Tag Archive | Obesity

The REALFOOD.ORG READER: Understanding Weight Regulation – Endocrinology Over Arithmetic


(The Versailles Paradox? Increased leisure, plentiful cheap food, noticeable lack of obesity.)

[Editor: This was previously published in The Marcus Reader]


Gary Taubes | The New York Times | 7 July 2002

The science behind the alternative hypothesis can be called Endocrinology 101, which is how it’s referred to by David Ludwig, a researcher at Harvard Medical School who runs the pediatric obesity clinic at Children’s Hospital Boston, and who prescribes his own version of a carbohydrate-restricted diet to his patients. Endocrinology 101 requires an understanding of how carbohydrates affect insulin and blood sugar and in turn fat metabolism and appetite. This is basic endocrinology, Ludwig says, which is the study of hormones, and it is still considered radical because the low-fat dietary wisdom emerged in the 1960’s from researchers almost exclusively concerned with the effect of fat on cholesterol and heart disease. At the time, Endocrinology 101 was still underdeveloped, and so it was ignored. Now that this science is becoming clear, it has to fight a quarter century of anti-fat prejudice.

The alternative hypothesis also comes with an implication that is worth considering for a moment, because it’s a whopper, and it may indeed be an obstacle to its acceptance. If the alternative hypothesis is right — still a big ”if” — then it strongly suggests that the ongoing epidemic of obesity in America and elsewhere is not, as we are constantly told, due simply to a collective lack of will power and a failure to exercise. Rather it occurred, as Atkins has been saying (along with Barry Sears, author of ”The Zone”), because the public health authorities told us unwittingly, but with the best of intentions, to eat precisely those foods that would make us fat, and we did. We ate more fat-free carbohydrates, which, in turn, made us hungrier and then heavier. Put simply, if the alternative hypothesis is right, then a low-fat diet is not by definition a healthy diet. In practice, such a diet cannot help being high in carbohydrates, and that can lead to obesity, and perhaps even heart disease. ”For a large percentage of the population, perhaps 30 to 40 percent, low-fat diets are counterproductive,” says Eleftheria Maratos-Flier, director of obesity research at Harvard’s prestigious Joslin Diabetes Center. ”They have the paradoxical effect of making people gain weight.”





Tara Parker Pope | The New York Times | 28 December 2011

Beginning in 2009, he and his team recruited 50 obese men and women. The men weighed an average of 233 pounds; the women weighed about 200 pounds. Although some people dropped out of the study, most of the patients stuck with the extreme low-calorie diet, which consisted of special shakes called Optifast and two cups of low-starch vegetables, totaling just 500 to 550 calories a day for eight weeks. Ten weeks in, the dieters lost an average of 30 pounds.

At that point, the 34 patients who remained stopped dieting and began working to maintain the new lower weight. Nutritionists counseled them in person and by phone, promoting regular exercise and urging them to eat more vegetables and less fat. But despite the effort, they slowly began to put on weight. After a year, the patients already had regained an average of 11 of the pounds they struggled so hard to lose. They also reported feeling far more hungry and preoccupied with food than before they lost the weight.

While researchers have known for decades that the body undergoes various metabolic and hormonal changes while it’s losing weight, the Australian team detected something new. A full year after significant weight loss, these men and women remained in what could be described as a biologically altered state. Their still-plump bodies were acting as if they were starving and were working overtime to regain the pounds they lost. For instance, a gastric hormone called ghrelin, often dubbed the “hunger hormone,” was about 20 percent higher than at the start of the study. Another hormone associated with suppressing hunger, peptide YY, was also abnormally low. Levels of leptin, a hormone that suppresses hunger and increases metabolism, also remained lower than expected. A cocktail of other hormones associated with hunger and metabolism all remained significantly changed compared to pre-dieting levels. It was almost as if weight loss had put their bodies into a unique metabolic state, a sort of post-dieting syndrome that set them apart from people who hadn’t tried to lose weight in the first place.

“What we see here is a coordinated defense mechanism with multiple components all directed toward making us put on weight,” Proietto says. “This, I think, explains the high failure rate in obesity treatment.”

Eventually, the Columbia subjects are placed on liquid diets of 800 calories a day until they lose 10 percent of their body weight. Once they reach the goal, they are subjected to another round of intensive testing as they try to maintain the new weight. The data generated by these experiments suggest that once a person loses about 10 percent of body weight, he or she is metabolically different than a similar-size person who is naturally the same weight.

The research shows that the changes that occur after weight loss translate to a huge caloric disadvantage of about 250 to 400 calories. For instance, one woman who entered the Columbia studies at 230 pounds was eating about 3,000 calories to maintain that weight. Once she dropped to 190 pounds, losing 17 percent of her body weight, metabolic studies determined that she needed about 2,300 daily calories to maintain the new lower weight. That may sound like plenty, but the typical 30-year-old 190-pound woman can consume about 2,600 calories to maintain her weight — 300 more calories than the woman who dieted to get there.

Read More…

Bariatric surgery may be about metabolic health rather than limiting consumption

The Los Angeles Times reports on the results of a new study of the benefits of bariatric surgery”

The study randomly assigned 150 overweight and obese people with Type 2 diabetes to one of three groups. Those in the control group had their diabetes managed with medications and daily blood-glucose monitoring. They also received intensive counseling about diet and exercise, including regular weigh-ins to monitor their progress. After three years, they had lost an average of 9.5 pounds.

