For decades now we have reviewed all kinds of dietary research. Some seemed interesting and some meaningless, but one point has often struck us: Researchers make very little effort to tie in consumer reports of purchase and consumption with actual evidence of purchase and consumption.
This always struck us as more than a little problematic. When we heard of a researcher questioning the use of uncorroborated self-reporting by consumers, we asked Pundit Investigator and Special Projects Editor Mira Slott to find out more:
Edward Archer, Ph.D., MS
Obesity Theorist and Computational Physiologist
Nutrition and Obesity Research Center & Office of Energetics
University of Alabama at Birmingham
Q: We’re intrigued by your illuminating and hard-hitting research, The Inadmissibility of What We Eat in America and NHANES Dietary Data in Nutrition and Obesity Research and the Scientific Formulation of National Dietary Guidelines. We have written many pieces over the years on the importance and challenges of producing fact-based evidence and scientifically approached research to justify and support programs to increase produce consumption.
Editor’s note: here are some examples:
What was the impetus behind this study? Could you provide context by sharing some information on your background — what inspired your career path, and why you embarked on this research?
A: My coauthors and I wrote our paper because for over 50 years, government-funded researchers have been presenting uncorroborated anecdotal evidence as if it were scientific data. Given that this anecdotal evidence constitutes the empirical basis for federal nutrition guidelines, we think the greatest problem in nutrition and obesity research is not ignorance; it is the illusion of knowledge created by pseudoscientific methods.
The data derived from these methods have been repeatedly demonstrated to be “physiologically implausible” and therefore incompatible with life.(2,4) [Editor’s note: Archer provides references to his research and related studies to support points he makes during this interview, which can be found at the end of this Q&A]. As such, we think this evidence (i.e., uncorroborated anecdotes) have no place in the scientific literature and should not be used to inform public policy. [See Archer et al., PLoS One. 2013;8(10):e76632 for empirical support and a brief review. (3)]
Importantly, nutrition epidemiologic researchers dismiss any concerns regarding the rigor of their methods, but the shifting sands of recommendations on salt, cholesterol, fat, saturated fat, etc., clearly demonstrate how flawed their memory-based methods (M-BM) are. Science is not akin to fashion and should not be reversing itself every few decades.
I think science can improve the human condition, but only if we are actually doing science; collecting anecdotes is not science.
When I first began my research career, I worked with HIV-positive, homeless, African American females. While that research was effective, and working with that population was immensely rewarding, HIV is now a manageable disease. Because I wanted to make an important contribution to human health, I shifted my research focus to nutrition and obesity.
Q: You say the reliance on memory-based dietary assessment methods to inform dietary policy continues despite decades of unequivocal evidence that M-BM data bear little relation to actual energy and nutrient consumption. What are the key reasons why M-BMs are “fundamentally and fatally flawed”? Are all M-BMs essentially the same, or are some methods more accurate than others?
A: The pseudoscientific nature of M-BMs is due to the fact that it is impossible to discern and quantify what percentage of the recalled foods and beverages are completely false reports, grossly inaccurate, or reports that are somewhat congruent with actual consumption. Therefore it is impossible to know the validity and the error associated with each dietary report. As such, all M-BMs (i.e., self-reported dietary data collection) are fatally flawed, pseudoscientific, and inadmissible in scientific research.
With respect to determining fact from fiction, a relevant example that I often use is that of drunk driving. It is extremely important to keep drunk drivers off our nation’s roads. To accomplish this task, do police officers merely ask the driver if s/he has been drinking and accept their word for it (i.e., their anecdotal evidence)? Or does the police officer use an objective biomarker of alcohol consumption (e.g., a breathalyzer)?
Are our nation’s dietary guidelines any less important? I do not think so and ask why nutrition researchers accept the anecdotes as evidence? It defies common and scientific sense to formulate our dietary guidelines on anecdotes.
Q: Why do you think M-BMs continue to be used to inform national dietary guidelines?
A: The confluence of self-interest, institutional inertia, and scientific incompetence has led to the continued use of M-BMs. If researchers are not trained in rigorous science, they will continue to use the methods with which they are familiar; whether or not those methods are valid. In many ways, we are experiencing a version of Lysenkoism: a policy tactic named after a politically successful pseudoscientist in the Soviet Union who manipulated evidence and controlled research output to reach pre-determined conclusions that were in line with Soviet ideology.
