Are Chemicals Making You Fat?

Many people say the obesity epidemic could be solved if we just got off our butt to hit the gym and stopped eating so many Big Macs. Diet and exercise do play a huge role in what we weigh, of course, but there’s one glitch with this theory: Over the past quarter century, the incidence of obesity has risen most markedly—by a whopping 74 percent—not in adults or children, but in infants.

In fact, six-month-olds today are fatter than they were in 1980, despite the fact that birth weights overall have been decreasing—a finding that makes some scientists wonder whether environmental chemicals could be causing babies to rapidly gain weight after birth. Bruce Blumberg, Ph.D., a biologist at the University of California-Irvine, is so concerned that these chemicals play a significant role in the rise in obesity that he considers them “obesogens.” “Not too long ago, no one would’ve believed there was such a thing as an obesogen and that anything except eating too much could make you fat,” he says. But in Blumberg’s research, TBT, a common chemical used to make PVC plastic (of the sort found in some shower curtains), caused mice to develop extra fat cells. And when Blumberg exposed pregnant mice to the chemical, their pups grew to be up to 15 percent fatter than mice that hadn’t been exposed.

Now, this is animal research, and no one knows just how widely humans are exposed to TBT, which hasn’t been tested extensively in humans. But last year researchers at the University at Albany in New York found traces of the chemical in every single sample of house dust they analyzed.

BPA and phthalates, chemicals used to make plastic flexible, may also impact your weight. Boston University research found that teen girls with greater levels of a certain phthalate in their urine were at higher BMIs than those without. Another study found that Americans who were most exposed to both chemicals were more at risk of developing diabetes. As a double whammy, BPA and some pesticides may even disrupt our body’s ability to regulate blood sugar and hunger—two key factors in losing weight. “For me, there’s no doubt common chemicals are playing a role in obesity and related diseases,” says Richard Stahlhut, M.D., an environmental health scientist at the University of Rochester in New York. “Some overweight people have been taking a beating for diseases that are not their fault.”

The good news, some researchers say, is that we may be able to lose weight not by starving ourselves but by avoiding obesogens. While researching his book The New American Diet, journalist Stephen Perrine asked 400 people to cut their obesogen exposure for six weeks. “We had them swap out foods that tended to be high in obesogens, such as canned foods and grain-fed meats, for versions of these foods with lower chemical loads,” Perrine says. They were still allowed to eat burgers and pork chops, just ones that were free-range and hormone-free. After six weeks, the subjects had lost, on average, 15 pounds. Filling your plate with (organic) green leafy vegetables like spinach and kale, which are high in folate, also helps.

Ginger and Lentil Soup

This anti-inflammatory, healing soup is perfect for a cool fall day. As we transition from summer to fall, try adding warming foods to your diet.

Healing Ginger and Lentil Soup

2 tablespoons extra virgin olive oil
1 large onion, chopped small
3 to 6 cloves garlic, minced
3 to 4 tablespoons ginger, grated or
nely diced
3 cups water
3 to 4 carrots, sliced
1 pound French lentils
6 cups vegetable or chicken broth
2 teaspoons ground cumin
1/4 teaspoon cayenne pepper (or to
taste)
1 tablespoon fresh lemon juice
salt and pepper to taste
grated Gruyere cheese for serving
(optional)
cooked quinoa for serving

Sift through the lentils for rocks and pebbles. Place in a colander and rinse with cool water. Set aside.
Chop onions and garlic, grate ginger, and chop carrots.
Place a large pot over medium heat. Add oil. When oil is hot, add onions. Cook until transparent and slightly browned. Add garlic, ginger, carrots and cook, while stirring,for 1 minute.
Add cumin and cayenne pepper and cook for 30 seconds.
Add the water to the hot pot and scrape the browned bits off the bottom of the pot as the liquid sizzles.
Add lentils and broth and simmer for about 45 minutes, until
lentils have softened.
Taste and season with salt and pepper. Finish with lemon.
Serve with grated cheese and/or quinoa.
The soup will last in an airtight container in the fridge for about a week. It’s also great to keep in the freezer.

10 ways to help your child grow their best brain

1. Help your child learn to sing or play music or learn a second language.
2. Make sure he or she has plenty of physical activity; whenever possible, outdoors is best.
3. Cut down on sugar, especially soda and diet soda.
4. Make sure they get plenty of protein.
5. Be consistent about hours for eating, sleeping and waking.
6. Help your child set goals and respect limits.
7. Feed various ways of learning. Take them to a science fair one weekend and an art fair the next. Take them to a sports competition another week and a play the next.
8. Provide opportunities for social interaction with people of all ages.
9. Remember that one-third of the brain is set up to execute and two-thirds, to receive information. Make room for quiet time.
10. If your child studies or reads all the time, plays computer games all the time, or plays sports all the time, know that too much of anything is too much. The brain needs balance and harmony.


Lee Gerdes
Author of Limitless You:
The Infinite Possibilities of a Balanced Brain

More muscle mass can protect against insulin resistance and prediabetes.

In a cross-sectional study, every 10% increase in the ratio of skeletal muscle mass to total body weight was associated with an 11% reduction in risk of insulin resistance and a 12% drop in risk of transitional, prediabetes, or overt diabetes.  Over 13,000 people were studied via an analysis of the National Health and Nutrition Examination Survey (NHANES) III data. The findings point to the importance of gauging muscle mass, in addition to body mass index (BMI) and waist circumference, when assessing a patient's metabolic health, the researchers said.

Foods for Colon Health

A new study from a California research team suggests that eating more legumes (dried beans, dried peas and lentils) at least three times a week can cut the risk of developing colon polyps (which can lead to cancer) by 33 percent. Brown rice reduces the risk, too, by 40 percent. Researchers at Loma Linda University also found that eating cooked green vegetables at least once a day, and dried fruit at least three times a week offers additional protection. The researchers analyzed data from more than 2,800 adults in the Adventist Health Study-1 performed in 1976-77, including information on participants who responded to a follow up study 26 years later. The first study asked participants how often they consumed specific foods. The investigators also considered other factors that could influence colon cancer risk, including family history of the disease, education, physical activity level, and constipation. They also checked alcohol intake, how often the participants ate sweets, used pain medication and took multivitamins. The study was published in the May 2011 issue of Nutrition and Cancer.

Vitamin D Reduces Diabetes Risk

Higher levels of vitamin D in the blood appear to be associated with a reduced risk of diabetes among people at high risk for the disease, according to a new report. In a study of over 2,000 people with prediabetes, it was seen that the higher the level of vitamin D in the blood, the lower the risk of developing type 2 diabetes.

Dr. Pittas of Tuft's University says that vitamin D might play a role in diabetes by improving insulin secretion and insulin sensitivity. Though this has been seen over the years in a few other studies, this is the first one that reflects the benefit of a long-term vitamin D status.

The research showed that for every 5 nanograms per milliliter (ng/mL) increase in vitamin D levels, the risk of developing diabetes dropped by 8%.

Thyroid Health Affected by Nutritional Status and Stress Hormones

I recently had the privilege of hearing Dr. Chris Meletis at an Advanced Hormone Module sponsored by the Institute for Functional Medicine, According to Dr. Meletis, "the clinical evidence is clear that prior to offering thyroid replacement, identifying underlying triggers for thyroid dysfunction is a must. The First Approach ideally incorporates ensuring that the adrenal function is sufficient as defined by adequate cortisol levels, along with DHEA sulfate and pregnenolone levels. Relative to specific nutritional supplements ensuring that there are sufficient ferritin levels of at least 70 to 100 is a must, along with adequate serum selenium of at least 90 mcg/L. In addition making sure that zinc status is optimal is foundational, as low zinc can also lower both T4/T3 levels. Iodine is certainly a must as well, with a minimum of 150 mcg daily, with at least 1000 mcg per day a common initial therapeutic dosing. It has also been noted that 40% of hypothyroid patients are B12 deficient."

