‘We’re fat because . . .’

Special to The Times

Call IT Fattergate. Americans are getting scandalously big for their britches (and shirts and skirts and dresses and suits). And scientists would like to know why, so they can make it stop. After all, this sharp trend toward a well-rounded population has some pretty hefty (and heinous) consequences for public health.

There’s a simple explanation for the weight gain, of course: People consume more calories than they burn. The favorite explanation: They eat bigger portions of less nutritional foods at easier-to-get-to fast food places, even as they hunker down more and more faithfully in front of their TV and computer screens. “Most of us say it is a combination of reduced energy expenditures plus dietary intake not declining enough,” says Barry Popkin, a nutrition professor at the University of North Carolina at Chapel Hill.

But why does that happen far more often now than 30 years ago? It’s not obvious, says Susan Roberts, a senior scientist at the Human Nutrition Research Center on Aging at Tufts University in Boston: “There is definitely no definitive answer on ‘what went wrong.’ ”

Even as researchers try to refine the eat-too-much-move-too-little theory, some are entertaining other ideas (obesity virus, anyone?). Read on for some of their theories, as well as a weigh-in from our panel of obesity researchers.



The theory: High-fructose corn syrup (HFCS) was introduced in the 1970s, about the time the obesity epidemic was first taking off. Maybe the syrup has some special, inimical quality that makes it wreak havoc with our fat cells.


The research: Made from corn, HFCS comes in two forms, 42% fructose or 55% fructose, the rest being primarily glucose. Regular table sugar (sucrose) is 50% fructose and 50% glucose.

Consumption of HFCS took off like a shot when it was introduced, but because it generally replaced sugar in foods and beverages, stats from the U.S. Department of Agriculture show that consumption of sugar dropped just about the same amount, says, a website dedicated to all things HFCS and associated with the Corn Refiners Assn. Because the composition of sugar and HFCS is quite similar, the mix of glucose and fructose in foods and beverages is close to what it was 30 years ago, according to the site.

There have been several reviews of the HFCS-obesity link. Last month, the American Medical Assn. issued a report on HFCS and obesity after conducting a review of articles published through 2007. The authors concluded the evidence didn’t support a special obesity link and wrote, “Because the composition of HFCS and sucrose are so similar, particularly on absorption by the body, it appears unlikely that HFCS contributes more to obesity or other conditions than sucrose.” Some recent data raise new questions. Peter Havel of UC Davis presented a study at an Endocrine Society meeting last month in which he followed 33 overweight and obese adults as they dieted for 12 weeks. During the last 10 weeks, half of them got 25% of their calories from fructose, and half got 25% from glucose. Though both groups gained the same amount of weight -- 3.3 pounds -- those who had the fructose had an increase in the least-desirable fat (the kind that wraps around internal organs, causes a pot belly and is linked to higher risk of diabetes and heart disease) while the others did not.

The fructose-eaters (but not the glucose-eaters) also had heightened levels of triglycerides and cholesterol and decreased insulin sensitivity, a danger sign for diabetes.

Our experts weigh in: “A number of recent studies . . . have convinced me that HFCS does not affect weight gain,” says Barry Popkin of the University of North Carolina, who was an early proponent of the HFCS-obesity hypothesis. “At the same time, there is a new body of research that suggested HFCS might be linked with higher triglyceride levels and other health effects. This research is too preliminary to make any conclusion.”

Adds Dr. Julie Lumeng of the University of Michigan: “By exposing children to more sweet foods . . . you may be inducing a long-term preference for sweets that leads to excessive caloric consumption.”



The theory: The pollution in our environment can poison our chances to lose weight.

The research: In a 2004 study published in the International Journal of Obesity, 15 obese people lost an average of 23 pounds on a 15-week diet. When researchers compared blood samples at the end of the diet with ones taken before the diet began, they found two differences: Concentrations of leptin -- the hormone that usually keeps hunger in check -- were 33% lower. And concentrations of industrial chemicals called organochlorines were 23% higher.

The researchers also compared the dieters’ metabolic rates before and after dieting. In general, as people lose weight their metabolism slows, in what seems to be the body’s attempt not to lose weight (which makes sense for our evolutionary past but seems rather perverse to anyone trying to drop a few pounds). But in this study, the dieters’ metabolisms slowed way down .

