(The Versailles Paradox? Increased leisure, plentiful cheap food, noticeable lack of obesity.)
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.
Robert Lustig MD | The Huffington Post
We asked the question, “What in the world’s food supply explains diabetes rates, country-by-country, over the last decade?” We melded databases from the Food and Agriculture Organization (FAOSTAT), which measures food availability, the International Diabetes Federation (IDF), which measures diabetes prevalence, the World Bank World Development Economic Indicators, and the World Health Organization Global Infobase. We assessed total calories; meat (protein); oils (fat); cereals (glucose); pulses, nuts, vegetables, roots, and tubers (fiber); fruit excluding wine (natural sugar); and sugar, sugarcrops, and sweeteners (added sugar). We controlled for poverty, urbanization, aging, and most important, obesity and physical activity.
Bottom line — only changes in sugar availability explained changes in diabetes prevalence worldwide; nothing else mattered.
Total caloric availability was unrelated to diabetes prevalence; for every extra 150 calories per day, diabetes prevalence rose by only 0.1 percent. But if those 150 calories per day happened to be a can of soda, diabetes prevalence rose 11-fold, by 1.1 percent (and Americans on average consume the added sugar equivalent of 2.5 cans of soda per day, so that’s 2.75 percent!). And this effect of sugar was exclusive of obesity; controlling for body mass index did not negate the effect. Even more important, we showed that the change in sugar availability preceded the change in diabetes (that’s cause, not effect); and we showed directionality — those countries where sugar availability rose showed increases in diabetes, while those where sugar availability fell showed decreases in diabetes. This is a very robust signal, with little noise. While epidemiology can’t prove scientific causation, the data allow for objective inference. Sugar drives diabetes worldwide, and unrelated to its calories.
Robert Lustig MD | Youtube
Robin Marantz Henig | The New York Times | 13 April 2006
One of Atkinson’s most memorable patients was Janet S., a bright, funny 25-year-old who weighed 348 pounds when she finally made her way to U.C.L.A. in 1975. In exchange for agreeing to be hospitalized for three months so scientists could study them, Janet and the other obese research subjects (30 in all) each received a free intestinal bypass. During the three months of presurgical study, the dietitian on the research team calculated how many calories it should take for a 5-foot-6-inch woman like Janet to maintain a weight of 348. They fed her exactly that many calories — no more, no less. She dutifully ate what she was told, and she gained 12 pounds in two weeks — almost a pound a day.
“I don’t think I’d ever gained that much weight that quickly,” recalled Janet, who asked me not to use her full name because she didn’t want people to know how fat she had once been. The doctors accused her of sneaking snacks into the hospital. “But I told them, ‘I’m gaining weight because you’re feeding me a tremendous amount of food!’ ”
The experience with Janet was an early inkling that traditional ideas about obesity were incomplete. Researchers and public-health officials have long understood that to maintain a given weight, energy in (calories consumed) must equal energy out (calories expended). But then they learned that genes were important, too, and that for some people, like Janet, this formula was tilted in a direction that led to weight gain. Since the discovery of the first obesity gene in 1994, scientists have found about 50 genes involved in obesity. Some of them determine how individuals lay down fat and metabolize energy stores. Others regulate how much people want to eat in the first place, how they know when they’ve had enough and how likely they are to use up calories through activities ranging from fidgeting to running marathons. People like Janet, who can get fat on very little fuel, may be genetically programmed to survive in harsher environments. When the human species got its start, it was an advantage to be efficient. Today, when food is plentiful, it is a hazard.
This is typical of people who have lost weight — not only a lot of weight, as Janet has, but even a little weight. According to Rudolph Leibel, an obesity researcher at Columbia University who was involved in the discovery of the first human gene implicated in obesity, if you take two nonobese people of the same weight, they will require different amounts of food depending on whether or not they were once obese. It goes in precisely the maddening direction you might expect: formerly fat people need to eat less than never-fat people to maintain exactly the same weight. In other words, a 150-pound woman who has always weighed 150 might be able to get away with eating, say, 2,500 calories a day, but a 150-pound woman who once weighed more — 20 pounds more, 200 pounds more, the exact amount doesn’t matter — would have to consume about 15 percent fewer calories to keep from regaining the weight. The change occurs as soon as the person starts reducing, Leibel said, and it “is not proportional to amount of weight lost, and persists over time.”
For many people, then, losing weight and keeping the weight off requires a constant state of hunger — and when you’re hungry, you’re miserable. You think of nothing but food every moment of the day. All morning you think about lunch, all afternoon you think about dinner, and when you’re asleep, you dream of food.
