New FDA Warnings On Statins

Statins are not the only way to lower cholesterol

Possible Side Effects: Memory Loss, High Blood Sugar, Diabetes

The Food and Drug Administration recently announced that statin drugs, used by millions of Americans to lower cholesterol, must carry warnings on their labels about the following potential side effects:

  • Memory loss and mental confusion
  • Risk of high blood sugar
  • Risk of being diagnosed with Type 2 diabetes

“The value of statins in preventing heart disease has been clearly established,” said Amy G. Egan, M.D., M.PH., deputy director for safety in FDA’s Division of Metabolism and Endocrinology Products. “Their benefit is indisputable, but they need to be taken with care and knowledge of their side effects.”

“The effects of the Pritikin Program are all positive. With lifestyle changes, you don’t have to worry about negative side effects,” notes Dr. Scheib.Cardiologist Ronald Scheib, MD, Medical Director of the Pritikin Longevity Center, agrees. “Statins have important benefits like lowering cholesterol and perhaps reducing the inflammation in blood vessel walls that are associated with the development of cholesterol-related plaque. But statins are drugs, and drugs, by their very nature, have both risks and benefits. It is wrong to assume that any drug is 100 percent ‘safe.’”

“Individualization of statin therapy is necessary,” continues Dr. Scheib. “For each patient, the decision-making process regarding the risk/benefit ratio must take into consideration several factors, including the occurrence of a previous coronary event and multiple risk factors. For many, the benefits of statins outweigh the potential negative side effects.”

Lifestyle Change – No Risks

One form of cholesterol-lowering therapy that is side-effect-free is lifestyle change, such as the food, fitness, and lifestyle program taught by the physicians, registered dietitians, and other faculty at the Pritikin Longevity Center. “The effects of the Pritikin Program are all positive. With lifestyle changes, you don’t have to worry about negative side effects,” notes Dr. Scheib.

Key lifestyle actions of the Pritikin Program for lowering total and LDL (bad) cholesterol levels:
  • Eat far fewer saturated fats (such as butter, palm oil, coconut oil, meat fats, and milk fats); trans fats (partially hydrogenated oils); and dietary cholesterol.
  • Eat far more fiber-rich foods, especially soluble fiber from food such as beans, yams, oats, barley, and berries.
  • Eat vegetable proteins (such as tofu and beans) in place of animal protein like meat and poultry.
  • Eat fewer refined sugars and refined grains (such as white flour).
  • Exercise regularly: 1) Aerobic exercise daily, a minimum of 30 minutes, alternating moderate-intensity days with vigorous-intensity days; 2) Full-body resistance routine two to three times weekly; and 3) Stretching exercises two to three times weekly.
  • Lose excess weight, especially belly fat.

The results of the Pritikin Program in improving cholesterol levels and overall heart-health have been documented in more than 100 studies in peer-reviewed publications. One major study found that among more than 4,500 men and women attending the Pritikin Center for three weeks, total cholesterol levels fell on average 23 percent. LDL bad cholesterol also fell 23 percent. (Sources: The New England Journal of Medicine and the Annals of Internal Medicine.)

The evidence of the value of the Pritikin Program in reducing heart disease risk factors like cholesterol and preventing heart disease is so strong that recently the Pritikin Program was approved by Medicare for Intensive Cardiac Rehabilitation.

For more information from the FDA regarding its new warnings about statins, go to:


More Whole Grains, Less Belly Fat


Want a flatter, leaner tummy? Remove from your diet white, processed grains like white bread and white rice, and eat more whole grains such as oatmeal, barley, bulgar, 100% whole-wheat bread, whole-wheat pasta, and brown rice, research has found.

More Whole Grains, Less Belly FatStudying 50 obese men and women, scientists at Pennsylvania State University put all 50 subjects on a calorie-reducing diet for 12 weeks, but divided them into two groups. Half were instructed to eat whole grains; the other half were told to choose refined, processed grains, like white-flour foods.

After 12 weeks, average weight loss for both groups was about the same: 8 to 11 pounds. But the whole-grain group showed significantly greater reductions in the percentage of fat around the middle, the researchers reported in the American Journal of Clinical Nutrition.

That’s great news not only for a svelte tummy but also for health. Numerous studies published over the past two decades have found that belly fat is particularly harmful to our hearts and health. Abdominal fat is one of the characteristics of a now-epidemic condition in the U.S. called the metabolic syndrome, which is a collection of several risk factors for diabetes, heart disease, and stroke.

Belly fat is also linked with chronic low-level inflammation in the blood vessels, which in turn is a harbinger of heart attacks and strokes. Another risk factor that tumbled among the whole-grain eaters (and not the refined grain eaters) in the Pennylvania State University study was a key marker of chronic inflammation – C-reactive protein, or CRP.

Similarly, research on people who adopted the Pritikin Program found that CRP levels plummeted. Within two to three weeks, C-reactive protein decreased 45% among women, 39% among men, and 41% among children.Metabolism, 53: 377, 2004; Journal of Applied Physiology, 100: 1657, 2006; Atherosclerosis, 191: 98, 2007.

At the Pritikin Center, guests learn their fat-to-muscle ratio via DEXA Body Composition Scanning. After two to three weeks, follow-up scanning reveals how powerful Pritikin living is in shedding fat and increasing muscle.Studies have also found that among both adults and children, the Pritikin Program reversed the clinical diagnosis of metabolic syndrome.

“But please don’t feel complacent if you don’t have a pot belly,” urges Dr. Danine Fruge, Associate Medical Director at the Pritikin Longevity Center.

“There’s a tragic – and growing – problem in our country, and we doctors call this problem TOFI, which means thin on the outside and fat on the inside.”

You are a TOFI if your weight is normal, but your body mass shows a high ratio of fat to muscle. You may not see the fat, but it’s there, under the skin, and deposited around and inside the internal organs, including the heart, muscle, and liver. It’s largely the result of our sedentary lifestyles — our lack of muscle use — and our fatty, sugary, white-flour-focused calorie-dense diets.

At the Pritikin Longevity Center, guests learn their fat-to-muscle ratio via DEXA Body Composition Scanning. After two to three weeks, follow-up scanning reveals how powerful Pritikin living is in shedding fat and increasing muscle. The end result is a leaner, fitter, better toned body.

What does it mean to be a TOFI? “It means,” warns Dr. Fruge, “that despite normal weight, you are still at increased risk for diabetes, heart disease, and other diseases related to obesity.”

Bottom line: Excess body fat, whether it’s around your belly or deep within, is dangerous.

“So get up and get moving!” encourages Dr. Fruge. “And enjoy the many benefits of the Pritikin Eating Plan, rich in healthful whole foods like whole grains, fruits, vegetables, and beans.

“I know of nothing else in medicine that comes close to what a healthy lifestyle like Pritikin can do.”

Eating Well with Canada’s Food Guide

Eating Well with Canada’s Food Guide


Following Canada’s Food Guide recommendations will ensure that you’ll get your daily requirements for vitamins, minerals and other important nutrients, helping you to achieve overall good health and vitality.


Healthy eating recommendations:

  • Eating plenty of vegetables and fruit. Every day, include a dark green (such as broccoli, asparagus and romaine lettuce) and an orange (such as carrots and sweet potato) vegetable.
  • Making half of your grain products whole grain (such as brown and wild rice, bulgur, quinoa and oatmeal) each day.
  • Serving fish twice a week (such as rainbow trout, salmon and sardines). See Health Canada’s advice on limiting exposure to mercury from certain types of fish.
  • Including beans, lentils and tofu (meat alternatives) more often in your diet.
  • Drinking lower fat milk and milk alternatives such as fortified soy beverages. Be aware that other fortified drinks such as orange juice, rice, almond and potato do not contain the same level of protein found in milk or soy.
  • Using unsaturated oils such as canola, olive, and soybean as well as non-hydrogenated margarines (Include a small amount – 30 to 45 mL/2 to 3 tbsp a day).
  • Taking a Vitamin D supplement if you are over the age of 50. If you are planning on becoming pregnant, take a multivitamin that contains folic acid. Once pregnant, your supplements should also contain iron.
  • Adults (18 to 64) and older adults (65+) must get at least 150 minutes of moderate- to vigorous-intensity physical activity per week. Children need moderate to vigorous physical activity for at least 60 minutes every day.

What not to eat:

  • foods and beverages high in calories, fat, sugar or salt such as desserts, fried snack foods, alcohol and sugar sweetened beverages
  • saturated fats from fatty meats, butter, lard, shortening and hard margarines
  • trans fats found in such foods as doughnuts, cookies and other baked goods. 

Recommended number of servings per day:


Canada’s Food Guide also outlines the number of servings we should eat from each of the four food groups and provides guidance on portion sizes. The recommended number of serving sizes is based on age and gender. Look at the chart below to find your recommended number of Food Guide servings per day. Remember that it is just the average amount that people should try to eat each day.

Sugar/glucose-fructose is HFCS!

Public understanding of sugar is poor: Canadian Sugar Institute

Labeling: Making sense of sugar

Photograph by: Sun , graphics


Read more:

Ok HFCS is corn syrup that is converted from 100% glucose to a fructose/glucose mix.  It comes in three varieties HFCS 90 (baking), HFCS 55 (soft drinks) and HFCS 45 (sports drinks) with the number being the percent of fructose.

