When an overwhelmed pancreas produces little or no insulin or the cells stop responding to whatever insulin is produced, glucose builds up in the bloodstream. That’s what we call diabetes.
And because the refining process strips away all enzymes, vitamins, minerals, fiber and other nutrients, refined sweeteners comprise nothing but empty calories. The body can metabolize these sweeteners only by drawing upon its own micronutrient storehouses: in other words, by draining its reserves. This process hinders the body’s ability to metabolize fatty acids; increased fatty-acid storage leads to obesity.
In which case, refined sugars aren’t just not food. They’re arguably antifood.
“A lot of things being sold as foods have low or zero nutritional value aside from calories,” says Joel Kimmons, a nutritional epidemiologist with the CDC’s Division of Nutrition, Physical Activity and Obesity. “From a health and culinary perspective, the foods that we feed our children, our families and ourselves need to have more than calories—they should include a wide variety of vitamins, minerals, protein, phytonutrients and fiber. The problem with sugar and other refined foods is that they dilute the nutritional content of your diet overall. It becomes more difficult to meet your nutritional requirements within your calorie limits every time you add sugar.”
Yet we add so much. Those 22 teaspoons a day—which comprises all sweeteners put into foods during processing and preparation by the manufacturer and the consumer—amount to 156 pounds per person per year, according to the USDA. This figure is “shocking,” avows Anticancer author Servan-Schreiber, railing against what he calls “the sugar boom” and noting that in 1830, the average American ate only 11 pounds of sugar a year.
Right, but it’s everywhere. (Every four grams of sugar, as listed on food labels, equals about one teaspoonful.) And it goes by so many names. Maltodextrin, rice syrup, dextrose, galactose—to choose from two dozen. Especially ubiquitous, in a country whose government subsidizes corn production, is high-fructose corn syrup (HFCS), a lower-cost alternative to cane sugar that was first developed in the 1950s, entered the processed-food scene big time during the late 1970s, and now represents between 40 and 50 pounds of our annual 156.
Many food activists, including Michael Pollan, point damning fingers at the fact that the industrialized world’s recent rise in obesity coincides with the mainstreaming of HFCS. For this, many blame HFCS’s high fructose content: 55 percent as compared to white sugar’s 50 percent. Several studies, such as one performed at the University of Texas in 2008, suggest that fructose metabolizes differently than glucose does and transforms into body fat much more rapidly than glucose does. Yet many, including a 2007 University of Maryland project, argue the opposite. “Based on the currently available evidence,” reads the Maryland report, “the expert panel concluded that HFCS does not appear to contribute to overweight and obesity any differently than do other energy sources.”
In any case, the corn industry has a powerful public-relations department that, based on past experience, will track me down and send me another stern-but-upbeat missive denouncing HFCS’s bad press and insisting that, as cited on the industry’s Web site, SweetSurprise.com, “High fructose corn syrup is simply a kind of corn sugar. It has the same number of calories as sugar and is handled similarly by the body.”
The corn industry’s basic line is that HFCS “is no worse than sucrose,” aka white sugar, says the CDC’s Joel Kimmons. “The error they’re making is in saying, ‘We’re just as good as sucrose.’ Sweeteners are a problem simply because they provide calories without the concomitant required nutrients. Some researchers suggest that problem with sugar is fructose,” which has been blamed not just for weight gain but also for illness; one 2008 University of Florida study links fructose consumption with liver disease; a University of Cincinnati study that same year links it with kidney disease and hypertension.
A study published last year by the Minneapolis-based nonprofit Institute for Agriculture and Trade Policy reported detectable levels of mercury in 17 out of 55 food products containing HFCS that had been purchased the previous year. Even what appears innocent probably isn’t: While the body can easily handle the amount of fructose in a single piece of actual fruit, fruit juices—even those without added sweeteners—are a different story.
Kimmons says HFCS is probably not handled much differently by the body than sucrose, given the similarity between the molecular makeup of both sweeteners. “However, the functional properties of HFCS have led to its being in all sorts of foods into which traditionally we would never consider putting a sweetener. It’s even in bread,” Kimmons laments.
HFCS’s texture allows it to be used in ways that sugar can’t. “In addition to providing sweetness,” we read at SweetSurprise.com, HFCS “gives chewy breakfast bars their soft texture and also protects freshness. High fructose corn syrup keeps products fresh by maintaining consistent moisture.”
A five-minute wander through my own kitchen reveals the presence of HFCS or just-plain-corn-syrup in seven different “savory” products, including Del Monte tomato sauce and a loaf of Old Country Round Top Wheat and Bran Bread.
“I work with a lot of people who describe themselves as not being able to control their cravings for sugar,” says nutrition therapist Karen Scheuner, who helps clients with eating disorders at the My Weigh therapy center in Oakland, California. “It is clear that food marketers do a really good job of priming us to crave sugar in the sense that it is ubiquitous, easy to buy and relatively cheap. On one hand our culture tells us to eat it, and on the other, it tells us to feel guilty for having eaten the chocolate cake. … Sugar is both widely abundant and forbidden,” Scheuner says.
First admitting, then appreciating the differences in flavor is a key to reducing sugar consumption, says Mireille Guiliano, bestselling author of French Women Don’t Get Fat: The Secret of Eating for Pleasure (Knopf, 2004).
“Learn to enjoy the first three bites. That’s all you need. Eat slowly, savor. The bad sugar is in sodas, cakes, cookies—all the stuff with HFCS. Read labels and don’t buy anything with HFCS. It’s poison,” Guiliano tells me. “If you eat the bad stuff … your body will go into a sugar crave that can last a few hours to a few days. So think before you eat, pay attention to how fast you eat and remember that once you start eating, your brain, not your stomach, will signal satiety. Twenty minutes is required for the stomach to feel full and since most people gulp down the sweets much faster, it wastes calories and makes you fat.”
“On the other hand, don’t fool yourself and believe you can do totally without sugar—most people can’t,” she says. “If you like chocolate, try a little square at the end of a meal and have dessert once in a while.” Guiliano adds: “Find a balance and remember: If you have dessert tonight, then no pain au chocolat for breakfast tomorrow. It’s doable with a little practice.”
Guiliano recommends honey “because it’s so sweet, as well as divinely flavorful, [so] you can use less—in my case, about half the amount of processed sugar.”
That’s what all this advice from everyone except the soft-drink, fast-food, candy and corn industry boils down to: using less. In urging us to go from 22 teaspoons of sugar per day to six or nine, the American Heart Association is asking us to cut down on sugar by 70 percent.

