"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."
"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."
"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."
"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."
"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.”
"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."
http://www.nytimes.com/2011/04/17/magazine/mag-17Sugar-t.html?pagewanted=1&_r=1&src=twr
excellent article.
"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."
"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."
"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."
"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.”
"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."
http://www.nytimes.com/2011/04/17/magazine/mag-17Sugar-t.html?pagewanted=1&_r=1&src=twr
excellent article.
