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Dangers of Dieting a Body Adapted to Famine

Friday, March 2, 2012   (1 Comments)
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Shan Guisinger, PhD,  Clinical Psychologist

For F.E.A.S.T. March 2012

Shan Guisinger is a clinician with 25 years experience treating eating disorders. She received her Ph.D. from the University of California, Berkeley and completed postdoctoral work at the Yale University Eating Disorders Clinic. In her research and practice, she seeks to understand how biological, psychological, and social factors interact to create or ameliorate emotional problems. Shan has authored articles for Psychological Review and The American Psychologist on evolution of anorexia nervosa and interpersonal relatedness, and she is at work on a treatment manual for anorexia nervosa.


Dangers of Dieting a Body Adapted to Famine

Because our ancestors were adapted to survive famine, very low calorie diets can make dieters more obese, trigger eating disorders, and increase the risk of obesity and diabetes for their children and grandchildren.

Our bodies bring hundreds of millions of years of evolution to the problem of famine. In the New York Times Magazine (January 1, 2012) Tara Parker-Pope reported research showing that biological mechanisms cause dieters to regain their lost weight. This seems to come as a surprise to Parker-Pope, but her conclusion that, diets fail over the long-term, is not news. In the last decade review articles in Nature, Science, the New England Journal of Medicine, and The American Psychologist have concluded that diets are not the answer to obesity because over the long term the body responds to weight loss by storing more fat.

Diets do work initially. We seem to be able to tolerate and even enjoy short-term weight loss. This makes sense; when our ancestors lived as hunter-gatherers, there were times when the body needed to quiet hunger pangs and focus on migrating or getting by until spring. But over the longer term the body tries to return to its pre-diet weight, and because energy regulation is under neuroendocrine control, weight cannot be permanently controlled by conscious effort.

Information that food is scarce leads to changes in gene expression that alter every level of the body’s powerful energy regulation system. A network of chemical switches, collectively known as the epigenome, work like a volume knob on the gene, by make it easier or more difficult for the cell's protein-making machinery to read them. This allows organisms to respond to environmental conditions. Epigenetic chemical markers serve as a layer of genetic control on top of the DNA sequence—thus their name “epi” means “above.” The amount of food and regularity of eating feeds back to the genes via these epigenetic pathways. Some genetic mechanisms are hundreds of millions of years old. For example, one obesity gene, FTO, that is up-regulated by dieting in humans plays a similar role in energy utilization in yeast.

Genes can be permanently altered by the conditions an organism encounters. One extreme diet in adolescence can set up an individual for weight struggles the rest of his or her life. In a study of 14,972 American adolescents followed over three years, Field and colleagues found dieters gained more weight than non-dieters, even when researchers controlled for age, gender, BMI, calorie intake and physical activity. In other words, the diet made the body more efficient at using energy and storing it. Adolescents who were underweight or normal weight were as susceptible to weight gain as those who were overweight.

A recent review of 31 long-term diet plans published in The American Psychologist found dieters gained more weight than nondieters. The evidence convinced the authors to advise Medicare and Medicaid policymakers that diets are counterproductive for weight control. Mann and colleagues wrote, “Even in studies with the longest follow-up times (of four or five years postdiet), the weight gain trajectories did not typically appear to level off. It is important for policymakers to remember that weight regain does not necessarily end when researchers stop following study participants” (p221).

For hundreds of millions of years the biggest danger facing animals was starvation and our bodies are exquisitely sensitive to that threat. Deep in the brain an ancient region called the hypothalamus monitors nutritional status and manipulates our appetite to get us the things we need. The hypothalamus gets its information about protein, sugar, fat, salt and water levels from sampling the blood, not from the conscious mind. You could be sitting at a banquet, but if you restrict calories your hypothalamus figures you live with famine.

When starving, the hypothalamus turns up hunger so we can think of little but food; it keeps satiety (fullness) signals low so that when food becomes available we can gorge, and it quiets the part of the brain responsible for self-restraint. One study published this fall in the New England Journal of Medicine found that hunger signals were still significantly elevated a full year after obese people went on an eight-week, very low calorie diet. The dieted body can lower metabolic rate up to 40%, slow transit time in the gut to extract more of the nutrients from food, and divert calories from energy into fat storage.

Starvation turn up the brain’s rewards for eating to motivate food searches. Indeed, street drugs exploit reward systems that first evolved to insure that animals eat. For example, when starving opiate receptors are amplified so that eating pasta can feel like an addict’s fix. Increased cannabinoid receptors make food taste like you’re stoned. Dopamine, the brain chemical that plays a key role in orgasm and in addiction, surges when a starving person eats.

One popular explanation for the obesity epidemic is that people have learned to associate eating with a reward. Parker-Pope quotes Rena Wing, a psychiatry professor at Brown, “We’ve taught ourselves over the years that one of the ways to reward yourself is with food.” But people do not have to learn that eating is rewarding. Wing’s naïve statement illustrates the widespread ignorance of the body’s powerful energy regulation system, even among weight loss experts.