Killer superbug solution discovered in Norway

By Martha Mendoza and Margie Mason, Associated Press, Dec. 31, 2009

OSLO, Norway–Aker University Hospital is a dingy place to heal. The floors are streaked and scratched. A light layer of dust coats the blood pressure monitors. A faint stench of urine and bleach wafts from a pile of soiled bedsheets dropped in a corner.

Look closer, however, at a microscopic level, and this place is pristine. There is no sign of a dangerous and contagious staph infection that killed tens of thousands of patients in the most sophisticated hospitals of Europe, North America and Asia this year, soaring virtually unchecked.

The reason: Norwegians stopped taking so many drugs.

Twenty-five years ago, Norwegians were also losing their lives to this bacteria. But Norway’s public health system fought back with an aggressive program that made it the most infection-free country in the world. A key part of that program was cutting back severely on the use of antibiotics.

Now a spate of new studies from around the world prove that Norway’s model can be replicated with extraordinary success, and public health experts are saying these deaths–19,000 in the U.S. each year alone, more than from AIDS–are unnecessary.

“It’s a very sad situation that in some places so many are dying from this, because we have shown here in Norway that Methicillin-resistant Staphylococcus aureus (MRSA) can be controlled, and with not too much effort,” said Jan Hendrik-Binder, Oslo’s MRSA medical adviser. “But you have to take it seriously, you have to give it attention, and you must not give up.”‘

The World Health Organization says antibiotic resistance is one of the leading public health threats on the planet. A six-month investigation by The Associated Press found overuse and misuse of medicines has led to mutations in once curable diseases like tuberculosis and malaria, making them harder and in some cases impossible to treat.

Now, in Norway’s simple solution, there’s a glimmer of hope.

Dr. John Birger Haug shuffles down Aker’s scuffed corridors, patting the pocket of his baggy white scrubs. “My bible,” the infectious disease specialist says, pulling out a little red Antibiotic Guide that details this country’s impressive MRSA solution.

It’s what’s missing from this book–an array of antibiotics–that makes it so remarkable.

“There are times I must show these golden rules to our doctors and tell them they cannot prescribe something, but our patients do not suffer more and our nation, as a result, is mostly infection free,” he says.

Norway’s model is surprisingly straightforward. Norwegian doctors prescribe fewer antibiotics than any other country, so people do not have a chance to develop resistance to them.

