TCS Daily

The Skinny on Fat

By Sandy Szwarc - July 16, 2003 12:00 AM

A host of sinful foods have been demonized as the root of obesity and poor health of American adults and children. Fast food restaurants have been sued, accused of contributing to customers' obesity because their food tastes too good and they tempt us by advertising. Taxes are being proposed on foods deemed fattening or bad for us, namely, anything with meat or fat, that is fried or processed or that is sweet.

The Truth About Obesity
The Skinny on Fat
The Diet Problem
Dying to Be Thin
The War on Fat's Casualties
To Your Health
Where's the Epidemic?
To Do List
A Simple Plan
Mikey Doesn't Like It
Although these foods make intuitively appealing (and profitable) targets, the body of scientific evidence doesn't support the assertions. There is no scientific evidence that any specific food causes obesity. Like the American Dietetic Association (ADA), the American Council on Science and Health's (ACSH) position is: "There are no good foods or bad foods. The problem is not any one food, but one of dietary immoderation, imbalance and lack of variety." That's true for children as well as adults. The American Heart Association (AHA) Medical Scientific Statement, "Understanding Obesity in Youth," concluded, "Studies of diet composition in children do not identify the cause of obesity."

Let's consider the evidence about the supposedly most sinful culprits:

Sugar Too Sweet?

Sugar is frequently cited as a source of empty calories, but a U.S. Department of Agriculture (USDA) study published in the February 2001 Journal of the American College of Nutrition (JACN) found little difference in the quality of diets among those eating more or less added sugars.

"Sugar is not inherently a dietary villain," said David Klurfeld, Ph.D., professor and chairman of the Department of Nutrition and Food Science at Wayne State University, editor-in-chief of the JACN and Nutrition New Focus and scientific expert with the International Food Information Council. "The statistical relationships of sugar intake with the rest of the diet are small and probably not biologically meaningful."

A study in the September 2000 issue of the American Journal of Clinical Nutrition actually found sugar in the morning resulted in better mental performance in children and adults. Research has repeatedly demonstrated that sugar and the next culprit, sodas, do not cause diabetes, hyperactivity, addiction, tooth decay, bad bones, chronic diseases, or obesity.

Soda Pop Slop

Sodas have been made scapegoats, especially denied school children, without clinical evidence that they are to blame for obesity. The ADA stated in January 2002, "There is no nutritional reason why soft drinks ... and juices should not be made available to students. All these beverages, consumed in moderation, fall within the Dietary Guidelines established by the USDA and ADA."

Studies this year analyzing the National Health and Nutrition Examination Survey (NHANES III) by the U.S. Department of Health and Human Services (HHS) and the USDA's Continuing Survey of Food Intake by Individuals found no relationship between consumption of soft drinks and the overall quality of diets or the BMIs in adolescents. In fact, teen boys who drank the most carbonated beverages also exercised the most, and the thinnest kids tended to be the biggest pop drinkers.

"As long as young children or teens consume a well-balanced, healthful diet, moderate consumption of soda does not threaten their health or nutritional well being," said ACSH President Elizabeth Whelan, Sc.D., M.P.H. "Too much of anything -- even a food as innocuous as apple juice -- can compromise nutritional status."

Fat and 'Junk' Food Bunk

Throughout the war on fat, the low-fat message has been most taken to heart. Shunning dietary fat seems to make sense, in a simplistic sort of way: fat makes you fat.

Except the data simply doesn't support the link. As total fat consumption among American adults dropped from 1965, obesity rates soared.

In children, the evidence is absent, as well. Cara Ebbeling, Ph.D., and colleagues at the Division of Endocrinology at Children's Hospital Boston questioned the relationship between dietary fat and fatness in the Aug. 10, 2002, issue of Lancet, noting: "Findings of epidemiological studies do not consistently show an association between dietary fat and adiposity in children and young adults."

The science also doesn't conclusively support low-fat eating as being healthful for most people, as Gary Taubes' extensive thesis in Science magazine on March 30, 2001, documented. One example among a significant body of evidence against eating low fat is the clinical trials led by Laura A. Corr, M.D., Ph.D., published in European Heart Journal in 1997. Researchers found "little support for such [low-fat] recommendations and it may be that far more valuable messages for the dietary and non-dietary prevention of coronary heart disease are getting lost in the immoderate support of the low-fat diet." In the conclusions, Dr. Corr wrote: "Dietary advice to reduce saturated fat and cholesterol intake, even combined with intervention to reduce other risk factors, appears to be relatively ineffective for the primary prevention of coronary heart disease and has not been shown to reduce mortality."

