If you are what you eat, then what does it mean that the average American consumes 130 pounds of sugar a year? Sanjay Gupta reports on new research showing that beyond weight gain, sugar can take a serious toll on your health, worsening conditions ranging from heart disease to cancer. Some physicians go so far as to call sugar a toxin.

The following script is from “Sugar” which aired on April 1, 2012. Dr. Sanjay Gupta is the correspondent. Denise Schrier Cetta and Sumi Aggarwal, producers

The chances are good that sugar is a bigger part of your daily diet than you may realize which is why our story tonight is so important. New research coming out of some of America’s most respected institutions is starting to find that sugar, the way many people are eating it today, is a toxin and could be a driving force behind some of this country’s leading killers, including heart disease.

As a result of these findings, an anti-sugar campaign has sprung up, led by Dr. Robert Lustig, a California endocrinologist, who believes the consumption of added sugars has plunged America into a public health crisis.

Dr. Sanjay Gupta: Is sugar toxic?

Dr. Robert Lustig: I believe it is.

Dr. Sanjay Gupta: Do you ever worry that that’s– it just sounds a little bit over the top?

Dr. Robert Lustig: Sure. All the time. But it’s the truth.

Dr. Robert Lustig is a pediatric endocrinologist at the University of California, San Francisco and a pioneer in what is becoming a war against sugar.

Motivated by his own patients — too many sick and obese children – Dr. Lustig has concluded that sugar, more than any other substance, is to blame.

Dr. Sanjay Gupta: What are all these various diseases that you say are linked to sugar?

Dr. Robert Lustig: Obesity, type II diabetes, hypertension, and heart disease itself.

Lustig says the American lifestyle is killing us.

Dr. Sanjay Gupta: And most of it you say is preventable?

Dr. Robert Lustig: Seventy-five percent of it is preventable.

While Dr. Lustig has published a dozen scientific articles on the evils of sugar, it was his lecture on YouTube, called “Sugar: The Bitter Truth,” that brought his message to the masses.

By “bad food” Dr. Lustig means the obvious things such as table sugar, honey, syrup, sugary drinks and desserts, but also just about every processed food you can imagine, where sugar is often hidden: yogurts and sauces, bread, and even peanut butter. And what about the man-made, often vilified sweetener, high fructose corn syrup?

Dr. Sanjay Gupta: Is it worse than just table sugar?

Dr. Robert Lustig: No. ‘Cause it’s the exact same. They are basically equivalent. The problem is they’re both bad. They’re both equally toxic.

Since the 1970s, sugar consumption has gone down nearly 40 percent, but high fructose corn syrup has more than made up the difference. Dr. Lustig says they are both toxic because they both contain fructose — that’s what makes them sweet and irresistible.

Dr. Robert Lustig: We love it. We go out of our way to find it. I think one of the reasons evolutionarily is because there is no food stuff on the planet that has fructose that is poisonous to you. It is all good. So when you taste something that’s sweet, it’s an evolutionary Darwinian signal that this is a safe food.

Dr. Sanjay Gupta: We were born this way?

Dr. Robert Lustig: We were born this way.

Central to Dr. Lustig’s theory is that we used to get our fructose mostly in small amounts of fruit — which came loaded with fiber that slows absorption and consumption — after all, who can eat 10 oranges at a time? But as sugar and high fructose corn syrup became cheaper to refine and produce, we started gorging on them. Americans now consume 130 pounds per person a year — that’s a third of a pound every day.

Dr. Lustig believes those sweeteners are helping fuel an increase in the most deadly disease in America: heart disease. For years, he’s been a controversial voice.

But now, studies done by Kimber Stanhope, a nutritional biologist at the University of California, Davis are starting to back him up. She’s in the middle of a groundbreaking, five-year study which has already shown strong evidence linking excess high fructose corn syrup consumption to an increase in risk factors for heart disease and stroke. That suggests calories from added sugars are different than calories from other foods.

Dr. Sanjay Gupta: The mantra that you hear from most nutritionists is that a calorie is a calorie is a calorie.

Kimber Stanhope: And I think the results of the study showed clearly that is not true.

Stanhope’s conclusions weren’t easy to come by. Nutrition studies are expensive and difficult. Stanhope has paid groups of research subjects to live in this hospital wing for weeks at a time, under a sort of 24-hour lockdown. They undergo scans and blood tests – every calorie they ingest, meticulously weighed and prepared.

Kimber Stanhope: They’re never out of our sight. So we do know that they are consuming exactly what we need them to consume.

Dr. Sanjay Gupta: And they’re not sneaking any candy bars on the side.

Kimber Stanhope: Yeah, right, exactly.

For the first few days, participants eat a diet low in added sugars, so baseline blood levels can be measured.

Then, 25 percent of their calories are replaced with sweetened drinks and Stanhope’s team starts drawing blood every 30 minutes around the clock. And those blood samples? They revealed something disturbing.

Dr. Sanjay Gupta: And what are you starting to see?

Kimber Stanhope: We found that the subjects who consumed high fructose corn syrup had increased blood levels of LDL cholesterol and other risk factors for cardiovascular disease.

Dr. Sanjay Gupta: How quickly did these changes occur?

Kimber Stanhope: Within two weeks.

Kimber Stanhope’s study suggests that when a person consumes too much sweet stuff, the liver gets overloaded with fructose and converts some of it into fat. Some of that fat ends up in the bloodstream and helps generate a dangerous kind of cholesterol called small dense LDL. These particles are known to lodge in blood vessels, form plaque and are associated with heart attacks.

Dr. Sanjay Gupta: Did it surprise you when you first got these results back?

Kimber Stanhope: I would have to say I was surprised because when I saw our data, I started drinking and eating a whole lot less sugar. I would say our data surprised me.

So imagine, for these healthy young people, drinking a sweetened drink might be just as bad for their hearts as the fatty cheeseburgers we’ve all been warned about since the 1970s. That’s when a government commission mandated that we lower fat consumption to try and reduce heart disease.

Dr. Sanjay Gupta: So with the best of intentions, they say, “Time to reduce fat in the American diet?”

Dr. Robert Lustig: Exactly. And we did. And guess what? Heart disease, metabolic syndrome, diabetes and death are skyrocketing.

