The Low-Fat Myth
How the sugar lobby made America obese
An Addendum to Michael Pollan’s “Nutritionsim Defined” Essay
In “Nutritionism Defined” by Michael Pollan, Pollan produces the argument that “nutritionism” and nutritional science are two separate entities. Nutritionism, according to Pollan is an ideology that emphasizes “quantifying the nutrients contained in foods” (492) — that is to say, exercising scientific reductionism that “encourages us to take a simple mechanistic view” (Pollan 496) of nutrition such that all qualitative aspects are removed in favor of a blandly transactional and often incomplete approach. Pollan further cements this premise by pointing out the many times scientists were wrong about nutrition in the past, citing the different evolutions that nutritional science has gone through, each time having left scientists more convinced that their understanding was surely complete that time (scientists do not actually think like this). Yes, the reduction of food to its summary parts, in an effort to make sweeping generalizations, is in fact problematic. As Marion Nestle, a New York University nutritionist, puts it, this practice “takes the nutrient out of the context of the food, the food out of the context of the diet, and the diet out of the context of the lifestyle.” (Pollan 495). And Pollan’s overarching thesis regarding the proliferation of “bad science” (495) is mostly correct. However, it is incomplete for three reasons. First, because he understates the influence corporations have historically had and continues to have on academia alongside the corresponding journalism that selects which parts of it to publish, and secondly because he takes a dismissive, almost callous stance towards nutritional science. While the validity of looking in hindsight at the ever-sprawling tree of science as evidence for future inevitable incomplete understandings is arguably fallible, there is one nutrient, if you can call it that, that is still impervious to this retrospective logic: sugar. Thus, culminating in Pollan’s third critical omission and or mischaracterization; the well-established danger of sugar, specifically refined sugars (in all its 56 purposefully deceptive forms, see healthline.com below) and carbohydrates and the role they play in the undue demonization of fats.
Demonizing Fats Was the Prelude
To understand how things got so bad as Pollan iterates, one must look at the corporate influence that has loomed over nutritional science for the last century. Pollan touches on this with his mention of imitation foods not having to be listed as such starting in the 1970s — undoubtedly carried out because of continued pressure from the food industry. Ten companies control the entire world’s food supply and with a highly consolidated food conglomerate, regulatory capture and academic capture to a degree become not just more trouble-free but expected. Throughout the 1960s the sugar industry heavily funded research that highlighted hazards of fat while minimizing the hazards of sugars (Kearns, et al.) (NPR.org). For every expert Pollan says got it wrong last century it is possible to produce a scientist who was in fact right but often underfunded or suppressed. Pollan acknowledges that fats in fact are not the boogeyman they are propped up as and correctly asserts that not all fats are created equal but fails to mention the correspondent nature that sugar and refined carbohydrates play in the demonization of fats in the Western diet. Although Pollan assigns the label of ‘bad science’ to all thinking that unduly isolates nutrients, he himself is guilty of this practice because he isolates the components of the sugar-fat relationship.
Much of the entire anti-fat and subsequent pro-sugar craze began, however, with one man, Ancel Keys. In the late 1950s, Keys began work on a multi-national longitudinal epidemiological study — the same type of study Pollan is understandably skeptical of — which sought to find a correlation between fat consumption and elevated cholesterol levels as well as heart disease. This is known as the diet-heart hypothesis (note: this was never proven true). His famous study, the Seven Countries Study plotted seven countries — the U.S, Canada, Australia, England/Wales (which were concatenated into a single datum, virtually making the study a six-country study), Japan, and Italy’s total fat percentage of diet consumption against coronary heart disease (CHD) death rates.
The data when graphed showed a strong correlation between the two variables. The problem with this oversimplification is that data existed for twenty-two countries in total, which, when plotted on the same graph provides a smorgasbord of data points with no discernible relationship. Whether or not Keys purposefully omitted most of the data is unknown. Nevertheless, he rushed to have his ideas accepted by the United States Department of Agriculture (USDA), American Medical Association (AMA), American Heart Association (AHA), and American Diabetes Association (ADA) and was successful in doing so. Dr. George Mann, one of the doctors who worked on the Framingham heart study, initially worked to bolster Keys’ diet-heart hypothesis, but later admitted that, during the 1950s and 60s, “[t]o be a dissenter was to be unfunded because the peer-review system rewards conformity and excludes criticism.” (Mann 645).