Current public-health messages deny this harsh reality. They make losing weight sound easy, just a simple matter of doing the math and applying some willpower. A pound of fat contains 3,500 calories, government documents say, and if you cut down a week’s worth of food intake or increase exercise by a total of 3,500 calories, then, voilà — you lose a pound. “To lose weight, you must use more energy than you take in,” states the Web site of the Office of the Surgeon General. “A difference of one 12-oz. soda (150 calories) or 30 minutes of brisk walking most days can add or subtract approximately 10 pounds to your weight each year.”
But if genes or viral infection or gut microflora are involved, then for some people 3,500 calories might not equal a pound of fat, and 150 fewer calories a day might not mean they’ll lose 10 pounds in a year. As scientists continue to investigate how obese people are different, we can only hope that a side benefit will be a more largehearted understanding of what it means to be fat and how hard it is to try to become, and to remain, less fat.
Shanna Williams | Institute for Translational Medicine | University of Chicago | 7 January 2013
“It’s known that insulin sensitivity shows a marked improvement in most bariatric surgery patients, even before significant long-term weight loss occurs,” Brady said. “What’s not known is why the sensitivity to insulin improves.”
“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.”
Gretchen Reynolds | The New York Times | 16 April 2010
“In general, exercise by itself is pretty useless for weight loss,” says Eric Ravussin, a professor at the Pennington Biomedical Research Center in Baton Rouge, La., and an expert on weight loss. It’s especially useless because people often end up consuming more calories when they exercise. The mathematics of weight loss is, in fact, quite simple, involving only subtraction. “Take in fewer calories than you burn, put yourself in negative energy balance, lose weight,” says Braun, who has been studying exercise and weight loss for years.
The mechanisms that control appetite and energy balance in the human body are elegantly calibrated. “The body aims for homeostasis,” Braun says. It likes to remain at whatever weight it’s used to. So even small changes in energy balance can produce rapid changes in certain hormones associated with appetite, particularly acylated ghrelin, which is known to increase the desire for food, as well as insulin and leptin, hormones that affect how the body burns fuel.
The effects of exercise on the appetite and energy systems, however, are by no means consistent. In one study presented last year at the annual conference of the American College of Sports Medicine, when healthy young men ran for an hour and a half on a treadmill at a fairly high intensity, their blood concentrations of acylated ghrelin fell, and food held little appeal for the rest of that day. Exercise blunted their appetites. A study that Braun oversaw and that was published last year by The American Journal of Physiology had a slightly different outcome. In it, 18 overweight men and women walked on treadmills in multiple sessions while either eating enough that day to replace the calories burned during exercise or not. Afterward, the men displayed little or no changes in their energy-regulating hormones or their appetites, much as in the other study. But the women uniformly had increased blood concentrations of acylated ghrelin and decreased concentrations of insulin after the sessions in which they had eaten less than they had burned. Their bodies were directing them to replace the lost calories. In physiological terms, the results “are consistent with the paradigm that mechanisms to maintain body fat are more effective in women,” Braun and his colleagues wrote. In practical terms, the results are scientific proof that life is unfair. Female bodies, inspired almost certainly “by a biological need to maintain energy stores for reproduction,” Braun says, fight hard to hold on to every ounce of fat. Exercise for many women (and for some men) increases the desire to eat.
Gretchen Reynolds | The New York Times | 16 April 2012
And as another provocative new study of brain activity after exercise found, some overweight, sedentary people respond to exercise by revving their food-reward systems, not dampening them.
In that study, published last year in The Journal of Obesity, 34 heavy men and women began a supervised, five-day-a-week exercise program, designed so that each participant would burn about 500 calories per workout. They were allowed to eat at will throughout the experiment. Twelve weeks later, 20 of the group had lost considerable weight, about 11 pounds on average. But 14 had not, dropping only a pound or two, if any.
Those 14, dubbed nonresponders, also had displayed the highest brain responses to food cues following exercise when the study began. After three months, they retained that undesirable lead. Their food-reward networks lit up riotously after exercise at the sight of food, and in fact showed more enthusiasm now than at the start of the study. The responders’ brains, in contrast, responded with a relative ‘meh’ to food pictures after exercise.
Tara Parker-Pope | The New York Times | 18 March 2013
During the first week of the study, half the people were allowed to sleep nine hours a night while the other half stayed up until about midnight and then could sleep up to five hours. Everyone was given unlimited access to food. In the second week, the nine-hour sleepers were then restricted to five hours of sleep a night, while the sleep-deprived participants were allowed an extra four hours.