It’s the high levels of fructose that you body converts into triglycerides when your intake levels are higher then your body’s needs (glucose is also turned to fat via insulin).

Now sugar (table sugar/sucrose) is 50% glucose/50% fructose, honey’s ratio of glucose/fructose is 45% glucose/55% fructose (same as HFCS 55).

But here is where we get to the problem of sugar, that it’s a problem when you eat to much of it.  It really doesn’t matter which kind of either (though honey does has some anti-oxidant properties it will still raise triglycerides) in the end added sugar is added sugar

Avoid this toxic mix at all costs. Fructose is very unhealthy for your well being.

Called glucose/fructose in Canada

High fructose corn syrup

From Wikipedia, the free encyclopedia

Structural formulae of fructose (left) and glucose (right)

High-fructose corn syrup (HFCS)—also called glucose/fructose in Canada,[1]glucose–fructose syrup (GFS) in the EU,[2][3] and high-fructose maize syrup in other countries—comprises any of a group of corn syrups that has undergoneenzymatic processing to convert some of its glucose into fructose to produce a desired sweetness.

The 7 Basic Food Bullets to Eat and Live By Nutrient Rich Principles

superfoodsbig check markIn this post I want to cover the most basic healthy eating plan; the 7 basic food bullets to eat and live by that you will want to check off each day to ensure you are always eating healthy, or more accurately put “nutrient rich”.

[See below] but first read the lead in so that you appreciate these, “the magnificent 7”,  even more.

Amidst an endless flurry of new and existing foodstuffs “designed” to seduce us, highjack our taste buds and subsequently our health; it is the following 7-point-plan that will ensure you’re body is optimally nourished, flooded with the micronutrients that make a healthy eating style “healthy” and able to function right.

Now, I know this may seem like just another set of food guidelines; another list of “superfoods” you now need to eat on top of all the others you’ve read about. And if you were to think that you would be partly true. It is a list, but it’s not “another” list. This is not any ole’ list of superfoods. This is the simplest version of The Most Basic Way to Eat Nutrient Rich and it alone can satisfy your body every day!

needle in haystackWhat? That’s all it takes to satisfy your body?

Yep, at a basic and balanced level. Of course, if you are an athlete, among countless other factors, this may change, but this is the most basic way to eat nutrient rich and it is true, it’s can feel like the needle in a haystack given how many other foodstuffs there are to choose from.

Of course the food industry is not interested in you figuring out what or where “the needle” is. Making sure YOU, do not know much about it, is what drives confusion and consumption of anything and everything that’s promoted; Save, the amazing work done by today’s food revolutionaries (like us and many others) who are telling the real story.

The food industry (particularly the meat and dairy and fast and convenience food industries) want you to believe it’s all “healthy” so to speak, as determined by the people promoting it. Cheese Pizza is even considered a vegetable in the government’s eyes because it has tomato sauce on it rich in lycopene; one phytochemical (albeit a powerful one) out of thousands!

Of course, just add low fat to a muffin and it too is healthy!

Unfortunately, we have gotten so far away from what’s actually healthy with too many foodstuffs that have the buy-in from many industries who are vested in keeping confusion, consumption and disease alive; we, the people stay on an endless treadmill (figuratively speaking) chasing lots of protein, vitamin C, and other “popular nutrients” with foods stuffs that never really serve our nutrient needs, the way whole, plant based, nutrient rich “superfoods” always will.

So to help you find that needle in the big cluttered haystack of nutrient poor foods that we are virtually swimming in…

Here are the 7 Basic Food Bullets to Eat and Live By Nutrient Rich Principles.

Just start adding these “modules” of foods to your current eating style, then you will begin to change the way you eat. Eventually you’ll challenge yourself and make the Switch to a Nutrient Rich Healthy Eating style, but eating 90% or More Plant Based Nutrient Rich for 90 Day’s or More! After that, you’ll rarely go back to nutrient poor ways of eating.

  1. Eat a Nutrient Rich, vegetable-based diet. This means you want vegetables at the base of your food pyramid in your mind, or first and foremost on your plate. It doesn’t mean eat only vegetables. It just means base your diet on vegetables since they are the most nutrient rich and calorie appropriate foods in existence. Leafy, green and colored vegetables both nutrify and detoxify the body and by virtue of the fact that they don’t contain cholesterol, saturated fat and other refined and added unnatural ingredients (salt, oil and sugar, chemicals) that you have no need for from food; they will protect your body from inflammation – from the most visible inflammation – weight gain – to the invisible atherosclerotic plaque buildup.
  2. Eat approx 3-4 Fruits Every Day. The antioxidants in berries and pomegranates, such as anthocyanin and punicalagin, are especially effective in lowering your LDL cholesterol and blood pressure, according to the nutritional research of Joel Fuhrman M.D. [2]
  3. Include, mushrooms, onions, tomatoes, garlic, scallions, leeks, broccoli, Brussels sprouts and other cruciferous vegetables in your meals that are known to substantially decrease cancer incidence. Beyond their properties for health promotion they are also so incredibly flavorful! [3]
  4. Aim to limit animal foods and refined carbohydrates to 10% or less of total food consumption.Refined carbohydrates have been found to be just as damaging to the cardiovascular system as saturated fats. [4, 5]
  5. Eat at least one ounce of raw nuts and seeds daily. Regular consumption of nuts and seeds like pistachios and walnuts has been shown to regulate body weight and satiety when they replace nutrient poor food stuffs of equal caloric value, and protect against type II diabetes among others. Nuts and seeds are also superfoods. [6]
  6. Eat 1 cup to one can’s worth of beans each day. A high-fiber bean-rich diet is as effective as a low-carbohydrate diet for weight loss, although, only a bean-rich diet lowered atherogenic lipids [7]. Not only are beans very tasty, they are also very satisfying and nutrient rich.
  7. Add 1 Tbsp. of ground flax seeds or chia seeds each day. These contain cardioprotective omega-3 fats, lignans, flavonoids, sterols, and fiber. [8]

Bonus Bullet: Supplement Intelligently. Even eating a high nutrient density diet, full of super nutrient-rich foods, it’s a good idea to supplement various substances known to be limited no matter what eating style you have due to modern food production and limited access to sunlight, and depending on the nutritional quality of your previous usual eating style[9]. – Vitamin B12, Vitamin D, and a well-designed multivitamin that does not contain substances such as vitamins A & E… Learn More Here > .

Eating healthy “Nutrient Rich” is not difficult. It can actually be so simple, quick and easy that it may even make eating today’s modern fast and convenient foods seem like too much work and too expensive. It’s easier to eat, easier to digest and you will get no distractions after you eat in this most basic way, because you won’t create weight and health complications you then have to deal with.

The hard part is getting unhooked from the foodstuffs that have a hold on you. Which is why the 90 / 90 Challenge is so Powerful. (You’ll learn more about this as we move forward together). You don’t need to be perfect, but if you want to be healthy and drop the weight of the past for good…, understanding The 7 Basic Food Bullets to Eat and Live By Nutrient Rich Eating Principles is essential.

Maximize Your Health and Life Potential,

John Allen Mollenhauer, NET, CPLC

Performance Lifestyle Trainer and Coach.


This Common Food Ingredient Can Really Mess Up Your Metabolism


What if you were to learn that every day, 25 percent of your calories came from a poison, disguised as a food?            

And what if you discovered that this chemical imposter was responsible for your insulin resistance and weight gain?

And elevated blood pressure …

And elevated triglycerides and LDL …

And depletion of vitamins and minerals …

And even gout, heart disease and liver damage?

What if you were to discover that this toxic substance had been dumped into your food in gradually increasing quantities for the last thirty years, with the full knowledge and blessings of the American Heart Association, the American Medical Association, the USDA and the FDA?

Would you be angry?

I wish I could tell you that this is just a dramatic plot from some fiction novel, but it’s actually a shocking reality.

The substance dealing such a crushing blow to your health and responsible for many, if not most of the chronic diseases that are so rampant in our society, is sugar — and more specifically, fructose.

We now know without a doubt that sugar in your food, in all its myriad of forms, is taking a devastating toll on the health of this nation.

By the end of this article, you will have a solid understanding of how and why this has happened. In order to really grasp this material, you’ll have to learn a little of the biochemistry of energy, which is rather technical. But hang in there — the knowledge you’re about to gain, and the impact it will have on your health, will be well worth the effort.

I will try my best to make the more technical aspects as simple as I can for you.

Big Gulp, Meet Big Belt

We are eating far more than we were 25 years ago.

On average, men are consuming 187 more calories per day, and women 335 more calories. People who were never heavy before are becoming overweight, and the obese are becoming more so. We are now a “supersized” population.

But why?

Modern science has shown that the obesity epidemic isn’t simply about lack of self-control, but rather a phenomenon driven by biochemical changes that have altered the way your body regulates energy.

Something has caused your appetite regulation system to go awry. Leptin, the hormone responsible for satiety, isn’t working. It isn’t simply a matter of calories in and calories out. Six-month old babies are the latest victims of the obesity epidemic–diet and exercise cannot explain that.

So, what are you eating now that you weren’t eating thirty years ago? What are you doing to yourself that started the day you were born?

Studies show that all of those extra calories are coming in the form of carbohydrates.

What carbohydrates in particular?

Sugar — specifically, sugared drinks. Soft drinks (41 percent) and fruit drinks (35 percent) make up the majority of these extra calories.