A study in the April 1997 American Journal of Clinical Nutrition by Dr. Jorgen Jeppesen and colleagues at the Stanford University School of Medicine demonstrated that low-fat diets in adult women were actually unhealthful, as they raised triglycerides, lowered good HDL-cholesterol, and worsened insulin resistance. Dr. Ronald Krauss, head of the AHA Nutrition Committee, admitted studies have found that for two-thirds of consumers low-fat diets increased the risk of heart disease or didn't help them. Since establishing their 2000 Dietary Guidelines, the AHA has recommended diets moderate in fat intake for healthy Americans.

For children, there is evidence that restricting fat before age five could be dangerous, while there's little evidence it may be beneficial, said Bruce Watkins, Ph.D., professor of Lipid Chemistry and Metabolism at Purdue University.

In a 1998 scientific review of all available information, researchers at Purdue concluded that dietary recommendations for adults had been inappropriately applied to children, who have different physiological and growth needs. Not only can low-fat diets retard growth and development, they said, but they may actually stimulate the enzyme that synthesizes cholesterol, which appears to be normally suppressed by high-fat diets. The American Academy of Pediatrics recommends 30 to 40 percent of calories in a normal child's diet should come from fat and there be no restriction in dietary fats before the age of two.

"During the past 30 years, avoiding dietary fat has been the mantra for most of the public and many scientists," Klurfeld, in a July 15, 2001, Nutrition News Focus, said. "However, a significant number of disbelievers among researchers were ignored by the media and their peers."

It's becoming clearer that data simply doesn't link fat intake with a major impact on heart disease, most types of cancer, or weight. The 2001 findings of the Nutrition Committee of the AHA's Scientific Conference on Dietary Fatty Acids and Cardiovascular Health recognized the changing science and the need for increased understanding of how fatty acids affect health.

But wait, diet evangelists such as Marion Nestle and Michael Jacobson tell us, all the bad things in fast foods and growing restaurant portion sizes are undeniably to blame -- it's "intuitively obvious." Despite such pervasive clamors of a potential cause, Ebbeling concluded, there's no clinical evidence that either fast-food content or portion sizes cause obesity. "There is little research into the effects of portion size on food intake," she reported. In fact, a clinical study found younger children ate the same amount irrespective of portion size, and that didn't change until children were older and into the age group already seeing obesity and diabetes. Likewise, "there are no data on fast food and obesity in children."

The Stealth Fat

Concerning the latest demon fat in the news, Klurfeld wrote in a July 2, 1999, Nutrition News Focus that scientists still don't agree on how bad trans fatty acids actually are and the associations for them being harmful are weak. The Nurses Health Study of 90,000 nurses over 20 years, he cited as an example, has failed to find a link between trans fats or any other dietary fats and heart disease. A study on butter versus margarine published in the Dec. 6, 2000, Journal of the American Medical Association (JAMA), showed that moderate intake of trans fat is not harmful, according to Dr. Klurfeld.

A critical examination of the scientific evidence on trans fats was done by Steven Milloy, adjunct scholar at Cato Institute and publisher of, who concurred in a May 16, 2003, column for Fox News: "None of eight human population studies comes close to linking trans fat with heart disease... [merely that it] temporarily increased cholesterol levels," Milloy wrote. Even trans fatty acids aren't all the same; some are natural in milk and appear to have no detrimental health effects and may be actually healthful, according to a study in the March 10, 2001, issue of Lancet.

Yet, the growing publicity to ban this "stealth fat hiding in our foods" has made even an Oreo cookie out to be deadly. "In part to a citizen petition from the Center for Science in the Public Interest (CSPI) on Feb 14, 1994" and the subsequent 1,720 letters it received, the FDA issued a ruling on the labeling of trans fats on July 9, 2003. Their review of the scientific evidence concluded that consumption of trans fatty acids increased LDL-cholesterol, a heart disease risk factor, like saturated fats, and advised "consumers choose foods low in both saturated and trans fats as part of a healthful diet."

But the FDA specifically stated that trans fats need not be eliminated from the diet. And it's noteworthy that deep in the 260-page ruling, the agency noted: "[I]nformation on trans fat content in foods is limited ... information on trans fat intake is limited, ... but average saturated fat intake in the United States is about 5 times greater than average trans fat intake ... and the rate of heart disease mortality and morbidity in the United States has been decreasing for several decades."

