1977. Coca-Cola Funds Scientists Who Shift Blame for Obesity Away From Bad Diets

By Anahad O'Conner, The New York Times, August 9, 2015

Coca-Cola, the world’s largest producer of sugary beverages, is backing a new “science-based” solution to the obesity crisis: To maintain a healthy weight, get more exercise and worry less about cutting calories.

The beverage giant has teamed up with influential scientists who are advancing this message in medical journals, at conferences and through social media. To help the scientists get the word out, Coke has provided financial and logistical support to a new nonprofit organization called the Global Energy Balance Network, which promotes the argument that weight-conscious Americans are overly fixated on how much they eat and drink while not paying enough attention to exercise.

“Most of the focus in the popular media and in the scientific press is, ‘Oh they’re eating too much, eating too much, eating too much’ — blaming fast food, blaming sugary drinks and so on,” the group’s vice president, Steven N. Blair, an exercise scientist, says in a recent video announcing the new organization. “And there’s really virtually no compelling evidence that that, in fact, is the cause.”

Health experts say this message is misleading and part of an effort by Coke to deflect criticism about the role sugary drinks have played in the spread of obesity and Type 2 diabetes. They contend that the company is using the new group to convince the public that physical activity can offset a bad diet despite evidence that exercise has only minimal impact on weight compared with what people consume.

This clash over the science of obesity comes in a period of rising efforts to tax sugary drinks, remove them from schools and stop companies from marketing them to children. In the last two decades, consumption of full-calorie sodas by the average American has dropped by 25 percent.

“Coca-Cola’s sales are slipping, and there’s this huge political and public backlash against soda, with every major city trying to do something to curb consumption,” said Michele Simon, a public health lawyer. “This is a direct response to the ways that the company is losing. They’re desperate to stop the bleeding.”

Coke has made a substantial investment in the new nonprofit. In response to requests based on state open-records laws, two universities that employ leaders of the Global Energy Balance Network disclosed that Coke had donated $1.5 million last year to start the organization.

Since 2008, the company has also provided close to $4 million in funding for various projects to two of the organization’s founding members: Dr. Blair, a professor at the University of South Carolina whose research over the past 25 years has formed much of the basis of federal guidelines on physical activity, and Gregory A. Hand, dean of the West Virginia University School of Public Health.

Records show that the network’s website, gebn.org, is registered to Coca-Cola headquarters in Atlanta, and the company is also listed as the site’s administrator. The group’s president, James O. Hill, a professor at the University of Colorado School of Medicine, said Coke had registered the website because the network’s members did not know how.

“They’re not running the show,” he said. “We’re running the show.”

Coca-Cola’s public relations department repeatedly declined requests for an interview with its chief scientific officer, Rhona Applebaum, who has called attention to the new group on Twitter. In a statement, the company said it had a long history of supporting scientific research related to its beverages and topics such as energy balance.

“We partner with some of the foremost experts in the fields of nutrition and physical activity,” the statement said. “It’s important to us that the researchers we work with share their own views and scientific findings, regardless of the outcome, and are transparent and open about our funding.”

Dr. Blair and other scientists affiliated with the group said that Coke had no control over its work or message and that they saw no problem with the company’s support because they had been transparent about it.

But as of last week, the group’s Twitter and Facebook pages, which promote physical activity as a solution to chronic disease and obesity while remaining largely silent on the role of food and nutrition, made no mention of Coca-Cola’s financial support. So far, the social media campaign has failed to gain much traction: As of Friday, the group had fewer than 1,000 followers on Twitter.

The group’s website also omitted mention of Coke’s backing until Dr. Yoni Freedhoff, an obesity expert at the University of Ottawa, wrote to the organization to inquire about its funding. Dr. Blair said this was an oversight that had been quickly corrected.

“As soon as we discovered that we didn’t have not only Coca-Cola but other funding sources on the website, we put it on there,” Dr. Blair said. “Does that make us totally corrupt in everything we do?”

Coke’s involvement in the new organization is not the only example of corporate-funded research and advocacy to come under fire lately. The American Society for Nutrition and the Academy of Nutrition and Dietetics have been criticized by public health advocates for forming partnerships with companies such as Kraft Foods, McDonald’s, PepsiCo and Hershey’s. Dietitians have also faced criticism for taking payments from Coke to present the company’s soda as a healthy snack.

Critics say Coke has long cast the obesity epidemic as primarily an exercise problem. “The message is that obesity is not about the foods or beverages you’re consuming, it’s that you’re not balancing those foods with exercise,” Dr. Freedhoff of the University of Ottawa said.