It is essential to ask the clinical question of why a tissue or gland has become insufficient. Optimizing nutritional status is always the first step, while making sure that an acute or chronic adrenal stress response has not down-regulated the TSH and Free T4 and Free T3 is an absolute consideration. In addition, thyroid hormone levels are dynamic as reflected in the 2007 survey published in the Archives of Internal Medicine,which showed that values spontaneously returned to normal in more than 50% of patients with abnormal TSH levels when the test was repeated at a later date.

So the bottom line is have your physician check adrenal functioning and nutritional status first before putting you on thyroid replacement hormone. Once on a replacement hormone, such as Synthroid, the thyroid may shut down, which necessitates being on thyroid replacement therapy for life.

What's the Best Way to Do a Dietary Cleanse?

Faddish juice fasts can shed pounds speedily … but experts agree that a slower, whole-foods approach to cleansing is healthier and more sustainable

One thing’s for certain. The juice cleanse has gone mainstream.

Celebrities like Julia Roberts and Beyoncé have gone public with their affection for juice delivery services like NYC’s Blueprint Cleanse and that old dieting stalwart, the Master Cleanse.

But are they effective? Depends on the goal.

“The motivation for these cleanses is typically weight loss,” says Bonnie Taub-Dix, a NYC-based nutritionist and author of Read It Before You Eat It, who points out that most people who lose weight on trendy cleanses tend to gain it back.

For those looking for more of a digestive tune-up – following, say, an overindulgent summer barbecue – the experts are split when it comes to endorsing the recent spate of pricey juice and raw-food cleanses to get back on track.

But they’re all in agreement that easy lifestyle fixes (read: inexpensive) can be just as effective. Here are 5 simple expert-endorsed tips to cleansing and getting your systems back on track.

1) Find the right time to do it.
Timing is everything, and that applies to cleansing as well. Don’t pick the week a big work project is due to focus on detoxing.

Dr. Ron Stram, Director at the Center for Integrative Health and Healing, cites a low-stress environment as being necessary for optimal results. “Activity level should be moderate and you should feel relaxed,” he says.

And let’s not forget sleep. Pamela Salzman, a holistic health counselor based in Los Angeles, states that sleep is when detoxification and physical restoration occurs. Plus, “people who are under-rested are more susceptible to illness and tend to make poor dietary choices,” says Monica Reinagel, nutritionist and author of Nutrition Diva’s Secrets for a Healthy Diet.

Taub-Dix agrees, saying, “You end up reaching for a cookie instead of a nap.” She also says sustained wellness comes from practicing the trifecta of exercise, healthy diet, and sleep: “Think of a 3-legged stool. Take away one of those legs and the stool won’t be stable.”

2) Create a sustainable cleanse.
Most experts who aren’t fans of juice cleanses point out it’s not feasible to sustain them and their effects for a prolonged period of time.

“Healthful cleansing has just as much to do with moderation as overeating,” says Taub-Dix, who suggests taking an overall look at your diet and eating habits to assess what’s missing and what you really need to add for good health.

Set goals that can be integrated into your life, such as planning, shopping for, and eating a well-balanced breakfast for a week to combat the mid-morning slump. “The reality is that fad diets are based on some sort of truth that go off the deep end,” she says.

Apply common-sense principles, such as eliminating processed foods and caffeine or eating more raw food. Avoid extremes and look for sustainable change.

Reinagel also says that a 24-hour fast may be useful for people who are overly dependent on food and need to “break the cycle,” adding that a fast has “little to do with resting the digestive organs, but can reduce inflammation and improve immune response.”

No matter what, fasting for a prolonged period of time or drastically reducing your caloric intake aren’t good ideas. “Your body actually needs food to cleanse and won’t be able to function properly while fasting,” says Salzman.

3) Up your intake of fruits and vegetables.
Certain powerhouse fruits and veggies will offer more benefits on a cleanse than others. Salzman favors dark green, leafy vegetables, like kale and parsley, as they’re “rich in chlorophyll, one of nature’s natural detoxifiers.” She also recommends adding lemon juice to your water and food, as it “breaks up and draws out stagnant mucus in the body.”

Dr. Stram advocates consuming cruciferous vegetables such as cabbage, cauliflower, and bok choy, all of which contain compounds that help the liver detoxify. “Fruits and vegetables promote healthy colon function,” adds Reinagel, meaning that they help flush out toxins.

4) Chug more water.
The easiest, fastest way to jumpstart a cleanse is to properly hydrate. “Water hydrates the cells and helps flush your circulatory and lymph systems,” says Dr. Stram.

Translation: Your internal system of checks and balances won’t function at its best unless you’re drinking enough water.

Plus, “cleansing is about eliminating toxins,” says Salzman. “Once your body releases toxins, you must up your intake of water to dilute them and flush them out.”

5) Give it time to kick in.
Most people find the first few days the most challenging. “Sometimes you feel worse before you feel better,” says Salzman. “Many people experience symptoms of withdrawal from sugar, caffeine or chemicals in foods. Headaches and irritability are very common as toxins enter the bloodstream.”

Dr. Stram will advise patients combating caffeine withdrawal to switch to green tea for a few days.

If you’re sticking to healthful, “clean” foods, drinking lots of water, aiming for adequate sleep, and still feeling rotten, give your body the time needed to expel the toxins first, before turning to more drastic, less balanced fad cleanses.

Written by by Teri Tsang Barrett for Vital Choice Newsletter

Does Menu Diversity Lead to Overeating?

Repeatedly being offered the same foods may lead to food ‘boredom’ and decrease energy intakes in women, but variety may actually increase caloric intake, suggests a new study.

A study with obese and non-obese women showed that, when macaroni and cheese was offered daily, the energy consumed decreased by about 100 calories a day. When the mean was provided only weekly, caloric intake increased by about 30 calories per day.

Researchers from the University at Buffalo and the University of Vermont report their findings in the American Journal of Clinical Nutrition .

The findings support dietary advice for people to try to eat the same food every day, “in which case habituation may develop that would reduce the likelihood of overeating and subsequent obesity”, according to the researachers.

Led by Buffalo’s Leonard Epstein, the researchers note that monotony is known to reduce food acceptability and consumption, but their study “provide[s] the first evidence in humans that habituation may provide a theoretical explanation for why repeatedly consuming the same food will lead to reduced consumption.

“Long-term habituation, in terms of a faster rate of habituation and reduced energy intake, was observed for the daily group but not for the weekly group.

“Repeated presentations once a day compared with once a week provide a reference point for the interval between food presentations that could lead to long-term habituation,” added Epstein and his co-workers.

Results showed that women in the daily group consumed less calories per day, whereas the weekly food exposure increased the caloric intake, and the results were the same for both obese and non-obese women.

“It is of interest that obese subjects and non-obese subjects showed similar long-term habituation to daily presentations of the same food
“These results suggest that repeated presentations of the same [main meal] over days would equally effective for obese and non-obese women,” wrote the researchers.Commenting on the study, Avena and Gold said the work was “very important” but limited due to only including women.

“Thus, it will be important to further explore whether the findings obtained in the present study extend to men.”

Source: American Journal of Clinical Nutrition
Volume 94, Pages 371-376
“Long-term habituation to food in obese and nonobese women”
Authors: L.H. Epstein, K.A. Carr, M.D. Cavanaugh, R.A. Paluch, M.E. Bouton

Editorial: American Journal of Clinical Nutrition
Volume 94, Pages 367-368
“Variety and hyperpalatability: are they promoting addictive overeating?”
Authors: N.M. Avena, M.S. Gold

Now tell me what you think? Does diversity in food choices lead to overeating? Maybe it depends upon what's being served. I could eat dark chocolate 365 days a year.

Deficiency in D major: Did vitamin deficiency led to Mozart’s untimely death?

A lack of exposure to sun and the resulting deficiency in vitamin D may have been behind the early demise of Wolfgang Amadeus Mozart, suggests a new analysis.