Today, 55 percent of sweeteners used in food and beverage manufacturing are made from corn, and the number one source of calories in America is soda, in the form of high fructose corn syrup (HFCS). In fact, the average American drinks 60 gallons of soda every year.

High Fructose Corn Syrup Has Only Been Around One Generation!

HFCS was invented in 1966 in Japan and introduced to the American market in 1975. Food and beverage manufacturers began switching their sweeteners from sucrose (table sugar) to corn syrup when they discovered that high fructose corn syrup (HFCS) was far cheaper to make — sucrose costs about three times as much as HFCS.

HFCS is about 20% sweeter than table sugar. HFCS is either 42% or 55% fructose, and sucrose is 50% fructose, so it’s a wash in terms of sweetness.

Still, the switch from sugar to fructose drastically altered the average American diet. The statistics are beyond alarming:

  • Corn syrup is now found in every type of processed, pre-packaged food you can think of. In fact, the use of HFCS in the U.S. diet increased by a whopping 10,673 percent between 1970 and 2005, according to a report by the USDA[i].
  • The current annual consumption of sugar is 141 pounds per person, and 63 pounds of that is HFCS.
  • Adolescents are taking in 73 grams per day of fructose, mostly from soft drinks and juice drinks — and 12 percent of their total caloric intake is from fructose alone.
  • In the past century, fructose consumption has increased 5-fold.
  • Processed foods account for more than 90 percent of the money Americans spend on meals.

You’ve probably heard the statistic that one soda a day is worth 15 pounds of fat per year. However, one soda today does not equal one soda of yesteryear. The original coke bottle was 6.5 ounces. Now, you have 20-ounce bottles and a 44-ounce Big Gulp.

Tragically, many infant formulas are more than 50 percent sugar — 43 percent being corn syrup solids. You might as well be giving your baby a bottle of Coke or Pepsi.

No wonder there is an obesity epidemic.

The War on Fat

Sugar’s rise to power was really an accidental by-product of three political winds, beginning with the Nixon administration:

  1. In 1972, Richard Nixon wanted to reduce food costs as part of his “war on poverty.” He partnered with the USDA to do whatever means necessary to bring food costs down.
  2. In 1975, HFCS was introduced, replacing sugar because it was cheap and readily available.
  3. In the mid 1970s, dietary fats were blamed for heart disease (more about this later), giving rise to the “low-fat craze.” Market response was an explosion of processed convenience foods, all nonfat and low fat, most of which tasted like sawdust unless sugar was added. Fructose was used to make fat-free products more palatable.

In 1982, the American Heart Association (AHA), the American Medical Association (AMA), and the United Stated Department of Agriculture (USDA) reduced fats from 40 percent of your diet to 30 percent. You eagerly complied, believing you were lowering your risks for both obesity and cardiovascular disease.

Yet, as the low-fat craze spread, so did rates of heart disease, diabetes, and obesity — the very illnesses you thought you were preventing. Clearly, the plan wasn’t working.

Justification for Low-Fat Diet

But how did the war on fat start, in the first place?

It began with a study called the Seven Countries study by Ancel Keys[ii], a Minnesota epidemiologist who used multivariate regression analysis to examine diet and disease. He compared the diets of seven countries, and his main conclusion was that saturated fats were responsible for cardiovascular disease. After much heated public debate, this notion that saturated fats caused heart disease was widely adopted, especially once he made the cover of Time Magazine in 1980.

Keys’ study laid the foundation for nutrition science, education, and public policy for the next three decades.

There was only one problem. His conclusions were dead wrong.

Keys’ neglected to perform the converse analysis demonstrating that the effect of saturated fat on cardiovascular disease wasindependent of sucrose. In other words, sucrose and saturated fat were co-mingled into his data. In retrospect, it is impossible to tease out the relative contributions of sucrose versus saturated fat on cardiovascular disease in this study because the original data is long gone and Keys has passed on.

Additionally he never separated out the issue of how the fat was consumed. There is a major difference in raw and cooked animal fat, especially fat cooked at high temperatures, which clearly produces known carcinogens.

Nevertheless, lowering fat (without regard to sugar) became the nutritional model that persists to this day, despite copious evidence that it doesn’t work.

As your fats went from 40 percent to 30 percent, your carbohydrates went from 40 percent to 55 percent. And this carbohydrate increase was of the worst possible kind: SUGAR.

Proof that Sugar Cause Obesity

The American Beverage Association claims there is “no association between high fructose corn syrup and obesity.”[iii]

However, a long lineup of scientific studies suggest otherwise:

  • Dr. David Ludwig of Boston Children’s Hospital did a study of the effects of sugar-sweetened drinks on obesity in children[iv]. He found that for each additional serving of a sugar-sweetened drink, both body mass index and odds of obesity increased in the children he studied.
  • Dr. Kelly Brownell of Yale University did a systematic review and meta-analysis of 88 studies about the association between soft drink consumption and health outcomes[v]. He found clear associations between soft drink consumption and higher body weight.
  • The Fizzy Drink Study in Christchurch, England explored the effects on obesity when soda machines were removed from schools for one year. In the schools where the machines were removed, obesity stayed constant. In the schools where soda machines remained, obesity rates continued to rise[vi].
  • A study by Schulze in JAMA in 2004[vii] provides further evidence that sugared drinks cause type II diabetes.
  • A similar study in 2008 of African American women[viii] demonstrated higher intake of both sugar-sweetened soft drinks and fruit drinks leads to higher rates of type II diabetes.
  • In a very recent study[ix], sixteen volunteers were fed a controlled diet including high levels of fructose. Ten weeks later, the volunteers had produced new fat cells around their hearts, livers and other digestive organs. They also showed signs of food-processing abnormalities linked to diabetes and heart disease. A second group of volunteers who were fed a similar diet, but with glucose replacing fructose, did not have these problems.

But it doesn’t stop at soft drinks.

Sweetened fruit drinks are contributing to your expanding waistline as well. High fruit juice intake (sucrose) is associated with childhood obesity, especially in low-income families[x].

What is it in soft drinks and juice drinks that is damaging your health?

Primarily, it’s the fructose. Read on to discover exactly how and why this is so.

Fructose is NOT the Same as Glucose

Glucose is the form of energy you were designed to run on. Every cell in your body, every bacterium — and in fact, every living thing on the Earth — uses glucose for energy.

glucose, fructose, sugars

Fructose is not the same molecule. Glucose is a 6-member ring, but fructose is a 5-member ring. Sucrose (table sugar) is 50 percent glucose and 50 percent fructose, and HFCS is 42-55 percent fructose.

If you received your fructose only from vegetables and fruits (where it originates) as most people did a century ago, you’d consume about 15 grams per day — a far cry from the 73 grams per day the typical adolescent gets as a bolus from sweetened drinks. In vegetables and fruits, it’s mixed in with fiber, vitamins, minerals, enzymes, and beneficial phytonutrients, all which moderate the negative metabolic effects.

It isn’t that fructose itself is bad — it is the MASSIVE DOSES you’re exposed to that make it dangerous.

Before you can understand the differences between how your body metabolizes glucose and fructose, you have to have a basic understanding of LDL.

There are Two Types of LDL — and Only One is Bad

In the 1970s, low-density lipoproteins (LDLs) were discovered. LDLs were found to be higher in people with cardiovascular disease, so the focus of medicine and nutrition became lowering your LDLs.

One of the crucial pieces of the puzzle that wasn’t recognized at the time was that there are two kinds of LDL: Pattern A and Pattern B.

  1. Pattern A LDLs are large, light, buoyant “floating” LDLs that don’t get under your endothelial cells, and they don’t cause plaque formation. They are harmless.
  2. Pattern B LDL (or VLDLs) are smaller, denser LDLs that are able to wedge themselves under your epithelial cells and therefore roughen surfaces and stimulate plaque formation. These are the bad guys.

Unfortunately, when you get a standard lipid profile at your annual check-up, the LDL measured is a combination of both types. Lab measurements lump them together unless you have a very specialized panel, which most physicians don’t order.

To decipher whether or not you have an excess of the bad type, you can look at your triglycerides and high-density lipoprotein (HDL) levels. (HDL, or “high density lipoprotein is commonly called “good cholesterol.”)

Here is a simple way to determine if you have too much bad LDL:

  1. If your triglycerides are low and your HDL is high, then the LDL you have is the good variety.
  2. If your triglycerides are high and your HDL is low, then the LDL you have is the bad variety. The triglyceride-to-HDL ratio is a far better indicator of cardiovascular disease than the total cholesterol-to-HDL ratio that everyone uses.

Now, here’s the bottom line: Dietary fat raises your large, buoyant LDL — the one that is harmless. Dietary sugar raises your small, dense LDL — the one that correlates with heart disease!

So, what has happened over the past 30 years was that sugar was added to our low-fat foods to improve palatability — in the form of either HFCS or sucrose — and a high-carb, high-risk diet was created — simply the worst combination for your health.

And the fiber was eliminated.

Fiber Foregone

Fiber is an important nutrient (although not acknowledged as such by the government) and offers many health benefits, particularly if the fiber comes from vegetables.

A high-fiber diet may offer some protection from colorectal cancer, although the research is unclear exactly how this works and what all the factors are. The benefits of vegetable fiber are not yet completely understood. We do know that the risk ofcolorectal cancer is lower among populations with high intakes of vegetables and fruits, and there is some evidence that vegetable fiber may offer some protection from prostate cancer.