Patients with MRSA are isolated and medical staff who test positive stay at home.

Doctors track each case of MRSA by its individual strain, interviewing patients about where they’ve been and who they’ve been with, testing anyone who has been in contact with them.

Haug unlocks the dispensary, a small room lined with boxes of pills, bottles of syrups and tubes of ointment. What’s here? Medicines considered obsolete in many developed countries. What’s not? Some of the newest, most expensive antibiotics, which aren’t even registered for use in Norway, “because if we have them here, doctors will use them,” he says.

He points to an antibiotic. “If I treated someone with an infection in Spain with this penicillin I would probably be thrown in jail,” he says, “and rightly so because it’s useless there.”

Norwegians are sanguine about their coughs and colds, toughing it out through low-grade infections.

“We don’t throw antibiotics at every person with a fever. We tell them to hang on, wait and see, and we give them a Tylenol to feel better,” says Haug.

Convenience stores in downtown Oslo are stocked with an amazing and colorful array–42 different brands at one downtown 7-Eleven–of soothing, but non-medicated, lozenges, sprays and tablets. All workers are paid on days they, or their children, stay home sick. And drug makers aren’t allowed to advertise, reducing patient demands for prescription drugs.

In fact, most marketing here sends the opposite message: “Penicillin is not a cough medicine,” says the tissue packet on the desk of Norway’s MRSA control director, Dr. Petter Elstrom.

He recognizes his country is “unique in the world and best in the world” when it comes to MRSA. Less than 1 percent of health care providers are positive carriers of MRSA staph.

But Elstrom worries about the bacteria slipping in through other countries. Last year almost every diagnosed case in Norway came from someone who had been abroad.

“So far we’ve managed to contain it, but if we lose this, it will be a huge problem,” he said. “To be very depressing about it, we might in some years be in a situation where MRSA is so endemic that we have to stop doing advanced surgeries, things like organ transplants, if we can’t prevent infections. In the worst case scenario we are back to 1913, before we had antibiotics.”

Forty years ago, a new spectrum of antibiotics enchanted public health officials, quickly quelling one infection after another. In wealthier countries that could afford them, patients and providers came to depend on antibiotics. Trouble was, the more antibiotics are consumed, the more resistant bacteria develop.

Norway responded swiftly to initial MRSA outbreaks in the 1980s by cutting antibiotic use. Thus while they got ahead of the infection, the rest of the world fell behind.

In Norway, MRSA has accounted for less than 1 percent of staph infections for years. That compares to 80 percent in Japan, the world leader in MRSA; 44 percent in Israel; and 38 percent in Greece.

In the U.S., cases have soared and MRSA cost $6 billion last year. Rates have gone up from 2 percent in 1974 to 63 percent in 2004. And in the United Kingdom, they rose from about 2 percent in the early 1990s to about 45 percent, although an aggressive control program is now starting to work.

About 1 percent of people in developed countries carry MRSA on their skin. Usually harmless, the bacteria can be deadly when they enter a body, often through a scratch. MRSA spreads rapidly in hospitals where sick people are more vulnerable, but there have been outbreaks in prisons, gyms, even on beaches. When dormant, the bacteria are easily detected by a quick nasal swab and destroyed by antibiotics.

Dr. John Jernigan at the U.S. Centers for Disease Control and Prevention said they incorporate some of Norway’s solutions in varying degrees, and his agency “requires hospitals to move the needle, to show improvement, and if they don’t show improvement they need to do more.”

And if they don’t? “Nobody is accountable to our recommendations,” he said, “but I assume hospitals and institutions are interested in doing the right thing.”

But can Norway’s program really work elsewhere?

The answer lies in the busy laboratory of an aging little public hospital about 100 miles outside of London. It’s here that microbiologist Dr. Lynne Liebowitz got tired of seeing the stunningly low Nordic MRSA rates while facing her own burgeoning cases.

So she turned Queen Elizabeth Hospital in Kings Lynn into a petri dish, asking doctors to almost completely stop using two antibiotics known for provoking MRSA infections.

One month later, the results were in: MRSA rates were tumbling. And they’ve continued to plummet. Five years ago, the hospital had 47 MRSA bloodstream infections. This year they’ve had one.

“I was shocked, shocked,” says Liebowitz, bouncing onto her toes and grinning as colleagues nearby drip blood onto slides and peer through microscopes in the hospital laboratory.

When word spread of her success, Liebowitz’s phone began to ring. So far she has replicated her experiment at four other hospitals, all with the same dramatic results.