Dr. Lustig believes that’s primarily because we replaced a lot of that fat with added sugars.

Dr. Robert Lustig: Take the fat out of food, it tastes like cardboard. And the food industry knew that. So they replaced it with sugar.

Dr. Sanjay Gupta: This idea that sugar increases this particularly bad LDL, the small dense particles that are associated with heart disease. Do most doctors– do they know this?

Dr. Robert Lustig: No, they do not know this. This is new.

And it turns out, sugar has become a major focus in cancer research too. Lewis Cantley, is looking at the connection.

Dr. Sanjay Gupta: If you limit your sugar you decrease your chances of developing cancer?

Lewis Cantley: Absolutely.

Cantley, a Harvard professor and the head of the Beth Israel Deaconess Cancer Center, says when we eat or drink sugar, it causes a sudden spike in the hormone insulin, which can serve as a catalyst to fuel certain types of cancers.

Lewis Cantley: What we’re beginning to learn is that insulin can cause adverse effects in the various tissues. And of particular concern is cancer.

Why? Nearly a third of some common cancers — including breast and colon cancers — have something called insulin receptors on their surface. Insulin binds to these receptors and signals the tumor to start consuming glucose.

Lewis Cantley: This is your body…

Every cell in our body needs glucose to survive. But the trouble is, these cancer cells also use it to grow.

Lewis Cantley: So if you happen to have the tumor that has insulin receptors on it then it will get stimulated to take up the glucose that’s in the bloodstream rather than go into fat or muscle, the glucose goes into the tumor. And the tumor uses it to grow.

Dr. Sanjay Gupta: So you’ve just seen that tumor turn blue which is essentially reflective of glucose going into it.

Lewis Cantley: That’s right.

Dr. Sanjay Gupta: So these cancers, much in the same way that muscle will say, “Hey, I’d like some of that glucose, the fat says, “I would like some of that glucose,” the cancers have learned how to do this themselves as well?

Lewis Cantley: Yes. So they have evolved the ability to hijack that flow of glucose that’s going by in the bloodstream into the tumor itself.

Lewis Cantley’s research team is working on developing drugs that will cut off the glucose supply to cancer cells and keep them from growing. But until there’s a breakthrough, Cantley’s advice? Don’t eat sugar. And if you must, keep it to a minimum.

Lewis Cantley: In fact– I– you know, I live my life that way. I rarely eat sugar.

Dr. Sanjay Gupta: When you see a sugary drink or if I were to offer you one, what– with all that you know, what’s going through your mind?

Lewis Cantley: I probably would turn it down and get a glass of water.

But for most of us, that’s easier said than done…

Eric Stice: It turns out sugar is much more addictive than I think we had sort of realized early on.

Eric Stice, a neuroscientist at the Oregon Research Institute, is using functional MRI scanners to learn how our brains respond to sweetness.

Eric Stice: Sugar activates our brain in a special way. That’s very reminiscent of, you know, drugs like cocaine.

That’s right. Cocaine.

Dr. Sanjay Gupta: Let’s give it a shot…

I climbed into the MRI scanner to see how my brain would respond. That’s a straw that’s been rigged to deliver a tiny sip of soda into my mouth.

Eric Stice: Stay as still as you can, ok?

Just as it hit my tongue, the scanner detected increased blood rushing to certain regions of my brain. In these images, the yellow areas show that my reward region is responding to the sweet taste. Dopamine – a chemical that controls the brain’s pleasure center – is being released, just as it would in response to drugs or alcohol.

Dr. Sanjay Gupta: So dopamine is released. That sort of makes me feel good. I’m experiencing some pleasure from having this Coke.

Eric Stice: Right, that euphoric effect.

Dr. Sanjay Gupta: So far be it for people to realize this ’cause sugar is everywhere, but you’re saying this is one of the most addictive substances possibly that we have?

Eric Stice: It certainly is very good at firing the reward regions in our brain.

Eric Stice says by scanning hundreds of volunteers, he’s learned that people who frequently drink sodas or eat ice cream or other sweet foods may be building up a tolerance, much like drug users do. As strange as it sounds, that means the more you eat, the less you feel the reward. The result: you eat more than ever.

Eric Stice: If you overeat these on a regular basis it causes changes in the brain that basically it blunts your reward region response to the food, so then you eat more and more to achieve the same satisfaction you felt originally.

With all this new science emerging, we wanted to hear from the sugar industry, so we visited Jim Simon, who’s on the board of the Sugar Association, at a sugar cane farm in Louisiana.

Dr. Sanjay Gupta: Would it surprise you that almost every scientist that we talked to in researching this story told us they are eliminating all added sugars. They’re getting rid of it because they’re concerned about the health impacts.

Jim Simon: To say that the American consuming public is going to completely omit, eliminate, sweeteners out of their diet I don’t think gets us there.

Simon cautions that eliminating sugar wrongly vilifies one food, rather than working towards the long-term solution of reducing calories and exercising.

Dr. Sanjay Gupta: You know, a lot of people, Jim, are saying that sugar is different. That it is bad for your heart and is causing a lot of the problems we’re talking about. It is addictive and in some cases might even fuel cancers. What would you – I mean you’ve looked at this. You must have looked at some of these studies. What do you say about that?

Jim Simon: The science is not completely clear here.

Dr. Sanjay Gupta: But some of that’s, but some of these studies exist. I mean, what is a consumer, what are they to make of all that?

Jim Simon: Well, I would say to them, that they’ve got to approach, their diet in balance.

Dr. Robert Lustig agrees — we need a balanced diet — but his idea of balance is a drastic reduction in sugar consumption. To that end he co-authored an American Heart Association report recommending men should consume no more than 150 calories of added sugars a day. And women, just 100 calories. That’s less than the amount in just one can of soda.

Dr. Robert Lustig: Ultimately this is a public health crisis. And when it’s a public health crisis, you have to do big things and you have to do them across the board. Tobacco and alcohol are perfect examples. We have made a conscious choice that we’re not going to get rid of them, but we are going to limit their consumption. I think sugar belongs in this exact same wastebasket.