Fiber has three important roles:

  • It reduces the rate of intestinal carbohydrate absorption, reducing your insulin response.
  • It increases the speed of transit of intestinal contents to your ileum, which speeds up release of satiety hormones.
  • It inhibits absorption of some free fatty acids to your colon, which would become short chain fatty acids, which suppress insulin.

Thousands of years ago your ancestors likely consumed 100 to 300 grams of fiber every day. Now, you are lucky to get 12 grams daily.

Why is this?

  • Fiber-less foods are cheap.
  • They have a longer shelf life and are easier to ship. This makes them easier to export to other countries.
  • Fiber-rich foods take too long to prepare and eat, and are often less appealing to the general public.

The standard American diet (SAD) is typically loaded with processed foods full of sugar, and devoid of most nutrients and fiber. Sounds like the perfect recipe for an explosion of chronic disease.

The Molecule that Makes Fat Stick to You

Obesity is a disorder of excess fat accumulation. But what regulates fat accumulation?

Fat is a metabolically active tissue. Your adipose tissue is in a perpetual state of flux with free fatty acids (FFAs) being converted into triglycerides and back again, in an ongoing cycle.

FFAs can move in and out of your cells, across cell membranes, but triglycerides (three fatty acid molecules plus one glycerol molecule) are too big to cross. Fat enters and exits a cell as FFA, but is stored as a triglyceride. When fuel is needed, the triglyceride is broken down into FFAs, which can then be burned as fuel.

The glycerol molecule, which is a primary component of a triglyceride, comes from something called glycerol-3-phosphate (g-3-p), or “activated glycerol,” which originates from the metabolism of glucose. The amount of G-3-p you make determines the rate that FFAs are “esterified” into triglycerides inside your fat cells[xi].

The rate of deposition of fat into your fat cells is dependent on the presence of g-3-p. The more g-3-p that is available, the more fat is deposited.

Carbohydrate Biochemistry 101

I promised you a crash course in biochemistry — so here we go.

Much of the following information comes from the important work of Dr. Robert Lustig[xii] Professor of Pediatrics in the Division of Endocrinology at the University of California, San Francisco.

In order to appreciate just how damaging fructose is to your body, it is crucial to have a basic understanding of how different types of carbohydrates are metabolized.

We’ll start with glucose since it’s the basic carbohydrate energy source for all living cells.

I. Glucose Metabolism

Glucose is the basic fuel for living organisms, from bacteria to humans, and is the primary energy source for your brain. It is a product of photosynthesis and is found in rice, corn and other grains, and bread and pasta.

Once you take in glucose from a meal — like, say, from two slices of bread — 80 percent of it is used by all of the organs of your body — every single cell. The remaining 20 percent goes to your liver to be metabolized and stored.

The following is what happens to that 20 percent, once it reaches your liver:

  • Whatever glucose your body doesn’t need immediately gets converted into glycogen for storage in the liver. Glycogen is your body’s non-toxic short-term energy storage package, where it can be easily converted to energy when you need it. Your liver has no limit to how much glycogen it can store without detrimental effects. (That is what athletes take advantage of when they “carbo-load.”)
  • A small amount of pyruvate is produced, which ends up being converted to ATP (the chemical storage form of energy) and carbon dioxide. An even smaller quantity of citrate is produced from this process through the “citrate shuttle,” which ends up as VLDL (very low density lipoproteins, the bad ones) in a process known as de novo lipogenesis — but we’re talking about a very small amount (less than one calorie from two slices of bread).
  • Insulin is released by your pancreas in response to the rise in blood glucose (i.e., blood sugar), which helps the glucose get into your cells. Without insulin, your cells would not be able to process the glucose and therefore would have no energy for movement, growth, repair, or other functions. Insulin is key to unlocking the door of the cell to allow the glucose to be transferred from the bloodstream into the cell.
  • When you consume 120 calories of glucose, less than one calorie contributes to adverse metabolic outcomes.

This is all very normal, and it’s how you were designed to operate.

II. Ethanol Metabolism

Ethanol, or ethyl alcohol, is the favorite carbohydrate of many. But it is also a carbohydrate that undergoes a very different metabolic process, leaving in its wake a trail of toxins a mile long.

Ethanol is an acute central nervous system toxin and a chronic hepatotoxin due to the fact that it must be metabolized almost completely in the liver.

After consuming an alcoholic beverage, 10 percent of the ethanol gets broken down by the stomach and intestine as a “first pass” effect, and another 10 percent is metabolized by the brain and other organs. The fact that ethanol is partially metabolized in your brain is the reason you experience that familiar “buzz.”

The remaining 80 percent hits the liver, where it must be broken down. This is four times the load on the liver as the same number of calories from glucose.

But the metabolic process in the liver is quite different from that of glucose.

This metabolic cascade can be summarized as follows:

  • The liver converts ethanol to aldehydes, which produce free radicals that damage proteins in the liver.
  • Some of these aldehydes are converted to glucose, but a large amount of excess citrate is formed in the process, stimulating “junk chemicals” that result in free fatty acids (FFAs), VLDL and triglycerides. As compared to the 1 calorie from glucose that was converted to VLDL (see previous section), the same caloric intake from ethanol produces 30 calories of VLDL that are transported to your fat cells and contribute to your obesity, or participate in plaque formation. This is what leads to the dyslipidemia of alcoholism.
  • The resulting lipids, together with the ethanol, lead to an enzyme that begins an inflammation cascade, which in turn causes hepatic insulin resistance, liver inflammation and cirrhosis.
  • Fat globules accumulate in the liver as well, which can lead to fatty liver disease.
  • Free fatty acids (FFAs) leave the liver and cause your skeletal muscles to become insulin resistant. This is a worse form of insulin resistance than hepatic insulin resistance and can lead to type II diabetes.
  • After a 120-calorie bolus of ethanol, a large fraction (about 40 calories) can contribute to disease.

Why am I including a discussion of ethanol metabolism in a report about fructose?

Because, in nearly every way, fructose is metabolized the same way as ethanol, creating the same toxins in your body.

III. Fructose Metabolism

Now we finally come to fructose.

When you consume fructose, 100 percent of it goes directly to your liver to be metabolized. This is why it is a hepatotoxin — it overloads the liver. Fructose metabolism creates the following adverse effects:

  • Fructose is immediately converted to fructose-1-phosphate (F1P), depleting your liver cells of phosphates.
  • The above process produces waste products in the form of uric acid. Uric acid blocks an enzyme that makes nitric oxide. Nitric oxide is your body’s natural blood pressure regulator, so when it is blocked, your blood pressure rises — leading tohypertension. Elevated uric acid levels can also cause gout.
  • Almost all of the F1P is turned into pyruvate, ending up as citrate, which results in de novo lipogenesis, the end products of which are FFAs, VLDLs, and triglycerides. The result — hyperlipidemia.
  • Fructose stimulates g-3-p (activated glycerol), which you will recall is the crucial molecule for turning FFAs into triglycerides within the fat cells. Remember, the rate of deposition of fat into fat cells is dependent on the presence of g-3-p. The more g-3-p that is available, the more fat is deposited. Fructose is the carbohydrate most efficiently converted into g-3-p11. In other words, fructose is the most lipophilic carbohydrate.
  • FFAs are exported from the liver and taken up in skeletal muscle, causing skeletal muscle insulin resistance.
  • Some of the FFAs stay in the liver, leading to fat droplet accumulation, hepatic insulin resistance and nonalcoholic fatty liver disease (NAFLD)[xiii][xiv].
  • Insulin resistance stresses the pancreas, which pumps out more insulin in response to rising blood sugar as your cells are unable to get the sugar out of your bloodstream, and this can progress to type II diabetes.
  • As with a bolus dose of ethanol, a 120-calorie bolus of fructose results in a large fraction (again, about 40 calories) that directly contributes to disease.

Do these symptoms sound a bit familiar to you? Hypertension, lipogenesis and dyslipidemia, obesity, inflammation, insulin resistance, and central nervous system leptin resistance?

If you are thinking it sounds a lot like classic metabolic syndrome, you are dead on!

The point to take away is: consuming fructose is consuming fat. Fructose is not really a carbohydrate — a high fructose diet is a HIGH FAT diet. A high-fat diet that creates a vicious cycle of consumption that won’t turn itself off.

You can see by comparing the metabolism of fructose with the metabolism of ethanol that they are very similar. In fact, when you compare the metabolism of 150 calories of soda with 150 calories of beer (a 12 ounce can of each), about 90 calories reach the liver in either case. Fructose causes most of the same toxic effects as ethanol because both come from sugar fermentation.

Both ethanol metabolism and fructose metabolism lead to visceral adiposity (belly fat), insulin resistance and metabolic syndrome.

Studies are accumulating that bear this out.

For example, high-fructose diets were shown to cause dyslipidemia in healthy people with and without a family history of type II diabetes, a recent study showed[xv].

Two other studies were done using medical students, both looking at biological responses to fructose loading. In the first, the med students were given either a large glucose load or a large fructose load. In the students given fructose, almost 30 percent of the calories ended up as fat. In the students given glucose, almost none ended up as fat.

In the second study, medical students were given a high-fructose diet for 6 days. In just that short time, their insulin resistance and triglycerides doubled!

The Neurochemical Basis for Gluttony

You eat as a result of the activation of the “reward pathway” (also known as the hedonic pathway) of your brain.