All work and no play (outside), made Wolfgang a sick boy
Mozart passed away at the tender age of 35 having suffered from a list of infectious diseases throughout his lifetime, including pneumonia and sepsis, heart disease, and kidney disease, all of which have a link to vitamin D deficiency, according to a letter to the journal Medical Problems of Performing Artists.

William Grant, PhD, from the Sunlight, Nutrition, and Health Research Center (SUNARC) in San Francisco and Stefan Pilz, MD, from the Medical University of Graz in Austria report that weak sunlight for six months of the year in Salzburg and Vienna would have made it impossible for a person to make vitamin D from sun exposure.

Add to this that Mozart did the majority of his composing at night – and therefore slept during the day – and you have a new hypothesis to explain Mozart’s death.

“While understanding the causes of Mozart’s death cannot bring him back,” wrote Grant and Pilz, “it does have an important lesson for those living at higher latitudes in Europe and elsewhere regarding the importance of vitamin D.

“Emerging science indicates that the serum 25(OH)D level [the storage form of vitamin D in the body] for optimal health is 75 to 100 nmol/L or slightly higher. Mainly attributable to reduced sunlight-induced vitamin D synthesis in the skin, the population mean value for those living at mid-to-high latitudes is between 40 and 65 nmol/L.

“To increase serum 25(OH)D levels to over 100 nmol/L could take 2500 to 5000 IU of vitamin D per day.”

Source: Medical Problems of Performing Artists
June 2011, Volume 26, Number 2, Page 117
“Vitamin D deficiency contributed to Mozart's death”
Authors: W.B. Grant, S. Pilz

"Chemical Calories" May Be Making Us Fat

Hair-raising theory: Scientists say chemicals in beauty products can make us put on weight by altering our hormone balance

Read more: http://www.dailymail.co.uk/femail/article-2013283/Is-shampoo-making-FAT-The-truth-chemical-calories-beauty-products.html#ixzz1RqpBRWQE

By Peta Bee

When it comes to losing weight, most of us are aware of the three factors at play: genetics, the number of calories we consume and the energy we are prepared to expend sweating our way into shape.

We can’t choose our parents but, according to the dieting mantra, eat healthily, exercise regularly and the pounds will eventually drop off.

But what if your body stubbornly refuses to remove excess fat, despite concerted efforts to shift it? Emerging evidence suggests that a more sinister reason than food and activity could be contributing to weight problems and that so-called ‘chemical calories’ lurking in everyday beauty products such as shampoo, body lotions and soap could be to blame.

Doctors at the Mount Sinai Medical Center in New York claim that phthalates, chemical ingredients in 70 per cent of cosmetics as well as many household cleaning products, have been shown to throw the body’s natural weight control system, a delicate balance of hormones, off kilter.

They suggest that exposure to phthalates through daily use may be linked to childhood obesity and weight problems in adults.

In their long-term study on girls living in the inner city area of East Harlem, the Mount Sinai team measured exposure to phthalates by analysing the children’s urine.

‘The heaviest girls have the highest levels of phthalates in their urine,’ says Professor Philip Landrigan, a paediatrician and the study author. ‘It goes up as the children get heavier, but it’s most evident in the heaviest kids.’

Phthalates have been widely used as gelling agents in cosmetics, cleaning products and to make plastic bottles for more than half a century, but it has only just come to light that there may be possible health risks.
Another substance, Bisphenol-A (BPA), also present in containers and bottles, has also been found to provide ‘chemical calories’.

It’s the fact they are absorbed into the body that causes most concern. Billed as ‘endocrine disruptors’, they are known to affect the glands and hormones that regulate numerous bodily functions.

Studies on animals have shown consistently that the chemicals depress testosterone levels, known to be a risk factor for weight gain. They have also been found to mimic the effects of oestrogen, which have been linked to weight gain and early puberty.

Further research on humans linked phthalates with poor semen quality in men and with subtle alterations in the reproductive organs of male babies. And now come the latest revelations that they may also influence weight.

In numerous studies, mice exposed to such ‘endocrine disruptors’ became obese. But could the same effect occur in people?

Zoe Harcombe, nutritionist and author of the Obesity Epidemic, says that even the slightest disruption to hormone levels ‘is very bad news’ for someone trying to lose weight.

‘In men, phthalates and other chemicals have an anti-testosterone capacity that has been linked to obesity,’ she says. ‘In women they mess up our basic genetic hormone balance so that you get disruptions similar to those that might occur during the menopause or at puberty.’

Using phthalate-containing cosmetics when you are dieting could make matters worse. ‘Women who follow a low-fat diet are likely to suffer the most from adverse side-effects to these chemicals,’ says Harcombe:
‘By reducing the fat they consume, they also reduce the fat-soluble vitamins in their body. That often leaves them with dry skin. They slather on moisturisers to rectify that problem without realising they are unwittingly causing another by supplying chemical calories through the skin.’

Among those at the forefront of tackling obesity, the influence of chemicals is a hot topic.


Tam Fry, a spokesperson for the National Obesity Forum, says many obesity doctors accept that the hormonal disruption caused by exposure to chemicals does play a part in weight problems. While under-activity and over-eating remain the major causes of obesity, Fry says more work needs to be done to confirm the links.

‘There is particular concern about whether these chemicals with an oestrogenic effect are contributing to earlier puberty in girls,’ Fry says.


‘Girls reach puberty when they are at a weight that can support the reproductive cycle and this is getting earlier and earlier. Whether that’s a result of straightforward over-eating by a generation of young girls or whether there is an additional chemical effect, we don’t yet know.’

It’s not just girls who seem susceptible to the phthalate effect. In 2007, researchers at the University of Rochester school of medicine in New York found the same class of chemicals were contributing to abdominal obesity and insulin resistance, a precursor to diabetes, in men.

Adding Soluble Fiber to the Diet May Reduce Abdominal Fat

Increased soluble fibre consumption may reduce the amount of deep belly fat that we accumulate, according to new research.
The study, published in Nature’s journal Obesity, found that for every 10-gram increase in soluble fiber eaten per day, deep belly visceral fat, known to be more dangerous than subcutaneous fat found near the skin, was reduced by 3.7 per cent over five years.

In addition, the authors reported that increased moderate activity resulted in a 7.4 per cent decrease in the rate of visceral fat accumulation over the same time.

“Our study is valuable because it provides specific information on how dietary fiber, especially soluble fiber, may affect weight accumulation through abdominal fat deposits,” said Dr Kristen Hairston, assistant professor of internal medicine at Wake Forest Baptist Medical Center.

In the longitudinal study, Hairston and her team examined whether lifestyle factors, including diet and frequency of exercise, were associated with a five-year change in abdominal fat of African Americans and Hispanic Americans – populations who are at a disproportionally higher risk for developing high blood pressure and diabetes and accumulating visceral fat.

Central obesity has been associated with hypertension, blood lipid imbalances, insulin resistance, fatty liver disease, and type-2 diabetes.

Non-alcoholic Fatty Liver Disease

The growing culprit behind liver disease

By Elizabeth Cohen, CNN Senior Medical Producer
June 17, 2011 6:22 a.m. EDT

(CNN) -- The first time Wilson Alvarado got lost on the way to a neighborhood park, he told his wife, Patricia, not to worry about it -- he was 62, he told her, and just getting a little forgetful.

Patricia thought it was strange, considering the park was only a half-mile away, and he'd driven there every week for more than 30 years. Then Wilson got lost again on the way to the park. A few months later, he called Patricia from the supermarket, asking why he was there.

"I thought, well, maybe he really is just getting old," Patricia recalls. "My mother has Alzheimer's, and I thought maybe that was it."

It was easy to overlook the little memory lapses until several years later when the situation reached a head. While her husband was visiting relatives in Puerto Rico, Patricia received a phone call from his cousin saying they'd taken Wilson to the hospital because he "wasn't making any sense" and was acting so aggressive the hospital put him in restraints.

"It was really horrifying," she says.