As a result, Soviet biology failed to progress while Lysenko and his students/acolytes were in power. The state of US nutrition research is very similar: no scientific progress over 50 years.
Currently, government-funded nutrition researchers control the field by funding only those researchers that use the same flawed methods; they stifle progress by rejecting contradictory evidence and immediately impugn the integrity and competence of researcher who disagree. Importantly, M-BMs are the textbook example of how to perpetuate a vicious cycle of equivocal and ambiguous findings leading to the ever-growing federal funding of nutrition and obesity research.
Q: Are these M-BMs also used as a core component in determining dietary policy outside of the U.S., in Europe, for instance? Are results noticeably different?
A: Unfortunately, most countries base their dietary policy either on US policy or use their own M-BMs. As we detail in our paper, M-MBs from across the world produce physiologically implausible data. In fact, both the United Nations (UN) and World Health Organization (WHO) use M-BM data to inform their policies, and some of the largest epidemiologic surveys in the world are based on M-BM. For example, The EPIC study has exhibited significant misreporting with 10-13% identified as “extreme underreporters.”(5)
Q: What other methods, scientific data, health information, politics, etc., are also used in coming up with guidelines and policy?
A: The answer to this question could fill a number of texts. My colleagues and I focus primarily on the data from M-MBs because they constitute the majority of the evidence the Dietary Guidelines Advisory Committee (DGAC) uses to inform their report. The NHANES data are speciously used to provide all population-level estimates of consumption.
Given the evidence of “Lysenkoism’ in nutrition research, it is not surprising that the majority of the evidence is from the least rigorous methods. This is true because ambiguous findings can be manipulated statistically to arrive at predetermined politically correct conclusions.
Q: You pull no punches. What are the biggest flaws in the national dietary recommendations? Do you have evidence that the dietary recommendations are actually harmful in any way? In terms of health and nutrition, and/or in terms of diverting resources that could be used in other ways…?
A: The greatest error is that the DGAC uses physiologically implausible anecdotal data to generate correlations that are then used to generate recommendations. The DGAC ignore the obvious fact that correlations provide no information as to causation (especially if the data are meaningless; e.g., physiologically implausible).
Stated simply, without causal evidence there should not be any recommendations.
Importantly, I argue that fears sell better than facts. The DGAC are selling fears that misdirect attention and resources away from the actual causes of disease. The DGAC states that Americans are under-consuming nutrients, yet this is directly contradicted by the objective evidence that 80% are not at risk for any dietary deficiencies, nor do Americans have the actual diseases or the deficiencies themselves.6The fears generated by the guidelines cause us to ignore the real causes of obesity and type II diabetes mellitus (i.e., nongenetic inheritance and evolution (7,8)).
Q: Could you provide a layman’s definition of non-genetic inheritance, and elaborate a bit more on this point, for some of us less versed in scientific and medical terminology!
A: The real cause of obesity and type II diabetes mellitus is ‘maternal effects”, a form of non-genetic inheritance and evolution(7,8).
In evolutionary biology, the term ‘maternal effects’ defines how a mother’s characteristics such as her body size, adiposity (i.e., fatness), and behaviors (e.g., her exercise and TV viewing habits) are ‘passed on’ (i.e., inherited) by her children and grandchildren, independent of her genes. For example, when a pregnant woman is physically active, the increased energy demands of physical activity redirect calories and nutrients to her muscles and away from her developing child. This competition between the mother’s exercising muscles and the developing child’s fat cells produces leaner, healthier children, who grow up to be leaner, healthier parents. In other words, how a pregnant woman spends her day affects not only her health and that of her children, but also the health of future generations (i.e., grandchildren and great-grandchildren)(7,8).
Q: Are you saying then that maternal effects, such as body composition and bad behavior during pregnancy, are “the” real cause of obesity and type II diabetes mellitus, or “a” real cause? Are there other real causes for obesity and type II diabetes mellitus due to non-genetic inheritance and evolution? And what role do genetics play in obesity?
A: Prenatal and postnatal maternal effects (i.e., non-genetic inheritance and evolution) are the cause for the twin epidemics of obesity and T2DM. There are other predisposing factors but they are relatively trivial.
There are rare genetic-based disorders that cause obesity (e.g., Prader-Willis, Leptin deficiency), but these account for <1%.
