As fall approaches, many students are preparing to return back to school, where they will encounter the challenges and everyday stressors of academic life. Along with those stressors comes plentiful access to comfort foods in campus cafeterias, with their meal plans and “all you care to eat” dining policies. Adhering to a healthy diet in such an environment can be a challenge as the specter of the dreaded “freshman 15” looms. But what exactly is a healthy diet, anyway?
There are few areas of science more controversial than the science of diet, exercise, and weight loss. Indeed, self-identified “experts” in diet and nutrition make specious yet highly scientific-sounding claims that back their firm recommendations about the best ways to diet and lose weight. Unfortunately, much of the public accepts these claims uncritically, failing to investigate any of the underlying evidence, which is usually sparse and unconvincing. The idea that dietary fat is fattening and should be “used sparingly” has become nothing less than a pop culture truism, something seemingly self-evident. However, the idea that dietary fat is the primary culprit in the U.S. obesity epidemic is a surprisingly recent invention.
C. Everett Koop, speaking in his capacity as Surgeon General, proclaimed in 1988 that the high-fat American diet represented a major public health crisis, going so far as to compare the risks associated with consuming a high-fat diet to those associated with smoking tobacco. In his introduction to the Surgeon General's Report on Nutrition and Health, he wrote that the “depth of the science base underlying its findings is even more impressive than that for tobacco and health in 1964, with animal and clinical evidence adding to the epidemiologic studies.”
Where exactly was all the evidence for such a strong claim? Double-blinded randomized controlled trials? Systematic reviews with extensive meta-analyses? Decades of case-controlled prospective studies? Could a U.S. Surgeon General really get the facts wrong?
Unfortunately, scientists and doctors rarely follow the excellent advice that serves as the motto of the oldest scientific academy in existence, the Royal Society, which is “nullius in verba,” Latin for “on the word of no one.” Instead, Koop, like the architects of the food pyramid with their recommendations of 6-11 servings of carbohydrate per day with fats used only sparingly, succumbed to a sort of scientific group-think. Koop and the food pyramid architects listened to self-proclaimed experts who had concluded that dietary fat was the culprit in the obesity and heart disease epidemic based on weak observational studies and animal studies with questionable designs and dubious relevance. The idea that dietary fat caused obesity sounded like it should be true, and many experts seemingly allowed the apparent logic of the claim to cloud their judgment of the evidence for it when assessing its validity.
The loudest voice proclaiming that dietary fat was the enemy in the obesity epidemic, and the man who influenced Koop and other policy makers during the 1970s and 1980s, was a nutritional science researcher named Ancel Keys. Keys rose to prominence during World War II, when he was in charge of the K-rations provided to GIs abroad. In the 1950s, Keys promulgated his theory that Americans were suffering from an epidemic of obesity, heart disease, and diabetes because they were consuming much more dietary fat than any humans ever had previously. Keys famously showed that the Western, high-fat diet correlated with elevated risks of heart disease, whereas the relatively low-fat Japanese diet correlated with reduced risk. Keys included four other countries in his assessment, and showed a strong correlation between dietary fat and incidence of heart disease. Though few people questioned the ideas Keys presented at the time, we now know that Keys was very far off-base.
Firstly, the “epidemic” of heart disease Keys had observed in the 1950s and 1960s was what is often called a “paper epidemic,” which refers to an epidemic that occurs only on paper as new cases of an already common disease are reported, usually because of increased surveillance or the development of more sensitive diagnostic tools. At the time Keys completed his studies in the mid-1950s and 1960s, Americans were living longer as infectious diseases and war claimed fewer lives, and age-related cases of heart disease were more readily diagnosed by improving clinical methods.
Secondly, there’s no real evidence that earlier diets were any leaner than the high-fat American diet of the 1950s and 1960s. In the 19th century, Americans got as just as many or more of their calories from meat and animal products.