The second group in the trial got Roux-en-Y gastric bypasses, in which the stomach is reshaped and relocated to divert most food past much of the lower intestine, where nutrients and calories are largely absorbed. The third group got a procedure called sleeve gastrectomy, which staples some 80% of the stomach closed, creating a banana-shaped tube where once a large pouch existed. Patients who had surgery received intensive medical management and lifestyle counseling as well.

Three years later, those who had the Roux-en-Y bypass had lost an average of nearly 58 pounds, and those who had sleeve gastrectomy lost an average of 47 pounds.

More importantly, Schauer said, the patients in the surgery groups were much more likely to have their diabetes under control — 58% of those who had Roux-en-Y and 33% of those who had sleeve gastrectomy were able to stop taking diabetes medications. Only 5% of patients in the control group achieved the same endpoint after three years, and none were able to discontinue medications completely.

In addition, study volunteers who had gastric bypass whittled their daily number of blood pressure and cholesterol-lowering medications from 2.73 to 0.96, on average. And subjects who had sleeve gastrectomy reduced their average number of cardiovascular medications from 2.18 to 1.35 three years later.

The medication tally for the control group didn’t budge.

Sadly, the report does not discuss the possible mechanism(s) responsible for this result. The theory behind bariatric surgery was that it would work simply by restricting the volume of food that the patient could consume. It turns out that it seems to be driven more by the way it resets metabolic health in general and insulin sensitivity in particular.

Once he was awarded funding, Brady began collecting fat samples from bariatric surgery patients with the help of a research assistant. The samples were collected two weeks before the surgery, and then again two weeks after the surgery.

“We added varying dosages of insulin to the samples to test the sensitivity, to create a dose-response curve,” Brady said. “And what we found that there was a huge increase in both insulin sensitivity and responsiveness just two weeks after the procedure.”

Brady found that these results could be reproduced in each patient undergoing a Roux-en-Y or duodenial switch.

Bariatric surgery seems to ‘reboot’ fat cells so that they do their job properly, absorbing and retaining the lipids,” Brady said. “However, there are likely to be more subtle molecular and metabolic differences between the two procedures. This is something we’re hoping to examine in a larger study.”

It would be great to see the conversation about type 2 diabetes and obesity shift further away from the overeating paradigm to a metabolic health paradigm.

Occam’s Razor and Endocrine Disruptors

David Epstein has quick and interesting look at research into the possible role of endocrine disrupting chemicals might be playing a role in weight gain both in humans and in animals. Cats and dogs, rats and mice, apes and chimps are all gaining weight in captivity (this is also seen in feral rats with access to people food). The research is credible, but it raises to issues for me.

The first is that it seems a little too convenient that ALL the endocrine disruptors in the environment are only causing our metabolisms to partition energy into fat storage rather than vice versa. In fact some of them are chemicals used for weight gain. I’d have liked to have seen that addressed in the article.

More centrally, I tend to approach the obesity crisis keeping Occam’s Razor in mind. As guideline, Occam’s Razor holds “among competing hypotheses, the hypothesis with the fewest assumptions should be selected.” The first step is to try to limit the number of possible variable instead of multiplying them. Instead of asking what is causing THIS OBESITY EPIDEMIC and then trying to account for all the variables that make this period of time different than the period that preceded it, you should ask what causes OBESITY EPIDEMICS IN GENERAL and the look at what they have in common. Gary Taubes outlines examples in “Why Do We Get Fat”

1961-63 Trinidad West Indies
A team of nutritionist from the US reports that malnutrition is a serious problem on the island, but so is obesity. Nearly a third of the women older than twenty five are obese. The average caloric intake among these women is estimated a fewer than 2000 calories a day.

1963 Chile
Obesity is described as “the main nutritional problem of Chilean adults.” 22% of military personnel and 32 % of white collar workers are obese. Among factory workers, 35% of males and 39% of females are obese.

1964-65 Johannesburg South Africa
Researchers from the South African Institute for Medical Research study urban Bantu “pensioners” older than 60 – “the most indigent of the elderly Bantu,” which means the poorest members of an exceedingly poor population. The women in this population average 165 pounds. 30% of them are “severely overweight.” The average weight of “poor white'” women is also reported to be 165 pounds.

1969 Ghana
25% of the women and 7% of the men attending medical outpatient clinics in Accra are obese, including half of all women in their 40s. “It may be reasonably concluded that severe obesity is common in women aged 30 to 60,” writes an associate professor at the University of Ghana Medical School, and it is “fairly common knowledge that many market women in the coastal towns of West Africa are fat.”

1970 Lagos Nigeria
5% of men are obese, as are nearly 30% of the women. Of women between 55 and 65, 40% are “grossly obese.”

Cheap refined flours, sugars and oils are sufficient to explain previous obesity epidemics, and I’m don’t see why they are not sufficient to explain this one.

There are some observations in the Epstein article and a longer one by David Berreby in Aeon that can’t be explained the flour, sugar, oil hypothesis. The research around endocrine disruptors is certainly interesting and bears a closer look. I look forward to the EFSA report on BpA later next year. In the meantime, a diet of lots of fruit and vegetables, pulses and whole grains with minimal, minimally processed foods has enough to recommend it without getting overly chemophobic. Obviously, for anyone with an endocrine disorder, a whole different set of criteria are warranted for assessing risk, but for myself, I will continue to believe that the canned tomatoes in my diet are a net plus nutritionally.