Your brain’s pleasure center (aka ventral tegmental area, or VTA, and nucleus accumbens, or NA) is the root of all behavior, driven by chemical messengers that are intimately tied into the energy processes I have outlined above.

The part of your brain that responds to what you eat is the same part that responds to nicotine, morphine, amphetamine, ethanol, sex and exercise! That is why people taking narcotics tend to overeat.

Leptin and insulin are modulators of these reward responses, decreasing this VTA-NA activity. In other words, leptin and insulin cause your brain to send you signals to stop eating.

Fructose undermines these normal satiety signals, increasing caloric consumption both directly and indirectly:

  1. Fructose does not stimulate a leptin rise, so your satiety signals are diminished.
  2. Glucose suppresses ghrelin (the hunger hormone—it makes you want more food), but fructose does not.
  3. By raising triglycerides, fructose reduces the amount of leptin crossing your blood-brain barrier.
  4. Fructose increases insulin levels, interfering with the communication between leptin and your hypothalamus, so your pleasure signals aren’t extinguished. Your brain senses starvation and prompts you to eat more.
  5. Fructose decreases the production of malonyl-CoA, which may help promote a sense of energy adequacy.

Along with causing insulin resistance, fructose alters the hedonic response to food thereby driving excessive caloric intake, setting up a positive feedback loop for overconsumption.

Big Fat Lies From the Corn Industry

Now that scientific studies have shown the metabolic similarity between HFCS and sucrose, the Corn Refiners Association has embarked on a vociferous campaign to convince the public that their product is equal to table sugar, that it is “natural” and safe.

Of course, many things are “natural” — cocaine is natural, but you wouldn’t want to use 141 pounds of it each year.

The food and beverage industry doesn’t want you to realize how truly pervasive HFCS is in your diet — not just from soft drinks and juices, but also in salad dressings and condiments and virtually every processed food. The introduction of HFCS into the Western diet in 1975 has been a multi-billion dollar boon for the corn industry.

Now the corn industry has come up with another product it’s using in beverages called “crystalline fructose.” This is produced by allowing the fructose to crystallize from a fructose-enriched corn syrup, resulting in a product that is 99.5 percent pure fructose — a fructose level twice as high as regular HFCS!

Clearly, all the health problems associated with HFCS could become even more pronounced with this product.

Making matters worse, crystalline fructose may also contain arsenic, lead, chloride and heavy metals — a virtual laundry list of toxic agents you should clearly avoid. In fact, more than one study has detected unsafe mercury levels in HFCS[xvi]. If you have children, all of these contaminants can impact your child’s development and long-term health.

Why doesn’t the FDA regulate fructose since it poses the same health risks as ethanol — and it regulates ethanol?

The FDA doesn’t touch chronic toxins. They regulate only acute toxins, and ethanol falls into that category because it produces immediately toxic neurological effects. Fructose doesn’t get metabolized in the brain, so it’s effects, although damaging, are cumulative and magnify over time.

Also realize that nearly all HFCS is made from genetically modified corn, which comes with its own set of risks.

The FDA classifies fructose as GRAS: Generally Regarded As Safe. Which pretty much means nothing and is based on nothing.

It is interesting to note that soda taxes[xvii] have recently been proposed both in New York and California, and legislation for the removal of soft drinks from schools has been enacted in several states.

What’s a Sugarholic to Do?

Ideally, I recommend that you avoid as much sugar as possible. This is especially important if you are overweight or have diabetes, high cholesterol, or high blood pressure.

In fact, I believe that the positive health impacts of breaking the country’s sugar addiction would be even greater than if everyone stopped smoking, because elevated insulin levels are the foundation of nearly every chronic disease known to man, from cancer and arthritis to cardiovascular disease.

I also realize you don’t live in a perfect world, and following rigid dietary guidelines is not always practical or even possible.

If you want to use a sweetener occasionally, this is what I recommend:

  1. Use the herb stevia
  2. Use organic cane sugar in moderation
  3. Use organic raw honey in moderation

Avoid ALL artificial sweeteners, which can damage your health even more quickly than HFCS.

And I don’t recommend agave syrup since it is a highly processed sap that is almost all fructose. Your blood sugar will spike just as it would if you were consuming regular sugar or HFCS. Agave has gained meteoric popularity due to a great marketing campaign, but any health benefits present in the original agave plant are processed away.

Be sure to eat your sugar with fiber … as in a piece of fruit. As Dr. Lustig says, “When God made the poison, he packaged it with the antidote: fiber.”

Wait 20 minutes before second portions at meals, giving your brain a chance to receive satiety signals.

And exercise regularly. Dr. Ludwig recommends you “buy your screen time with physical activity.”

Exercise is important for several reasons, some of which might surprise you:

  • Exercise improves skeletal muscle insulin sensitivity (insulin works best in your muscles)
  • Exercise reduces stress and lowers cortisol, which decreases appetite
  • Exercise suppresses ghrelin, thereby decreasing appetite
  • Exercise speeds up metabolic cycles, reducing citrate levels, thus reducing fat production
  • Exercise can make you sharper, reduce arthritis, lift your mood, strengthen your bones, and even slow down aging

Avoid so-called energy drinks and sports drinks because they are loaded with sugar, sodium and chemical additives.

Rehydrating with pure, fresh water is a better choice.

If you or your child is involved in athletics, I recommend you read my article Energy Rules for some great tips on how to optimize your child’s energy levels and physical performance through good nutrition.

A Word of Warning About Infant Formula

And finally, be extremely careful about the infant formula you are feeding your baby. Nearly all infant formulas have as much or more high fructose corn syrup than a can of soda — in addition to many other things that are extremely detrimental to your baby’s health and development.

You have learned that, metabolically, there is very little difference between ethanol and sugar, so by giving your infant formula, you might as well be giving him a bottle of beer or soda!

And studies have shown that the earlier you expose kids to sweets, the more they crave them later.

It is important for pregnant women to keep their blood sugars well managed not only for their own health, but also for the long-term health of their children.

Researchers have found that children born to mothers with gestational diabetes (high blood sugar during pregnancy) had an 82 percent chance of becoming obese between the ages of 5 and 7 through a phenomenon called “metabolic imprinting.” Even mothers with elevated blood sugar, short of gestational diabetes, had children with a significantly increased risk for obesity.[xviii]

I advocate breastfeeding if at all possible — it is by far the healthiest option.

One of the most clear-cut, non-debatable topics in health care is that breast milk is the best source of nutrition for newborns. The benefits to the baby and the new mom are enormous. Breastfed infants have shown lower obesity rates in later childhood[xix].

What Else Does the Science Say about the Health Impact of Fructose?

According to, scientific studies have linked fructose to about 30 different specific diseases and health problems. Select the hyperlinks provided to review how fructose may:

Raise your blood pressure, and cause nocturnal hypertension Insulin resistance / Type 2 Diabetes Non-alcoholic fatty liver disease(NAFLD)
Raise your uric acid levels, which can result in gout and/ormetabolic syndrome Accelerate the progression of chronic kidney disease Intracranial atherosclerosis(narrowing and hardening of the arteries in your skull)
Exacerbate cardiac abnormalities if you’re deficient in copper Have a genotoxic effect on the colon Promote metastasis in breast cancer patients
Cause tubulointerstitial injury(injury to the tubules and interstitial tissue of your kidney) Promotes obesity and related health problems and diseases Promotes pancreatic cancer growth


I would like to thank Dr. Robert H. Lustig, Professor of Pediatrics in the Division of Endocrinology at University of California, San Francisco, for sharing his incredibly important insights, without which this article would not have been possible. Much of the above information came directly from Dr. Lustig’s work related to central regulation of energy balance, and I am very grateful for his willingness to share it with me so that I can pass it along to you.

[i] Wells H.F. and Buzby J. c. “Dietary assessment of major trends in U.S. food consumption, 1970-2005. USDA Economic Research Service, Economic Information Bulletin Number 33, March 2008.

[ii] “Ancel Keys—villain or hero?” Stop Trans Fats.

[iii] American Beverage Association, News Release, March 25, 2004

[iv] Ludwig D.S., Peterson, K.E. and Gortmaker, S.L. “Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis” The Lancet Feb 17, 2001 Volume 357, Issue 9255, pp 505-508

[v] Vartanian L.R., Schwartz M.B. and Brownell K.D. “Effects of soft drink consumption on nutrition and health: A systematic review and meta-analysis” AJPH April 2007, vol 97, No. 41, pp 667-675.

[vi] Esterbrook J. “Schools that can soda cut obesity,” CBS News Health April 23, 2004

[vii] Apovian C.M. “Sugar-sweetened soft drinks, obesity, and type 2 diabetes” JAMA 2004;292:978-979

[viii] Palmer J.R., Boggs D.A., Krishnan S., Hu F.B., Singer M., and Rosenberg L. “Sugar-sweetened beverages and incidence of type 2 diabetes mellitus in African American women” Arch Intern Med. 2008;168(14):1487-1492.

[ix] Stanhope K.L., et al. “Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans” J Clin Invest. 2009 May 1;119(5):1322-1334

[x] Faith M.S., Dennison B.A., Edmunds L.S., Stratton H.H. “Fruit juice intake increased adiposity gain in children from low-income families: weight status by environment interaction” Pediatrics 118:2066-2075.