“It’s really very upsetting that some patients are dying from infections which could be prevented,” she says. “It’s wrong.”

Around the world, various medical providers have also successfully adapted Norway’s program with encouraging results. A medical center in Billings, Mont., cut MRSA infections by 89 percent by increasing screening, isolating patients and making all staff–not just doctors–responsible for increasing hygiene.

In Japan, with its cutting-edge technology and modern hospitals, about 17,000 people die from MRSA every year.

Dr. Satoshi Hori, chief infection control doctor at Juntendo University Hospital in Tokyo, says doctors overprescribe antibiotics because they are given financial incentives to push drugs on patients.

Hori now limits antibiotics only to patients who really need them and screens and isolates high-risk patients. So far his hospital has cut the number of MRSA cases by two-thirds.

In 2001, the CDC approached a Veterans Affairs hospital in Pittsburgh about conducting a small test program. It started in one unit, and within four years, the entire hospital was screening everyone who came through the door for MRSA. The result: an 80 percent decrease in MRSA infections. The program has now been expanded to all 153 VA hospitals, resulting in a 50 percent drop in MRSA bloodstream infections, said Dr. Robert Muder, chief of infectious diseases at the VA Pittsburgh Healthcare System.

“It’s kind of a no-brainer,” he said. “You save people pain, you save people the work of taking care of them, you save money, you save lives and you can export what you learn to other hospital-acquired infections.”

How to Train the Aging Brain

By Barbara Strauch, NY Times, December 29, 2009

I love reading history, and the shelves in my living room are lined with fat, fact-filled books. There’s “The Hemingses of Monticello,” about the family of Thomas Jefferson’s slave mistress; there’s “House of Cards,” about the fall of Bear Stearns; there’s “Titan,” about John D. Rockefeller Sr.

The problem is, as much as I’ve enjoyed these books, I don’t really remember reading any of them. Certainly I know the main points. But didn’t I, after underlining all those interesting parts, retain anything else? It’s maddening and, sorry to say, not all that unusual for a brain at middle age: I don’t just forget whole books, but movies I just saw, breakfasts I just ate, and the names, oh, the names are awful. Who are you?

Brains in middle age, which, with increased life spans, now stretches from the 40s to late 60s, also get more easily distracted. Start boiling water for pasta, go answer the doorbell and–whoosh–all thoughts of boiling water disappear.

Indeed, aging brains, even in the middle years, fall into what’s called the default mode, during which the mind wanders off and begin daydreaming.

Given all this, the question arises, can an old brain learn, and then remember what it learns? Put another way, is this a brain that should be in school? As it happens, yes. While it’s tempting to focus on the flaws in older brains, that inducement overlooks how capable they’ve become. Over the past several years, scientists have looked deeper into how brains age and confirmed that they continue to develop through and beyond middle age.

Many longheld views, including the one that 40 percent of brain cells are lost, have been overturned. What is stuffed into your head may not have vanished but has simply been squirreled away in the folds of your neurons.

One explanation for how this occurs comes from Deborah M. Burke, a professor of psychology at Pomona College in California. Dr. Burke has done research on “tots,” those tip-of-the-tongue times when you know something but can’t quite call it to mind. Dr. Burke’s research shows that such incidents increase in part because neural connections, which receive, process and transmit information, can weaken with disuse or age.

But she also finds that if you are primed with sounds that are close to those you’re trying to remember–say someone talks about cherry pits as you try to recall Brad Pitt’s name–suddenly the lost name will pop into mind. The similarity in sounds can jump-start a limp brain connection. (It also sometimes works to silently run through the alphabet until landing on the first letter of the wayward word.)

This association often happens automatically, and goes unnoticed. Not long ago I started reading “The Prize,” a history of the oil business. When I got to the part about Rockefeller’s early days as an oil refinery owner, I realized, hey, I already know this from having read “Titan.” The material was still in my head; it just needed a little prodding to emerge.

Recently, researchers have found even more positive news. The brain, as it traverses middle age, gets better at recognizing the central idea, the big picture. If kept in good shape, the brain can continue to build pathways that help its owner recognize patterns and, as a consequence, see significance and even solutions much faster than a young person can.

The trick is finding ways to keep brain connections in good condition and to grow more of them.

“The brain is plastic and continues to change, not in getting bigger but allowing for greater complexity and deeper understanding,” says Kathleen Taylor, a professor at St. Mary’s College of California, who has studied ways to teach adults effectively. “As adults we may not always learn quite as fast, but we are set up for this next developmental step.”