Patricia had him put back on a plane to Buffalo, near their home in Cheektowaga, New York. His doctors explained that liver disease was behind Wilson's memory lapses and erratic behavior.

"When you think about this kind of thing, you think about dementia or Alzheimer's," she says. "You don't think about the liver."

Wilson had cirrhosis, just like alcoholics get, but in his case, fat, not alcohol, was the culprit. At 5 feet 8 inches and 185 pounds, Wilson is overweight, and too much fat in his liver eventually caused it to malfunction.

According to the Centers for Disease Control and Prevention, a third of Americans are either overweight or obese, and doctors say they're seeing more and more patients like Wilson Alvarado.

"It's overwhelming how many patients we're seeing with this problem," says Dr. Naim Alkhouri, a hepatologist at the Cleveland Clinic.

Dr. William Carey, also a hepatologist at the Cleveland Clinic, adds, "This is huge. We didn't even know this disease existed 30 years ago. Now it's the most common liver disease in America."

'We won't have the ability to treat all these patients'

About a third of the U.S. population has nonalcoholic fatty liver disease, according to Dr. Michael Curry, a hepatologist at the Beth Israel Deaconess Medical Center in Boston.

Curry said most of those people -- about 80% -- will not develop significant liver disease. The other 20% will develop a disease called nonalcoholic steatohepatitis, or NASH. Of those, about 20-30% will go on to develop cirrhosis and end-stage liver disease, where the only real treatment is a liver transplant.

"That's about 6 million people. We won't have the ability to treat all those patients," Curry says. "If we even have a fraction of that number of patients, it will overwhelm liver transplant programs."

Laundry in the refrigerator

NASH is often silent, according to the National Institutes of Health. While some people have pain in the right side of their abdomen, most do not. Liver enzyme tests are sometimes normal, and even ultrasounds and CT scans don't always pick up on the disease.

"Symptoms are few and far between," the Cleveland Clinic's Carey says.

"It can sneak up on you," says Dr. Kevin Mullen, a hepatologist at the Case Western Reserve University School of Medicine. "Even your doctor might miss it."

Often symptoms don't show up until the disease has progressed. Sometimes, the first sign is a swollen stomach or ankles, or vomiting blood.

Some patients, such as Wilson Alvarado, develop brain changes called hepatic encephalopathy. As the disease progresses, the liver has a hard time filtering out toxins, which can go to the brain and cause problems such as memory lapses, trouble sleeping at night and lack of coordination.

"It might start out with minimal changes, like a few more dents in the car," Curry says.

Later, the changes can become more disturbing.

"I had a patient who put his laundry in the refrigerator," Carey says. "Another one couldn't remember the family party that had just happened that very day."

Curry adds, "One of my patients got into the shower and turned on boiling hot water and couldn't figure out how to switch it off."

Mullen says, "It really can be bizarre. They might try to sell their house for $100 or walking around the neighborhood unclothed."

Preventing nonalcoholic fatty liver disease

If a patient loses weight, eats better and exercises, he or she can often reverse the disease in its earlier stages.

"That's why we like to find these people early," says Alkhouri of the Cleveland Clinic.

However, by the time the disease has advanced to the point of cirrhosis, it's usually irreversible, he adds.

Alvarado had to have a liver transplant last month at the Cleveland Clinic, and his wife says his thinking has become more clear.

Non-alcoholic fatty liver disease is associated with sugar intake, not fat.

Olive Oil Consumption May Lower Risk of Stroke

A diet high in olive oil may help protect older people against strokes, which are the third leading cause of death in the United States after heart disease and cancer. The findings are in a study published in the journal Neurology.

A stroke occurs when an artery within the brain, or leading to the brain, becomes blocked by a clot or bursts. The brain becomes deprived of blood and oxygen carried in the arteries and begins to die. Strokes become more common as we age – stroke risk doubles for each decade of life after age 55, according to the American Heart Association.

University of Bordeaux researchers examined the medical records and olive oil consumption of 7,625 study participants, which included people age 65 and older from the French cities of Bordeaux, Dijon and Montpellier. None of the participants had any history of stroke when the study began. Olive oil use was classified as “no use”, “moderate use” – meaning using olive oil for cooking or as dressing or with bread, or “intensive use” which means olive oil was used for cooking and as dressing or with bread.

Participants had follow-up exams at 2, 4, and six years and stroke incidents were recorded and verified. 148 stokes occurred after slightly more than five years. Compared to those who didn’t use olive oil, people who had “intensive use” of olive oil had a 41% lower risk for stroke.

Many previous studies have reported health benefits from eating a Mediterranean-type of diet. "Olive oil is a component of the Mediterranean Diet which has been shown to have beneficial effects on cardiovascular disease and stroke. It can be included in a healthy eating plan as one of the oils that contains the least amount of saturated or bad fat,“ according to Dr. Ralph Sacco, President of the American Heart Association.

However, while numerous studies have linked the eating pattern to health benefits including lower rates of heart disease, cancer, diabetes, Alzheimer’s and Parkinson disease, Dr. Larry B. Goldstein of the Duke [University] Stroke Center, and a spokesman for the American Heart Association, is quick to note that the findings of the Neurology study show only an association between lower stroke risk and eating a diet high in olive oil, not proof that a diet high in olive oil will lower stroke risk. “There’s no reason you shouldn’t use olive oil paired with other heathy lifestyle behaviors including a diet high in fruits and vegetables, maintaining a healthy weight, regular exercise, and not smoking cigarettes,” which Goldstein says are known to reduce stroke risk by 80%.

Mindfulness Meditation Helps Hot Flashesl

It takes some training, but practicing mindfulness meditation does seem to help ease hot flashes, night sweats and insomnia in menopausal women, according to study results from the University of Massachusetts. Researchers there taught mindfulness meditation to 55 women between the ages of 47 and 69. A comparable group of 55 women of the same age who had the same symptoms were placed on a "waiting list" for training. The women in the first group attended classes once a week for eight weeks and also had a full day of training in mindfulness meditation, which involves focusing on the present. When the study began, the women reported five or more moderate to severe hot flashes or night sweats daily. After nearly two years of practice, the meditating women reported their symptoms bothered them about 15 percent less than they had at the outset, compared to a decrease of only 7 percent in the women who were on the waiting list. The study was published in the June 2011 issue of Menopause.

Broccoli Extract can Selectively Target Cancer Cells

The safety, and cancer-targeting ability of the broccoli extract sulforaphane, has been backed by a new study finding that it can selectively target cancer cells.

The research, published in Molecular Nutrition and Food Research, reports for the first time that sulforaphane – one of the primary phytochemicals in broccoli and other cruciferous vegetables – is able to selectively target and kill cancer cells, while leaving normal cells healthy and unaffected.

“It is well documented that sulforaphane can target cancer cells through multiple chemopreventive mechanisms," said the authors, led by Dr Emily Ho, associate professor at the Linus Pauling Institute at Oregon State University, USA.

“Here we show for the first time that sulforaphane selectively targets benign hyperplasia cells and cancerous prostate cells while leaving the normal prostate cells unaffected,” they added.

The tissue of cruciferous vegetables, such as broccoli, cauliflower, and cabbage, contain high levels of the plant chemicals glucosinolates. These are metabolized by the body into isothiocyanates (such as sulforaphane), which have been suggested to be powerful anti-cancer agents.

Moderate to Intense Exercise May Protect the Brain

Older people who regularly exercise at a moderate to intense level may be less likely to develop the small brain lesions, sometimes referred to as “silent strokes,” that are the first sign of cerebrovascular disease, according to a new study published in the June 8, 2011, online issue of Neurology®, the medical journal of the American Academy of Neurology (AAN).

“These ‘silent strokes’ are more significant than the name implies, because they have been associated with an increased risk of falls and impaired mobility, memory problems and even dementia, as well as stroke,” said study author Joshua Z. Willey, MD, MS, of Columbia University in New York and a member of the American Academy of Neurology. The research was also completed at the Univerisy of Miami in Florida. “Encouraging older people to take part in moderate to intense exercise may be an important strategy for keeping their brains healthy.”