Source: CBS News

When the state of California added the compound 4-methylimidazole, also known as 4-MI or 4-MEI, to its list of known carcinogens in 2011, it created a problem for the soda industry.

The caramel color they used to give colas that distinctive, brown hue contained levels of 4-MI that would have warranted a cancer warning label on every can sold in the state.

And this wasn’t the industry’s only challenge. The Center for Science in the Public Interest petitioned the U.S. Food and Drug Administration to ban ammonia-sulfite caramel color. It’s a request the CSPI repeated this week after finding 4-MI in samples of Coke and Pepsi.

“This is nothing more than CSPI scare tactics, and their claims are outrageous,” writes the American Beverage Association in a statement released to the media.

“The science simply does not show that 4-MEI foods or beverages is a threat to human health,” the statement continues.

And the FDA seems to agree.

FDA spokesman Douglas Karas wrote in a statement that the FDA is currently reviewing the CSPI petition, but “it is important to understand that a consumer would have to consume well over a thousand cans of soda a day to reach the doses administered in the studies that have shown links to cancer in rodents.”

But in order to meet the requirements of California law — and avoid cancer warning labels on cans — soda manufacturers have come up with a solution: switch to a new, low 4-MI formulation of caramel coloring. Coca-Cola tells The Salt they’ve already begun the change.

“The company did make the decision to ask its caramel suppliers to make the necessary manufacturing process modifications to meet the requirement of the State of California,” Diana Garza Ciarlante, a Coca-Cola spokeswoman, wrote in an email.

Garza Ciarlante says caramel coloring in all Coke products has always been safe.

“The fact is that the body of science about 4-MEI in foods or beverages does not support the erroneous allegations that CSPI would like the public to believe,” she writes. Outside of California, no regulatory agency concerned with protecting the public’s health has stated that 4-MI is a human carcinogen.

“Caramel color is now — and has always been — safe and harmless” says Ted Nixon, CEO of D.D. Williamson, the world’s largest supplier of caramel color.

He explained that in order to modify the caramel color to reduce the levels of 4-MI, he sent his scientists back to the drawing board to change the manufacturing process.

“We did have to change these various inputs of temperature, pressure and the various ingredients we’re using in order to change [4-MI concentrations],” Nixon says.

And Nixon says he’ll be able to meet the demand of all of his soda clients, in rolling out this modified caramel color in products nationwide, and worldwide.

Coke says it will expand the use of the low-4-MI caramel color nationally, though Garza Ciarlante says it’s important to note that the modifications will not change Coca-Cola products.

Source: WBUR.org

*See Also: Coke, Pepsi make changes to avoid cancer warning (boston.com)

We physicians with all our training, knowledge and authority often acquire a rather large ego that tends to make it difficult to admit we are wrong. So, here it is. I freely admit to being wrong. As a heart surgeon with 25 years experience, having performed over 5,000 open-heart surgeries, today is my day to right the wrong with medical and scientific fact.

I trained for many years with other prominent physicians labelled “opinion makers.” Bombarded with scientific literature, continually attending education seminars, we opinion makers insisted heart disease resulted from the simple fact of elevated blood cholesterol.

The only accepted therapy was prescribing medications to lower cholesterol and a diet that severely restricted fat intake. The latter of course we insisted would lower cholesterol and heart disease. Deviations from these recommendations were considered heresy and could quite possibly result in malpractice.

It Is Not Working!

These recommendations are no longer scientifically or morally defensible. The discovery a few years ago that inflammation in the artery wall is the real cause of heart disease is slowly leading to a paradigm shift in how heart disease and other chronic ailments will be treated.

The long-established dietary recommendations have created epidemics of obesity and diabetes, the consequences of which dwarf any historical plague in terms of mortality, human suffering and dire economic consequences.

Despite the fact that 25% of the population takes expensive statin medications and despite the fact we have reduced the fat content of our diets, more Americans will die this year of heart disease than ever before.

Statistics from the American Heart Association show that 75 million Americans currently suffer from heart disease, 20 million have diabetes and 57 million have pre-diabetes. These disorders are affecting younger and younger people in greater numbers every year.

Simply stated, without inflammation being present in the body, there is no way that cholesterol would accumulate in the wall of the blood vessel and cause heart disease and strokes. Without inflammation, cholesterol would move freely throughout the body as nature intended. It is inflammation that causes cholesterol to become trapped.

Inflammation is not complicated — it is quite simply your body’s natural defence to a foreign invader such as a bacteria, toxin or virus. The cycle of inflammation is perfect in how it protects your body from these bacterial and viral invaders. However, if we chronically expose the body to injury by toxins or foods the human body was never designed to process,a condition occurs called chronic inflammation. Chronic inflammation is just as harmful as acute inflammation is beneficial.

What thoughtful person would willfully expose himself repeatedly to foods or other substances that are known to cause injury to the body? Well, smokers perhaps, but at least they made that choice willfully.

The rest of us have simply followed the recommended mainstream diet that is low in fat and high in polyunsaturated fats and carbohydrates, not knowing we were causing repeated injury to our blood vessels. This repeated injury creates chronic inflammation leading to heart disease, stroke, diabetes and obesity.

Let me repeat that: The injury and inflammation in our blood vessels is caused by the low fat diet recommended for years by mainstream medicine.

What are the biggest culprits of chronic inflammation? Quite simply, they are the overload of simple, highly processed carbohydrates (sugar, flour and all the products made from them) and the excess consumption of omega-6 vegetable oils like soybean, corn and sunflower that are found in many processed foods.

Take a moment to visualize rubbing a stiff brush repeatedly over soft skin until it becomes quite red and nearly bleeding. you kept this up several times a day, every day for five years. If you could tolerate this painful brushing, you would have a bleeding, swollen infected area that became worse with each repeated injury. This is a good way to visualize the inflammatory process that could be going on in your body right now.

Regardless of where the inflammatory process occurs, externally or internally, it is the same. I have peered inside thousands upon thousands of arteries. A diseased artery looks as if someone took a brush and scrubbed repeatedly against its wall. Several times a day, every day, the foods we eat create small injuries compounding into more injuries, causing the body to respond continuously and appropriately with inflammation.