Notably, the researchers found that staying up late and getting just five hours of sleep increased a person’s metabolism. Sleep-deprived participants actually burned an extra 111 calories a day, according to the findings published last week in The Proceedings of the National Academy of Sciences.
Last fall, The Annals of Internal Medicine reported on a study by University of Chicago researchers, who found that lack of sleep alters the biology of fat cells. In the small study — just seven healthy volunteers — the researchers tracked the changes that occurred when subjects moved from 8.5 hours of sleep to just 4.5 hours. After four nights of less sleep, their fat cells were less sensitive to insulin, a metabolic change associated with both diabetes and obesity.
“Metabolically, lack of sleep aged fat cells about 20 years,” said Matthew Brady, an associate professor of medicine at the University of Chicago and the senior author on the study.
“These subjects were in their low 20s but it’s as if they were now middle-aged in terms of their response. We were surprised how profound the effects were.”
Jennifer LaRue Huget | Washington Post | 5 April 2011
Gearhardt and her team used functional MRI to record brain activity as the women were shown images of yummy chocolate shakes and of a clear, taste-free solution. MRI images were also recorded while the women actually sampled those beverages. (The study explains that the clear formula was made to replicate saliva, as the taste of water actually triggers activity in some brain receptors.)
As was expected, the parts of the brain associated with anticipation and craving were activated by the image of the chocolate shake among women with symptoms of food addiction. But once they tasted the shake, the parts of their brain that should signal them to slow down showed decreased activity, essentially encouraging them to seek more chocolate shake.
Tara Parker-Pope | The New York Times
Princeton University and University of Florida researchers have found that sugar-binging rats show signs of opiatelike withdrawal when their sugar is taken away — including chattering teeth, tremoring forepaws and the shakes. When the rats were allowed to resume eating sugar two weeks later, they pressed the food lever so frantically that they consumed 23 percent more than before. Scientists in California and Italy last year reported that the digestive systems of rats on a fatty liquid diet began producing endocannabinoids, chemicals similar to those produced by marijuana use.
Earlier this year, scientists at the Oregon Research Institute conducted brain-scan studies on children who looked at pictures of chocolate milkshakes and later consumed shakes. Their findings suggest that just as drug abusers and alcoholics need increasingly larger doses over time, children who are regular ice-cream eaters may require more and more ice cream for the reward centers of their brains to indicate that they are satisfied.
Michael Moss | The New York Times | 20 February 2013
I called on Steven Witherly, a food scientist who wrote a fascinating guide for industry insiders titled, “Why Humans Like Junk Food.” I brought him two shopping bags filled with a variety of chips to taste. He zeroed right in on the Cheetos. “This,” Witherly said, “is one of the most marvelously constructed foods on the planet, in terms of pure pleasure.” He ticked off a dozen attributes of the Cheetos that make the brain say more. But the one he focused on most was the puff’s uncanny ability to melt in the mouth. “It’s called vanishing caloric density,” Witherly said. “If something melts down quickly, your brain thinks that there’s no calories in it . . . you can just keep eating it forever.”
David Kessler: The End of Overeating
Kimfuhi | Yahoo Voices | 21 July 2005
A 7 year old girl who was 220% over her ideal weight. She lived with her mother who used food stamps. Her mother said that during 2 weeks out of a month she didn’t have enough food and was unable to provide her daughter with low calorie, high density (filling) foods that she needed. Alternately, during the two weeks of the month when she had food, she would purchase high fat foods that were filling. The two weeks when there was not enough food, Dr. Dietz said her body stored the extra fat. Dr. Dietz proposed that the body has an internal physiological adaptation to retain fat when it is consumed a lot, when episodic food shortages exist. Dr. Dietz suggested that, to prevent obesity, impoverished populations require increased food supplementation, not food restriction. In 1995, Dr. William Dietz published these results in the professional journal, Pediatrics”Does Hunger Cause Obesity?”
Meredith Melnick | Time | 8 December 2011
In a recent study, presented at the San Antonio Breast Cancer Symposium, British researchers found that women who eliminated carbohydrate-rich foods like bread, pasta, potatoes and rice two days a week and ate their normal diet the rest of the time lost an average of 9 lb. over four months. Meanwhile, women in a similar group who ate a 1,500-cal.-per-day Mediterranean-style diet for the same time period lost only 5 lb.
Women on the intermittent diet not only lost more weight but also showed greater improvements on other markers of health, including levels of insulin and leptin.