The study involved 1,238 people who had never had a stroke. Participants completed a questionnaire about how often and how intensely they exercised at the beginning of the study and then had MRI scans of their brains an average of six years later, when they were an average of 70 years old.

A total of 43 percent of the participants reported that they had no regular exercise; 36 percent engaged in regular light exercise, such as golf, walking, bowling or dancing; and 21 percent engaged in regular moderate to intense exercise, such as hiking, tennis, swimming, biking, jogging or racquetball.

The brain scans showed that 197 of the participants, or 16 percent, had small brain lesions, or infarcts, called silent strokes. People who engaged in moderate to intense exercise were 40 percent less likely to have the silent strokes than people who did no regular exercise. The results remained the same after the researchers took into account other vascular risk factors such as high blood pressure, high cholesterol and smoking. There was no difference between those who engaged in light exercise and those who did not exercise.

“Of course, light exercise has many other beneficial effects, and these results should not discourage people from doing light exercise,” Willey said.

The study also showed that the benefit of moderate to intense exercise on brain health was not apparent for people with Medicaid or no health insurance. People who exercised regularly at a moderate to intense level who had Medicaid or no health insurance were no less likely to have silent infarcts than people who did no regular exercise. “It may be that the overall life difficulties for people with no insurance or on Medicaid lessens the protective effect of regular exercise,” Willey said.

The Healthy Mind Platter

Just as we now have a Healthy Food Plate, which the government recently released to replace the Food Pyramid, why not also adopt a Healthy Mind Platter. (Courtesy of Dr. Dan Siegel)

Seven daily essential mental activities to optimize brain matter and create well-being:
Focus Time. When we closely focus on tasks in a goal-oriented way, we take on challenges that make deep connections in the brain.
Play Time. When we allow ourselves to be spontaneous or creative, playfully enjoying novel experiences, we help make new connections in the brain.
Connecting Time. When we connect with other people, ideally in person, and when we take time to appreciate our connection to the natural world around us, we activate and reinforce the brain's relational circuitry.
Physical Time. When we move our bodies, especially aerobically, we strengthen the brain in many ways.
Time In. When we quietly reflect internally, focusing on sensations, images, feelings and thoughts, we help to better integrate the brain.
Down Time. When we are non-focused, without any specific goal, and let our mind wander or simply relax, we help the brain recharge.
Sleep Time. When we give the brain the rest it needs, we consolidate learning and recover from the experiences of the day.

Social Connections Influence Our Genes

Scientists are discovering that the environment plays a powerful role in biology, including influencing gene expression. For example, researchers found that social circumstances influenced gene expression in cancer cells. More than 220 genes were turned on in the cancer cells of women with low levels of social support and high levels of depression. These genes were not active in women with good social support. Some of the genes that were turned on were associated with higher rates of cancer spreading from one organ to another. These and other studies are showing that at a molecular level, social and emotional factors relate to physical health. These scientists are studying "the psychology of cells" and proving that genes and the environment are linked. Your genetic capacity can be compared to a sandbox of possibilities, but what kind of castle you build depends upon your experiences.

Carrageenan May Be Carcinogenic

Carrageenan, a common and food additive that comes from red seaweed, is used as a thickener and emulsifier in many processed foods, such as ice cream, yogurt, cottage cheese, soy milk and other processed food products. Many of these products may be so-called health foods. Based on results of animal studies, it has been tagged by some as an unsafe product that may cause ulcerations and cancers of the gastrointestinal tract. According to Dr Andrew Weil, the evidence is compelling enough to avoid carrageenan in any product, especially if you have GI disorders such as irritable bowel disease.

Omega-3s May Reduce Symptoms of Depression in the Elderly

According to findings published in The Journal of Nutrition, Health & Aging, depressed women who received daily supplements containing 2.5 grams of omega-3 experienced significant reductions in their symptoms.

In addition, researchers from the University of Pavia also report that omega-3 supplements providing a daily EPA (eicosapentaenoic acid) dose of 1.67 grams and a daily DHA (docosahexaenoic acid) dose of 0.83 grams reported improvements in the ‘quality of life’.

“This [quality of life] observation has never been achieved before and it appears of great value from the clinical point of view, due to the importance of these aspects in the elderly population,” wrote the researchers.

“The concept of quality of life is defined as a perceived global satisfaction and satisfaction within a number of key domains, with special emphasis on well-being.

“Therefore, the amelioration of quality of life in depressed elderly patients after supplementation with omega-3 long-chain polyunsaturated fatty acids is an important finding,” they added.

Jury’s still out?

The link between omega-3 and mood is complex and data to date is contradictory. For example, in researchers from Norway reported that regular and long-term intake of omega-3 fatty acid-rich cod liver oil may protect people from symptoms of depression (Journal of Affective Disorders).

Moreover, a joint Anglo-Iranian study reported that depression ratings were cut by 50 per cent following daily one gram supplements of EPA, an effect similar to that obtained by the antidepressant drug fluoxetine, according to findings published in the Australian and New Zealand Journal of Psychiatry.

Despite this growing number of studies, the science overall is unsufficient to support a link between omega-3 and depression, said the British Medical Journal's Drug and Therapeutics Bulletin (DTB) in February 2007.

"Despite observational evidence linking depression with reduced intake of long-chain omega-3 fatty acids, there is no convincing basis for using these nutrients as a [means of alleviating] the condition," stated the DTB.

Commenting on the findings, Harry Rice, PhD, VP regulatory & scientific affairs for the Global Organization for EPA and DHA Omega-3s (GOED) welcomed the findings and said that they were not only statistically significant, “but clinically significant in that long-chain omega-3 intake improved quality of life while decreasing the severity of depression in elderly females not taking any antidepressant medication”.

“The logical next question is ‘Do the results hold up in elderly men not taking antidepressant medication?’

“While the results are exciting with potential clinical utility, it’s a stretch to conclude that the results support the theory that depression is a manifestation of a decrease in the omega-3 to omega-6 ratio caused by excessive omega-6 intake.

“For now, what can be concluded is that long-chain omega-3 supplementation reduced depressive symptoms, while improving quality of life, in elderly women. The public health implications of such findings are widespread,” added Dr Rice.

L-theanine May Increase Concentration and Promote Relaxation

Daily supplements of L-theanine, an amino acid found in tea, may help people with anxiety focus on their daily activities, suggests a new study from Japan.
On the other hand, people with minimal anxiety levels did not experience any benefits from supplementation, according to findings published in the Journal of Functional Foods.

“Given that L-theanine is a relaxant, it is directly or indirectly involved at the neurochemical level and thus it is impacted by a number of neurotransmitter systems,” wrote the scientists from the University of Shiga Prefecture and Taiyo Kagaku.

“Therefore, 200 mg of L-theanine intake may help normal people with high anxiety propensity to concentrate on their daily activities.”

The study used Taiyo Kagaku’s Suntheanine-branded L-theanine ingredient, and the Japanese company funded the study.

L-theanine, an amino acid found in tea leaves, is thought to help reduce stress, promote relaxation and improve the quality of sleep. L-theanine is found in tea leaves in low concentrations (less than 2 percent), which means that effective dosage levels (of 100 – 200mg/day) cannot be delivered from drinking tea.

Various health effects have been associated with L-theanine, including relaxation, neuroprotective effects, and improved attention.

During rest, L-theanine increases alpha activity in EEG models - suggesting greater relaxation. Whilst the amino acid is known to induce changes in alpha activity that indicates increased attentional processing during tasks that require attention.

The new study confirmed the dose of 200 mg for “enhanced performance in visual attention task, and reaction time response, among the subjects with higher anxiety propensity symptoms”.