Next the researchers correlated the metabolic slowdowns for the dieters with the two main changes in their blood samples, the reduction in leptin and the elevation in organochlorines. Leptin is known to raise metabolic rates, so a decrease in it might well be connected with a decrease in metabolic rates. But as it turned out, the link with an increase in organochlorines was stronger.

The team hypothesized that organochlorines, which are stored in fat cells, get squeezed into the blood as the fat cells shrink during dieting. Then the body, worried about being poisoned, lowers its metabolic rate to keep the cells from letting any more out.

Theoretically, this same process could happen in everybody since everybody is polluted with organochlorines, says Angelo Tremblay of Laval University in Quebec, a study coauthor. But it’s more likely to happen in obese people because their fat cells are storing more poisons. Are there more pollutants in the environment now than there used to be? Well, duh.

Our experts weigh in: “I am intrigued,” says James Hill of the University of Colorado. Adds Tremblay, “I hesitate to say it’s a major determinant of obesity. But you know, there are not only unhealthy eating and sedentariness. There are also real toxins.”



The theory: Call it the Goldilocks Syndrome. If people rarely get too cold or too hot, but almost always stay “just right” in their temperature comfort zone -- as Americans do, these days, year-round -- they will gain weight.

The research: Environmental temperature can affect weight. A 2002 study of Dutch men found they burned more calories when in a room that was a chilly 61 degrees than when it was a cozier 72 degrees.

That same year, a study with Dutch women found they consumed fewer calories in a too-toasty 81-degree room than in a 72-degree room, because they chose lower-calorie foods to eat. That fits with other science. Studies of people (and pigs) have found they eat less in hot environments.

If the effects seen in short-term experiments hold over time, you’d expect that people who experience sizable temperature variations would be thinner than people who live in conditions that always suit them.

This could only be implicated in the widespread widening of Americans if they’re staying in their comfort zone more than they did 30 years ago -- and it seems that they are. Although most homes were heated in the 1970s, better units and better insulation now help keep people in those homes warmer in winter. But greater progress has probably been made in beating the summer heat. Data from the Air-Conditioning, Heating and Refrigeration Institute show that nearly 90% of new homes are now built with central air conditioning, while only about one-third were in the 1970s. And Americans are even more likely to stay cool on the road. Almost every new car has AC now, whereas only about 60% used to back then.

Our experts weigh in: “I am very skeptical about this one,” says James Hill of the University of Colorado, and Susan Roberts of Tufts University calls it “small stuff.” But Dr. George Bray of Louisiana State University thinks there may be something to it. He notes that temperature affects energy intake and output -- so the more the temperature varies, the more a person’s energy balance may bounce around.



The theory: The low-fat food fad made us fatter. We ate high-carb foods that weren’t as satisfying -- and, by gosh, we ate more as a result.

The research: In 1990, federal health officials recommended for the first time that Americans should eat less fat to lower their risk of heart disease. Many people believe that they’ve gained weight on such diets. Low-fat diets are generally high-carb diets. And, Dr. David Ludwig of Harvard Medical School would say that too often they have a high glycemic load.

When people diet successfully, their metabolism slows down. That slows down any continued weight loss they might hope to have. But research with mice and people has shown that how much your metabolism slows down depends on what you eat.

In one study, Ludwig and his colleagues found that metabolism slowed down about twice as much for those on a low-fat diet compared with those on a diet with a low-glycemic load (meaning foods that are digested and absorbed slowly, producing only gradual rises -- not rushes -- in blood sugar and insulin).

Those on the low-glycemic load diet also felt less hungry, perhaps because of fewer blood sugar crashes.

Our experts weigh in: Everybody has a body weight “set point,” Ludwig says. “If your weight falls below that point, the body has compensation mechanisms to try to kick it back up.” A diet with a low-glycemic load lowers the set point, he adds, “so you don’t run into a brick wall so soon.”