[xi] Taubs G. Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease, 2007, Knopf; and Medical Grand Rounds presentation, Datmouth-Hitchcock,

[xii] Robert H. Lustig, MD: UCSF faculty bio page, and YouTube presentation “Sugar: The bitter truth” ; and “The fructose epidemic”The Bariatrician, 2009, Volume 24, No. 1, page 10)

[xiii] Lim J.S., Mietus-Snyder M.L., Valente A., Schwartz J.M., and Lustig R.H. “Fructose, NAFLD, and metabolic syndrome,” Dept. of Pediatrics and Medicine, University of California, San Francisco 2009

[xiv] Ouyang X., Cirillo P., Sautin Y., McCall S., Bruchette J.L., Diehl A.M. Johnson R.J., Abdelmalek M.F. “Fructose consumption as a risk factor for non-alcoholic fatty liver disease” J. Hepatol. 2008 Jun;48(6):993-9

[xv] Le K.A., Ilth M., Kreis R., Faeh D., Bortolotti M., Tran C., Boesch C., and Tappy L. “Fructose overconsumption causes dyslipidemia and ectopic lipid deposition in healthy subjects with and without a family history of type 2 diabetes” Am J Clin Nutr. 2009 Jun;89(6):1760-5

[xvi] “Why is the FDA unwilling to study evidence of mercury in high-fructose corn syrup?” 20 Feb 2009, Grist

[xvii] Brownstein J. “Public health leaders propose soda tax” ABCNews/Health, September 17, 2009

[xviii] Hillier T.A., Pedula K.L., Schmidt B.A., Mullen J.A., Charles M., Pettitt D.J. “Childhood obesity and metabolic imprinting: The ongoing effects of maternal hyperglycemia” Diabetes Care September 2007 vol. 30 no. 9 pages 2287-2292

[xix] U.S. Department of Health and Human Services, Administration for Children and Families, Early Childhood Learning and Knowledge Center (ECLKC) “Prevention of overweight and obesity in infants and toddlers

HFCS: High Fructose Corn Syrup

HFCS, high fructose corn syrup, is the missing piece in the puzzle that explains why Americans, in particular, are becoming obese. The rest of the world is catching up to us, though, as we export this poison to other countries in the form of soft drinks, fast foods, and other processed foods.

It is not simply because we are eating more that we have become a nation that is about 68% overweight or obese. We are eating and drinking more calories — and gaining a LOT more weight — because fructose has been substituted for sucrose in our processed food and beverages.

According to Dr. Robert Lustig’s research, fructose by-passes our body’s normal hormonal signal that tells us when we are “full.”

Fructose not only helps to explain our growing obesity (which began to skyrocket after this sweetener was introduced in the USA in 1975), but also our high rate of heart disease, liver disease, kidney disease, hypertension, and more.

This is new information that needs to be factored into what T.Colin Campbell, PhD,(author of The China Study) and Dr. Caldwell Esselstyn have to say about the dangers of a high-fat diet(specifically, from animal fat).

Quitting animal products — meat, poultry, milk and cheese, fish and eggs — is not the whole solution to our weight problems, cardiovascular disease, kidney and liver disease and cancer. HFCS is the missing key that opens Pandora’s Box of modern society’s diseases. Watch this video, please.

The processed food industry and their clever lobbyists would like you to remain confused about why you can’t seem to lose weight or control your appetite as long as you eat their products. They create Web sites like and the TV commercials it contains to argue that HFCS is just like “good-‘ol cane sugar.”

Don’t believe it!

If you want the truth, so you can protect your health and that of your family, you need to read this Web page from Dr. Mercola’s blog and especially watch the video of Dr. Robert Lustig, a prominent pediatric endocrinologist, lecturing at the University of California, San Francisco.

HFCS is the key to the obesity epidemic

While it may be difficult to get through the entire presentation on HFCS by doctor Lustig, it is important to be exposed to the proven scientific facts.

I try to base my decisions on health matters on the basis of a consensus view of the best scientific research — and NOT the research that is funded by the fructose industry, as in the case of Websites like or pharmaceutical industy pawns like

If you want to be healthy, it is critical to be able to discern if the information you accept is tainted and influenced by a financial connection with those industries that are being investigated.

Men like Dr. Mercola and Dr. Lustig don’t take a controversial position like this lightly. They have a lot to lose in terms of their professional reputation if they were found to be wrong about such an important point as HFCS represents.

So I have a lot more confidence in the truth of their conclusions about fructose than I do about an industry-funded Web site like or any number of mainstream dieticians(who are generally parroting what they learned in heavily food-industry-influenced schools).

My motto is “Consider the source!” Where is this information coming from? Who benefits? If it is the industry whose profits depend on your continued purchases of their products, BEWARE!





Is Sugar Toxic?

Kenji Aoki for The New York Times
Published: April 13, 2011
 On May 26, 2009, Robert Lustig gave a lecture called “Sugar: The Bitter Truth,” which was posted on YouTube the following July. Since then, it has been viewed well over 800,000 times, gaining new viewers at a rate of about 50,000 per month, fairly remarkable numbers for a 90-minute discussion of the nuances of fructose biochemistry and human physiology.

What the average American consumes in added sugars:

Kenji Aoki for The New York Times

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 alsoportrayed 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 themajor, risk factor for heart disease and diabetes. The Centers for Disease Control and Prevention now estimate that some 75 million Americans have metabolic syndrome. For those who have heart attacks, metabolic syndrome will very likely be the reason.

The first symptom doctors are told to look for in diagnosing metabolic syndrome is an expanding waistline. This means that if you’re overweight, there’s a good chance you have metabolic syndrome, and this is why you’re more likely to have a heart attack or become diabetic (or both) than someone who’s not. Although lean individuals, too, can have metabolic syndrome, and they are at greater risk of heart disease and diabetes than lean individuals without it.

Having metabolic syndrome is another way of saying that the cells in your body are actively ignoring the action of the hormone insulin — a condition known technically as being insulin-resistant. Because insulin resistance and metabolic syndrome still get remarkably little attention in the press (certainly compared with cholesterol), let me explain the basics.

You secrete insulin in response to the foods you eat — particularly the carbohydrates — to keep blood sugar in control after a meal. When your cells are resistant to insulin, your body (your pancreas, to be precise) responds to rising blood sugar by pumping out more and more insulin. Eventually the pancreas can no longer keep up with the demand or it gives in to what diabetologists call “pancreatic exhaustion.” Now your blood sugar will rise out of control, and you’ve got diabetes.

Not everyone with insulin resistance becomes diabetic; some continue to secrete enough insulin to overcome their cells’ resistance to the hormone. But having chronically elevated insulin levels has harmful effects of its own — heart disease, for one. A result is higher triglyceride levels and blood pressure, lower levels of HDL cholesterol (the “good cholesterol”), further worsening the insulin resistance — this is metabolic syndrome.

When physicians assess your risk of heart disease these days, they will take into consideration your LDL cholesterol (the bad kind), but also these symptoms of metabolic syndrome. The idea, according to Scott Grundy, a University of Texas Southwestern Medical Center nutritionist and the chairman of the panel that produced the last edition of the National Cholesterol Education Program guidelines, is that heart attacks 50 years ago might have been caused by high cholesterol — particularly high LDL cholesterol — but since then we’ve all gotten fatter and more diabetic, and now it’s metabolic syndrome that’s the more conspicuous problem.

This raises two obvious questions. The first is what sets off metabolic syndrome to begin with, which is another way of asking, What causes the initial insulin resistance? There are several hypotheses, but researchers who study the mechanisms of insulin resistance now think that a likely cause is the accumulation of fat in the liver. When studies have been done trying to answer this question in humans, says Varman Samuel, who studies insulin resistance at Yale School of Medicine, the correlation between liver fat and insulin resistance in patients, lean or obese, is “remarkably strong.” What it looks like, Samuel says, is that “when you deposit fat in the liver, that’s when you become insulin-resistant.”

That raises the other obvious question: What causes the liver to accumulate fat in humans? A common assumption is that simply getting fatter leads to a fatty liver, but this does not explain fatty liver in lean people. Some of it could be attributed to genetic predisposition. But harking back to Lustig, there’s also the very real possibility that it is caused by sugar.

As it happens, metabolic syndrome and insulin resistance are the reasons that many of the researchers today studying fructose became interested in the subject to begin with. If you want to cause insulin resistance in laboratory rats, says Gerald Reaven, the Stanford University diabetologist who did much of the pioneering work on the subject, feeding them diets that are mostly fructose is an easy way to do it. It’s a “very obvious, very dramatic” effect, Reaven says.

By the early 2000s, researchers studying fructose metabolism had established certain findings unambiguously and had well-established biochemical explanations for what was happening. Feed animals enough pure fructose or enough sugar, and their livers convert the fructose into fat — the saturated fatty acid, palmitate, to be precise, that supposedly gives us heart disease when we eat it, by raising LDL cholesterol. The fat accumulates in the liver, and insulin resistance and metabolic syndrome follow.

Michael Pagliassotti, a Colorado State University biochemist who did many of the relevant animal studies in the late 1990s, says these changes can happen in as little as a week if the animals are fed sugar or fructose in huge amounts — 60 or 70 percent of the calories in their diets. They can take several months if the animals are fed something closer to what humans (in America) actually consume — around 20 percent of the calories in their diet. Stop feeding them the sugar, in either case, and the fatty liver promptly goes away, and with it the insulin resistance.