Now, public health advocates say, Coca-Cola is going a step further, recruiting reputable scientists to make the case for them.

Dr. Hill, the nonprofit’s president, is a co-founder of the National Weight Control Registry, a long-term study of people who have lost weight, and has served on committees for the World Health Organization and the National Institutes of Health. The American Society for Nutrition refers to him as “a leader in the fight against the global obesity epidemic.”

Barry M. Popkin, a professor of global nutrition at the University of North Carolina at Chapel Hill, said Coke’s support of prominent health researchers was reminiscent of tactics used by the tobacco industry, which enlisted experts to become “merchants of doubt” about the health hazards of smoking.

Marion Nestle, the author of the book “Soda Politics” and a professor of nutrition, food studies and public health at New York University, was especially blunt: “The Global Energy Balance Network is nothing but a front group for Coca-Cola. Coca-Cola’s agenda here is very clear: Get these researchers to confuse the science and deflect attention from dietary intake.”

Funding from the food industry is not uncommon in scientific research. But studies suggest that the funds tend to bias findings. A recent analysis of beverage studies, published in the journal PLOS Medicine, found that those funded by Coca-Cola, PepsiCo, the American Beverage Association and the sugar industry were five times more likely to find no link between sugary drinks and weight gain than studies whose authors reported no financial conflicts.

On its website, the new nonprofit promises to be “the voice of science” in discussions about healthy lifestyles and contends that the concept of energy balance provides “a new science-based framework” for achieving a stable body weight.

The group says there is “strong evidence” that the key to preventing weight gain is not reducing food intake — as many public health experts recommend — “but maintaining an active lifestyle and eating more calories.” To back up this contention, the group provides links to two research papers, each of which contains this footnote: “The publication of this article was supported by The Coca-Cola Company.”

In March, Dr. Hill, Dr. Blair, and Dr. Hand announced the creation of the organization in an editorial in the British Journal of Sports Medicine. They argued that the public and many scientists largely overlooked physical inactivity as a cause of obesity. They said they were creating the Global Energy Balance Network to raise awareness “about both sides of the energy balance equation.”

The editorial contained a disclosure that the group had received an “unrestricted education gift” from Coca-Cola.

In response to a request made under the state Freedom of Information Act, the University of South Carolina disclosed that Dr. Blair had received more than $3.5 million in funding from Coke for research projects since 2008.

The university also disclosed that Coca-Cola had provided significant funding to Dr. Hand, who left the University of South Carolina last year for West Virginia. The company gave him $806,500 for an “energy flux” study in 2011 and $507,000 last year to establish the Global Energy Balance Network.

It is unclear how much of the money, if any, ended up as personal income for the professors.

“As long as everybody is disclosing their potential conflicts and they’re being managed appropriately, that’s the best that you can do,” Dr. Hand said. “It makes perfect sense that companies would want the best science that they can get.”

The group’s president, Dr. Hill, also has financial ties to Coca-Cola. The company last year gave an “unrestricted monetary gift” of $1 million to the University of Colorado Foundation. In response to a request made under the Colorado Open Records Act, the university said that Coca-Cola had provided the money “for the purposes of funding” the Global Energy Balance Network.

Dr. Hill said he had sought money from Coke to start the nonprofit because there was no funding available from his university. The group’s website says it is also supported by a few universities and ShareWIK Media Group, a producer of videos about health. Dr. Hill said that he had also received a commitment of help from General Mills, as well as promises of support from other businesses, which had not formally confirmed their offers.

He said he believed public health authorities could more easily change the way people eat by working with the food industry instead of against it.

On its website, the group recommends combining greater exercise and food intake because, Dr. Hill said, “ ‘Eat less’ has never been a message that’s been effective. The message should be ‘Move more and eat smarter.’ ”

He emphasized that weight loss involved a combination of complex factors and that his group’s goal was not to play down the role of diet or to portray obesity as solely a problem of inadequate exercise.

“If we are out there saying it’s all about physical activity and it’s not about food, then we deserve criticism,” he said. “But I think we haven’t done that.”

But in news releases and on its website, the group has struck a different tone.

“The media tends to blame the obesity epidemic on our poor eating habits,” one recent news release states. “But are those french fries really the culprit? Dr. Steve Blair explains that you shouldn’t believe everything you see on TV.”

In the news release, Dr. Blair suggests that sedentary behavior is a bigger factor.

