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[silk] Is sugar toxic?

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  • Udhay Shankar N
    I am posting teh entire long piece below as I think it is an important discussion to have - I wanted the opinions of the folks here, some of whom have been
    Message 1 of 86 , Apr 18, 2011
      I am posting teh entire long piece below as I think it is an important
      discussion to have - I wanted the opinions of the folks here, some of
      whom have been saying similar things for many years.

      Udhay

      http://www.nytimes.com/2011/04/17/magazine/mag-17Sugar-t.html?_r=2&pagewanted=all

      April 13, 2011
      Is Sugar Toxic?
      By GARY TAUBES

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

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

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

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

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

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

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

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

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

      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@...) 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@...).



      --
      ((Udhay Shankar N)) ((udhay @ pobox.com)) ((www.digeratus.com))
    • Udhay Shankar N
      ... ​Some more disquieting data: http://www.theage.com.au/interactive/2017/what-sugar-does-to-your-brain/ What sugar does to your brain Why sugar could be to
      Message 86 of 86 , Jan 3 12:00 AM
        On Fri, Apr 4, 2014 at 11:22 AM, Udhay Shankar N <udhay@...> wrote:

        > http://www.nytimes.com/2011/04/17/magazine/mag-17Sugar-t.
        > html?_r=2&pagewanted=all
        >
        > Another interesting long read, even if the language sometimes is a
        > little too wide-eyed.
        >
        > http://ngm.nationalgeographic.com/2013/08/sugar/cohen-text


        ​Some more disquieting data:

        http://www.theage.com.au/interactive/2017/what-sugar-does-to-your-brain/

        What sugar does to your brain

        Why sugar could be to blame for your bad memory – and can it get you hooked?

        To tell the story of what sugar does to your brain, you have to start with
        the thought that triggers your need for a hit of sweetness.

        It often happens in the afternoon when your brain, which runs on sugar,
        starts to get hungry.

        To satiate the craving your brain activates a string of neurons, often
        referred to as the reward pathway, which pump the chemical dopamine into
        your brain.

        All of a sudden you need a chocolate bar or that sweet pastry you saw at
        lunchtime.

        If you act on that craving, the reward pathway then switches mode, pumping
        chemicals such as beta-endorphins into your brain, generating feelings of
        pleasure.

        Your brain thanks you for the sugar hit by making the chocolate bar
        literally taste sweeter, says Dr Zane Andrews, a scientist at Monash
        University who studies how our brains regulate control of our diets.

        But if you respond to the brain’s need for sugar too often, the reward
        pathway can develop tolerance to the stimulus.

        “That means we need to eat more to get the same feeling. That’s a classic
        feature of addiction,” says Dr Andrews.

        The prefrontal cortex acts as the brain's “brakes” but it's weakened by too
        much sugar (and fat).

        You do possess the ability to resist cravings - it’s called willpower.

        That ability to stop yourself comes in part from a network of neurons
        called inhibitory neural circuits. These circuits occur throughout your
        brain, but are particularly concentrated in the parts involved in
        decision-making, impulse control and delaying gratification.

        “They are kind of like the brain’s brakes,” explains RMIT sugar scientist
        Dr Amy Reichelt.

        But if you find you can’t resist that craving for a chocolate bar don’t be
        ashamed – you may be able to blame it on the sugar.

        In world-first research using rats, Dr Reichelt has shown that high-sugar
        diets can alter decision-making and the ability to control behaviour.

        Her studies revealed that rats fed on high-sugar diets suffered a loss of
        those willpower neurons.

        “When you’re consuming these high-sugar diets and you’re told to stop
        consuming them, you’ve made alterations to your behavioural control – and
        that can lead to your diet falling apart,” she says. “You’re literally
        unable to resist that cake.”

        Much of the research, though, on sugar’s impact on the brain has yet to be
        replicated in people.

        In another study conducted last year, a team led by Professor Richard
        Stevenson from Macquarie University asked a group of volunteers to rate how
        much they wanted to eat several snack foods when they were feeling hungry
        versus when they were sated.

        They found that the volunteers who regularly ate a high-fat, high-sugar
        diet were much more likely to crave snack foods even when they weren’t
        hungry.

        The scientists suggest the high-sugar and fat diet was actually impairing
        the ability of the brain to block food cravings.

        “We’re all prone to try to excuse our behaviour by claiming we’re addicted.
        Which is rubbish.”
        Professor Margaret Morris

        Can you get hooked on sugar?
        Let’s say you manage to use your willpower to get on top of your craving
        for that chocolate bar. But the feeling does not go away.

        Your mouth runs dry. You can taste the first bite. Your work performance
        drops. It’s just like ... (you think wistfully to yourself) ... craving a
        cigarette.

        Maybe the similarities run deeper than that.

        In world-first research, Queensland University of Technology neuroscientist
        Professor Selena Bartlett claims to have found evidence that high-sugar
        diets act on the brain in very similar ways to tobacco, alcohol or other
        physically addictive substances.

        Her work targets the basolateral amygdala, a small region in the brain that
        is linked to fear and stress, and the prefrontal cortex, which sits at the
        front of the brain.

        She found that mice who had binged on sugar had far fewer links between the
        neurons in these regions and looked a lot like animals addicted to alcohol.