While we savor the tantalizing taste of a sweet roll, our bodies respond alarmingly as if a foreign invader arrived declaring war. Foods loaded with sugars and simple carbohydrates, or processed with omega-6 oils for long shelf life have been the mainstay of the American diet for six decades. These foods have been slowly poisoning everyone.

How does eating a simple sweet roll create a cascade of inflammation to make you sick?

Imagine spilling syrup on your keyboard and you have a visual of what occurs inside the cell. When we consume simple carbohydrates such as sugar, blood sugar rises rapidly. In response, your pancreas secretes insulin whose primary purpose is to drive sugar into each cell where it is stored for energy. If the cell is full and does not need glucose, it is rejected to avoid extra sugar gumming up the works.

When your full cells reject the extra glucose, blood sugar rises producing more insulin and the glucose converts to stored fat.

What does all this have to do with inflammation? Blood sugar is controlled in a very narrow range. Extra sugar molecules attach to a variety of proteins that in turn injure the blood vessel wall. This repeated injury to the blood vessel wall sets off inflammation. When you spike your blood sugar level several times a day, every day, it is exactly like taking sandpaper to the inside of your delicate blood vessels.

While you may not be able to see it, rest assured it is there. I saw it in over 5,000 surgical patients spanning 25 years who all shared one common denominator — inflammation in their arteries.

Let’s get back to the sweet roll. That innocent looking goody not only contains sugars, it is baked in one of many omega-6 oils such as soybean. Chips and fries are soaked in soybean oil; processed foods are manufactured with omega-6 oils for longer shelf life. While omega-6′s are essential -they are part of every cell membrane controlling what goes in and out of the cell — they must be in the correct balance with omega-3′s.

If the balance shifts by consuming excessive omega-6, the cell membrane produces chemicals called cytokines that directly cause inflammation.

Today’s mainstream American diet has produced an extreme imbalance of these two fats. The ratio of imbalance ranges from 15:1 to as high as 30:1 in favor of omega-6. That’s a tremendous amount of cytokines causing inflammation. In today’s food environment, a 3:1 ratio would be optimal and healthy.

To make matters worse, the excess weight you are carrying from eating these foods creates overloaded fat cells that pour out large quantities of pro-inflammatory chemicals that add to the injury caused by having high blood sugar. The process that began with a sweet roll turns into a vicious cycle over time that creates heart disease, high blood pressure, diabetes and finally, Alzheimer’s disease, as the inflammatory process continues unabated.

There is no escaping the fact that the more we consume prepared and processed foods, the more we trip the inflammation switch little by little each day. The human body cannot process, nor was it designed to consume, foods packed with sugars and soaked in omega-6 oils.

There is but one answer to quieting inflammation, and that is returning to foods closer to their natural state. To build muscle, eat more protein. Choose carbohydrates that are very complex such as colorful fruits and vegetables. Cut down on or eliminate inflammation- causing omega-6 fats like corn and soybean oil and the processed foods that are made from them.

One tablespoon of corn oil contains 7,280 mg of omega-6; soybean contains 6,940 mg. Instead, use olive oil or butter from grass-fed beef.

Animal fats contain less than 20% omega-6 and are much less likely to cause inflammation than the supposedly healthy oils labelled polyunsaturated. Forget the “science” that has been drummed into your head for decades. The science that saturated fat alone causes heart disease is non-existent. The science that saturated fat raises blood cholesterol is also very weak. Since we now know that cholesterol is not the cause of heart disease, the concern about saturated fat is even more absurd today.

The cholesterol theory led to the no-fat, low-fat recommendations that in turn created the very foods now causing an epidemic of inflammation. Mainstream medicine made a terrible mistake when it advised people to avoid saturated fat in favor of foods high in omega-6 fats. We now have an epidemic of arterial inflammation leading to heart disease and other silent killers.

What you can do is choose whole foods your grandmother served and not those your mom turned to as grocery store aisles filled with manufactured foods. By eliminating inflammatory foods and adding essential nutrients from fresh unprocessed food, you will reverse years of damage in your arteries and throughout your body from consuming the typical American diet.

Source: Signs of the Times

They say there is mounting research that it is the type of oil used, and whether or not it has been used before, that really matters.

The Weston A. Price Foundation (WAPF) has warned the FDA that plans for salt restriction pose a health threat to Americans of all ages, in comments submitted to the agency yesterday.

The Weston A. Price Foundation is a non-profit nutrition education foundation dedicated to accurate scientific information about diet and health.

WAPF noted that by entitling their document “Approaches to Reducing Sodium Consumption,” the FDA has signaled that it has already decided that Americans’ sodium consumption should be reduced. But neither history nor the scientific evidence support this approach.

“A study from 1991 indicates that people need about one and one-half teaspoons of salt per day,” says Sally Fallon Morell, president of the Weston A. Price Foundation. “Anything less triggers a cascade of hormones to recuperate sodium from the waste stream, hormones that make people vulnerable to heart disease and kidney problems. This is proven biochemistry. Yet, FDA as well as USDA want to mandate drastically restricted sodium consumption at about one-half teaspoon per day.”

WAPF testimony noted that salt plays a critical role in body physiology and brain function. In the elderly, lack of salt is associated with increased hip fractures and cognitive decline; low salt diets in growing children predisposes to poor neurological development.

Proposals to restrict salt cite benefits to hypertension. But only 30 percent of the population experiences a slight reduction in blood pressure on a salt restricted diet, while 70 percent show no benefit.

“These statistics don’t justify a population-wide policy of salt reduction,” says Fallon Morell

Recent studies show a correlation of salt restriction with increased heart failure and with insulin resistance leading to diabetes. Studies show that even modest reductions in salt cause an increased risk of cardiovascular disease. Higher incidence of inflammatory markers and altered lipoproteins are also found by researchers evaluating those on salt reduced diets. These factors are precursors to metabolic syndrome, which predicts heart problems and diabetes.

Both sodium and chloride, the components of salt, are needed for digestion. These elements form the basis of cellular metabolism and our only source of adequate intake is salt.

The Foundation also cautions the FDA that salt reductions will increase food safety risks. Salt is a traditional food preservation medium with an excellent track record. Artisan cheeses, preserved meats like salami and traditional pickled foods like sauerkraut require salt to prevent contamination by pathogens.