Good Fats, Bad Fats?

Marking fatty foods for punitive measures doesn't stand up to an evidence-based approach to public health policy. Not all fats are bad, nor is any particular type of fat all bad. In fact, eating a variety in moderation offers healthful benefits, beyond supplying essential fatty acids.

A type of polyunsaturated fatty acid, omega-3s found mostly in fish, for example, appears to help our immune system, promotes eye health, and reduces our risk of heart disease and strokes by decreasing blood clotting and lowering triglyceride levels.

Even naughty saturated fats, shunned by some low-fat diet proponents for raising bad LDL-cholesterol levels, also raise the good HDL-cholesterol, leaving other nutrition experts to claim it a wash. About one-third of the saturated fatty acids we consume are stearic acid, found mainly in red meat and cocoa butter, which acts like favored monounsaturated fats (in nuts, avocados and olive oil) in lowering bad LDL-cholesterol levels while raising the good HDL-cholesterol.

The fact is that any diet -- be it low-fat to high-carb -- that restricts or eliminates certain foods is more likely to be unhealthful. A study of more than 14,000 American children and adults by the University of Nevada published in the Journal of the American Dietetic Association this past May found those eating a variety of high-fat and low-fat foods had healthier diets -- higher in vitamins, calcium, fiber, iron, zinc and other minerals -- than those eating low-fat diets.

"All foods fit into a healthful eating plan," Connie Diekman, a registered dietician with the ADA, has said. "People don't have to feel guilty about eating their favorite foods, so long as they are eating a balance of foods as well as getting regular physical activity."

So, if no one food or group of foods is the real culprit in the obesity epidemic, what is?

The Truth is in Ourselves

Most Americans scoff at the notion of a genetic component to obesity, thinking fat people can overcome their genes. But it's much more significant and involved than most realize.

The breadth of our individual differences is seen in all our physical attributes, not just skin and eye color, but also our body shape and size. The estimates on the degree of inheritability of weight are at least as strong as that of height. Like height, genes are more significant in the expression of the attribute than environment, but cannot be separated from it. Estimates of the inheritability of height from studies of different populations have ranged from 56 to 80 percent, varying by researcher and study design. By comparison, M. Borjeson's famous 1976 twin studies in Scandinavia estimated the inheritability of obesity to be 88 percent. Subsequent studies, and reviews of all existing family and twin studies done by researchers at the Virginia Institute of Psychiatric and Behavioral Genetics in Richmond, Va., have consistently shown genes responsible for 50 to 90 percent of our adiposity (fatness).

The genetic reality is that some of us have bodies that are naturally plumper than others. Such individuals are genetically designed to hold onto fat no matter how much they starve themselves. Much like Archie Andrew's comic pal, Jughead, others can eat everything in sight, never move from the couch, and never gain a pound.

In a range of studies using different methodologies, people living in similar environments and gorging on the same excessive high-calorie diet often weigh radically differently. Some individuals plump up quickly, while others remain gangly, and everything in between. That variability was dramatically demonstrated in the classic 1970s prison study, published in Clinics in Endocrinology and Metabolism, where volunteers tried to gain weight, but some couldn't no matter how much they ate, including one inmate who was eating almost 10,000 calories a day. Meanwhile, identical twins, whether raised separate or together and no matter what they eat, won't ever significantly differ in weight.

Our genetic differences regarding weight are evident at birth. In studies of children by Michael Loewy, Ph.D., those with fat parents have 10 percent lower metabolic rates than do children of non-obese parents, and the rates are 20 percent lower during infancy.

But Robert Olsen, M.D., Ph.D., professor emeritus of Medicine at State University of New York (SUNY)-Stony Brook noted that the dissimilarities go far beyond metabolism. "Individuals with strong genetic traits for obesity have a different pattern of fat deposition or mobilization" than others, he wrote in Health Priority. Multiple researchers have found they convert glucose and other energy sources to body fat more efficiently, their muscles burn fat less readily, their fat cells more readily multiply, and genetic insulin resistance is seen in their skeletal muscles unrelated to their body weight or pancreatic defects.

Other physiological differences stacked against the obese, noted by doctors at the University of California at Davis, included hormonal changes and changes at sites in the brain that control satiety -- the sense of feeling full -- particularly in the hypothalamus.