Susan Roberts of Tufts University thinks low-glycemic diets are a legitimate option for losing weight, but she doubts that high-glycemic load diets are a cause of the obesity epidemic. “Just think about the 1950s,” she says. “Everyone was eating white bread, meatloaf (made with white breadcrumbs), potatoes and rice -- and were much thinner than today.”

Barry Popkin of the University of North Carolina says there’s plenty of evidence that a variety of dietary patterns will sustain weight loss -- low-fat and high in complex carbs; low-carb and high in lean proteins; diets higher in fat. “The issue is cutting calories,” he says. “All do work for the short term and few work for the long term without strong self-control, family support, and exercise.”



The theory: Chronic stress leads to weight gain, and chronic stress is at epidemic levels (just like obesity).

The research: Whole books have been written to explain how stress leads to weight gain -- “The Cortisol Connection: Why Stress Makes You Fat and Ruins Your Health -- and What You Can Do About It”; “Fat Around the Middle: How to Lose That Bulge for Good.”

Cortisol is often called the “stress hormone” because it’s part of the body’s fight-or-flight response. It’s a good thing when you’re being chased by a lion (or chewed out by an angry boss), but many doctors and scientists believe that chronic stress is anything but good.

Studies have shown that cortisol makes people crave rich sweets in the worst way -- and pile on pounds in the worst place, around the middle, putting a body at risk for bad cholesterol, heart attacks and strokes. One study compared women with high waist-to-hip ratios to women with low waist-to-hip ratios and found that the former secreted more cortisol in stressful lab situations and self-reported more stressful feelings.

In 2007, researchers introduced a different notion of how stress is related to weight gain. Their study compared stressed mice (who had to live either in cold cages or with a bunch of mean cousins) and unstressed mice (who, relatively speaking, had the life of Stuart Little before all that bad stuff happened). When fed a high-fat, high-sugar diet, all the mice gained weight, but the stressed mice gained twice as much. The scientists found that a molecule in the stressed mice -- neuropeptide Y -- activated a gene in fat cells, causing the cells to grow in size and number. When that gene was blocked for two weeks, the mice lost 40% of the weight they had gained.

Are we more stressed these days? “I would say that modernity . . . provides more factors that are a source of stress,” says Angelo Tremblay of Laval University in Quebec.

Our experts weigh in: Susan Roberts of Tufts University says lots of research shows changes in food preferences for animals under stress. And Dr. Julie Lumeng of the University of Michigan says studies have shown that obese people are less likely than others to be drug addicts or alcoholics -- “the thought being that if you use food to ‘soothe your mood,’ you will be less likely to need to use alcohol or drugs to ‘soothe your mood.’ ”


STUDYING ‘INFECTOBESITY’The theory: Certain viruses may put people at greater risk of becoming obese.

The research: At least 10 viruses are believed to cause obesity in animals, and two have been tenuously linked to people. Antibodies against one (SMAM-1, which causes obesity in chickens) were found in about 20% of a group of 50 obese people tested in 1992. (Scientists don’t know how many non-obese people would have antibodies to this virus as well.) In 2005, in a study of 500 people tested, antibodies to Ad-36 -- a virus that causes symptoms similar to the common cold -- were found in about 30% of obese people, but only in 11% of non-obese people. And in a 2005 test of 89 twin pairs, if one had antibodies and the other didn’t, the one who did was generally heavier.

After exposure to Ad-36, chickens, mice, monkeys and rats hardly act under the weather at all, but their body fat increases, sometimes even doubling. Strangely, though, their total cholesterol, “bad” cholesterol and triglyceride levels go down. People who have antibodies for Ad-36 also have better metabolic profiles than people who don’t.

It’s unknown whether more people are exposed to Ad-36 now than 30 years ago since no one was tested then.

Our experts weigh in: “Obesity due to infection is possible in some people. How big the group is I don’t know. . . . Not all obesity is due to viral infection,” says Nikhil Dhurandhar of Louisiana State University, who has studied SMAM-1 and Ad-36 and coined the term “infectobesity” for “obesity of infectious origin.”

“I think the data are new and emerging, and we just don’t know yet,” says Dr. Julie Lumeng of the University of Michigan, while Dr. George Bray of Louisiana State University says, “The jury is out on whether these are important in humans.”