It is no secret among the scientific community that Keys’ hypothesis is flawed. Pollan even notes the fact that construing saturated fats as the enemy was misguided, stating that
Like most of us, they [diet-heart researchers] assumed that a bad outcome like heart disease must have a bad cause, like saturated fat or cholesterol . . . Of course thanks to the low-fat-diet fad (inspired by the same reductionist hypothesis about fat), it is entirely possible to slash your intake of saturated fat without greatly reducing your consumption of animal protein. . . Unfortunately, the focus on nutrients didn’t tell us much about foods
(Emphasis in original) (Pollan 498)
Here in the essay is a prime opportunity for Pollan to mention the work of scientists who did get it right. Writing in The American Journal of Clinical Nutrition in 1971, for instance, Charlotte Young and Sonia Scanlan found fat-loss to be inversely related to the carbohydrate level in the diet. The study also found the low-carbohydrate diets tested were more effective in controlling hunger and ultimately concluded a low-carbohydrate diet to be “most suitable for long-term use” (Young, et al.). There is also the work of John Yudkin who in 1972 aptly warned of the dangers of rising sugar consumption in the American diet and its effects, issuing possible causations for obesity, diabetes, liver disease, gout, and more in his book Pure, White, and Deadly — all of which have now been shown to be true.
Unsurprisingly, after 1977 when the USDA released the now ubiquitous “food pyramid” and dietary guidelines which sought to cut fats from the diet in favor of grains and starches, census data showed an almost immediate increase in obesity, CHD — which is still the leading cause of death worldwide today — and diabetes rates (CDC.gov) that have not slowed down ever since. Published in the British Medical Journal, one peer-reviewed systematic meta-analysis of randomized control trials (RCTs) — the true gold-standard in nutritional research — reviewed RCTs published prior to 1983 and found that “No RCT had tested government dietary fat recommendations before their introduction” (Harcombe et al.). The meta-review concluded that
The current available evidence found no significant difference in all-cause mortality or CHD mortality, resulting from dietary fat interventions. RCT evidence currently available does not support the current dietary fat guidelines
(Harcombe et al.)
Zero-Sum Relationship
One might ask what sugar and fat have to do with each other and why reducing calories from fat seems to inherently make people more predisposed to conditions that are less likely to occur in a person eating more fat and not less. The answer can be found in the zero-sum relationship of food which Pollan elegantly describes as a principle wherein “If you eat a lot of one thing, you’re probably not eating a lot of something else.” (498). In the case of sugar and fat, this is known as the “sugar-fat seesaw”(Sadler, et al.). The sugar industry was keenly aware of this phenomenon when funding their anti-fat campaign. With the crusade on fats underway in the 1970s, food manufacturers became pressured to reduce fats from their products to appease consumers. With the removal of calorically energy-dense fats from foods and from the diet, the sugar industry was left free to fill the gap with added sugars simply because the removal of fat from a food (e.g. low-fat yogurt), reduces its tastiness, causing the product to sell less and prompting manufacturers to compensate by pumping added sugars into foods. Manufacturers refer to a product’s equilibrium sweetness level where it sells the most as its “Bliss Point” (nytimes.com).
However, zooming out in the spirit of utilizing Pollan’s more holistic approach of looking at foods versus sole nutrients, one very clear difference between sugar and fat presents itself: satiety. Ethan Sims, a professor of medicine at the University of Vermont from 1950 until his death in 2010, conducted a study in the 1960s at a state prison on inmate “volunteers” who deliberately overate. Sims was curious about what would happen when a thin person deliberately tried to become obese. What he found was that the “calories-in: calories-out” axiom was not actually an axiom as it ignores hormonology. Ethical concerns aside, what he found was that inmates were able to consume upwards of 10,000 calories (Lester, et al 1009) when carbohydrates became the main macronutrient in the diet and that the same group of inmates struggled to eat 800 calories of fats. This is because of the satiety that fats provide. Refined carbs and sugars are not just empty in terms of how full they make a person feel, they are also hormonally destructive as they elevate blood sugar causing beta cells within the pancreas to produce insulin, the main fat-storing hormone. Overtime these beta cells weaken due to overuse, leading to insulin resistance and with enough damage, type II diabetes, non-alcoholic fatty liver disease, etc. (Stanislaw 00:02:10–00:03:30+). As of 2015, there were over 84 million Americans living with prediabetes, a condition that if not treated often leads to type II diabetes within five years (CDC.gov). By looking at the dietary context surrounding nutrients as Pollan suggests, it is clear that overeating on a high-fat, low-carb/sugar diet, is even more difficult than overeating on the opposite diet.