Although the genetic link to obesity is obvious, the exact relationship between genes and the susceptibility to gain weight isn't straightforward, states the Centers for Disease Control's (CDC) Office of Genomics and Disease Prevention. Several studies have noted the genetic elements are seldom traced back to a single gene. In fact, the interaction of multiple genes appear to contribute to obesity, wrote Timothy Aitman, M.D., Ph.D. in the May 22, 2003, New England Journal of Medicine. And, these genes and alliances have proven very hard to identify.

The number of genes, markers and chromosomal regions that have been linked or associated with human obesity is now well above 200, Dr. Miina Ohman at the Departments of Molecular Medicine and Medical Genetics at the University of Helsinki, Finland, has reported. But the human obesity gene map is continually being expanded, with updates in Obesity Research. Genetic obesity research is still in its infancy, advancing vigorously just since the 1994 discovery of leptin, a hormone that diminished with certain genetic mutations and was thought to potentially trigger obesity.

Genes or the Environment?

Of course, neither genes alone nor the environment alone may explain the surge in obesity. But their interactions might.

We hear a lot about a "toxic environment" from trial lawyers and those fighting the war on obesity. Their definition: the too ready abundance and convenience of tasty fattening foods and workplaces, schools and neighborhoods that discourage activity. But the real toxic environment may be the very thing these advocates are promoting: dieting.

In the August 2000 issue of Journal of Lipid Research, researchers from Israel, London, and Seattle summarized a number of studies that found "some genes are 'switched on' in response to specific environmental factors and remain continuously active." And these genes may not manifest themselves until years later or even subsequent generations.

A gene currently receiving researchers' attention for its role in obesity is one that codes for lipoprotein lipase, an enzyme produced in fat cells that encourages the body to collect fat and move it into cells for storage. It's also the major enzyme that raises LDL-cholesterol, triglycerides, and lowers HDL-cholesterol. A 1997 meta-analysis of 14 studies, representing 15,000 subjects, in the International Journal of Clinical Laboratory Research not surprisingly linked activation of this gene with heart disease risk. Lipogenic enzymes are potential targets for new research and the future development of some extremely profitable drug therapies for obesity.

Of particular note to individuals considering going on a diet or those promoting them, this gene appears to be activated by -- dieting. Researchers from Cedars-Sinai Medical Center, Los Angeles, in an April 12, 1990, New England Journal of Medicine study found that lipase levels rose 25 times normal in fat people and stayed elevated for 6 months, long after they'd stopped dieting. This activation is believed to be a reason why those who have dieted gain weight more easily than those who haven't and then have a harder time losing weight again, as the FDA's "Guide to Dieting" published in FDA Consumer, reported in 1991.

Most diet enthusiasts would be shocked at the idea that dieting can actually cause genetic changes or trigger certain genes to make some of us fatter and endanger our health. But, this knowledge could help explain rising body weights seen during our recent diet-obsessed decades, despite lowered calorie and fat intake and unchanged physical activity levels. Those naturally plump aren't necessarily unhealthy, but compelling them to diet appears to contribute to their health risks.

Even more frightening, is the growing body of evidence of genetic changes before birth and in early infancy contributing to childhood obesity and diabetes; as well as to adult obesity and chronic weight-associated diseases. "The implications of these findings are formidable," Ebbeling said. According to her, the complex interactions of genes in fat building "indicate that environmental and perhaps perinatal factors must underlie the childhood obesity epidemic."

Since it's evident the real culprits in the obesity epidemic aren't "unhealthy" foods or portions, why are the diet and health food industries, government policy-makers, advocacy groups, and healthcare institutions all blaming food? Why, in the face of a ponderous body of evidence to the contrary do they continue to spread fear about "bad" foods and the dangers of obesity, while espousing thinness, dieting and weight loss?

Those at the forefront of this war on obesity -- Marion Nestle, John F. Banzhaf III, Anthony Robbins, Kelly Brownell, Michael F. Jacobson, William H. Dietz, and others -- have even created a new coalition to fight obesity using legislation and litigation against food companies. Increasingly this battle appears more about politics and profits, than philanthropy. Considering how unscientific pontifications can wrongly identify the causes of obesity and promote remedies that threaten the health and welfare of consumers, maybe its time for the facts to take precedence before allowing those with the most money, media presence or political correctness to do more harm.

Coming Friday: The missing link to obesity, or how the diet industry makes people fat.

© 2003 Sandy Szwarc. All rights reserved.

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