“I don’t buy into these at all,” says Susan Roberts of Tufts University.



The theory: It’s the meds. Many drugs have the added side effect of endowing people who take them with added pounds.

And this happens more now because, in general, these drugs are much more widely used than they were 30 years ago (when some didn’t even exist).

The research: Weight gain is a known side effect of many drugs, including powerful antipsychotics, over-the-counter antihistamines, antidepressants, diabetes drugs, beta blockers and corticosteroids. Oral contraceptives have often been implicated too, though a 2006 review paper found no evidence of a connection.

Reasons for this burgeoning embonpoint aren’t yet clear, though at least some drugs seem to make patients hungrier, and beta blockers may lower a patient’s metabolic rate.

A 2000 review article found weight gain can be a sign that antidepressants are working if patients who lost weight when they started being depressed gain some back when they stop (though no one thinks that’s the whole story).

Not all drugs of any one type are equally fattening. For instance, metformin is one diabetes drug not associated with weight gain, and some newer beta blockers aren’t either, but older ones are.

Antipsychotics are probably the biggest problems -- leading some patients to gain as much as 100 pounds in a year.

Use of these prescription drugs has increased a lot. Some drugs associated with weight gain weren’t even on the market 30 years ago. Others are prescribed much more than they used to be.

One 2003 study showed that U.S. use of oral antidiabetics more than doubled from 1990 to 2001.

Our experts weigh in: The consensus is that, yes, drugs can cause weight gain. But just as with smoking, even if effects are big in subgroups of the population, they don’t necessarily pack much of a punch in the population as a whole.

“This is a contribution to the obesity epidemic, but again, I would not say this is a big contributor,” says James Hill of the University of Colorado.



The theory: A baby’s risk for future obesity can be affected by his or her mother’s health and habits during pregnancy.

The research: If a woman has diabetes or smokes during her pregnancy, or is poorly nourished during the pregnancy’s early stages, the risk that her baby will be obese or overweight as a child or adolescent is 1.4 to 2 times greater than it would be otherwise, according to a 2007 study that reviewed the scientific literature from 1975 through 2005.

The same researchers are now trying to figure out the physiological mechanisms behind these effects. Dr. Michael Lu of UCLA, a study coauthor, suggests the following pattern for a mother with diabetes: Her blood sugar is high, and that sugar crosses into her baby through the placenta. So the baby produces excess insulin, and in response lays down a lot of fat cells. The extra insulin also programs the baby to always need too much insulin and not “listen” when the hormone leptin sends instructions to hold down insulin production. (Leptin, a “stop eating” hormone, also tells the pancreas to stop producing insulin.) Together, these events predispose the baby to a lifetime of being overweight or obese as well as toward developing Type 2 diabetes.

A study published this year in the journal Diabetes Care found that the number of women who had diabetes (Type 1 or Type 2) when they became pregnant doubled from 1999 to 2005. For teenagers, the number grew to five times higher.

Lu’s study also found that malnourishment in the early stages of a mother’s pregnancy increases the risk that her baby will become an overweight or obese child. And the frequency of low birth weight babies, which correlates with malnourished mothers, has been rising since about 1985.

Our experts weigh in: “Babies’ vital organs and systems are being programmed during pregnancy,” Lu says. “The seeds of their future health are being planted in the womb.” Dr. George Bray of Louisiana State University notes that long-term effects of mothers’ health on their children’s have been seen historically. “Whether they contribute in today’s surfeit of food is unclear to me,” he says.



The theory: People get less sleep these days, and this can mess up their hormones in a way that makes them eat (and eventually weigh) too much.

The research: How much people sleep can affect how much they weigh. A 2007 study of 785 elementary school students conducted by Dr. Julie Lumeng of the University of Michigan found that the less sixth-graders slept, the more likely they were to be overweight. And for every extra hour of sleep they got per night, the risk of being overweight was reduced by 20%. Among third-graders, the less they slept, the more likely they were to be overweight in sixth grade -- every additional hour of sleep reduced the risk by 40%.