Most public health experts say that energy balance is an important concept, because weight gain for most people is about calories in vs. calories out. But the experts say research makes it clear that one side of the equation has a far greater effect.

While people can lose weight in several ways, many studies suggest that those who keep it off for good consume fewer calories. Growing evidence also suggests that maintaining weight loss is easier when people limit their intake of high glycemic foods such as sugary drinks and other refined carbohydrates, which sharply raise blood sugar.

Physical activity is important and certainly helps, experts say. But studies show that exercise increases appetite, causing people to consume more calories. Exercise also expends far fewer calories than most people think. A 12-ounce can of Coca-Cola, for example, contains 140 calories and roughly 10 teaspoons of sugar. “It takes three miles of walking to offset that one can of Coke,” Dr. Popkin said.

In one of the most rigorous studies of physical activity and weight loss, published in the journal Obesity, scientists recruited 200 overweight, sedentary adults and put them on an aggressive exercise program. To isolate the effects of exercise on their weight, the subjects were instructed not to make any changes in their diets.

Participants were monitored to ensure they exercised five to six hours a week, more than double the 2.5 weekly hours of exercise recommended in federal guidelines. After a year, the men had lost an average of just 3.5 pounds, the women 2.5. Almost everyone was still overweight or obese.

“Adding exercise to a diet program helps,” said Dr. Anne McTiernan, the lead author of the study and a researcher at the Fred Hutchinson Cancer Center in Seattle. “But for weight loss, you’re going to get much more impact with diet changes.”

But much like the research on sugary drinks, studies of physical activity funded by the beverage industry tend to reach conclusions that differ from the findings of studies by independent scientists.

Last week, the Pennington Biomedical Research Center in Louisiana announced the findings of a large new study on exercise in children that determined that lack of physical activity “is the biggest predictor of childhood obesity around the world.”

The news release contained a disclosure: “This research was funded by The Coca-Cola Company.”

Kelly D. Brownell, dean of the Sanford School of Public Policy at Duke, said that as a business, Coke “focused on pushing a lot of calories in, but then their philanthropy is focused on the calories out part, the exercise.”

In recent years, Coke has donated money to build fitness centers in more than 100 schools across the country. It sponsors a program called “Exercise is Medicine” to encourage doctors to prescribe physical activity to patients. And when Chicago’s City Council proposed a soda tax in 2012 to help address the city’s obesity problem, Coca-Cola donated $3 million to establish fitness programs in more than 60 of the city’s community centers.

The initiative to tax soda ultimately failed.

“Reversing the obesity trend won’t happen overnight,” Coca-Cola said in an ad for its Chicago exercise initiative. “But for thousands of families in Chicago, it starts now, with the next push-up, a single situp or a jumping jack.”

1490. About the Shrimp on the Menu

By Mangrove Action Project, April 9, 2013

Portion of a mangove forest

Introduction: This a short, educational clip about how shrimp farming destroys mangroves key to integrity of ecosystems on which much life and livelihood depends.  Also, it shows how farmed shrimp is bad for your health.  I urge you to give up eating shrimp entirely, however. A vegan diet is best for your health and for the world. For a a discussion see "How Veganism Can Help Save the World".  KN.

1439. Meat Consumption and Cancer Risk

By Physician Committee for Responsible Medicine, June 8, 2014

Graph is from "Meat and Cancer: Country Comparisons" by AnthonyWilson, May 6, 2012

The World Health Organization has determined that dietary factors account for at least 30 percent of all cancers in Western countries and up to 20 percent in developing countries. When cancer researchers started to search for links between diet and cancer, one of the most noticeable findings was that people who avoided meat were much less likely to develop the disease. Large studies in England and Germany showed that vegetarians were about 40 percent less likely to develop cancer compared to meat eaters.^1-3 In the United States, researchers studied Seventh-day Adventists, a religious group that is remarkable because, although nearly all members avoid tobacco and alcohol and follow generally healthful lifestyles, about half of the Adventist population is vegetarian, while the other half consumes modest amounts of meat. This fact allowed scientists to separate the effects of eating meat from other factors. Overall, these studies showed significant reductions in cancer risk among those who avoided meat.⁴ In contrast, Harvard studies showed that daily meat eaters have approximately three times the colon cancer risk, compared to those who rarely eat meat.