“Our biggest concern is that with FDA dictates against salt, manufacturers will add imitation salt flavors like Senomyx to processed foods,” says Fallon Morell. ”Marketed as a food, so it does not require testing, and added in amounts so small that is does not need to be labeled, this neurotropic compound can interfere with our natural taste for salt, leading to severe deficiencies. Or, people will become obese as they eat more and more, trying to satisfy the body’s need for salt.”

The Weston A. Price Foundation fully referenced commentary is posted  at http://www.westonaprice.org/images/pdfs/wapf-comments-fda-salt.pdf.

Source: www.westonaprice.org

Patricia Cochran, an Inupiat from Northwestern Alaska, is talking about the native foods of her childhood: “We pretty much had a subsistence way of life. Our food supply was right outside our front door. We did our hunting and foraging on the Seward Peninsula and along the Bering Sea.

“Our meat was seal and walrus, marine mammals that live in cold water and have lots of fat. We used seal oil for our cooking and as a dipping sauce for food. We had moose, caribou, and reindeer. We hunted ducks, geese, and little land birds like quail, called ptarmigan. We caught crab and lots of fish—salmon, whitefish, tomcod, pike, and char. Our fish were cooked, dried, smoked, or frozen. We ate frozen raw whitefish, sliced thin. The elders liked stinkfish, fish buried in seal bags or cans in the tundra and left to ferment. And fermented seal flipper, they liked that too.”

Cochran’s family also received shipments of whale meat from kin living farther north, near Barrow. Beluga was one she liked; raw muktuk, which is whale skin with its underlying blubber, she definitely did not. “To me it has a chew-on-a-tire consistency,” she says, “but to many people it’s a mainstay.” In the short subarctic summers, the family searched for roots and greens and, best of all from a child’s point of view, wild blueberries, crowberries, or salmonberries, which her aunts would mix with whipped fat to make a special treat called akutuq—in colloquial English, Eskimo ice cream.

Now Cochran directs the Alaska Native Science Commission, which promotes research on native cultures and the health and environmental issues that affect them. She sits at her keyboard in Anchorage, a bustling city offering fare from Taco Bell to French cuisine. But at home Cochran keeps a freezer filled with fish, seal, walrus, reindeer, and whale meat, sent by her family up north, and she and her husband fish and go berry picking—“sometimes a challenge in Anchorage,” she adds, laughing. “I eat fifty-fifty,” she explains, half traditional, half regular American.

No one, not even residents of the northernmost villages on Earth, eats an entirely traditional northern diet anymore. Even the groups we came to know as Eskimo—which include the Inupiat and the Yupiks of Alaska, the Canadian Inuit and Inuvialuit, Inuit Greenlanders, and the Siberian Yupiks—have probably seen more changes in their diet in a lifetime than their ancestors did over thousands of years. The closer people live to towns and the more access they have to stores and cash-paying jobs, the more likely they are to have westernized their eating. And with westernization, at least on the North American continent, comes processed foods and cheap carbohydrates—Crisco, Tang, soda, cookies, chips, pizza, fries. “The young and urbanized,” says Harriet Kuhnlein, director of the Centre for Indigenous Peoples’ Nutrition and Environment at McGill University in Montreal, “are increasingly into fast food.” So much so that type 2 diabetes, obesity, and other diseases of Western civilization are becoming causes for concern there too.

Today, when diet books top the best-seller list and nobody seems sure of what to eat to stay healthy, it’s surprising to learn how well the Eskimo did on a high-protein, high-fat diet. Shaped by glacial temperatures, stark landscapes, and protracted winters, the traditional Eskimo diet had little in the way of plant food, no agricultural or dairy products, and was unusually low in carbohydrates. Mostly people subsisted on what they hunted and fished. Inland dwellers took advantage of caribou feeding on tundra mosses, lichens, and plants too tough for humans to stomach (though predigested vegetation in the animals’ paunches became dinner as well). Coastal people exploited the sea. The main nutritional challenge was avoiding starvation in late winter if primary meat sources became too scarce or lean.

These foods hardly make up the “balanced” diet most of us grew up with, and they look nothing like the mix of grains, fruits, vegetables, meat, eggs, and dairy we’re accustomed to seeing in conventional food pyramid diagrams. How could such a diet possibly be adequate? How did people get along on little else but fat and animal protein?

What the diet of the Far North illustrates, says Harold Draper, a biochemist and expert in Eskimo nutrition, is that there are no essential foods—only essential nutrients. And humans can get those nutrients from diverse and eye-opening sources.

One might, for instance, imagine gross vitamin deficiencies arising from a diet with scarcely any fruits and vegetables. What furnishes vitamin A, vital for eyes and bones? We derive much of ours from colorful plant foods, constructing it from pigmented plant precursors called carotenoids (as in carrots). But vitamin A, which is oil soluble, is also plentiful in the oils of cold-water fishes and sea mammals, as well as in the animals’ livers, where fat is processed. These dietary staples also provide vitamin D, another oil-soluble vitamin needed for bones. Those of us living in temperate and tropical climates, on the other hand, usually make vitamin D indirectly by exposing skin to strong sun—hardly an option in the Arctic winter—and by consuming fortified cow’s milk, to which the indigenous northern groups had little access until recent decades and often don’t tolerate all that well.

As for vitamin C, the source in the Eskimo diet was long a mystery. Most animals can synthesize their own vitamin C, or ascorbic acid, in their livers, but humans are among the exceptions, along with other primates and oddballs like guinea pigs and bats. If we don’t ingest enough of it, we fall apart from scurvy, a gruesome connective-tissue disease. In the United States today we can get ample supplies from orange juice, citrus fruits, and fresh vegetables. But vitamin C oxidizes with time; getting enough from a ship’s provisions was tricky for early 18th- and 19th-century voyagers to the polar regions. Scurvy—joint pain, rotting gums, leaky blood vessels, physical and mental degeneration—plagued European and U.S. expeditions even in the 20th century. However, Arctic peoples living on fresh fish and meat were free of the disease.