Thirdly, and perhaps most damningly for Keys’s theory, the correlation Keys found between dietary fat consumption and heart disease rates was an artifact of sampling error; had Keys looked at data from a larger subset of countries, the correlation would have disappeared completely. Examples of cultures with high-fat diets and low risks of heart disease abound. For example, Eskimo cultures derive almost all of their calories from fat and animal products, and have low rates of heart disease, and the French, who consume diets famously high in fat (think Julia Child, of Julie & Julia fame), also suffer from relatively low rates of heart disease and obesity.
Of course, not all contemporary scientists were immediately swayed by Keys’s flawed studies. In 1957, the American Heart Association wisely proclaimed that the theory linking heart disease to dietary fat consumption failed to “stand up to critical examination.” Sadly, when Keys was appointed to the committee making the AHA’s recommendations only three years later, it entirely reversed itself, and a half-century of nutritional science ‘truthiness’ was born.
Fortunately, in the decades since the alarmingly off-base food pyramid guidelines were issued, many observational studies and “gold-standard” randomized, controlled trials of dietary fat reduction and heart disease risk have been performed. The current understanding of the association between heart disease risk and dietary fat consumption is, quite frankly, that the association does not exist.
The Cochrane Heart Group has published an Intervention Review on the matter, synthesizing the results of all randomized controlled trials that tested the hypothesis that dietary fat consumption produces heart disease. The plain-language summary of their findings is as follows (emphasis added):
“Modifying fat in our food (replacing some saturated (animal) fats with plant oils and unsaturated spreads) may reduce risk of heart and vascular disease, but it is not clear whether monounsaturated or polyunsaturated fats are more beneficial. There are no clear health benefits of replacing saturated fats with starchy foods (reducing the total amount of fat we eat). Heart and vascular disease includes heart attacks, angina, strokes, sudden cardiovascular death and the need for heart surgery. Modifying the fat we eat seems to protect us better if we adhere in doing so for at least two years. It is not clear whether people who are currently healthy benefit as much as those at increased risk of cardiovascular disease (people with hypertension, raised serum lipids or diabetes for example) and people who already have heart disease, but the suggestion is that they would all benefit to some extent.”
It would seem, then, that dietary fat has more or less been exonerated, after more than 50 years spent on death row. The question to be asked, then, is which dietary criminal remains at large? If not fat, what is causing the epidemic of obesity, diabetes, heart disease, stroke, and other metabolic diseases that currently plagues the United States?
Although the Cochrane group’s systematic review alludes to one potential culprit — certain types of saturated fats found in animal products — the evidence that these fats produce metabolic syndrome is very poor; instead, the evidence points more directly to these saturated fats acting something like accomplices once metabolic syndrome has already set in.
While a “smoking gun” has yet to be found for the obesity epidemic — for the most part because randomized controlled trials investigating hypothesized causative agents other than fat have largely yet to be conducted — there is suggestive evidence pointing to excessive consumption of carbohydrates, particularly simple sugar. Thus, in a severe case of irony, the nutritional recommendations that advised people to cut fat from their diets and encouraged them to consume more carbohydrates to compensate — think about those 6-11 servings of carbs sitting at the base of the food pyramid — may have actually exacerbated the obesity epidemic.
What evidence points to carbohydrates’ being particularly fattening? The evidence comes from two main lines of argument.
Firstly, carbohydrate consumption produces less of a satiety response than does fat consumption. Overeating carbohydrates and refined sugar displaces other, more nutritionally beneficial foods from our diet, such as vegetables, fruits, and meats. And, because refined carbohydrates aren’t as filling as the fats, proteins, and fibers they replace, they tend to be over-consumed, leading to a caloric imbalance and weight gain.
Secondly, it turns out consuming lots of carbohydrates has a negative effect on our bodies’ regulation of metabolism. The old adage that “a calorie is a calorie” no matter where it comes from isn’t quite right. Some calories are worse than others. So, not only do we have to worry about eating “empty carbs” that supply little nutritional value on their own, we might actually need to be thinking about “toxic carbs,” as childhood obesity researcher Robert Lustig would have it. Lustig demonizes fructose consumption in particular, describing the unique metabolic effects fructose has on the body; according to Lustig, eating large quantities of fructose, found in common sweeteners such as table sugar and high-fructose corn syrup, is incredibly fattening.