A number of hypotheses have been advanced to explain the connection between meat consumption and cancer risk. First, meat is devoid of fiber and other nutrients that have a protective effect. Meat also contains animal protein, saturated fat, and, in some cases, carcinogenic compounds such as heterocyclic amines (HCA) and polycyclic aromatic hydrocarbons (PAH) formed during the processing or cooking of meat. HCAs, formed as meat is cooked at high temperatures, and PAHs, formed during the burning of organic substances, are believed to increase cancer risk. In addition, the high fat content of meat and other animal products increases hormone production, thus increasing the risk of hormone-related cancers such as breast and prostate cancer.

In 2007, the American Institute for Cancer Research (AICR) published their second review of the major studies on food, nutrition, and cancer prevention. For cancers of the oesophagus, lung, pancreas, stomach, collorectum, endometrium, and prostate, it was determined that red meat (beef, pork, or lamb) and processed meat consumption possibly increased cancer risk. For colorectal cancer, a review of the literature determined that there is convincing scientific evidence that red meat increased cancer risk and that processed meat, saturated/animal fat, and heavily cooked meat were also convincing of increased risk.⁵

Carcinogenic Compounds in Cooked Meat

Heterocyclic Amines
HCAs, a family of mutagenic compounds, are produced during the cooking process of many animal products, including chicken, beef, pork, and fish. Even meat that is cooked under normal grilling, frying, or oven-broiling may contain significant quantities of these mutagens.^6,7,8 The longer and hotter the meat is cooked, the more these compounds form. In some studies, grilled chicken has formed higher concentrations of these cancer-causing substances than other types of cooked meat.⁹

The major classes of heterocyclic amines include amino-imidazo-quinolines, or amino-imidazo-quinoxalines (collectively called IQ-type compounds), and amino-imidazo-pyridines such as PhIP. IQ-type compounds and PhIP are formed from creatine or creatinine, specific amino acids, and sugars.¹⁰ All meats (including fish) are high in creatine, and HCA formation is greatest when cooking meat at high temperatures, as is most common with grilling or frying. Consumption of well-done meat and PhIP has been associated with increased risk of breast cancer and colon cancer, as discussed in greater detail below. A recent case-control study at the University of Utah that included 952 subjects with rectal cancer and 1205 controls found that men and women with the highest consumption of processed or well-cooked meat had an increased risk of rectal cancer.¹¹

Polycyclic Aromatic Hydrocarbons

Grilling or broiling meat over a direct flame results in fat dropping on the hot fire and the production of polycyclic aromatic hydrocarbon-containing flames. Polycyclic aromatic hydrocarbons (PAHs) adhere to the surface of food, and the more intense the heat, the more PAHs are present.5 They are widely believed to play a significant role in human cancers.¹² A fairly consistent association between grilled or broiled, but not fried, meat consumption and stomach cancer implies that dietary exposure to PAHs may play a role in the development of stomach cancer in humans.⁵

Breast Cancer

Countries with a higher intake of fat, especially fat from animal products, such as meat and dairy products, have a higher incidence of breast cancer.^13,14,15 In Japan, for example, the traditional diet is much lower in fat, especially animal fat, than the typical western diet, and breast cancer rates are low. In the late 1940s, when breast cancer was particularly rare in Japan, less than 10 percent of the calories in the Japanese diet came from fat.¹⁶ The American diet is centered on animal products, which tend to be high in fat and low in other important nutrients, with 30 to 35 percent of calories coming from fat. When Japanese girls are raised on westernized diets, their rate of breast cancer increases dramatically. Even within Japan, affluent women who eat meat daily have an 8.5 times higher risk of breast cancer than poorer women who rarely or never eat meat.¹⁷ One of the proposed reasons is that fatty foods boost the hormones that promote cancer.

According to new findings from the Shanghai Women's Health Study, soy food intake provides protection against premenopausal breast cancer when consumed during adolescence and as an adult. The usual dietary intake of 73,223 Chinese women during adulthood and adolescence was assessed after a mean follow-up of 7.4 years. Those with the highest intake of soy protein or isoflavone versus those with the lowest had about half the risk of premenopausal breast cancer regardless of age at time of consumption. No significant association with soy foods was found for postmenopausal breast cancer.¹⁸

The consumption of high-fat foods such as meat, dairy products, fried foods, and even vegetable oils causes a woman’s body to make more estrogens, which encourage cancer cell growth in the breast and other organs that are sensitive to female sex hormones. This suggests that, by avoiding fatty foods throughout life, hormone-related cancer risk decreases. A 2003 study, published in the Journal of the National Cancer Institute, found that when girls ages eight to ten reduced the amount of fat in their diet—even very slightly—their estrogen levels were held at a lower and safer level during the next several years. By increasing vegetables, fruits, grains, and beans, and reducing animal-derived foods, the amount of estradiol (a principal estrogen) in their blood dropped by 30 percent, compared to a group of girls who did not change their diets.¹⁹