Impressed, the explorer Vilhjalmur Stefansson adopted an Eskimo-style diet for five years during the two Arctic expeditions he led between 1908 and 1918. “The thing to do is to find your antiscorbutics where you are,” he wrote. “Pick them up as you go.” In 1928, to convince skeptics, he and a young colleague spent a year on an Americanized version of the diet under medical supervision at Bellevue Hospital in New York City. The pair ate steaks, chops, organ meats like brain and liver, poultry, fish, and fat with gusto. “If you have some fresh meat in your diet every day and don’t overcook it,” Stefansson declared triumphantly, “there will be enough C from that source alone to prevent scurvy.”

In fact, all it takes to ward off scurvy is a daily dose of 10 milligrams, says Karen Fediuk, a consulting dietitian and former graduate student of Harriet Kuhnlein’s who did her master’s thesis on vitamin C. (That’s far less than the U.S. recommended daily allowance of 75 to 90 milligrams—75 for women, 90 for men.) Native foods easily supply those 10 milligrams of scurvy prevention, especially when organ meats—preferably raw—are on the menu. For a study published with Kuhnlein in 2002, Fediuk compared the vitamin C content of 100-gram (3.55-ounce) samples of foods eaten by Inuit women living in the Canadian Arctic: Raw caribou liver supplied almost 24 milligrams, seal brain close to 15 milligrams, and raw kelp more than 28 milligrams. Still higher levels were found in whale skin and muktuk.

As you might guess from its antiscorbutic role, vitamin C is crucial for the synthesis of connective tissue, including the matrix of skin. “Wherever collagen’s made, you can expect vitamin C,” says Kuhnlein. Thick skinned, chewy, and collagen rich, raw muktuk can serve up an impressive 36 milligrams in a 100-gram piece, according to Fediuk’s analyses. “Weight for weight, it’s as good as orange juice,” she says. Traditional Inuit practices like freezing meat and fish and frequently eating them raw, she notes, conserve vitamin C, which is easily cooked off and lost in food processing.

Hunter-gatherer diets like those eaten by these northern groups and other traditional diets based on nomadic herding or subsistence farming are among the older approaches to human eating. Some of these eating plans might seem strange to us—diets centered around milk, meat, and blood among the East African pastoralists, enthusiastic tuber eating by the Quechua living in the High Andes, the staple use of the mongongo nut in the southern African !Kung—but all proved resourceful adaptations to particular eco-niches. No people, though, may have been forced to push the nutritional envelope further than those living at Earth’s frozen extremes. The unusual makeup of the far-northern diet led Loren Cordain, a professor of evolutionary nutrition at Colorado State University at Fort Collins, to make an intriguing observation.

Four years ago, Cordain reviewed the macronutrient content (protein, carbohydrates, fat) in the diets of 229 hunter-gatherer groups listed in a series of journal articles collectively known as the Ethnographic Atlas. These are some of the oldest surviving human diets. In general, hunter-gatherers tend to eat more animal protein than we do in our standard Western diet, with its reliance on agriculture and carbohydrates derived from grains and starchy plants. Lowest of all in carbohydrate, and highest in combined fat and protein, are the diets of peoples living in the Far North, where they make up for fewer plant foods with extra fish. What’s equally striking, though, says Cordain, is that these meat-and-fish diets also exhibit a natural “protein ceiling.” Protein accounts for no more than 35 to 40 percent of their total calories, which suggests to him that’s all the protein humans can comfortably handle.

This ceiling, Cordain thinks, could be imposed by the way we process protein for energy. The simplest, fastest way to make energy is to convert carbohydrates into glucose, our body’s primary fuel. But if the body is out of carbs, it can burn fat, or if necessary, break down protein. The name given to the convoluted business of making glucose from protein is gluconeogenesis. It takes place in the liver, uses a dizzying slew of enzymes, and creates nitrogen waste that has to be converted into urea and disposed of through the kidneys. On a truly traditional diet, says Draper, recalling his studies in the 1970s, Arctic people had plenty of protein but little carbohydrate, so they often relied on gluconeogenesis. Not only did they have bigger livers to handle the additional work but their urine volumes were also typically larger to get rid of the extra urea. Nonetheless, there appears to be a limit on how much protein the human liver can safely cope with: Too much overwhelms the liver’s waste-disposal system, leading to protein poisoning—nausea, diarrhea, wasting, and death.

Whatever the metabolic reason for this syndrome, says John Speth, an archaeologist at the University of Michigan’s Museum of Anthropology, plenty of evidence shows that hunters through the ages avoided protein excesses, discarding fat-depleted animals even when food was scarce. Early pioneers and trappers in North America encountered what looks like a similar affliction, sometimes referred to as rabbit starvation because rabbit meat is notoriously lean. Forced to subsist on fat-deficient meat, the men would gorge themselves, yet wither away. Protein can’t be the sole source of energy for humans, concludes Cordain. Anyone eating a meaty diet that is low in carbohydrates must have fat as well.

Stefansson had arrived at this conclusion, too, while living among the Copper Eskimo. He recalled how he and his Eskimo companions had become quite ill after weeks of eating “caribou so skinny that there was no appreciable fat behind the eyes or in the marrow.” Later he agreed to repeat the miserable experience at Bellevue Hospital, for science’s sake, and for a while ate nothing but defatted meat. “The symptoms brought on at Bellevue by an incomplete meat diet [lean without fat] were exactly the same as in the Arctic . . . diarrhea and a feeling of general baffling discomfort,” he wrote. He was restored with a fat fix but “had lost considerable weight.” For the remainder of his year on meat, Stefansson tucked into his rations of chops and steaks with fat intact. “A normal meat diet is not a high-protein diet,” he pronounced. “We were really getting three-quarters of our calories from fat.” (Fat is more than twice as calorie dense as protein or carbohydrate, but even so, that’s a lot of lard. A typical U.S diet provides about 35 percent of its calories from fat.)

Stefansson dropped 10 pounds on his meat-and-fat regimen and remarked on its “slenderizing” aspect, so perhaps it’s no surprise he’s been co-opted as a posthumous poster boy for Atkins-type diets. No discussion about diet these days can avoid Atkins. Even some researchers interviewed for this article couldn’t resist referring to the Inuit way of eating as the “original Atkins.” “Superficially, at a macronutrient level, the two diets certainly look similar,” allows Samuel Klein, a nutrition researcher at Washington University in St. Louis, who’s attempting to study how Atkins stacks up against conventional weight-loss diets. Like the Inuit diet, Atkins is low in carbohydrates and very high in fat. But numerous researchers, including Klein, point out that there are profound differences between the two diets, beginning with the type of meat and fat eaten.