Similar effects can be shown in humans, although the researchers doing this work typically did the studies with only fructose — as Luc Tappy did in Switzerland or Peter Havel and Kimber Stanhope did at the University of California, Davis — and pure fructose is not the same thing as sugar or high-fructose corn syrup. When Tappy fed his human subjects the equivalent of the fructose in 8 to 10 cans of Coke or Pepsi a day — a “pretty high dose,” he says —– their livers would start to become insulin-resistant, and their triglycerides would go up in just a few days. With lower doses, Tappy says, just as in the animal research, the same effects would appear, but it would take longer, a month or more.

Despite the steady accumulation of research, the evidence can still be criticized as falling far short of conclusive. The studies in rodents aren’t necessarily applicable to humans. And the kinds of studies that Tappy, Havel and Stanhope did — having real people drink beverages sweetened with fructose and comparing the effect with what happens when the same people or others drink beverages sweetened with glucose — aren’t applicable to real human experience, because we never naturally consume pure fructose. We always take it with glucose, in the nearly 50-50 combinations of sugar or high-fructose corn syrup. And then the amount of fructose or sucrose being fed in these studies, to the rodents or the human subjects, has typically been enormous.

This is why the research reviews on the subject invariably conclude that more research is necessary to establish at what dose sugar and high-fructose corn syrup start becoming what Lustig calls toxic. “There is clearly a need for intervention studies,” as Tappy recently phrased it in the technical jargon of the field, “in which the fructose intake of high-fructose consumers is reduced to better delineate the possible pathogenic role of fructose. At present, short-term-intervention studies, however, suggest that a high-fructose intake consisting of soft drinks, sweetened juices or bakery products can increase the risk of metabolic and cardiovascular diseases.”

In simpler language, how much of this stuff do we have to eat or drink, and for how long, before it does to us what it does to laboratory rats? And is that amount more than we’re already consuming?

Unfortunately, we’re unlikely to learn anything conclusive in the near future. As Lustig points out, sugar and high-fructose corn syrup are certainly not “acute toxins” of the kind the F.D.A. typically regulates and the effects of which can be studied over the course of days or months. The question is whether they’re “chronic toxins,” which means “not toxic after one meal, but after 1,000 meals.” This means that what Tappy calls “intervention studies” have to go on for significantly longer than 1,000 meals to be meaningful.

At the moment, the National Institutes of Health are supporting surprisingly few clinical trials related to sugar and high-fructose corn syrup in the U.S. All are small, and none will last more than a few months. Lustig and his colleagues at U.C.S.F. — including Jean-Marc Schwarz, whom Tappy describes as one of the three best fructose biochemists in the world — are doing one of these studies. It will look at what happens when obese teenagers consume no sugar other than what they might get in fruits and vegetables. Another study will do the same with pregnant women to see if their babies are born healthier and leaner.

Only one study in this country, by Havel and Stanhope at the University of California, Davis, is directly addressing the question of how much sugar is required to trigger the symptoms of insulin resistance and metabolic syndrome. Havel and Stanhope are having healthy people drink three sugar- or H.F.C.S.-sweetened beverages a day and then seeing what happens. The catch is that their study subjects go through this three-beverage-a-day routine for only two weeks. That doesn’t seem like a very long time — only 42 meals, not 1,000 — but Havel and Stanhope have been studying fructose since the mid-1990s, and they seem confident that two weeks is sufficient to see if these sugars cause at least some of the symptoms of metabolic syndrome.

So the answer to the question of whether sugar is as bad as Lustig claims is that it certainly could be. It very well may be true that sugar and high-fructose corn syrup, because of the unique way in which we metabolize fructose and at the levels we now consume it, cause fat to accumulate in our livers followed by insulin resistance and metabolic syndrome, and so trigger the process that leads to heart disease, diabetes and obesity. They could indeed be toxic, but they take years to do their damage. It doesn’t happen overnight. Until long-term studies are done, we won’t know for sure.

One more question still needs to be asked, and this is what my wife, who has had to live with my journalistic obsession on this subject, calls the Grinch-trying-to-steal-Christmas problem. What are the chances that sugar is actually worse than Lustig says it is?

One of the diseases that increases in incidence with obesity, diabetes and metabolic syndrome is cancer. This is why I said earlier that insulin resistance may be a fundamental underlying defect in many cancers, as it is in type 2 diabetes and heart disease. The connection between obesity, diabetes and cancer was first reported in 2004 in large population studies by researchers from the World Health Organization’s International Agency for Research on Cancer. It is not controversial. What it means is that you are more likely to get cancer if you’re obese or diabetic than if you’re not, and you’re more likely to get cancer if you have metabolic syndrome than if you don’t.

This goes along with two other observations that have led to the well-accepted idea that some large percentage of cancers are caused by our Western diets and lifestyles. This means they could actually be prevented if we could pinpoint exactly what the problem is and prevent or avoid that.

One observation is that death rates from cancer, like those from diabetes, increased significantly in the second half of the 19th century and the early decades of the 20th. As with diabetes, this observation was accompanied by a vigorous debate about whether those increases could be explained solely by the aging of the population and the use of new diagnostic techniques or whether it was really the incidence of cancer itself that was increasing. “By the 1930s,” as a 1997 report by the World Cancer Research Fund International and the American Institute for Cancer Research explained, “it was apparent that age-adjusted death rates from cancer were rising in the U.S.A.,” which meant that the likelihood of any particular 60-year-old, for instance, dying from cancer was increasing, even if there were indeed more 60-years-olds with each passing year.

The second observation was that malignant cancer, like diabetes, was a relatively rare disease in populations that didn’t eat Western diets, and in some of these populations it appeared to be virtually nonexistent. In the 1950s, malignant cancer among the Inuit, for instance, was still deemed sufficiently rare that physicians working in northern Canada would publish case reports in medical journals when they did diagnose a case.

In 1984, Canadian physicians published an analysis of 30 years of cancer incidence among Inuit in the western and central Arctic. While there had been a “striking increase in the incidence of cancers of modern societies” including lung and cervical cancer, they reported, there were still “conspicuous deficits” in breast-cancer rates. They could not find a single case in an Inuit patient before 1966; they could find only two cases between 1967 and 1980. Since then, as their diet became more like ours, breast cancer incidence has steadily increased among the Inuit, although it’s still significantly lower than it is in other North American ethnic groups. Diabetes rates in the Inuit have also gone from vanishingly low in the mid-20th century to high today.

Now most researchers will agree that the link between Western diet or lifestyle and cancer manifests itself through this association with obesity, diabetes and metabolic syndrome — i.e., insulin resistance. This was the conclusion, for instance, of a 2007 report published by the World Cancer Research Fund and the American Institute for Cancer Research — “Food, Nutrition, Physical Activity and the Prevention of Cancer.”

So how does it work? Cancer researchers now consider that the problem with insulin resistance is that it leads us to secrete more insulin, and insulin (as well as a related hormone known as insulin-like growth factor) actually promotes tumor growth.

As it was explained to me by Craig Thompson, who has done much of this research and is now president of Memorial Sloan-Kettering Cancer Center in New York, the cells of many human cancers come to depend on insulin to provide the fuel (blood sugar) and materials they need to grow and multiply. Insulin and insulin-like growth factor (and related growth factors) also provide the signal, in effect, to do it. The more insulin, the better they do. Some cancers develop mutations that serve the purpose of increasing the influence of insulin on the cell; others take advantage of the elevated insulin levels that are common to metabolic syndrome, obesity and type 2 diabetes. Some do both. Thompson believes that many pre-cancerous cells would never acquire the mutations that turn them into malignant tumors if they weren’t being driven by insulin to take up more and more blood sugar and metabolize it.

What these researchers call elevated insulin (or insulin-like growth factor) signaling appears to be a necessary step in many human cancers, particularly cancers like breast and colon cancer. Lewis Cantley, director of the Cancer Center at Beth Israel Deaconess Medical Center at Harvard Medical School, says that up to 80 percent of all human cancers are driven by either mutations or environmental factors that work to enhance or mimic the effect of insulin on the incipient tumor cells. Cantley is now the leader of one of five scientific “dream teams,” financed by a national coalition called Stand Up to Cancer, to study, in the case of Cantley’s team, precisely this link between a specific insulin-signaling gene (known technically as PI3K) and tumor development in breast and other cancers common to women.

Most of the researchers studying this insulin/cancer link seem concerned primarily with finding a drug that might work to suppress insulin signaling in incipient cancer cells and so, they hope, inhibit or prevent their growth entirely. Many of the experts writing about the insulin/cancer link from a public health perspective — as in the 2007 report from the World Cancer Research Fund and the American Institute for Cancer Research — work from the assumption that chronically elevated insulin levels and insulin resistance are both caused by being fat or by getting fatter. They recommend, as the 2007 report did, that we should all work to be lean and more physically active, and that in turn will help us prevent cancer.

But some researchers will make the case, as Cantley and Thompson do, that if something other than just being fatter is causing insulin resistance to begin with, that’s quite likely the dietary cause of many cancers. If it’s sugar that causes insulin resistance, they say, then the conclusion is hard to avoid that sugar causes cancer — some cancers, at least — radical as this may seem and despite the fact that this suggestion has rarely if ever been voiced before publicly. For just this reason, neither of these men will eat sugar or high-fructose corn syrup, if they can avoid it.