Blueberries May Help Reduce Fat Cells

The benefits of blueberry consumption have been demonstrated in several nutrition studies, more specifically the cardio-protective benefits derived from their high polyphenol content. Blueberries have shown potential to have a positive effect on everything from aging to metabolic syndrome. Recently, a researcher from Texas Woman's University (TWU) in Denton, TX, examined whether blueberries could play a role in reducing one of the world's greatest health challenges: obesity. Shiwani Moghe, MS, a graduate student at TWU, decided to evaluate whether blueberry polyphenols play a role in adipocyte differentiation, the process in which a relatively unspecialized cell acquires specialized features of an adipocyte, an animal connective tissue cell specialized for the synthesis and storage of fat. Plant polyphenols have been shown to fight adipogenesis, which is the development of fat cells, and induce lipolysis, which is the breakdown of lipids/fat.

Green Tea May Help Memory

Daily supplements of a green tea extract may boost mental alertness and enhance memory, according to a randomized, double-blind, placebo-controlled study from Korea.

Milk and sugar? Let me think about it...
A combination of a green tea extract with L-theanine was associated with improvements in immediate and delayed recall, and general memory, according to findings published in the Journal of Medicinal Foods.

“As a natural ingredient with a long history of consumption, LGNC-07 [ – a combination of green tea extract and L-theanine - ] should be considered as a potential nutraceutical candidate for enhancing cognitive performance,” according to the researchers.

The majority of science on tea has looked at green tea, with benefits reported for reducing the risk of Alzheimer's and certain cancers, improving cardiovascular and oral health, as well as aiding in weight management.

Green tea contains between 30 and 40 per cent of water-extractable polyphenols, while black tea (green tea that has been oxidized by fermentation) contains between 3 and 10 per cent. Oolong tea is semi-fermented tea and is somewhere between green and black tea. The four primary polyphenols found in fresh tea leaves are epigallocatechin gallate (EGCG), epigallocatechin, epicatechin gallate, and epicatechin.

Sugar and Fatty Foods as Addictive as Drugs

The brain's response to the tempting appeal of a sugary, fatty milkshake or to a bag of salty, greasy snack chips appears to be the same response a drug addict's brain exhibits when anticipating the next "hit," suggests a new study published in the journal Archives of General Psychiatry. Ashley Gearhardt of Yale University and her colleagues found that the addictive nature of many junk foods is literally the same as the addictive nature of drugs.

The team analyzed the brains of a group of 48 young women, who were tempted with either a chocolate milkshake or a tasteless beverage solution. Based on data gathered using functional magnetic resonance imaging (fMRI), the team discovered that the women's anterior cingulate cortex and the medial orbitofrontal cortex -- two areas of the brain known to respond to drug addiction -- both responded to sensory cravings for the milkshake, regardless of the women's weight.

Gluten Intolerance: The Hidden Epidemic

899
Share


Get Health Ranger daily news via email

Your email privacy is 100% protected.
(NaturalNews) Gluten is the common protein found in wheat, barley, oats, spelt, kamut, & rye. Gluten is a sticky, storage protein that when combined with water becomes sort of `gluey.` Inside of the digestive tract, this reaction can lead to gluten binding to the small intestinal wall where it can cause digestive and immune system disorders. Gluten sensitivity is an epidemic that is a major contributing factor with many of today`s health problems.

Gliadins are the glycoprotein portion of the gluten molecule that is responsible for the negative effects. Researchers have found that certain gliadin compounds can bind to a chemo attractant receptor and increase a certain factor that destroys tight junctions. These junctions tie the small intestinal cells together and prevent leakage of food particles into the body. This gliadin reaction has been linked to increased intestinal permeability and leaky gut syndrome.

When the gut is permeable and food particles are able to cross into the blood stream it creates a stress response in the body. As a result of this, the body very often forms an immune response to the circulating molecules as well as to the toxic culprits causing havoc in the gut.

This immune reaction begins with the body forming T-lymphocyte recognition of gluten peptides in circulation and gluten peptides that are bound to tissue. Once this recognition is formed the second immune interaction results in the production of Anti-Gliadin anti-bodies (AGA). Over time this process creates a dramatic increase in gut inflammation and finally toxic destruction to the villi of the small intestine as seen in Celiac disease.

Experts now believe that celiac disease represents just one extreme of a broad spectrum of gluten intolerance that includes millions of people with less severe -- but nevertheless problematic -- reactions to the protein. While celiac disease affects about 1% of the U.S. population, certain experts believe that 3-15% of the population have elevated AGA levels and may or may not have any diagnosed symptoms. This is a syndrome entitled non-celiac gluten intolerance (NCGI). There are many others who have negative AGA levels but may still have gluten sensitive reactions.

When it comes to celiac disease and gluten intolerance, scientists look at HLA DQ genes. According to gluten researcher Dr. Kenneth Fine, 90% of people with celiac have the DQ2 gene. This gene is mostly found in individuals with Northern European background. 9% have the DQ8 gene which is more common among those of European/Mediterranean descent. The DQ 1 & DQ3 genes are associated more with gluten intolerance than celiac disease.

"This is something that we're just beginning to get our heads around," says Daniel Leffler, M.D., an assistant professor of medicine at Harvard Medical School and a gastroenterologist at Beth Israel Deaconess Medical Center, in Boston. "There is a tight definition of celiac disease, but gluten intolerance has been a moving target."

Dr. Kenneth Fine`s research estimates that Americans are genetically susceptible to celiac disease by 43% while 81% are predisposed to gluten intolerances. While some may have digestive discomfort, most do not. Many may instead experience inflammation in the skin (eczema & psoriasis), joints (arthritis), respiratory tract (asthma, allergies) and brain (brain fog, poor memory, dizziness, etc.).

"Gluten is fairly indigestible in all people," Leffler says. "There's probably some kind of gluten intolerance in all of us." Untreated or undiagnosed individuals with elevated AGA are at an increased risk for lymphoid cancers and other auto-immune disorders such as Sjogren`s syndrome & Hashimoto`s Thyroiditis. Anyone with chronic inflammatory conditions should immediately consider removing gluten from their diet. Brown rice and quinoa are much better choices.

(Many of my patients with depression improve significantly when they remove gluten from their diet.)

This article was recently featured in NaturalNewsTV.com

Low Vitamin D Linked to Moew Aggressive Breast Cancers

Breast cancer patients with suboptimal vitamin D levels were more likely to have tumors with more aggressive tumor profiles, worse prognostic markers (ER- and triple-negative tumors), and higher recurrence risk (Oncotype scores), lending support to previous research that found decreased breast cancer survival among vitamin D deficient individuals."

Losing Weight Improves Cognitive Functioning

A study at Kent State University found that overweight patients who had gastric bypass surgery scored much better on tests of memory and cognitive function after shedding about 50 pounds in the months following the operations. The investigation included 150 patients all of whom were tested initially to assess their mental abilities; then 109 participants underwent the surgery.

Green Tea Consumption May Reduce Belly Fat

Compelling evidence presented in the journal Nutrition Research makes the irrefutable connection among green tea consumption, lowered body weight and reduced levels of dangerous belly fat. Drinking between 5 and 8 cups of green tea each day was shown to lower body weight by 5.6% and to decrease abdominal fat stores by 17.8% over a period of 8 weeks. Green tea consumption has long been associated with lowered risk of cancer, metabolic syndrome and heart disease. This research provides compelling evidence that green tea boosts metabolism to target fat stores and assists weight loss efforts.

Green tea extracts have been researched extensively over the past decade and are shown to dramatically lower the risk of Alzheimer`s disease and dementia, cardiovascular disease and many forms of cancer. Additional studies have shown that the polyphenols in green tea are a significant factor in improved oral health and can provide necessary support for weight management and control. Green tea is composed of four primary polyphenols (epigallocatechin gallate (EGCG), epigallocatechin, epicatechin gallate, and epicatechin) that are shown to influence genetic signaling and metabolic rate.