Q: You’ve stimulated a vibrant discussion. Could certain hormones be transferred from one generation to the other so perhaps the hormone regulating sense of hunger or desire for sweetness is transferred? Then again, are hormones emitted through glands that are genetically predisposed to excrete them?
A: With respect to hormones, maternal effects alter insulin production in the child [Editor’s note: See Archer’s papers here and here, and his article in The Washington Post: The Real Reason People are Obese]. So the hormones per se are not ‘transferred’ but the mother’s prenatal metabolism permanently alters the fetus’ insulin function and therefore metabolism.
Q: In speaking about behavioral inheritance of obesity, how important are environmental effects, such as poverty or external stress levels?
A: Another of my articles answers your questions about poverty and stress: The Family Trends Behind the Rise of Childhood Obesity. My theory suggests that the proximate cause of the increasing disparity in childhood obesity and metabolic diseases is the increased frequency of negative maternal health behaviors, which result not just from environmental changes but also from the time demands imposed by absentee fathers.
These negative health behaviors and the consequent obesity are passed down from mothers to children to grandchildren. If we as a nation are to break this cycle of inactivity, obesity, and metabolic disease, we first need to address the cultural and societal influences that drive women to become single, overburdened mothers and cause men to be absent from the lives of their children.
Q: What are the key challenges in conducting scientific studies and implementing objective, fact-based measurements to accurately inform policies to eradicate obesity?
A: The greatest impediment to progress is the current scientific and research paradigms. The idea that “we are what we eat” is an anachronism and unproductive. It is akin to geo-centrism (i.e., thinking the sun revolves around the Earth); while it may appear ‘obvious,’ when viewed from a scientific perspective, it is naïve and wholly incorrect.
The current food-centric paradigm keeps people focused on eating and on food while ignoring the actual causes of chronic non-communicable diseases. As I stated in the previous question, nongenetic evolutionary forces are driving most of our nation’s morbidity and mortality, not gluttony or genes. (7,8)
There are two fatally flawed assumptions (i.e., unsupported by evidence) that drive the politics behind the dietary guidelines. The first is that the American diet is a major risk factor for chronic non-communicable diseases (NCDs) and the second is that a “one-size-fits-all” recommendation will be accurate and not have unintended consequences.
Our current diet is not a major risk factor for disease and “one-size-fits-all” recommendations on specific nutrients are hopelessly unscientific.
Q: Those are powerful points. What are the best methods to use, and why? Do you have any examples you could share of effective strategies? What are the main obstacles to more widespread implementation of such strategies? Is it a matter of cost and resources, training, having the right expertise, etc.?
A: We need to be careful not to fall into the “we are what we eat” trap. Ceteris paribus (all else being equal), active people will burn more calories and therefore eat more food, be better nourished and maintain their weight much more easily than inactive people. This has been known for more than 50 years. Therefore, knowing how much someone eats is tangential to examinations of health and disease.
Importantly, inactive people risk nutrient deficiencies because they may eat less to avoid weight gain, and most importantly, inactivity dramatically increases the risk of cardiovascular disease, type II diabetes mellitus (T2DM), and cancer.(9-12) If the inactive person is a pregnant woman, she significantly increases the risk of these diseases and obesity in future generations.(7,8)
That said, the best technique for energy expenditure (and energy consumption if the participant is in energy balance) is the doubly-labelled water technique (DLW; i.e., non-radioactive isotopes to measure CO2 production). Cost of the isotopes is the greatest obstacle to its widespread use, but the economies of scale would significantly lower the cost if the resources that are currently wasted on subjective protocols (i.e., anecdotal data, asking people what they eat) were redirected.
The expertise needed also is extensive but it is relatively inexpensive to contract a lab to perform analyses compared to the cost of the isotopes.
Accelerometry-based physical activity monitors are acceptable for estimating physical activity, but these devices are a poor measure of energy expenditure.
Q: Aren’t there advances in technology and scientific methods that can be used to more accurately inform national dietary guidelines? What innovative methods are being employed, or in the pipeline?
A: The major issue with M-BMs is that it relies on people being honest and reliable with respect to the estimation of consumption. History clearly demonstrates that people are neither honest nor reliable with respect to their food and beverage consumption. In the context of a study, it is the researcher’s responsibility to select a method that minimizes the error associated with human nature and not the responsibility of the participant to generate an accurate representation of reality. Nevertheless, nutrition researchers have put the cart-before-the-horse and have abandoned their scientific responsibility to ensure accurate measurements.