        A pyramidal neuron in the brain of a rat fed a normal diet. Photo: Courtesy
        Dr Arnauld Belmer, QUT A pyramidal neuron in the brain of a rat fed a
        normal diet. Photo: Courtesy Dr Arnauld Belmer, QUT A pyramidal neuron in
        the brain of a rat that has been bingeing on sugar for 10 weeks. Photo:
        Courtesy Dr Arnauld Belmer, QUT A pyramidal neuron in the brain of a rat
        that has been bingeing on sugar for 10 weeks. Photo: Courtesy Dr Arnauld
        Belmer, QUT
        More remarkably, when her researchers gave mice a medication used to treat
        nicotine addiction, they stopped eating as much sugar.

        “What we discovered in the last five years is that sugar is as addictive as
        alcohol. We nailed a very specific set of circuits in the brain that
        alcohol and nicotine bind to,” Professor Bartlett says.

        “We showed sugar using the same protocols could change the brain in exactly
        the same way as alcohol and nicotine do, which labels it into the addictive
        pathway.”

        In a hotly contested field, claims about sugar’s addictive qualities are
        among the most fraught.

        “When we look at obesity, we’re not finding those addictive qualities at
        all. Where’s the evidence for that?,” says Professor John Dixon, a
        researcher with the Baker Heart and Diabetes Institute.

        “More than any other disease, people believe they know what causes obesity.
        They don’t.”

        Even University of NSW Professor Margaret Morris, one of the leading
        proponents of the theory that sugar can damage the brain, says the evidence
        for actual addiction is weak.

        “We did a review of the evidence and we had to conclude, on the balance of
        evidence, that there was no strong evidence for sugar addiction in humans.

        “We’re all prone to try to excuse our behaviour by claiming we’re addicted.
        Which is rubbish.”

        In animals, and men and women, a high-sugar diet seems to impair the
        hippocampus, which controls memory.

        “Sugar seems to adversely impact the hippocampus and longer-term brain
        structures that are involved in decision-making and pleasure.”
        Professor Richard Stevenson

        I can’t forget but I don’t remember what
        Most research on sugar’s impact focuses on a small horseshoe-shaped region
        in the middle of the brain, about level with your ear, called the
        hippocampus. It is responsible for memory formation and navigation; to do
        that, it needs to be continually building new neurons or rewiring existing
        pathways.

        This role makes it vulnerable to external stresses – potentially such as
        diets high in sugar.

        In animals, the research is fairly clear: sugar damages their ability to
        make new memories.

        The first person to confirm that effect in humans was Professor Richard
        Stevenson, leading a team at Macquarie University, earlier this year.

        He had volunteers spend a week eating a high-fat, high-sugar breakfast.
        After just four days, their performance on memory tests fell dramatically.

        “Sugar seems to adversely impact the hippocampus and longer-term brain
        structures that are involved in decision-making and pleasure,” he says.

        The University of Sydney’s Dr Kieron Rooney once did a quick study –
        largely for a lark – on a small group of people who signed up to a popular
        quit sugar diet. He was surprised to find that their memories had
        significantly improved by the end of the diet.

        Professor Morris has spent more than 20 years putting rats on high-sugar
        diets. She says the results are consistent and repeatable. “Weight gain and
        a cognitive decline - it’s quite a large effect,” she says.

        Obesity is characterised by low-grade inflammation throughout the body. The
        theory, says Professor Morris, is that with excess sugar and fat in the
        diet inflammation also appears to affect the hippocampus, impairing its
        function.

        High-sugar diets also reduce the levels of a chemical needed for new neuron
        formation - which is crucially important to the hippocampus’s job of
        creating new memories.

        The most prominent and studied impact of sugar on the hippocampus is
        navigation. We use the hippocampus to build an internal map of our
        surroundings.

        Professor Morris found that navigation for rats fed a high-sugar diet is
        significantly impaired.

        She also makes it clear though that her research on sugar’s effects on the
        brain has not been replicated in people, so the link to how humans will
        react is not definite.

        “It’s probable but it’s far from confirmed,” sums up Professor Morris.

        The green flecks are new immature neurons in the hippocampus of a mouse but
        their number has been reduced by chronic sugar consumption. Photo: Courtesy
        Dr Arnauld Belmer, QUT The green flecks are new immature neurons in the
        hippocampus of a mouse but their number has been reduced by chronic sugar
        consumption. Photo: Courtesy Dr Arnauld Belmer, QUT

        What can we do?

        So, what can you do to protect your brain from sugar?

        Beyond trying to eat less of it, not much, experts say.

        To deal with the addictive powers of sugar, Professor Selena Bartlett
        suggests meditation exercises to build focus and willpower.

        Omega-3s, the fats contained in fish oil, have shown potential
        neuro-protective effects in some trials, plus the ability to bolster
        hippocampal function. Professor Morris suggests using them to supplement
        your diet.

        But ultimately, says Professor Morris, the only magic pill is exercise and
        following the Australian Dietary Guidelines, which recommend limiting your
        intake of added sugars.

        “There is no question that there is some ability of the system to reset. If
        people adopt a healthy diet, that could go some way to reversing the
        effect.”

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