Vitamin D May Lower Blood Sugar Levels

Researchers from the National Nutrition and Food Technology Research Institute in Iran discovered recently that when given extra vitamin D as part of their daily diets for several months, diabetics' blood sugar levels decreased.

Tirang Neyestani and colleagues divided 90 adult participants with diabetes into three test groups. The first group received plain yogurt with no added vitamin D, the second group received a vitamin D-fortified yogurt, and the final group received a vitamin D-fortified yogurt with added calcium. The vitamin D yogurt in the two latter groups contained a moderate 500 international units (IU) of the vitamin.

At the end of three months, the plain yogurt group experienced a nine percent average increase in blood sugar levels, while the two vitamin D groups actually experienced a seven percent decrease in blood sugar levels. And at the end of the entire 12-week study, Neyestani told Reuters that the vitamin D groups experienced a "relatively remarkable improvement" in their conditions.

(I typically recommend 1000 IUs of vitamin D3 in the summer and 2000 IUs during the winter months)

Fish Oil Supplementation Reduces Postpartum Depression

Eating fatty fish or other foods rich in healthy omega-3 fatty acids during pregnancy may help lower your risk of developing symptoms commonly seen in postpartum depression, a study suggested at the Experimental Biology 2011 annual meeting. The pregnant women took either a corn oil placebo pill or a fish oil capsule containing 300 milligrams of DHA for five days a week during the 24th to 40th weeks of their pregnancy. The amount of DHA contained in each capsule is the equivalent of about one-half serving of salmon. The researchers used a postpartum depression screening scale to determine if the women were showing any signs or symptoms of postpartum depression two weeks, six weeks, three months, and six months after delivery. Women who received the fish oil supplements scored lower on the scale and had significantly fewer postpartum depression symptoms than those who received the placebo. Women in the fish oil group were also less likely to report anxiety symptoms.

Is Sugar Toxic?

Is Sugar Toxic?

By GARY TAUBES

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

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

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

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

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

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

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

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

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

The history of the debate over the health effects of sugar has gone on far longer than you might imagine. It is littered with erroneous statements and conclusions because even the supposed authorities had no true understanding of what they were talking about. They didn’t know, quite literally, what they meant by the word “sugar” and therefore what the implications were.

So let’s start by clarifying a few issues, beginning with Lustig’s use of the word “sugar” to mean both sucrose — beet and cane sugar, whether white or brown — and high-fructose corn syrup. This is a critical point, particularly because high-fructose corn syrup has indeed become “the flashpoint for everybody’s distrust of processed foods,” says Marion Nestle, a New York University nutritionist and the author of “Food Politics.”

This development is recent and borders on humorous. In the early 1980s, high-fructose corn syrup replaced sugar in sodas and other products in part because refined sugar then had the reputation as a generally noxious nutrient. (“Villain in Disguise?” asked a headline in this paper in 1977, before answering in the affirmative.) High-fructose corn syrup was portrayed by the food industry as a healthful alternative, and that’s how the public perceived it. It was also cheaper than sugar, which didn’t hurt its commercial prospects. Now the tide is rolling the other way, and refined sugar is making a commercial comeback as the supposedly healthful alternative to this noxious corn-syrup stuff. “Industry after industry is replacing their product with sucrose and advertising it as such — ‘No High-Fructose Corn Syrup,’ ” Nestle notes.

But marketing aside, the two sweeteners are effectively identical in their biological effects. “High-fructose corn syrup, sugar — no difference,” is how Lustig put it in a lecture that I attended in San Francisco last December. “The point is they’re each bad — equally bad, equally poisonous.”

Refined sugar (that is, sucrose) is made up of a molecule of the carbohydrate glucose, bonded to a molecule of the carbohydrate fructose — a 50-50 mixture of the two. The fructose, which is almost twice as sweet as glucose, is what distinguishes sugar from other carbohydrate-rich foods like bread or potatoes that break down upon digestion to glucose alone. The more fructose in a substance, the sweeter it will be. High-fructose corn syrup, as it is most commonly consumed, is 55 percent fructose, and the remaining 45 percent is nearly all glucose. It was first marketed in the late 1970s and was created to be indistinguishable from refined sugar when used in soft drinks. Because each of these sugars ends up as glucose and fructose in our guts, our bodies react the same way to both, and the physiological effects are identical. In a 2010 review of the relevant science, Luc Tappy, a researcher at the University of Lausanne in Switzerland who is considered by biochemists who study fructose to be the world’s foremost authority on the subject, said there was “not the single hint” that H.F.C.S. was more deleterious than other sources of sugar.

The question, then, isn’t whether high-fructose corn syrup is worse than sugar; it’s what do they do to us, and how do they do it? The conventional wisdom has long been that the worst that can be said about sugars of any kind is that they cause tooth decay and represent “empty calories” that we eat in excess because they taste so good.

By this logic, sugar-sweetened beverages (or H.F.C.S.-sweetened beverages, as the Sugar Association prefers they are called) are bad for us not because there’s anything particularly toxic about the sugar they contain but just because people consume too many of them.

Those organizations that now advise us to cut down on our sugar consumption — the Department of Agriculture, for instance, in its recent Dietary Guidelines for Americans, or the American Heart Association in guidelines released in September 2009 (of which Lustig was a co-author) — do so for this reason. Refined sugar and H.F.C.S. don’t come with any protein, vitamins, minerals, antioxidants or fiber, and so they either displace other more nutritious elements of our diet or are eaten over and above what we need to sustain our weight, and this is why we get fatter.

Whether the empty-calories argument is true, it’s certainly convenient. It allows everyone to assign blame for obesity and, by extension, diabetes — two conditions so intimately linked that some authorities have taken to calling them “diabesity” — to overeating of all foods, or underexercising, because a calorie is a calorie. “This isn’t about demonizing any industry,” as Michelle Obama said about her Let’s Move program to combat the epidemic of childhood obesity. Instead it’s about getting us — or our children — to move more and eat less, reduce our portion sizes, cut back on snacks.

Lustig’s argument, however, is not about the consumption of empty calories — and biochemists have made the same case previously, though not so publicly. It is that sugar has unique characteristics, specifically in the way the human body metabolizes the fructose in it, that may make it singularly harmful, at least if consumed in sufficient quantities.

The phrase Lustig uses when he describes this concept is “isocaloric but not isometabolic.” This means we can eat 100 calories of glucose (from a potato or bread or other starch) or 100 calories of sugar (half glucose and half fructose), and they will be metabolized differently and have a different effect on the body. The calories are the same, but the metabolic consequences are quite different.

The fructose component of sugar and H.F.C.S. is metabolized primarily by the liver, while the glucose from sugar and starches is metabolized by every cell in the body. Consuming sugar (fructose and glucose) means more work for the liver than if you consumed the same number of calories of starch (glucose). And if you take that sugar in liquid form — soda or fruit juices — the fructose and glucose will hit the liver more quickly than if you consume them, say, in an apple (or several apples, to get what researchers would call the equivalent dose of sugar). The speed with which the liver has to do its work will also affect how it metabolizes the fructose and glucose.

In animals, or at least in laboratory rats and mice, it’s clear that if the fructose hits the liver in sufficient quantity and with sufficient speed, the liver will convert much of it to fat. This apparently induces a condition known as insulin resistance, which is now considered the fundamental problem in obesity, and the underlying defect in heart disease and in the type of diabetes, type 2, that is common to obese and overweight individuals. It might also be the underlying defect in many cancers.

If what happens in laboratory rodents also happens in humans, and if we are eating enough sugar to make it happen, then we are in trouble.

The last time an agency of the federal government looked into the question of sugar and health in any detail was in 2005, in a report by the Institute of Medicine, a branch of the National Academies. The authors of the report acknowledged that plenty of evidence suggested that sugar could increase the risk of heart disease and diabetes — even raising LDL cholesterol, known as the “bad cholesterol”—– but did not consider the research to be definitive. There was enough ambiguity, they concluded, that they couldn’t even set an upper limit on how much sugar constitutes too much. Referring back to the 2005 report, an Institute of Medicine report released last fall reiterated, “There is a lack of scientific agreement about the amount of sugars that can be consumed in a healthy diet.” This was the same conclusion that the Food and Drug Administration came to when it last assessed the sugar question, back in 1986. The F.D.A. report was perceived as an exoneration of sugar, and that perception influenced the treatment of sugar in the landmark reports on diet and health that came after.