Unfortunately, none of the recent developments in methodology, such as photography-based reporting and “bite-counters,” overcome this limitation. People will simply not take pictures of their food or take off the “bite-counter” when they eat foods deemed undesirable.
Again, the assumption that “food” in its broadest sense is the problem is mistaken. It is not our food, but rather how our bodies metabolize our food. Given this rather obvious fact, accurate measurement of food intake will be irrelevant to preventing and treating NCDs.
Q: In conducting your research, were you surprised by any of your findings? Did any results counter your expectations or go against your hypothesis?
A: The greatest surprise in my career has been the resistance to well-established facts. The data from M-MBs have been falsified on the population-level for 30 years and yet the nutrition community still defends these data as valid. The Dietary Guidelines Advisory Committee has actually asked the federal government to increase the funding of M-BMs.
I was a born skeptic and was completely agnostic when I began my research. I had no idea of what to expect but knew from my personal experience that eating more food did not lead to obesity. If it did, all my triathlete and bodybuilding friends would be massively obese.
In my experience, the most inactive people were the most obese. This is an example of reciprocal-causality because inactive people will gain more fat mass, and people suffering from obesity will be more inactive.
Q: Isn’t it challenging to change minds and reverse such an engrained, systemic paradigm, not to mention behaviors? After all, this is quite a complex topic.
A: I wrote a “lay person” version of my theory, “The Mother of All Problems, Don’t blame gluttony or genes for obesity. It’s our sedentary habits echoing down the generations,” which was published in the New Scientist magazine. A Washington Post article, The Real Reason People are Obese, on my theory targets a wider audience.
Q: Have you had a chance to see these two recent New York Times articles: “Health Law a Boon for Diet Clinics” and “Why is the Federal Government Afraid of Fat?” Since they are notably related to issues you raise, I thought it interesting and prudent to elicit your feedback…
A: Yes, I have read the NYT articles and am happy to share my thoughts on them. In regards to the piece, Health Law a Boon for Diet Clinics: The diet-industry is based on the unscientific and simplistic idea that if a person just eats less, he or she will overcome obesity. This mindset is unproductive for two reasons; first, the ‘move more and eat less’ mentality suggests that people suffering from obesity are lazy and make poor food choices; this is simply not true. Second, given my work on the inheritance of obesity, (7) people born predisposed to obesity will ‘move less and eat more’ simply because their bodies were designed that way ‘in utero. (7,8) Expecting them to ‘eat less’ is both stigmatizing and naive because willpower cannot compete with evolution.
Importantly, obesity is highly refractory to treatment precisely because the metabolic dysfunction that leads to obesity is established before birth. As such, it is no surprise that more than 95% of the people who attempt to lose weight will gain it back with additional fat mass in <5-10 years. (13-15) And many of these individuals will end up with impoverished body composition and health (e.g., diminished bone, organ, and skeletal muscle mass (16,18)), and predisposed to substantial gains in weight and fat mass. (19-21) This includes commercial and medically supervised dietary plans.(22) Even in the best weight-loss studies, the majority of participants suffering from obesity will still be classified as obese at two years. (23)
Given this reality, physician-sponsored diet-clinics are little more than insurance-sponsored quackery.
Q: I imagine you question the whole premise and reasoning of the second NYT article, “Why is the Government so Afraid of Fat?”
A: The authors of this article are a large part of the problem. They acknowledge that previous recommendations were flawed, but refuse to acknowledge that their data collection methods (i.e., M-BMs) were responsible for the error. As such, these authors continue to use the same fatally flawed method used over the past 50 years, yet expect different results.
As many have stated, the definition of insanity is doing the same thing over and over again and expecting different results. The question that remains to be answered is why do these researchers continue to use a pseudoscientific method that generated obviously flawed recommendations in the past?
Q: What advice do you have for executives in the produce industry looking to build a case for increasing produce consumption?
A: You are asking me to step outside my field of expertise, but as an educated consumer I can offer a few non-science-based suggestions! First, I eat a large amount of produce but avoid many types because there is a substantial lack of consistency in taste and value. For example, I can look at a banana and have a pretty good idea if it is ripe and worth eating, but it is much more difficult to ascertain the value of a peach. As such, I buy and eat more bananas than peaches despite the fact that I enjoy both when they are at the peak of ripeness and taste.