Educators say that, for adults, one way to nudge neurons in the right direction is to challenge the very assumptions they have worked so hard to accumulate while young. With a brain already full of well-connected pathways, adult learners should “jiggle their synapses a bit” by confronting thoughts that are contrary to their own, says Dr. Taylor, who is 66.

Teaching new facts should not be the focus of adult education, she says. Instead, continued brain development and a richer form of learning may require that you “bump up against people and ideas” that are different. In a history class, that might mean reading multiple viewpoints, and then prying open brain networks by reflecting on how what was learned has changed your view of the world.

“There’s a place for information,” Dr. Taylor says. “We need to know stuff. But we need to move beyond that and challenge our perception of the world. If you always hang around with those you agree with and read things that agree with what you already know, you’re not going to wrestle with your established brain connections.”

Such stretching is exactly what scientists say best keeps a brain in tune: get out of the comfort zone to push and nourish your brain. Do anything from learning a foreign language to taking a different route to work.

“As adults we have these well-trodden paths in our synapses,” Dr. Taylor says. “We have to crack the cognitive egg and scramble it up. And if you learn something this way, when you think of it again you’ll have an overlay of complexity you didn’t have before–and help your brain keep developing as well.”

Jack Mezirow, a professor emeritus at Columbia Teachers College, has proposed that adults learn best if presented with what he calls a “disorienting dilemma,” or something that “helps you critically reflect on the assumptions you’ve acquired.”

“As adults we have all those brain pathways built up, and we need to look at our insights critically,” he says. “This is the best way for adults to learn. And if we do it, we can remain sharp.”

Dickens vs. Darwin
Chuck Colson, BreakPoint, December 28, 2009
Two of the most famous books in the Western canon turned 150 years old in 2009–On the Origin of Species by Charles Darwin, and A Tale of Two Cities by Charles Dickens.
But these anniversaries were celebrated in vastly different ways. While Darwin’s book was honored around the globe with films and websites and much more, relatively few people took notice that Dickens’s book had reached the same milestone.
Why the difference? My colleague Gina Dalfonzo, in an article on BreakPoint Online, suggests that one reason might be “the difference in worldview.” Gina points out that Origin of Species is built on Darwin’s materialistic principles, while A Tale of Two Cities takes a more traditional and biblical view of things.
It’s easy to see how our educational and media elite would gravitate toward the work that more faithfully reflects their own views, even if they don’t fully realize why they’re doing it.
Both authors lived at a time when Western culture was transitioning from faith in God to faith in humanity and its progress. Darwin went along with the change, embracing materialism and seeing his own scientific studies in its light.
But Dickens resisted. His faith has been called “simple”–he was not openly interested in complex theological questions, and he did not always adhere to church doctrine. But he maintained his belief in a loving Creator to the end of his life.
Isn’t it interesting that it was Darwin who was swept up in some of the uglier trends of his day? Dr. Benjamin Wiker has recently pointed out Darwin’s interest in the theories of Thomas Malthus, who thought that the “surplus population”–the weak and the unfit–were holding humanity back. The influence of this belief can be seen in Origin of Species and in Darwin’s other works.
Personally, Darwin believed in helping the poor and sick, but his personal life did not fit with his actual ideas. His theory boiled down to “might makes right,” and that meant survival was the highest ethical good.
On the other hand, Dickens parodied Malthus in his works, and showed the moral bankruptcy of his theories. In A Tale of Two Cities, a novel about the French Revolution, Dickens shows a struggle for power between two families, a struggle that turns into a cycle of violence and revenge. Madame Defarge, a central figure in the cycle, has no mercy for her victims once she gets them in her power; in fact, you might call her a fully Darwinian figure. In the end, the cycle of violence can only be broken, and Madame Defarge disarmed, by another character’s self-sacrifice–the kind of act that would have no place in a Darwinian view of the world. But in Dickens’ biblically influenced view, this act of love and selflessness signifies the highest good of which humanity is capable. Both Darwin and Dickens were optimistic men, but in fundamentally different ways. Darwin’s vision of future perfection would be merely a race of physically and mentally strong beings. Dickens’ hope was for a fundamentally moral society where the sick and weak were cared for, not pushed out of the way.
As the 150th anniversary year comes to an end for these two books, it’s a good time to compare how these radically different worldviews worked out in practice. All you’ve got to do is look at the evidence of the last 150 years for a clear answer to which one was true.