The Sugar Association and the Corn Refiners Association have also portrayed the 1986 F.D.A. report as clearing sugar of nutritional crimes, but what it concluded was actually something else entirely. To be precise, the F.D.A. reviewers said that other than its contribution to calories, “no conclusive evidence on sugars demonstrates a hazard to the general public when sugars are consumed at the levels that are now current.” This is another way of saying that the evidence by no means refuted the kinds of claims that Lustig is making now and other researchers were making then, just that it wasn’t definitive or unambiguous.

What we have to keep in mind, says Walter Glinsmann, the F.D.A. administrator who was the primary author on the 1986 report and who now is an adviser to the Corn Refiners Association, is that sugar and high-fructose corn syrup might be toxic, as Lustig argues, but so might any substance if it’s consumed in ways or in quantities that are unnatural for humans. The question is always at what dose does a substance go from being harmless to harmful? How much do we have to consume before this happens?

When Glinsmann and his F.D.A. co-authors decided no conclusive evidence demonstrated harm at the levels of sugar then being consumed, they estimated those levels at 40 pounds per person per year beyond what we might get naturally in fruits and vegetables — 40 pounds per person per year of “added sugars” as nutritionists now call them. This is 200 calories per day of sugar, which is less than the amount in a can and a half of Coca-Cola or two cups of apple juice. If that’s indeed all we consume, most nutritionists today would be delighted, including Lustig.

But 40 pounds per year happened to be 35 pounds less than what Department of Agriculture analysts said we were consuming at the time — 75 pounds per person per year — and the U.S.D.A. estimates are typically considered to be the most reliable. By the early 2000s, according to the U.S.D.A., we had increased our consumption to more than 90 pounds per person per year.

That this increase happened to coincide with the current epidemics of obesity and diabetes is one reason that it’s tempting to blame sugars — sucrose and high-fructose corn syrup — for the problem. In 1980, roughly one in seven Americans was obese, and almost six million were diabetic, and the obesity rates, at least, hadn’t changed significantly in the 20 years previously. By the early 2000s, when sugar consumption peaked, one in every three Americans was obese, and 14 million were diabetic.

This correlation between sugar consumption and diabetes is what defense attorneys call circumstantial evidence. It’s more compelling than it otherwise might be, though, because the last time sugar consumption jumped markedly in this country, it was also associated with a diabetes epidemic.

In the early 20th century, many of the leading authorities on diabetes in North America and Europe (including Frederick Banting, who shared the 1923 Nobel Prize for the discovery of insulin) suspected that sugar causes diabetes based on the observation that the disease was rare in populations that didn’t consume refined sugar and widespread in those that did. In 1924, Haven Emerson, director of the institute of public health at Columbia University, reported that diabetes deaths in New York City had increased as much as 15-fold since the Civil War years, and that deaths increased as much as fourfold in some U.S. cities between 1900 and 1920 alone. This coincided, he noted, with an equally significant increase in sugar consumption — almost doubling from 1890 to the early 1920s — with the birth and subsequent growth of the candy and soft-drink industries.

Emerson’s argument was countered by Elliott Joslin, a leading authority on diabetes, and Joslin won out. But his argument was fundamentally flawed. Simply put, it went like this: The Japanese eat lots of rice, and Japanese diabetics are few and far between; rice is mostly carbohydrate, which suggests that sugar, also a carbohydrate, does not cause diabetes. But sugar and rice are not identical merely because they’re both carbohydrates. Joslin could not know at the time that the fructose content of sugar affects how we metabolize it.

Joslin was also unaware that the Japanese ate little sugar. In the early 1960s, the Japanese were eating as little sugar as Americans were a century earlier, maybe less, which means that the Japanese experience could have been used to support the idea that sugar causes diabetes. Still, with Joslin arguing in edition after edition of his seminal textbook that sugar played no role in diabetes, it eventually took on the aura of undisputed truth.

Until Lustig came along, the last time an academic forcefully put forward the sugar-as-toxin thesis was in the 1970s, when John Yudkin, a leading authority on nutrition in the United Kingdom, published a polemic on sugar called “Sweet and Dangerous.” Through the 1960s Yudkin did a series of experiments feeding sugar and starch to rodents, chickens, rabbits, pigs and college students. He found that the sugar invariably raised blood levels of triglycerides (a technical term for fat), which was then, as now, considered a risk factor for heart disease. Sugar also raised insulin levels in Yudkin’s experiments, which linked sugar directly to type 2 diabetes. Few in the medical community took Yudkin’s ideas seriously, largely because he was also arguing that dietary fat and saturated fat were harmless. This set Yudkin’s sugar hypothesis directly against the growing acceptance of the idea, prominent to this day, that dietary fat was the cause of heart disease, a notion championed by the University of Minnesota nutritionist Ancel Keys.

A common assumption at the time was that if one hypothesis was right, then the other was most likely wrong. Either fat caused heart disease by raising cholesterol, or sugar did by raising triglycerides. “The theory that diets high in sugar are an important cause of atherosclerosis and heart disease does not have wide support among experts in the field, who say that fats and cholesterol are the more likely culprits,” as Jane E. Brody wrote in The Times in 1977.

At the time, many of the key observations cited to argue that dietary fat caused heart disease actually support the sugar theory as well. During the Korean War, pathologists doing autopsies on American soldiers killed in battle noticed that many had significant plaques in their arteries, even those who were still teenagers, while the Koreans killed in battle did not. The atherosclerotic plaques in the Americans were attributed to the fact that they ate high-fat diets and the Koreans ate low-fat. But the Americans were also eating high-sugar diets, while the Koreans, like the Japanese, were not.

In 1970, Keys published the results of a landmark study in nutrition known as the Seven Countries Study. Its results were perceived by the medical community and the wider public as compelling evidence that saturated-fat consumption is the best dietary predictor of heart disease. But sugar consumption in the seven countries studied was almost equally predictive. So it was possible that Yudkin was right, and Keys was wrong, or that they could both be right. The evidence has always been able to go either way.

European clinicians tended to side with Yudkin; Americans with Keys. The situation wasn’t helped, as one of Yudkin’s colleagues later told me, by the fact that “there was quite a bit of loathing” between the two nutritionists themselves. In 1971, Keys published an article attacking Yudkin and describing his evidence against sugar as “flimsy indeed.” He treated Yudkin as a figure of scorn, and Yudkin never managed to shake the portrayal.

By the end of the 1970s, any scientist who studied the potentially deleterious effects of sugar in the diet, according to Sheldon Reiser, who did just that at the U.S.D.A.’s Carbohydrate Nutrition Laboratory in Beltsville, Md., and talked about it publicly, was endangering his reputation. “Yudkin was so discredited,” Reiser said to me. “He was ridiculed in a way. And anybody else who said something bad about sucrose, they’d say, ‘He’s just like Yudkin.’ ”

What has changed since then, other than Americans getting fatter and more diabetic? It wasn’t so much that researchers learned anything particularly new about the effects of sugar or high-fructose corn syrup in the human body. Rather the context of the science changed: physicians and medical authorities came to accept the idea that a condition known as metabolic syndrome is a major, if not the major, risk factor for heart disease and diabetes. The Centers for Disease Control and Prevention now estimate that some 75 million Americans have metabolic syndrome. For those who have heart attacks, metabolic syndrome will very likely be the reason.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Gary Taubes (gataubes@gmail.com) is a Robert Wood Johnson Foundation independent investigator in health policy and the author of “Why We Get Fat.” Editor: Vera Titunik (v.titunik-MagGroup@nytimes.com).


--