The question executives must answer is why would I risk buying something that is of indeterminate value? The answer is to find a simple method to inform consumers if the fruit is ripe and ready-to-eat. Why does the industry rely on the visual and/or olfactory skills of the customer? To me, this is archaic. Few successful industries conduct business in this manner.
If the scientific community can send a man to the moon and ascertain the presence of the Higgs-Boson particle, I think food scientists can devise a simple manner in which to inform their consumers of the value of their product.
With respect to health, people love fruits and vegetables as well as the juices associated with them. It is extremely unproductive for researchers and policy-makers to create a fear of juices (e.g., apple, etc.) because they contain carbohydrates and/or sugar (i.e., dietary components that have been part of a healthy diet since the dawn of time).
As I stated earlier, fears sell better than facts, and to generate a fear of foods that have been part of a healthy diet since the dawn of human history is not only inane, it is damaging to both the economic and personal health of our citizens.
Q: What are the biggest revelations from your work, and the most important lessons? What new questions have been raised by your research that you’d like to explore?
A: The “most important lesson” is that when someone says the “science is settled,” there is usually a political agenda. No one needs to assert that the law of gravity is “settled science.” The only context in which that phrase will be uttered is when the science is equivocal and there is a need to ‘sell’ that which is not empirically supported.
50 years ago, the “science” on the relationship between fat consumption and heart disease was “settled science.” But obviously, the actual science never supported a causal relationship. What was “settled” was the political debate for government control over the food industry.
Q: Will you be building on this research in the future? What projects do you have in the pipeline?
A: The most interesting question is how the nongenetic evolution of human energy metabolism has altered nutrient partitioning (i.e., the metabolic fate of the foods we consume) and led to obesity and risk of T2DM. (7,8) As a computational physiologist, I am now building virtual humans via computer code to examine the effects of body composition and physical activity and diet on nutrient partitioning and the intergenerational transmission of obesity.
Q: That’s fascinating. Please stay in touch with the latest developments. In exposing the flaws in the current methods for determining dietary guidelines, what recommendations do you have for policy-makers going forward to alleviate the problems?
A: The first rule for all policy-makers should be “Primum non nocere” (i.e., First, do no harm.) The second rule should be “fund both sides of the debate.” When the federal government began funding nutrition research 60 years ago, it established a perverse set of incentives that led to where we are today: a field awash in pseudoscience and confusion as to what constitutes a healthy diet.
Q: Thank you for this no-holds-barred, thought-provoking interview. It certainly will stimulate important discussion among our diverse and global readership.
[Editor’s Note: Below please find Archer’s references to points in this Q&A. You can also read an earlier critique of US national nutrition surveillance Archer cites in his answers.
1. Archer E, Pavela G, Lavie CJ. The Inadmissibility of ‘What We Eat In America’ (WWEIA) and NHANES Dietary Data in Nutrition & Obesity Research and the Scientific Formulation of National Dietary Guidelines. Mayo Clin Proc. Jun 5 2015.
2. Archer E. A Wolf in Sheep’s Clothing. The Scientist. 2013;Available at: http://www.the-scientist.com/?articles.view/articleNo/37918/title/Opinion–A-Wolf-in-Sheep-s-Clothing/.
3. Archer E, Hand GA, Blair SN. Validity of U.S. nutritional surveillance:National Health and Nutrition Examination Survey caloric energy intake data, 1971-2010. PLoS One. 2013;8(10):e76632.
4. Ioannidis JPA. Implausible results in human nutrition research. BMJ. 2013-11-14 10:11:10 2013;347.
5. Ferrari P, Slimani N, Ciampi A, et al. Evaluation of under- and overreporting of energy intake in the 24-hour diet recalls in the European Prospective Investigation into Cancer and Nutrition (EPIC). Public Health Nutr. Dec 2002;5(6B):1329-1345.
6. Pfeiffer CM, Sternberg MR, Schleicher RL, Haynes BM, Rybak ME, Pirkle JL. The CDC’s Second National Report on Biochemical Indicators of Diet and Nutrition in the U.S. Population is a valuable tool for researchers and policy makers. J Nutr. Jun 2013;143(6):938S-947S.
7. Archer E. The Childhood Obesity Epidemic as a Result of Nongenetic Evolution: The Maternal Resources Hypothesis. Mayo Clinic Proceedings. 1// 2015;90(1):77-92.