Harvard researchers recently conducted a prospective analysis of 90,655 premenopausal women, ages 26 to 46, enrolled in the Nurses’ Health Study II and determined that intake of animal fat, especially from red meat and high-fat dairy products, during premenopausal years is associated with an increased risk of breast cancer. Increased risk was not associated with vegetable fats.²⁰

In addition, researchers at the Ontario Cancer Institute conducted a meta-analysis of all the case-control and cohort studies published up to July 2003 that studied dietary fat, fat-containing foods, and breast cancer risk. Case-control and cohort study analyses yielded similar risk results, with a high total fat intake associated with increased breast cancer risk. Significant relative risks for meat and saturated fat intake also emerged, with high meat intake increasing cancer risk by 17 percent and high saturated fat intake increasing cancer risk by 19 percent.²¹

Several studies show meat intake to be a breast cancer risk factor, even when confounding factors, such as total caloric intake and total fat intake, are controlled.^22,23 Part of the reason may be that meat becomes a source of carcinogens and/or mutagens, such as HCAs, that are formed while cooking meat at high temperatures. A review of HCAs showed that certain HCAs are distributed to the mammary gland and that humans can activate HCAs metabolically.²⁴ As a consequence, frequent meat consumption may be a risk factor for breast cancer.²²

Colorectal Cancer

As with breast cancer, frequent consumption of meat, particularly red meat, is associated with an increased risk of colon cancer.^25,26 Total fat and saturated fat, which tend to be substantially higher in animal products than in plant-derived foods, and refined sugar, all heighten colon cancer risks. At Harvard University, researchers zeroed in on red meat, finding that individuals eating beef, pork, or lamb daily have approximately three times the colon cancer risk, compared to people who generally avoid these products.^26,27 A review of 32 case-control and 13 cohort studies concluded that meat consumption is associated with an increase in colorectal cancer risk, with the association being more consistently found with red meat and processed meat.¹² And, in the recently published Cancer Prevention Study II, involving 148,610 adults followed since 1982, the group with the highest red meat and processed meat intakes had approximately 30 to 40 percent and 50 percent higher colon cancer risk, respectively, compared to those with lower intakes.²⁸ In this study, high red meat intake was defined as 3 ounces of beef, lamb, or pork for men and 2 ounces for women daily, the amount in a typical hamburger. High processed meat intake (ham, cold cuts, hot dogs, bacon, sausage) was defined as 1 ounce eaten 5 or 6 times a week for men, and 2 or 3 times a week for women—the amount in one slice of ham. In addition, earlier studies have also indicated that those consuming white meat, particularly chicken, have approximately a threefold higher colon cancer risk, compared to vegetarians.²⁹

Secondary bile acids are probably part of the problem. In order to absorb fat, the liver makes bile, which it stores in the gallbladder. After a meal, the gallbladder sends bile acids into the intestine, where they chemically modify the fats eaten so they can be absorbed. Unfortunately, bacteria in the intestine turn these bile acids into cancer-promoting substances called secondary bile acids. Meats not only contain a substantial amount of fat; they also foster the growth of bacteria that cause carcinogenic secondary bile acids to form.

Cooking methods that promote the formation of HCAs are believed to play a significant role in colorectal cancer risk. A case-control study in North Carolina that analyzed meat intake by level of doneness, cooking method, and estimated intake of HCAs in 620 colon cancer patients and 1038 controls, found that not only was red meat intake positively associated with colon cancer risk, but also pan-frying was the riskiest way to prepare meat due to high HCA formation.³⁰ Confirmation of the link between frying and colorectal cancer risk was adduced in the review mentioned above, where high frying temperature was found to increase colon cancer risk almost twofold, and rectal cancer risk by 60 percent.¹²

Colorectal cancer is steadily becoming more common among young adults, according to an American Cancer Society analysis. Incidence rates among adults ages 20 to 49 increased 1.5 percent per year in men and 1.6 percent per year in women from 1992 to 2005. The increase may be tied to rising rates of obesity, a major risk factor for colorectal cancer. Increased consumption of meat (especially in fast food) over the past three decades could also be a key factor. Previous studies have suggested that diets free of red and processed meats and rich in plant-based foods may significantly reduce colorectal cancer risk.³¹   

