It’s not often that we’re lucky enough to get a new book or article from Gary Taubes, an award-winning medical and science journalist for the New York Times, a Robert Wood Johnson Foundation independent investigator in health policy, and the author of Why We Get Fat. But a new article appeared in this week’s NY Times Magazine, and it’s a doozy, because it ties together discussions on this blog in the last few weeks, especially about insulin and even more especially about hyperinsulinemia and non-alcoholic fatty liver disease (NAFLD). For those who have wondered “what reason” they could give to their doctors to get them to order a Fasting Insulin test when/if their A1c’s or Fasting Blood Glucose results are “normal” — wonder no more. Read the article below, print it out, and insist your doctor read it. Reassure them if you must that it’s only an article and not “a whole book!”
The article, Is Sugar Toxic?, is actually a two-fer, since it also provides a direct link to Taubes first article about the real causes of heart disease, What if It’s All Been a Big Fat Lie?, that appeared in a July, 2002 edition of the New York Times and set off a firestorm of controversy about eating fat. Both articles should be required reading for doctors, dietitians and nutritionists, even if they have to be tied down in chairs with their unwilling eyes propped open a la the protagonist of Kubrick’s A Clockwork Orange. They would probably need to be tied down after reading the first paragraph of 2002’s WIIABABFL:
“If the members of the American medical establishment were to have a collective find-yourself-standing-naked-in-Times-Square-type nightmare, this might be it. They spend 30 years ridiculing Robert Atkins, author of the phenomenally-best-selling ”Dr. Atkins’ Diet Revolution” and ”Dr. Atkins’ New Diet Revolution,” accusing the Manhattan doctor of quackery and fraud, only to discover that the unrepentant Atkins was right all along. Or maybe it’s this: they find that their very own dietary recommendations — eat less fat and more carbohydrates — are the cause of the rampaging epidemic of obesity in America. Or, just possibly this: they find out both of the above are true.”
And you’d likely have to tighten the restraints to get them through a few salient paragraphs in Is Sugar Toxic? [NOTE: which also has wider implications for anyone following Simeons’ original diet protocol, discussed in Part IV of that analysis], to wit:
“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. . . . 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.”
“. . . 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. . . . 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.”
“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.” . . . [Yudkin] 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. . . . 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.”
NOTE: Jane E. Brody has probably handed out more bad health advice than just about any journalist writing today. If she says “A” — do an immediate 180 toward “Z.”
“. . . 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. . . . For those who have heart attacks, metabolic syndrome will very likely be the reason. . . . 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. . . . 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.”
“. . . 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. What causes the liver to accumulate fat in humans? Harking back to Lustig, there’s also the very real possibility that it is caused by sugar.
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.
If it’s sugar that causes insulin resistance . . . 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.”
The implications of Lustig’s work, and now Taubes’ article, which I hope everyone will read from first word to last, are truly frightening for anyone with high blood glucose levels, but are ominous for anyone with high fasting levels of insulin. It’s bad enough to have impaired blood sugar control, in which the pancreas must pump out ever higher amounts of insulin to deal with the glucose/fructose (even from fruit, if you are insulin-resistant, especially high-fructose fruits like oranges) you eat. After reading this article, it’s clear to me at least that having insulin levels so high that they remain in the blood stream more or less at the same horrific levels 24/7 — even at night when you’re not eating anything — may be far worse. How do you know where you are in terms of Metabolic Syndrome? Test your fasting insulin level. And do it now.