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.
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.
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.
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.