Prostate Cancer

Prostate cancer is one of the leading cancers among men in the U.S., and researchers have explored a number of possible dietary factors contributing to prostate cancer risk. These include dietary fat, saturated fat, dairy products, and meat, as well as dietary factors that may decrease risk, such as the consumption of carotenoids and other antioxidants, fiber, and fruit. As with breast cancer risk, a man’s intake of dietary fat, which is abundant in meat and other animal products, increases testosterone production, which in turn increases prostate cancer risk. One of the largest nested case-control studies, which showed a positive association between prostate cancer incidence and red meat consumption, was done at Harvard University in an analysis of almost 15,000 male physicians in the Physicians’ Health Study.³² Although this study primarily analyzed plasma fatty acids and prostate cancer risk, the authors found that men who consumed red meat at least five times per week had a relative risk of 2.5 for developing prostate cancer compared to men who ate red meat less than once per week. The most comprehensive dietary cohort study on diet and prostate cancer risk reported on nearly 52,000 health professionals in Harvard’s Health Professionals Follow-Up Study, which completed food frequency questionnaires in 1986.³³ The report, based on 3 to 4 years of follow-up data, found a statistically significant relationship between higher red meat intake and the risk of prostate cancer, with red meat as the food group with the strongest positive association with advanced prostate cancer. These and other study findings suggest that reducing or eliminating meat from the diet reduces the risk of prostate cancer.³⁴

A new review published in the Journal of Human Nutrition and Dietetics assessed whether certain modifications in diet have a beneficial effect on the prevention of prostate cancer. Results suggest that a diet low in fat, red meat, dairy, and calcium, yet high in fruits and vegetables is beneficial in preventing and treating prostate cancer. Consumption of highly processed or charcoaled meats, dairy products, and fats seemed to be correlated with prostate cancer.³⁵

Other Cancers

Although not as extensively studied as breast, colon, and prostate cancer risk, a number of studies have concluded that meat consumption may play a significant role in kidney and pancreatic cancer risk. Three of eight case-control studies examining the relationship between renal cell carcinoma and meat consumption found a statistically significant increase in risk with a high consumption of meat. In addition, a prospective study in Japan found that people consuming meat daily had higher death rates from kidney cancer than those eating meat less frequently.⁵

Red meat and high glycemic index foods could be risk factors for kidney cancer, according to a 2009 study in the Journal of the American Dietetic Association.  Researchers studied food questionnaires for 335 people with renal cell carcinoma, the most common form of kidney cancer, and 337 healthy controls. They found that men and women who ate red meat five or more times a week were more than four times as likely to develop the disease, compared to those who consumed red meat less than once a week.  The study also found that white bread, white potatoes, and other high glycemic index foods increased the cancer risk threefold. High glycemic index foods affect insulin-like growth factors, which impact tumor development.³⁶ 

Pancreatic cancer is relatively uncommon, yet it is frequently fatal, with fewer than 20 percent of cases surviving for one full year. Daily meat intake has been shown to be associated with increased pancreatic cancer risk in a number of prospective, cohort, and case-control studies.⁵ Some of these studies have singled out beef and pork consumption and have concluded there is a higher risk for pancreatic cancer with a higher intake of these foods.⁵

According to a new study, fat from red meat and dairy products is associated with increased risk of pancreatic cancer. As part of the National Institutes of Health-AARP Diet and Health Study, researchers followed and analyzed the diets of more than 525,000 participants to determine whether there is an association between dietary fat and pancreatic cancer. This same study found no association between plant-food fat and pancreatic cancer.³⁷

A recent study in the British Journal of Cancer found that vegetarians are 12 percent less likely to develop cancer than meat-eaters.  After following 61,000 meat-eaters and vegetarians for over 12 years, researchers also discovered that cancers of the blood—such as leukemia, multiple myeloma, and non-Hodgkin lymphoma—were drastically reduced by as much as 45 percent for those following a vegetarian diet.  Although this study points to an overall reduced risk, this may well be an underestimate of the benefit of a vegetarian diet. Previous studies have shown as much as a 40 percent reduced risk for all cancers.³⁸

Conclusion

Two themes consistently emerge from studies of cancer from many sites: vegetables and fruits help to reduce risk, while meat, animal products, and other fatty foods are frequently found to increase risk. Consumption of dietary fat drives production of hormones, which, in turn, promotes growth of cancer cells in hormone-sensitive organs such as the breast and prostate. Meat is devoid of the protective effects of fiber, antioxidants, phytochemicals, and other helpful nutrients, and it contains high concentrations of saturated fat and potentially carcinogenic compounds, which may increase one’s risk of developing many different kinds of cancer.