Conclusions
Nutritional science is far from perfect, but to utilize “nutritionism” to diminish its credibility is dubious, considering much of what constitutes nutritionism is funded by corporations and or proliferated by the same media that Pollan is a part of. Pollan seems to agree with this sentiment at the beginning of “Nutritionism Defined” but by the end gradually veers towards confounding the informational value of the two entities while simultaneously trying to establish a clear line between them. He accomplishes this, perhaps unintentionally, by overinflating the amount of worth placed on epidemiological studies by nutritional scientists when such studies are merely viewed as solitary data points among a sea of others as opposed to a much more foundational framework. Furthermore, Pollan’s relative silence on refined carbohydrates/sugars considering the countless meta-analyses on the topic is worrisome and worth amending. Especially since minorities are at a much higher risk of developing type II diabetes, heart disease, liver disease (which sugar consumption is directly correlated to, see Umpleby, et al. 2564) and stroke (diabetes.org), this issue has important socio-economic implications. Overall, however, Pollan’s thesis on this matter of pop science is one of seemingly good intentions and sound logic, but incomplete conclusions.
Works Cited
American Diabetes Association (ADA). “Age, Race, Gender & Family History.” diabetes.org, 21 Mar. 2017, www.diabetes.org/are-you-at-risk/lower-your-risk/nonmodifiables.html#Race.
Bjarnadottir, Adda. “The 56 Most Common Names for Sugar (Some Are Tricky).” healthline.com, 3 June 2017, www.healthline.com/nutrition/56-different-names-for-sugar.
Center for Disease Control and Prevention. “Long-term Trends in Diabetes .” CDC’s Division of Diabetes Translation. , Apr. 2017, www.cdc.gov/diabetes/statistics/slides/long_term_trends.pdf.
Centers for Disease Control and Prevention. “New CDC report: More than 100 million Americans have diabetes or prediabetes.” cdc.gov, 18 July 2017, www.cdc.gov/media/releases/2017/p0718-diabetes-report.html.
Domonoske, Camila. “50 Years Ago, Sugar Industry Quietly Paid Scientists To Point Blame At Fat.” npr.org, 13 Sept. 2016, www.npr.org/sections/thetwo-way/2016/09/13/493739074/50-years-ago-sugar-industry-quietly-paid-scientists-to-point-blame-at-fat.
Harcombe, Zoë, et al. “Evidence from randomised controlled trials does not support current dietary fat guidelines: a systematic review and meta-analysis.” Openheart BMJ Journals, vol. 3, no. 2, 2016, pp. 1–9. William Madison Randall: Proquest, doi:10.1136/openhrt-2016–000409.
Kearns, Christin E., et al. “Sugar Industry and Coronary Heart Disease Research A Historical Analysis of Internal Industry Documents.” JAMA Intern Med, vol. 176, no. 11, 2016, pp. 1680–1685, doi:10.1001/jamainternmed.2016.5394.
Mann, George V. “Diet-Heart: End of an Era.” The New England Journal of Medicine, no. 297, 22 Sept. 1977, pp. 644–650, doi:10.1056/NEJM197709222971206.
Moss, Michael. “The Extraordinary Science of Addictive Junk Food.” nytimes.com, 20 Feb. 2013, www.nytimes.com/2013/02/24/magazine/the-extraordinary-science-of-junk-food.html?pagewanted=all.
Sadler, Michele J., et al. “Sugar-Fat Seesaw: A Systematic Review of the Evidence.” Critical Reviews in Food Science and Nutrition, vol. 55, 2 July 2013, pp. 338–356. William Randall Madison, doi:.org/10.1080/10408398.2011.654013.
Salans, Lester B., et al. Experimental Obesity in Man: Cellular Character of the Adipose Tissue. 05041, Dartmouth Hitchcock Medical Center and the University of Vermont Medical School, ca. 1965, pp.1005–1011. pdfs.semanticsholar.org, pdfs.semanticscholar.org/77a2/4c741388e67192aac52d8b442deabad865f9.pdf.
Stanislaw, Jody, narrator. Sugar is Not a Treat. TEDxSunValley, 12 Dec. 2017, www.youtube.com/watch?v=tic7X3ET4gE.
Umpleby, Margot A., et al. “Impact of liver fat on the differential partitioning of hepatic triacylglycerol into VLDL subclasses on high and low sugar diets.” Clinical Science, vol. 131, no. 21, 17 Oct. 2017, pp. 2561–2573, doi:10.1042/CS20171208.
Young, Charlotte M., et al. “Effect on body composition and other parameters in obese young men of carbohydrate level of reduction diet.” The American Journal of Clinical Nutrition, vol. 24, no. 3, Mar. 1971, pp. 290–296, doi:.org/10.1093/ajcn/24.3.290.
This essay was written in the spring of 2019 and awarded the Jo Ann Seiple Award for best Researched Argumentative Essay