A 2006 study of 422 grade-schoolers ages 5 to 10 found the risk of being overweight was 3.5 times higher for children who got fewer than 10 hours of sleep per night than for those who got 12 hours or more. Sleep affected weight more than physical activity and time with computer or TV.

A 2004 study found that after two nights with only four hours of sleep, males in their 20s were very hungry, especially for high-calorie goodies. And studies of people and rats show that sleep deprivation leads to less leptin, a hormone that says “stop stuffing your face,” and more ghrelin, one that says “time to chow down.”

Americans sleep one to two hours fewer these days than 40 years ago, and young adults are more than twice as likely to get fewer than seven hours of sleep -- 37% did in 2002, versus about 16% in 1960. Cellphones may contribute. In a study presented last month at a meeting of the Associated Professional Sleep Societies, excessive cellphone use in teens increased disrupted sleep, restlessness, stress and fatigue.

Our experts weigh in: “I think this is like a sleeper, pardon the pun,” says Dr. Wendy Slusser of UCLA. “It’s something you don’t really think about.” “I think there is something to this one,” adds James Hill of the University of Colorado. Adds Susan Roberts of Tufts University, “It’s part of the larger issue, that life is so rushed that healthy eating and home-prepared food take a back seat.”



The theory: Obesity rates are up at least partly because smoking rates are down. (Meaning we’d have less of a weight problem if we had more of a smoking problem -- not that anyone thinks that would be a good thing.)

Nonsmokers make up a greater proportion of the population now than they used to. And, on average, nonsmokers weigh more than smokers. It follows that the population as a whole should weigh more than it used to.

The research: Studies show that smokers burn more calories because nicotine speeds up their metabolic rates. It may also curb their enthusiasm for food. This may be why smokers tend to weigh less than nonsmokers and gain weight when they quit.

Smoking rates have gone way down. According to the National Health and Nutrition Examination Surveys for 1971-75 and 1999-2002 -- in which health professionals interviewed and examined thousands of people nationwide -- rates among men ages 25 to 39 fell from 50.4% to 32.3%. Among women that age, rates fell from 39.9% to 28.3%.

But a 2007 study found that the drop in smoking rates couldn’t well explain the rise in obesity. The author, Katherine Flegal of the federal Centers for Disease Control and Prevention, projected that if smoking rates hadn’t decreased, the obesity rate would have been 22.4% for men ages 25-39 in the 1999-2002 survey, compared with the actual rate of 23.8%. It would have been 30.2% for women in that age group -- again, just a skosh lower than the actual rate of 30.4%.

Yes, Flegal’s projected obesity rates were lower than actual rates in all age and gender groups, but never by much -- implying that even if smoking rates had stayed as high as in the past, obesity rates in the latest survey would have been hardly affected.

Our experts weigh in: Assessments of smoking’s role in today’s obesity rates range from “small” to “not big.” Susan Roberts of Tufts University says that, although people gain weight when they quit smoking, often they are gaining back weight they lost when they started. “It does contribute,” says James Hill of the University of Colorado, “but it is not a major determinant of the obesity epidemic.”


Theory credits

All research and writing for this article was done by Karen Ravn.

Interviewed for the article: Dr. George Bray, chief of clinical obesity and metabolism, Pennington Biomedical Research Center, Louisiana State University; Nikhil Dhurandhar, professor of infection and obesity, Pennington; James Hill, professor of pediatrics and medicine, University of Colorado in Denver, and director of the Center for Human Nutrition; Dr. Julie Lumeng, assistant research scientist, University of Michigan Center for Human Growth and Development; Dr. Michael Lu, professor of obstetrics and gynecology, David Geffen School of Medicine at UCLA; Dr. David Ludwig, professor of pediatrics, Harvard Medical School, and director of the obesity program at Children’s Hospital in Boston; Barry Popkin, director of the Obesity Center and professor of nutrition, School of Public Health, University of North Carolina at Chapel Hill; Susan Roberts, a senior scientist, Human Nutrition Research Center on Aging, Tufts University in Boston; Dr. Wendy Slusser, director of the UCLA Fit for Healthy Weight Program, Mattel Children’s Hospital UCLA; Angelo Tremblay, professor of social and preventive medicine, Laval University in Quebec.