Fats have been demonized in the United States, says Eric Dewailly, a professor of preventive medicine at Laval University in Quebec. But all fats are not created equal. This lies at the heart of a paradox—the Inuit paradox, if you will. In the Nunavik villages in northern Quebec, adults over 40 get almost half their calories from native foods, says Dewailly, and they don’t die of heart attacks at nearly the same rates as other Canadians or Americans. Their cardiac death rate is about half of ours, he says. As someone who looks for links between diet and cardiovascular health, he’s intrigued by that reduced risk. Because the traditional Inuit diet is “so restricted,” he says, it’s easier to study than the famously heart-healthy Mediterranean diet, with its cornucopia of vegetables, fruits, grains, herbs, spices, olive oil, and red wine.

A key difference in the typical Nunavik Inuit’s diet is that more than 50 percent of the calories in Inuit native foods come from fats. Much more important, the fats come from wild animals.

Wild-animal fats are different from both farm-animal fats and processed fats, says Dewailly. Farm animals, cooped up and stuffed with agricultural grains (carbohydrates) typically have lots of solid, highly saturated fat. Much of our processed food is also riddled with solid fats, or so-called trans fats, such as the reengineered vegetable oils and shortenings cached in baked goods and snacks. “A lot of the packaged food on supermarket shelves contains them. So do commercial french fries,” Dewailly adds.

Trans fats are polyunsaturated vegetable oils tricked up to make them more solid at room temperature. Manufacturers do this by hydrogenating the oils—adding extra hydrogen atoms to their molecular structures—which “twists” their shapes. Dewailly makes twisting sound less like a chemical transformation than a perversion, an act of public-health sabotage: “These man-made fats are dangerous, even worse for the heart than saturated fats.” They not only lower high-density lipoprotein cholesterol (HDL, the “good” cholesterol) but they also raise low-density lipoprotein cholesterol (LDL, the “bad” cholesterol) and triglycerides, he says. In the process, trans fats set the stage for heart attacks because they lead to the increase of fatty buildup in artery walls.

Wild animals that range freely and eat what nature intended, says Dewailly, have fat that is far more healthful. Less of their fat is saturated, and more of it is in the monounsaturated form (like olive oil). What’s more, cold-water fishes and sea mammals are particularly rich in polyunsaturated fats called n-3 fatty acids or omega-3 fatty acids. These fats appear to benefit the heart and vascular system. But the polyunsaturated fats in most Americans’ diets are the omega-6 fatty acids supplied by vegetable oils. By contrast, whale blubber consists of 70 percent monounsaturated fat and close to 30 percent omega-3s, says Dewailly.

Omega-3s evidently help raise HDL cholesterol, lower triglycerides, and are known for anticlotting effects. (Ethnographers have remarked on an Eskimo propensity for nosebleeds.) These fatty acids are believed to protect the heart from life-threatening arrhythmias that can lead to sudden cardiac death. And like a “natural aspirin,” adds Dewailly, omega-3 polyunsaturated fats help put a damper on runaway inflammatory processes, which play a part in atherosclerosis, arthritis, diabetes, and other so-called diseases of civilization.

You can be sure, however, that Atkins devotees aren’t routinely eating seal and whale blubber. Besides the acquired taste problem, their commerce is extremely restricted in the United States by the Marine Mammal Protection Act, says Bruce Holub, a nutritional biochemist in the department of human biology and nutritional sciences at the University of Guelph in Ontario.

“In heartland America it’s probable they’re not eating in an Eskimo-like way,” says Gary Foster, clinical director of the Weight and Eating Disorders Program at the Pennsylvania School of Medicine. Foster, who describes himself as open-minded about Atkins, says he’d nonetheless worry if people saw the diet as a green light to eat all the butter and bacon—saturated fats—they want. Just before rumors surfaced that Robert Atkins had heart and weight problems when he died, Atkins officials themselves were stressing saturated fat should account for no more than 20 percent of dieters’ calories. This seems to be a clear retreat from the diet’s original don’t-count-the-calories approach to bacon and butter and its happy exhortations to “plow into those prime ribs.” Furthermore, 20 percent of calories from saturated fats is double what most nutritionists advise. Before plowing into those prime ribs, readers of a recent edition of the Dr. Atkins’ New Diet Revolution are urged to take omega-3 pills to help protect their hearts. “If you watch carefully,” says Holub wryly, “you’ll see many popular U.S. diets have quietly added omega-3 pills, in the form of fish oil or flaxseed capsules, as supplements.”

Needless to say, the subsistence diets of the Far North are not “dieting.” Dieting is the price we pay for too little exercise and too much mass-produced food. Northern diets were a way of life in places too cold for agriculture, where food, whether hunted, fished, or foraged, could not be taken for granted. They were about keeping weight on.

This is not to say that people in the Far North were fat: Subsistence living requires exercise—hard physical work. Indeed, among the good reasons for native people to maintain their old way of eating, as far as it’s possible today, is that it provides a hedge against obesity, type 2 diabetes, and heart disease. Unfortunately, no place on Earth is immune to the spreading taint of growth and development. The very well-being of the northern food chain is coming under threat from global warming, land development, and industrial pollutants in the marine environment. “I’m a pragmatist,” says Cochran, whose organization is involved in pollution monitoring and disseminating food-safety information to native villages. “Global warming we don’t have control over. But we can, for example, do cleanups of military sites in Alaska or of communication cables leaching lead into fish-spawning areas. We can help communities make informed food choices. A young woman of childbearing age may choose not to eat certain organ meats that concentrate contaminants. As individuals, we do have options. And eating our salmon and our seal is still a heck of a better option than pulling something processed that’s full of additives off a store shelf.”

Not often in our industrial society do we hear someone speak so familiarly about “our” food animals. We don’t talk of “our pig” and “our beef.” We’ve lost that creature feeling, that sense of kinship with food sources. “You’re taught to think in boxes,” says Cochran. “In our culture the connectivity between humans, animals, plants, the land they live on, and the air they share is ingrained in us from birth.