8. Archer E. The Mother of All Problems. New Scientist. Vol 225. London,2015:32-33.
9. Blair SN, Kohl HW, 3rd, Barlow CE, Paffenbarger RS, Jr., Gibbons LW, Macera CA. Changes in physical fitness and all-cause mortality. A prospective study of healthy and unhealthy men. JAMA. 1995;273(14):1093-1098.
10. Blair SN, Kohl HW, III, Paffenbarger RS, Jr., Clark DG, Cooper KH, Gibbons LW. Physical Fitness and All-Cause Mortality: A Prospective Study of Healthy Men and Women. JAMA. November 3, 1989 1989;262(17):2395-2401.
11. Sui X, LaMonte MJ, Laditka JN, et al. Cardiorespiratory fitness and adiposity as mortality predictors in older adults. JAMA. Dec 5 2007;298(21):2507-2516.
12. LaMonte MJ, Blair SN, Church TS. Physical activity and diabetes prevention. J Appl Physiol. Sep 2005;99(3):1205-1213.
13. Mann T, Tomiyama AJ, Westling E, Lew AM, Samuels B, Chatman J. Medicare’s search for effective obesity treatments: diets are not the answer. Am Psychol. Apr 2007;62(3):220-233.
14. Franz MJ, VanWormer JJ, Crain AL, et al. Weight-loss outcomes: a systematic review and meta-analysis of weight-loss clinical trials with a minimum 1-year follow-up. J Am Diet Assoc. Oct 2007;107(10):1755-1767.
15. Kassirer JP, Angell M. Losing weight–an ill-fated New Year’s resolution. N Engl J Med. Jan 1 1998;338(1):52-54.
16. Weinheimer EM, Sands LP, Campbell WW. A systematic review of the separate and combined effects of energy restriction and exercise on fat-free mass in middle-aged and older adults: implications for sarcopenic obesity. Nutr Rev. Jul 2010;68(7):375-388.
17. Hinton PS, Rector RS, Linden MA, et al. Weight-loss-associated changes in bone mineral density and bone turnover after partial weight regain with or without aerobic exercise in obese women. Eur J Clin Nutr. May 2012;66(5):606-612.
18. Jensen LB, Kollerup G, Quaade F, Sorensen OH. Bone minerals changes in obese women during a moderate weight loss with and without calcium supplementation. J Bone Miner Res. Jan 2001;16(1):141-147.
19. Beavers KM, Lyles MF, Davis CC, Wang X, Beavers DP, Nicklas BJ. Is lost lean mass from intentional weight loss recovered during weight regain in postmenopausal women? Am J Clin Nutr. Sep 2011;94(3):767-774.
20. Lee JS, Visser M, Tylavsky FA, et al. Weight loss and regain and effects on body composition: the Health, Aging, and Body Composition Study. J Gerontol A Biol Sci Med Sci. Jan 2010;65(1):78-83.
21. Johannsen DL, Knuth ND, Huizenga R, Rood JC, Ravussin E, Hall KD. Metabolic slowing with massive weight loss despite preservation of fat-free mass. J Clin Endocrinol Metab. Jul 2012;97(7):2489-2496.
22. Wing RR. Treatment options for obesity: do commercial weight loss programs have a role? JAMA. Oct 27 2010;304(16):1837-1838.
23. Rock CL, Flatt SW, Sherwood NE, Karanja N, Pakiz B, Thomson CA. Effect of a free prepared meal and incentivized weight loss program on weight loss and weight loss maintenance in obese and overweight women: a randomized controlled trial. JAMA. Oct 27 2010;304(16):1803-1810.
We’re fortunate to have among our closest friends some pretty hard-hitting scientists in rigorous fields, and whenever we share the latest nutrition research we find our friends pointing out how weak the research is and how little we actually know about these subjects.
At the same time, we have found that when people such as Gary Taubes, author of among other things — Why We Get Fat: And What To Do About It, Good Calories, Bad Calories: Fats, Carbs, and the Controversial Science of Diet and Health, Diet Delusion, Bad Science: The Short Life and Weird Time of Cold Fusion, etc. — present theses outside the mainstream of science, they are often just ignored.
So we worry about politically correct ideas guiding research funding and the need to win grants dissuading researchers from stepping outside the conventional lines.
Dr. Archer’s views are far from mainstream but the core point: That people’s reports of diet are flawed is undoubtedly true, yet we constantly get research reports based on nothing more than consumer self-reporting. This seems likely to produce bad information and thus bad policy.