Scientists are finding that a very low calorie diet can also put our children and even grandchildren at higher risk for obesity and diabetes. Scientists first began to suspect that a mother’s diet could program her adult child for obesity by studying people born to mothers who were pregnant during the Dutch Hunger Winter of 1945. Hitler cut off food to Holland and thousands died of starvation. Women who were pregnant gave birth to infants that were smaller than normal, but epigenetic modifications prepared the children to survive famine by increasing their appetites and ability to store fat.

The offspring of rats who were undernourished during pregnancy also become obese adults. Rats turn out to be wonderful exemplars of human obesity and eating disorders. Rats and humans evolved in similar ecological niches as omnivorous, opportunistic nomadic foragers and the hypothalamus is structurally preserved through mammalian evolution. Like most animals, rats maintain a healthy weight in the wild and in the lab when allowed a normal diet and activity. But if given a rich diet and no exercise they will gain more weight. If they are dieted and then given a rich diet they become obese.

Epidemiologists believe epigenetic modification could help explain the obesity epidemic in China, where the children of mothers who starved during Mao’s Great Leap Forward are now obese in middle-age. Researchers believe that the same adaptations that allow individuals to utilize calories more efficiently under conditions of food scarcity contribute to diabetes and obesity when food is plentiful. Since the children grew up with plenty to eat, they become overweight and at greater risk of developing diabetes. Pregnant mothers who follow a very low calorie diet may signal the fetus that it will live with famine. 

Epigenetic adaptations to famine can be passed down at least two generations. The daughters of women who were pregnant during the Dutch famine gave birth to babies who were also smaller than average. Famine experienced by boys can even influence their grandchildren’s health. The Överkalix Cohort Study looked at the progeny of men in northern Sweden who had lived through a severe famine during their preadolescence. Researchers found increased risk of diabetes, obesity and cardiovascular disease for the men, their children and grandchildren.

Very low calorie diets also cause eating disorders. All the human eating disorders can be triggered in rats by restricting calories. If starved or if food is limited to one hour a day rats spontaneously develop anorexia behaviors where they ignore their food to run on a wheel. In the wild this activity would have helped them find food, but in the lab cage they can run themselves to death. Researchers have found that anorexia behaviors are triggered in both rats and humans by declining fat stores. Gorging, which is part of bulimia and binge eating disorder is a normal response to starvation. If you give stress dieted rats and give them access to sugar water, they binge eat.

Evolutionary adaptations to survive famine give form to the symptoms of anorexia nervosa, bulimia, and binge eating disorder. I believe eating disorders only make sense in the light of evolution, but most popular theories are derived from patients’ explanations of their behavior. Although only 2% of our brain is conscious, it tries to make sense of the actions of the other 98%--including activities of the hypothalamus--in psychological terms.

In the 1960s fewer people dieted and 15% of the population was obese and eating disorders were rare. Marilyn Monroe, wore a size 12. As weights of models and film stars began to decline, more people dieted and we became a nation obsessed with food. Today models are often a size 0, nearly 50% of the population dieted in the past year, eating disorders have tripled, and obesity rates have risen to 34%.

Given the evidence of diets inefficacy and perniciousness we should be asking, Why is the diet industry allowed to promote the very behavior that leads to greater obesity and to eating disorders?

According to a study of everyday stress, by the time they are middle-aged both men and women list unhappiness with their weight as their number one daily stressor. people who despise themselves for their failure to maintain their ideal weight often project their disdain onto those who are fatter. Prejudice against fat people is rationalized by the belief that fat is unhealthy, but for the middle 60% of the weight distribution there is no correlation between health and weight. In fact, people who are overweight, but not obese, have a lower risk of death than normal weight or underweight people.

Genetic studies have found that weight is as heritable as height, yet many people wake up everyday hating their weight and scorning those who are fatter. Although tallness and thinness are both valued, there isn’t widespread contempt of short people; height is seen as beyond the individual’s control. If a short person woke up every day hating her height we would question her sanity and values.

Is there no solution then to obesity and eating disorders? Actually there is. We should eat in a way to convince our bodies that they no longer, and will never again, live with famine. That means never go on a reduced calorie diet. Most people should eat more frequent, smaller meals beginning with breakfast. We should eat a diet closer to the one humans evolved with. There are no naturally occurring sweet fats or processed carbohydrates and our bodies don’t regulate as well with them. Follow Michelle Obama’s advice to substitute water for soft drinks, and increase fruits and vegetables. It is easier to do if you stop dieting. Find some physical activities you enjoy and make time for them. And then pray for the grace to accept the body you have.


Sarahfrancesyoung says...
Posted Saturday, December 19, 2015
Does that mean that those who recover from eating disorders can end up obese and keep gaining weight indefinitely?

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