Lustig cites biochemical evidence for his claims, noting that concentrated fructose is readily converted into fat by the liver, where it can accumulate and lead to insulin resistance, a dangerous condition commonly recognized to be at the heart of the “metabolic syndrome” that is a major risk factor in obesity, cardiovascular disease, diabetes, and certain cancers.
To properly understand insulin resistance and metabolic syndrome, it’s necessary to understand how insulin is produced and the effects it has on various cells within our bodies.
Insulin is the central hormone produced by the body in response to the food that we eat (complex carbohydrate and simple sugars in particular). Insulin’s job in the body is to control how much glucose (the simple sugar carbohydrates are digested into) circulates in the blood stream. It functions like a passport, allowing glucose to cross the border into cells to do energetic work when it is present, and not allowing glucose in when it is absent.
In the syndrome known as insulin resistance, important cells of the body such as muscle cells no longer allow glucose to enter when insulin is present — it is just as if a border guard refused to accept a passport as valid. To compensate for the rising levels of glucose in the blood, the pancreas produces more and more insulin. While muscle cells continue to ignore this flood of insulin, the signal is picked up by the fat cells, which interpret high insulin concentrations and blood glucose levels as a message telling them to store the glucose as fat and lock up the fat they’ve already stored. Fat cells bathed in insulin never allow the calories they’ve stored to leave; they begin to function more like a roach motel and less like a savings account.
Thus, during insulin resistance, it becomes very difficult to burn fat. The body is in a metabolic state that makes it receptive only to storing calories, and not to burning them. Because the circulating glucose is difficult for the body to use, and because fat cells aren’t allowed to liberate their stored calories, the body is left feeling constantly hungry, almost is if it were starving, despite having just eaten a carbohydrate-rich meal. This paradoxical hunger causes an increasingly overweight individual to become tired and lethargic, while consuming more and more food.
Based on this line of thinking, we have the causal relationship between inactivity and obesity backwards — it isn’t that inactivity makes us obese, but rather that obesity, by means of insulin resistance, makes us inactive.
Although the initial events that cause insulin resistance are not entirely understood, one leading hypothesis is that excessive storage of fat in the liver — a byproduct of sugar (and fructose) metabolism — is to blame.
There is extensive evidence for such biochemical pathways as the metabolism of fructose being relevant in insulin resistance and obesity, much of which comes from animal models (particularly rats and mice). Many nutritional researchers are presently reproducing studies of fructose consumption and insulin resistance in humans to determine if these mechanisms are equally relevant for us.
Initial results have been mixed; one systematic review found that fructose consumption did not lead directly to increased blood triglyceride levels, which are a marker for metabolic syndrome. Thus, in humans, fructose may not be any worse than other sugars. Another study concluded that fructose consumption produces insulin insensitivity independently of an effect on blood triglyceride levels. However, as the authors of the systematic review stated, “Most of the available trials were small, short, and of poor quality.” Longer studies with larger numbers of subjects and more measures of a larger set of clinical outcomes are required.
While we wait for more controlled intervention studies to be performed in humans, it might be a good idea to lay off of the soft drinks, candies, and baked goods. Unlike with fat, there is no good case to be made for eating lots of “empty carbs”; the debate ranges from “the evidence isn’t strong enough to say that eating sugars and empty carbohydrates is any worse for you than another source of calories would be” (a common food industry position) to “sugar is definitely toxic and leads directly to insulin resistance and metabolic syndrome” (something you might hear from Robert Lustig or Gary Taubes).
Based on all the evidence currently available, it would seem that a reasonable diet includes fats (mostly unsaturated fats, though saturated fat consumption may not be harmful if you are in good cardiovascular health) and complex carbohydrates, while limiting consumption of simple sugars. Following such diet advice might in fact be one way to stave off the freshman 15.
Editorial Note: The PhDish does not provide medical advice; you should discuss any diet or exercise program that you are considering with your doctor before making changes.