“I have eliminated refined sugar from my diet and eat as little as I possibly can,” Thompson told me, “because I believe ultimately it’s something I can do to decrease my risk of cancer.” Cantley put it this way: “Sugar scares me.”

Sugar scares me too, obviously. I’d like to eat it in moderation. I’d certainly like my two sons to be able to eat it in moderation, to not overconsume it, but I don’t actually know what that means, and I’ve been reporting on this subject and studying it for more than a decade. If sugar just makes us fatter, that’s one thing. We start gaining weight, we eat less of it. But we are also talking about things we can’t see — fatty liver, insulin resistance and all that follows. Officially I’m not supposed to worry because the evidence isn’t conclusive, but I do.

Gary Taubes ( is a Robert Wood Johnson Foundation independent investigator in health policy and the author of “Why We Get Fat.” Editor: Vera Titunik (

Glycaemic Index and Carbohydrates

The glycaemic index (GI) measures carbohydrates according to how quickly they are absorbed and raise the glucose level of the blood. A low GI diet may help weight loss and may also help energy levels for endurance sports.

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Food and drinks provide fuel for our body in the form of fat, protein, carbohydrates and alcohol. Carbohydrates are the body’s preferred fuel source. The glycaemic index (GI) is a way to rate carbohydrates according to how quickly they are absorbed and raise the glucose level of the blood. It has replaced classifying carbohydrates as either ‘simple’ or ‘complex’.

Foods that contain carbohydrates include bread, breakfast cereals, rice, pasta, legumes, corn, potato, fruit, milk, yoghurt, sugar, biscuits, cakes and lollies.

Digesting and absorbing carbohydrates

The digestive system breaks down carbohydrate-containing foods into simple sugars, mainly glucose. For example, both rice and soft drink will be broken down to simple sugars in your digestive system. This simple sugar is then carried to each cell through the bloodstream.

The pancreas secretes a hormone called insulin, which helps the glucose to migrate from the blood into the cells. Once inside a cell, the glucose is ‘burned’ along with oxygen to produce energy. Our muscles, brain and nervous system all rely on glucose as their main fuel to make energy.

The body converts excess glucose from food into another form called glycogen. This is stored inside muscle tissue and the liver, ready to supplement blood sugar levels if they drop between meals or during physical activity.

The glycaemic index

Carbohydrate-containing foods can be rated on a scale called the glycaemic index (GI). This scale ranks carbohydrate-containing foods based on their effect on blood sugar levels over a period of time – usually two hours. The GI compares foods that have gram-for-gram the same amount of carbohydrate.

Carbohydrate-containing foods are compared with glucose (although sometimes white bread can be used as a reference food), which is given a GI score of 100. Carbohydrates that break down quickly during digestion have the highest glycaemic indexes (GI more than 70). These high GI carbohydrates release their glucose into the blood quickly.

Carbohydrates that break down slowly release glucose gradually into the bloodstream. They have low glycaemic indexes (GI less than 55). The blood glucose response is slower and flatter.

Choosing between high and low GI foods

The best carbohydrate food to eat varies depending on the situation. For example, the rate at which porridge and cornflakes are broken down to glucose is different. People with type 2 diabetes or impaired glucose tolerance have become resistant to the action of insulin or cannot produce insulin rapidly enough to match the release of glucose into the blood after eating carbohydrate-containing foods. This means their blood glucose levels may rise above the normal level.

Porridge is digested to simple sugars much more slowly than cornflakes, so the body has a chance to respond with production of insulin, and the rise in blood glucose levels is less. For this reason, porridge is a better choice of breakfast cereal than cornflakes for people with type 2 diabetes. It will also provide more sustained energy for other people as well.

How much you eat is also important

The amount of the carbohydrate-containing food you eat will also affect your blood glucose levels. For example, even though pasta has a low GI, it is not advisable for people with diabetes or impaired glucose tolerance to have a large serve. This is because the total amount of carbohydrate, and therefore the kilojoules, will be too high.

The glycaemic load (GL) is a concept that builds on GI, as it takes into account both the GI of the food and the amount of carbohydrate in a portion. GL is based on the idea that a high GI food consumed in small quantities would give the same effect on blood glucose levels as larger quantities of a low GI food. GL is easily calculated by multiplying the GI by the number of grams of carbohydrate in a serving of food.

GI and weight loss

A low GI diet is commonly promoted as an effective way to help lose weight by controlling blood sugars and appetite. When high and low GI diets are compared head-to-head, however, scientific evidence has shown that there is no additional benefit for weight loss of a low GI diet over a similar diet of nutrient composition that is high GI.

While GI can be a useful guide in planning a diet, it should not be the only consideration. Both the serving size of foods and the nutritional quality of the diet are just as important to consider.

GI and exercise

Eating low GI foods two hours before endurance events, such as long-distance running, may improve exercise capacity. It is thought that the meal will have left your stomach before you start the event, but remains in your small intestine releasing energy for a few hours afterwards. On the other hand, high GI foods are recommended during the first 24 hours of recovery after an event to rapidly replenish muscle fuel stores (glycogen).

High GI foods are influenced by low GI foods

Generally, eating low GI foods and high GI foods at the same time has the effect of ‘averaging’ the GI. This is important, as most foods are eaten as part of a meal and this affects the GI value of foods. For example, eating cornflakes (a higher GI food) with milk (a lower GI food) will reduce the effect on blood sugar levels.

If a person with diabetes experiences a ‘hypo’, where the blood glucose levels fall below the normal range of 3.5–8mmol/L, they need to eat carbohydrate-containing foods (preferably those with a high GI) to restore their blood sugar levels to normal quickly. For example, eating five jellybeans will help to raise blood glucose levels quickly.

GI scale examples

Some examples of the GI rating of various carbohydrates include:

  • Low GI (less than 55) – soy products, beans, fruit, milk, pasta, grainy bread, porridge and lentils.
  • Medium GI (55 to 70) – orange juice, basmati rice and wholemeal bread.
  • High GI (greater than 70) – potatoes, white bread and long-grain rice (other than basmati).

Factors that affect the GI of a food

Factors such as the size, texture, viscosity (internal friction or ‘thickness’) and ripeness of a food affect its GI. For instance, an unripe banana may have a GI of 30, while a ripe banana has a GI of 51. Both ripe and unripe bananas have a low GI.

Fat, protein, soluble fibre, fructose (a carbohydrate found in fruit) and lactose (the carbohydrate in milk) also generally lower a food’s glycaemic response. Fat and acid foods (like vinegar, lemon juice or acidic fruit) slow the rate at which the stomach empties and so slow the rate of digestion, resulting in a lower GI. Other factors present in food, such as phytates in wholegrain breads and cereals, may also delay a food’s absorption and thus lower the GI.

Cooking and processing can also affect the GI – food that is broken down into fine or smaller particles will be more easily absorbed and so has a higher GI. Foods that have been cooked and allowed to cool (potatoes, for example) can have a lower GI when eaten cold than when cooked.

GI symbol on packaged foods

A food-packaging symbol for comparing the effect of different foods on blood sugar was launched in Australia in July 2002. The GI symbol, G – Glycemic index tested, indicates the GI rating of packaged food products in supermarkets. It ranks food products based on the speed at which they break down from carbohydrate to sugar in the bloodstream.

The GI symbol only appears on food products that meet certain nutrient criteria for that food category. High and intermediate GI soft drinks, cordials, syrups, confectionery and sugars are excluded. Jams, honey and other carbohydrate-containing spreads are not necessarily excluded.

Using the GI as a guide to healthy eating

The GI can be used as a guide to healthy eating, as long as you are aware of the limitations. For example, the GI of some fruits, vegetables and cereals can be higher than foods that are considered to be treats, such as biscuits and cakes. This does not mean we should replace fruit, vegetables and cereals with treats, because the first are rich in important nutrients and antioxidants and the treats are not. GI can be a useful concept in making good food substitution choices, such as having oats instead of cornflakes, or eating grainy bread instead of white bread.

It is not always possible or necessary to choose all low GI foods. There is room in a healthy diet for moderate to high GI foods and many of these foods can provide important sources of nutrients. If you mix a low GI food with a high GI food, you will get an intermediate GI for that meal.

Tips for healthy eating

Some practical suggestions include:

  • Use a breakfast cereal based on oats, barley or bran.
  • Use grainy breads or breads with soy.
  • Enjoy all types of fruit and vegetables.
  • Eat plenty of salad vegetables with vinaigrette dressing.
  • Eat a variety of carbohydrate-containing foods. If the main sources of carbohydrates in your diet are bread and potatoes then try lentils, legumes, pasta, basmati rice and pita breads.
  • Focus more on the serving size of foods, rather than just their GI rating.

Expert medical supervision

If you have a medical condition, such as diabetes, it is important to seek the advice of your doctor or specialist before making any changes to your diet.

Where to get help

  • Your doctor
  • Dietitians Association of Australia Tel. 1800 812 942
  • Nutrition Australia.

Things to remember

  • The glycaemic index (GI) rates carbohydrates according to how quickly they raise the glucose level of the blood.
  • The glycaemic load (GL) rates carbohydrates according to the glycaemic index and the amount of carbohydrate in the food.
  • A low GI rating of a food does not mean you can eat a larger serve of that food – the total amount of carbohydrate and kilojoules consumed are still important.
  • Choose a diet containing plenty of fruits, vegetables and legumes, but with smaller helpings of potatoes and less highly refined grain products and concentrated sugar.