Vegetarian diets and diets rich in high-fiber plant foods such as whole grains, legumes, vegetables, and fruits offer a measure of protection.⁵ Fiber greatly speeds the passage of food through the colon, effectively removing carcinogens, and fiber actually changes the type of bacteria that is present in the intestine, so there is reduced production of carcinogenic secondary bile acids. Plant foods are also naturally low in fat and rich in antioxidants and other anti-cancer compounds. Not surprisingly, vegetarians are at the lowest risk for cancer and have a significantly reduced risk compared to meat-eaters.³⁹

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1418. Always Hungry? Here Is Why

By David S. Ludwig and Mark. I. Friedman, The New York Times, May 16, 2014

For most of the last century, our understanding of the cause of obesity has been based on immutable physical law. Specifically, it’s the first law of thermodynamics, which dictates that energy can neither be created nor destroyed. When it comes to body weight, this means that calorie intake minus calorie expenditure equals calories stored. Surrounded by tempting foods, we overeat, consuming more calories than we can burn off, and the excess is deposited as fat. The simple solution is to exert willpower and eat less.

The problem is that this advice doesn’t work, at least not for most people over the long term. In other words, your New Year’s resolution to lose weight probably won’t last through the spring, let alone affect how you look in a swimsuit in July. More of us than ever are obese, despite an incessant focus on calorie balance by the government, nutrition organizations and the food industry.

But what if we’ve confused cause and effect? What if it’s not overeating that causes us to get fat, but the process of getting fatter that causes us to overeat?

The more calories we lock away in fat tissue, the fewer there are circulating in the bloodstream to satisfy the body’s requirements. If we look at it this way, it’s a distribution problem: We have an abundance of calories, but they’re in the wrong place. As a result, the body needs to increase its intake. We get hungrier because we’re getting fatter.

It’s like edema, a common medical condition in which fluid leaks from blood vessels into surrounding tissues. No matter how much water they drink, people with edema may experience unquenchable thirst because the fluid doesn’t stay in the blood, where it’s needed. Similarly, when fat cells suck up too much fuel, calories from food promote the growth of fat tissue instead of serving the energy needs of the body, provoking overeating in all but the most disciplined individuals.

We discuss this hypothesis in an article just published in JAMA, The Journal of the American Medical Association. According to this alternative view, factors in the environment have triggered fat cells in our bodies to take in and store excessive amounts of glucose and other calorie-rich compounds. Since fewer calories are available to fuel metabolism, the brain tells the body to increase calorie intake (we feel hungry) and save energy (our metabolism slows down). Eating more solves this problem temporarily but also accelerates weight gain. Cutting calories reverses the weight gain for a short while, making us think we have control over our body weight, but predictably increases hunger and slows metabolism even more.

Consider fever as another analogy. A cold bath will lower body temperature temporarily, but also set off biological responses — like shivering and constriction of blood vessels — that work to heat the body up again. In a sense, the conventional view of obesity as a problem of calorie balance is like conceptualizing fever as a problem of heat balance; technically not wrong, but not very helpful, because it ignores the apparent underlying biological driver of weight gain.

This is why diets that rely on consciously reducing calories don’t usually work. Only one in six overweight and obese adults in a nationwide survey reports ever having maintained a 10 percent weight loss for at least a year. (Even this relatively modest accomplishment may be exaggerated, because people tend to overestimate their successes in self-reported surveys.) In studies by Dr. Rudolph L. Leibel of Columbia and colleagues, when lean and obese research subjects were underfed in order to make them lose 10 to 20 percent of their weight, their hunger increased and metabolism plummeted. Conversely, overfeeding sped up metabolism.

For both over- and under-eating, these responses tend to push weight back to where it started — prompting some obesity researchers to think in terms of a body weight “set point” that seems to be predetermined by our genes.

But if basic biological responses push back against changes in body weight, and our set points are predetermined, then why have obesity rates — which, for adults, are almost three times what they were in the 1960s — increased so much? Most important, what can we do about it?

As it turns out, many biological factors affect the storage of calories in fat cells, including genetics, levels of physical activity, sleep and stress. But one has an indisputably dominant role: the hormone insulin. We know that excess insulin treatment for diabetes causes weight gain, and insulin deficiency causes weight loss. And of everything we eat, highly refined and rapidly digestible carbohydrates produce the most insulin.