“You truthfully can’t separate the way we get our food from the way we live,” she says. “How we get our food is intrinsic to our culture. It’s how we pass on our values and knowledge to the young. When you go out with your aunts and uncles to hunt or to gather, you learn to smell the air, watch the wind, understand the way the ice moves, know the land. You get to know where to pick which plant and what animal to take.

“It’s part, too, of your development as a person. You share food with your community. You show respect to your elders by offering them the first catch. You give thanks to the animal that gave up its life for your sustenance. So you get all the physical activity of harvesting your own food, all the social activity of sharing and preparing it, and all the spiritual aspects as well,” says Cochran. “You certainly don’t get all that, do you, when you buy prepackaged food from a store.

“That’s why some of us here in Anchorage are working to protect what’s ours, so that others can continue to live back home in the villages,” she adds. “Because if we don’t take care of our food, it won’t be there for us in the future. And if we lose our foods, we lose who we are.” The word Inupiat means “the real people.” “That’s who we are,” says Cochran.

Source: Discover Magazine

Her diet, based on the traditional diets of ancient humans provides her body with the healing ingredients necessary for healthful living.

Here she tells the story of her journey.

Visit Dr. Wahls’ Website: TerryWahls.com

A new study found that low-salt diets increase the risk of death from heart attacks and strokes and do not prevent high blood pressure, but the research’s limitations mean the debate over the effects of salt in the diet is far from over.

In fact, officials at the Centers for Disease Control and Prevention felt so strongly that the study was flawed that they criticized it in an interview, something they normally do not do.

Dr. Peter Briss, a medical director at the centers, said that the study was small; that its subjects were relatively young, with an average age of 40 at the start; and that with few cardiovascular events, it was hard to draw conclusions. And the study, Dr. Briss and others say, flies in the face of a body of evidence indicating that higher sodium consumption can increase the risk of cardiovascular disease.

“At the moment, this study might need to be taken with a grain of salt,” he said.

The study is published in the May 4 issue of The Journal of the American Medical Association. It involved only those without high blood pressure at the start, was observational, considered at best suggestive and not conclusive. It included 3,681 middle-aged Europeans who did not have high blood pressure or cardiovascular disease and followed them for an average of 7.9 years.

The researchers assessed the participants’ sodium consumption at the study’s start and at its conclusion by measuring the amount of sodium excreted in urine over a 24-hour period.  All the sodium that is consumed is excreted in urine within a day, so this method is the most precise way to determine sodium consumption.

The investigators found that the less salt people ate, the more likely they were to die of heart disease — 50 people in the lowest third of salt consumption (2.5 grams of sodium per day) died during the study as compared with 24 in the medium group (3.9 grams of sodium per day) and 10 in the highest salt consumption group (6.0 grams of sodium per day).  And while those eating the most salt had, on average, a slight increase in systolic blood pressure — a 1.71-millimeter increase in pressure for each 2.5-gram increase in sodium per day — they were no more likely to develop hypertension.

“If the goal is to prevent hypertension” with lower sodium consumption, said the lead author, Dr. Jan A. Staessen, a professor of medicine at the University of Leuven, in Belgium, “this study shows it does not work.”

But among the study’s other problems, Dr. Briss said, its subjects who seemed to consume the smallest amount of sodium also provided less urine than those consuming more, an indication that they might not have collected all of their urine in an 24-hour period.

Dr. Frank Sacks of the Harvard School of Public Health agreed and also said the study was flawed.

“It’s a problematic study,” Dr. Sacks said. “We shouldn’t be guiding any kind of public health decisions on it.”

Dr. Michael Alderman, a blood pressure researcher at Albert Einstein College of Medicineand editor of the American Journal of Hypertension, said medical literature on salt and health effects was inconsistent. But, Dr. Alderman said, the new study is not the only one to find adverse effects of low-sodium diets. His own study, with people who had high blood pressure, found that those who ate the least salt were most likely to die.

Dr. Alderman said that he once was an unpaid consultant for the Salt Institute but that he now did no consulting for it or for the food industry and did not receive any support or take any money from industry groups.

Lowering salt consumption, Dr. Alderman said, has consequences beyond blood pressure. It also, for example, increases insulin resistance, which can increase the risk of heart disease.

“Diet is a complicated business,” he said. “There are going to be unintended consequences.”

One problem with the salt debates, Dr. Alderman said, is that all the studies are inadequate. Either they are short-term intervention studies in which people are given huge amounts of salt and then deprived of salt to see effects on blood pressure or they are studies, like this one, that observe populations and ask if those who happen to consume less salt are healthier.

“Observational studies tell you what people will experience if they select a diet,” Dr. Alderman said. “They do not tell you what will happen if you change peoples’ sodium intake.”

What is needed, Dr. Alderman said, is a large study in which people are randomly assigned to follow a low-sodium diet or not and followed for years to see if eating less salt improves health and reduces the death rate from cardiovascular disease.

But that study, others say, will never happen.

“This is one of those really interesting situations,” said Dr. Lawrence Appel, a professor of medicine, epidemiology and international health at Johns Hopkins Medical Institutions. “You can say, ‘O.K., let’s dismiss the observational studies because they have all these problems.’ ” But, he said, despite the virtues of a randomized controlled clinical trial, such a study “will never ever be done.” It would be impossible to keep people on a low-sodium diet for years with so much sodium added to prepared foods.

Dr. Briss adds that it would not be prudent to defer public health actions while researchers wait for results of a clinical trial that might not even be feasible.

Dr. Alderman disagrees.

“The low-salt advocates suggest that all 300 million Americans be subjected to a low-salt diet. But if they can’t get people on a low-salt diet for a clinical trial, what are they talking about?”

He added: “It will cost money, but that’s why we do science. It will also cost money to change the composition of food.”

Source: New York Times

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’s lecture as posted on YouTube is viewable in its entirety at the bottom of this article.

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 avoidthat.

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.

Source: New York Times Magazine

Watch  “Sugar: The Bitter Truth,” Robert Lustig May 26, 2009: