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Unintended Consequences, Special Interests, and Our Problem with Sugar

Forty years ago this month, January 1977, the federal government entered the business of giving dietary advice, first with a Congressional report released by George McGovern’s bipartisan Select Committee on Hunger and Human Needs, which in turn prompted the first Dietary Guidelines from the U.S. Department of Agriculture.

With the perfect acuity of hindsight, two stories from those initiatives bear recalling. The first involves McGovern’s report, Dietary Goals for Americans, which was primarily controversial for its recommendation that Americans should reduce the fat content of their diets and compensate with more carbohydrates. After releasing the report, McGovern’s committee held a series of hearings to deal with the backlash, both from scientists and industry. While McGovern, his colleagues, and their committee staff may have all hoped the guidelines would lead to a nation eating, perhaps, as Michael Pollan would later memorably put it, (whole) food, “mostly plants and not too much,” that would not be the case. Hence story number one is about the dangers of unintended consequences.  

The Committee’s staff director later told me a story of how he got an inkling of what would eventually happen. As he recalled it, an economist pulled him aside after one of the hearings and gave him a lesson on market disincentives to healthy eating: ”He said if you create a new market with a brand-new manufactured food, give it a brand-new fancy name, put a big advertising budget behind it, you can have a market all to yourself and force your competitors to catch up. You can’t do that with fruits and vegetables. It’s harder to differentiate an apple from an apple.”

And this is indeed what happened. Supermarkets became full of low-fat food products—“foodlike substances,” to borrow again from Pollan—all with implicit or explicit health claims that they would lower cholesterol and bestow a longer and healthier life. Many of these products replaced fat with some variant of the 50-50 combination of glucose and fructose that makes up what we think of as sugar—most notably, high fructose corn syrup, which had just recently entered the food supply. While this transition was occurring, our nation and the world also experienced unprecedented increases in the prevalence of obesity and diabetes, raising the question of whether these two phenomena are causally related.

This brings us to story number two. McGovern’s Dietary Goals prompted Carol Foreman, an assistant secretary of agriculture appointed by President Jimmy Carter, to begin the process of codifying the goals as official government policy. As Foreman later told me, she was aware of scientific controversy on the nature of a healthy diet, but she believed that sufficient consensus existed to provide at least provisional recommendations. “Tell us what you know and tell us it’s not the final answer,” Foreman says would tell nutrition researchers at the time; “tell [us] what your best sense of the data is right now.”

The “best sense of the data,” however, will always depend on who is asked. And therein lies what may be the second problem with the last forty years of dietary guidance in the United States: The existence of a controversy in science implies that uncertainty exists about whether the consensus is correct. Clearly in the 1970s, the majority opinion among nutrition authorities was that dietary fat, particularly saturated fat, caused heart disease, and so probably diabetes and obesity as well. The three disorders are highly associated, suggesting a common cause. Since then, the dietary fat hypothesis has repeatedly failed confirmation in clinical trials, but the strong suspicion remains that fat consumption should be limited; it’s still a foundational assumption about the nature of a healthy diet, if not among public health authorities then among the public whose diet they have been trying to hard to influence.

Another unintended consequence emerged from the official embrace of the dietary fat consensus in the 1970s, however, and this may have had far more profoundly damaging implications. The dietary fat consensus negated the viability of a competing hypothesis that highly processed carbohydrates, and particularly sugars, are the macronutrients to worry about in the American diet. By this thinking, the modern diet damages our health not through cholesterol-related mechanisms (or the presence or absence of vitamins and minerals) but through disruptions of insulin signaling, in which diabetes and so premature death is the end state. Coronary heart disease is a consequence as well.

This hypothesis was actively studied and debated through the mid-1970s, but  then  it was disassociated from the likely causal link that pointed back to refined carbohydrates and sugar. This disassociation was a casualty of the consensus building of the 1970s, aided and abetted by the sugar industry itself, which was the party with the most to lose in the controversy.

The sugar industry worked diligently beginning in the mid-1960s to help shape the anti-fat consensus and assure that sugar was never perceived as anything more than a source of excess, if empty, calories. As influential nutritionists began to argue in the United States (Jean Mayer at the Harvard School of Public Health) and in the United Kingdom (John Yudkin, founder of the first dedicated nutrition department in Europe) that sugar was a very likely cause of heart disease and diabetes, they were in direct conflict with the great majority who believed fat was the problem. The sugar industry used that conflict to its advantage. It launched a methodical public relations campaign with the goal of assuring that no “confirmed scientific evidence link[ed] sugar” to chronic disease. To do so, it recruited and compensated influential researchers in the anti-fat camp (from Harvard, the University of Minnesota, the University of Washington, and elsewhere) to publish authoritative reviews and a 90-page journal supplement, Sugar in the Diet of Man, that reinforced the message that dietary fat was the problem and sugar was not. These documents played a pivotal role in the FDA’s 1976 preliminary assessment that sugar should retain its status as Generally Recognized as Safe (GRAS). And that decision, along with sugar-industry-funded research and industry-funded researchers, then played the critical role in forming the consensus that sugar was benign.

The first USDA Dietary Guidelines, released in 1980, cautioned against consuming “too much” sugar—a tautological statement that could apply to any food. They also stated that “too much sugar does not seem to cause diabetes,” acknowledging the possibility and some controversy. In 1985, the second edition of the Guidelines dropped the conditional and proclaimed unambiguously “too much sugar in your diet does not cause diabetes.” Worth noting is that much of the relevant research done on this question between 1980 and 1985 was carried out at the USDA’s own Carbohydrate Nutrition Laboratory, and the researchers involved vehemently disagreed with this conclusion. By then, though, researchers studying the question of sugar and health were already tarred with the perception of having crossed the line from legitimate science to quackery.

In 1986, the FDA officially concluded that sugar should retain its GRAS status on the basis that “no conclusive evidence demonstrates a hazard to the general public when sugars are consumed at the levels that are now current.” Seminal government reports that followed – from the Surgeon General’s Office (1988), the National Academy of Sciences (1989) and the British Committee on the Medical Aspects of Food Policy (1989) – all echoed this thinking. Dietary fat is a killer; sugar is a benign source of empty calories. To come to the latter conclusion, though, required that the authors of these reports equate “no conclusive evidence” with no evidence at all.  

By doing so, they successfully transformed a consensus of opinion into dogma. Among the consequences may have been the worldwide epidemics of obesity and diabetes. Had the nutrition research community and the public health authorities in the 1970s and 1980s understood that scientific controversy can only be resolved by careful experiment, not the assignment of truth to a consensus, then both our medical and public health approaches to obesity and diabetes might have had some effect. We cannot say. Should they understand it now, as I would hope to be the case, we’re still looking at perhaps 20 years of concerted research before definitive answers can be obtained. As such, we’re still in the position of the USDA in the late 1970s, having to act on incomplete and uncertain information, and still left having to make difficult decisions about who has the best sense of the data.    

At the core of this kind of nutrition controversy is a fundamental philosophical conflict between the requirements of an effective public health policy and the requirements of science. The belief that imminent action must be taken, that it would in fact be irresponsible not to act, may be incompatible with the institutionalized skepticism and rigor required to establish reliable knowledge. The urgency required to prevent imminent deaths can mean that public health authorities do not have the time to gather what they would often describe to me in my research as “definitive scientific evidence,” sometimes perceived naively as dotting the i’s and crossing the t’s.

Good scientists will argue that the absence of definitive scientific evidence means that the truth remains unknown and, therefore, so does any clearly beneficial path of action, one with minimal and acceptable risks. Science is about acknowledging uncertainty. Effective public health policy requires that the public be convinced to change their behavior for their own good, which requires that we believe such a change is based on the strongest possible evidence. These perspectives may be right in their particular fields of application, but they can also be mutually exclusive. In 1999, when I first began investigating these controversies for the journal Science, the then director of the NIH’s office of disease prevention, William Harlan, captured the conflict this way: “We’re all being pushed by people who say, ‘Give me the answer. Is it or isn’t it?’ They don’t want the answer after we finish a study in five years. They want it now. No equivocation …  [And so] we constantly get pushed into positions we may not want to be in and cannot justify scientifically.” A former director of the Center for Food Safety and Applied Nutrition at the FDA put it even more simply: “science,” he said, “is a destabilizing force in public policy.”

While the obesity and diabetes epidemics have finally motivated authorities, most notably the WHO, to advocate limited consumption of sugary beverages,­ they still do so based on the thinking that the sugar in these beverages provides only empty calories consumed in excess. As such, we’re back to the USDA’s admonishment from 1980: Avoid “too much sugar” and all will be well enough.

The minority opinion is much the same as it was forty years ago: sugar is far worse than a benign source of empty calories. It’s a toxin, albeit not a quick-acting toxin, but one that does its damage over years and decades. It may be the primary cause of diabetes, independent of its calories, and perhaps of obesity as well. If we didn’t consume sugar, by this thinking, both obesity and diabetes would be relatively rare conditions, just as lung cancer would be in the absence of cigarettes.

Another fact that has to be considered when institutions transform a consensus into a dogma is that reliable science not only should move slowly, but inevitably it does. The notion that sugar is a toxin is based on a scientific understanding that was evolving from the 1960s onward. It did so without the attention given to the also evolving research on dietary fat, cholesterol, and heart diseases. When the FDA, USDA, and other organizations embraced the dietary fat consensus, this research and its implications was still virtually unknown to those involved. Its transition to reliable textbook science only began afterward.  Only with the full awareness of the obesity epidemic that emerged in the late 1990s have the broader public health implications of this research come to be partially embraced, but by then these new implications had to be reconciled with the assumption that dietary fat is the real problem.

The sugar hypothesis is based on the fact that the fructose component of sugar (and high fructose corn syrup) is metabolized primarily in the liver, resulting in a chain of effects that is speculative but still compelling: first the liver converts the fructose into fat, and that fat accumulates in liver cells (hence a condition, now also epidemic, known as non-alcoholic fatty liver disease). This in turn results in a condition called insulin resistance, which is the fundamental defect in type 2 diabetes. And that insulin resistance is accompanied by a cluster of metabolic abnormalities (high blood pressure, low HDL cholesterol, glucose intolerance) that is now known as metabolic syndrome. It can be thought of as a pre-diabetic condition and is so strongly associated with obesity that it may play a causal role there as well. (The first symptom that a physician is instructed to look for in diagnosing metabolic syndrome is increasing central adiposity – i.e., the patient is getting fatter) The CDC estimates that 75 million Americans have metabolic syndrome. Insulin resistance and metabolic syndromes are powerful predictors of heart disease. So the assumption is that what causes one, causes all. Most authorities believe that metabolic syndrome, like obesity, is caused by excess calories – eating too much and sedentary behavior. Experiments in both animals and humans suggest that sugar-rich diets should be at least a prime suspect.

If sugar consumption does cause insulin resistance and metabolic syndrome, then the dietary prescriptions of the past forty years are tragically incorrect. The question is what we can do about it now, when the evidence is still ambiguous and when the sugar-is-toxic camp is still very much a minority. The research necessary to nail it down would take years to decades to complete and is not even on the radar screen of the funding agencies.

Once again we’re in the position of having to take action based on uncertain evidence amid what is now a public health crisis. The twin epidemics of obesity and diabetes worldwide are a “slow-motion disaster,” in the words of Margaret Chan, director general of the World Health Organization. Chan gave a keynote address at an October meeting of the National Academy of Medicine and predicted with virtual certainty that the situation would continue getting worse for the foreseeable future.

Whatever actions we take, though, are like to have unintended consequences. One of them is further ingraining the precedent for taking other actions that are likely to be wrong and damaging as well. Clearly rigorous research is necessary to clarify the inherent uncertainty in the nature of a healthy diet and specifically the role of sugar in human health and disease. We have to know beyond reasonable doubt the dietary triggers of obesity and diabetes. If sugar plays a unique role, then we have to act. But that research will take time and a concerted effort that is not even on the radar screen of the National Institutes of Health. If that research is guided by the same influential authorities who have overseen the last forty years of dietary guidance and the epidemics of obesity and diabetes coincident with them, and if that thinking is indeed wrong, further errors are likely to be propagated.

If this were any other crisis, if this were any other public health failure,  we would be assembling task forces of unbiased, independent researchers, perhaps from outside the field if necessary, to rigorously assess the evidence, determine what errors have indeed been made, and decide what to do next.  It’s the only solution I can see to an intractable problem.

Also from This Issue

Response Essays

  • Americans Eat Too Much Cake, but the Government Isn’t To Blame by Stephan Guyenet

    Stephan Guyenet says Americans can’t blame government nutrition advice for their overconsumption of sugar. Dietary guidelines issued in 1980 didn’t recommend substituting sugars for fats; they recommended decreasing consumption of both. Americans, however, started eating more sugar anyway. Nor is it clear that sugar is to blame for obesity, because American sugar consumption peaked in 1999 and has declined ever since. Meanwhile, obesity has continued on a steady upward trend. Sugar is one part of a larger picture that explains American obesity, diabetes, and heart disease; it is not the sole culprit.

  • Unintended Consequences, Special Interests, Sugar, and a View from the Clinical Trenches by Yoni Freedhoff

    Yoni Freedhoff says that the public policy debate about nutrition would benefit from a practical, clinical perspective. American’s eating habits have changed a lot since 1977, and while sugar is a part of that change, it’s only one part among many. Americans eat more meals outside the home. They eat more pre-packaged ready-to-eat meals. They eat larger portions. And they eat many more calories altogether. The case against fat in the 1970s and 1980s was certainly flawed, but those flaws can’t be blamed for Americans’ poor dietary choices in the meantime, and, what’s worse, today’s critics of sugar may be replicating some of the same mistakes.

  • Putting Nutrition Claims to the Test by Terence Kealey

    Terence Kealey praises Gary Taubes for being willing to submit his nutritional theories to empirical testing. Rather than trading on influence and suspicion, Taubes has articulated a hypothesis, namely that sugar is to blame for metabolic syndrome, and he has called for further research in the area: not panic, not grandstanding, but the same sort of testing that brought us to become skeptical of earlier conclusions that have now been rejected. If the sugar hypothesis is correct, it will stand the testing. If not, it deserves to be rejected. Public health and government guidelines should wait and see, and follow the research.