By this way of thinking, the increasing amount and processing of carbohydrates in the American diet has increased insulin levels, put fat cells into storage overdrive and elicited obesity-promoting biological responses in a large number of people. Like an infection that raises the body temperature set point, high consumption of refined carbohydrates — chips, crackers, cakes, soft drinks, sugary breakfast cereals and even white rice and bread — has increased body weights throughout the population.

One reason we consume so many refined carbohydrates today is because they have been added to processed foods in place of fats — which have been the main target of calorie reduction efforts since the 1970s. Fat has about twice the calories of carbohydrates, but low-fat diets are the least effective of comparable interventions, according to several analyses, including one presented at a meeting of the American Heart Association this year.

A recent study by one of us, Dr. Ludwig, and his colleagues published in JAMA examined 21 overweight and obese young adults after they had lost 10 to 15 percent of their body weight, on diets ranging from low fat to low carbohydrate. Despite consuming the same number of calories on each diet, subjects burned about 325 more calories per day on the low carbohydrate than on the low fat diet — amounting to the energy expended in an hour of moderately intense physical activity.

Another study published by Dr. Ludwig and colleagues in The Lancet in 2004 suggested that a poor-quality diet could result in obesity even when it was low in calories. Rats fed a diet with rapidly digesting (called high “glycemic index”) carbohydrate gained 71 percent more fat than their counterparts, who ate more calories over all, though in the form of slowly digesting carbohydrate.

These ideas aren’t entirely new. The notion that we overeat because we’re getting fat has been around for at least a century, as described by Gary Taubes in his book “Good Calories, Bad Calories.” In 1908, for example, a German internist named Gustav von Bergmann dismissed the energy-balance view of obesity, and hypothesized that it was instead caused by a metabolic disorder that he called “lipophilia,” or “love of fat.”

But such theories have been generally ignored, perhaps because they challenge entrenched cultural attitudes. The popular emphasis on calorie balance reinforces the belief that we have conscious control over our weight, and that obesity represents a personal failure because of ignorance or inadequate willpower.

In addition, the food industry — which makes enormous profits from highly processed products derived from corn, wheat and rice — invokes calorie balance as its first line of defense. If all calories are the same, then there are no bad foods, and sugary beverages, junk foods and the like are fine in moderation. It’s simply a question of portion control. The fact that this rarely works is taken as evidence that obese people lack willpower, not that the idea itself might be wrong.

UNFORTUNATELY, existing research cannot provide a definitive test of our hypothesis. Several prominent clinical trials reported no difference in weight loss when comparing diets purportedly differing in protein, carbohydrate and fat. However, these trials had major limitations; at the end, subjects reported that they had not met the targets for complying with the prescribed diets. We wouldn’t discard a potentially lifesaving cancer treatment based on negative findings, if the research subjects didn’t take the drug as intended.

There are better ways to do this research. Studies should provide participants with at least some of their food, to make it easier for them to stick to the diets. Two studies that did this — one by the Direct Group in 2008 and the other by the Diogenes Project in 2010 — reported substantial benefits associated with the reduction of rapidly digestible carbohydrate compared with conventional diets. We need to invest much more in this research. With the annual economic burden of diabetes — just one obesity-related complication — predicted to approach half a trillion dollars by 2020, a few billion dollars for state-of-the-art nutrition research would make a good investment.

If this hypothesis turns out to be correct, it will have immediate implications for public health. It would mean that the decades-long focus on calorie restriction was destined to fail for most people. Information about calorie content would remain relevant, not as a strategy for weight loss, but rather to help people avoid eating too much highly processed food loaded with rapidly digesting carbohydrates. But obesity treatment would more appropriately focus on diet quality rather than calorie quantity.

People in the modern food environment seem to have greater control over what they eat than how much. With reduced consumption of refined grains, concentrated sugar and potato products and a few other sensible lifestyle choices, our internal body weight control system should be able to do the rest. Eventually, we could bring the body weight set point back to pre-epidemic levels. Addressing the underlying biological drive to overeat may make for a far more practical and effective solution to obesity than counting calories.

David S. Ludwig directs the New Balance Foundation Obesity Prevention Center at Boston Children’s Hospital and is a professor of pediatrics at Harvard Medical School. Mark I. Friedman is vice president of research at the Nutrition Science Initiative.