The Demonization of ‘Diet’ Is Nothing New

ArticleinProgress in Cardiovascular Diseases 61(3) · August 2018with 42 Reads
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Abstract
...The demonization of ‘diet’ dates to the dawn of recorded history. And while pre-scientific proscriptions were driven by magico-religious motives and made no pretense to rigor, modern conjectures can and should be judged solely on scientific scholarship. As I detail comprehensively, ‘diet-centrism’ is a fundamentally flawed and unscientific perspective that engendered a great deal of illiterate nonsense. For example, modern diet-centric speculations led to the quaint but questionable and at times dangerous notions about the benefits of ‘raw foods’, ‘real foods’, ‘super foods’, ‘whole foods’, ‘organic foods’, ‘detox foods’, ‘vegan diets’, and ‘clean eating’...

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  • Article
    Full-text available
    Controversies regarding the putative health effects of dietary sugar, salt, fat, and cholesterol are not driven by legitimate differences in scientific inference from valid evidence, but by a fictional discourse on diet-disease relations driven by decades of deeply flawed and demonstrably misleading epidemiologic research. Over the past 60 years, epidemiologists published tens of thousands of reports asserting that dietary intake was a major contributing factor to chronic non-communicable diseases despite the fact that epidemiologic methods do not measure dietary intake. In lieu of measuring actual dietary intake, epidemiologists collected millions of unverified verbal and textual reports of memories of perceptions of dietary intake. Given that actual dietary intake and reported memories of perceptions of intake are not in the same ontological category, epidemiologists committed the logical fallacy of ‘Misplaced Concreteness’. This error was exacerbated when the anecdotal (self-reported) data were impermissibly transformed (i.e., pseudo-quantified) into proxy-estimates of nutrient and caloric consumption via the assignment of ‘reference’ values from databases of questionable validity and comprehensiveness. These errors were further compounded when statistical analyses of diet-disease relations were performed using the pseudo-quantified anecdotal data. These fatal measurement, analytic, and inferential flaws were obscured when epidemiologists failed to cite decades of research demonstrating that the proxy-estimates they created were often physiologically implausible (i.e., meaningless) and had no verifiable quantitative relation to the actual nutrient or caloric consumption of participants. In this critical analysis, we present substantial evidence to support our contention that current controversies and public confusion regarding diet-disease relations were generated by tens of thousands of deeply flawed, demonstrably misleading, and pseudoscientific epidemiologic reports. We challenge the field of nutrition to regain lost credibility by acknowledging the empirical and theoretical refutations of their memory-based methods and ensure that rigorous (objective) scientific methods are used to study the role of diet in chronic disease.
  • Available at:Mercatus Centerhttps:// www.mercatus.org/publications/government-dietary-guidelines-public-healthpolicy
    • E Archer
    • M Marlow
    • R Williams
    Archer E, Marlow M, Williams R. Government dietary guidelines: uncertain science leads to questionable public health policy. Available at:Mercatus Centerhttps:// www.mercatus.org/publications/government-dietary-guidelines-public-healthpolicy 2017. Accessed April 30, 2017.
  • Sedentary behavior and health: concepts, assessment & interventionHuman Kinetics
    • E Archer
    • E G Artero
    • Sedentary Behavior Blair
    • Disease Cardiovascular
    Archer E, Artero EG, Sedentary Behavior Blair SN, Disease Cardiovascular. In: Zhu W, Owen N, eds. Sedentary behavior and health: concepts, assessment & interventionHuman Kinetics. Champaign, IL: Human Kinetics; 2017. p. 203-225.
    • E Archer
    • S N Blair
    • Reply
    • Freedman
    Archer E, Blair SN. Reply to LS Freedman et al. Adv Nutr 2015;6:489-490.
  • Article
    There is a politically expedient but problematic fiction that ‘consensus’ matters in medicine and science. Since a million matching opinions do not constitute a fact, a ‘consensus’, either real or apparent, is simply an exercise in groupthink. For example, early in the 20th century there was an unfounded ‘consensus’ that women were inferior and unfit to be trained as physicians. Yet over the next century, the consensus shifted to the converse. Thus, a ‘consensus’ is not a statement about facts, but merely the status quo made explicit...
  • Article
    The debate on the relative contributions of presumptive etiologic factors in the development of obesity is becoming increasingly speculative, insular, and partisan. As the global prevalence of obesity continues to rise, the sheer volume of unfounded conjecture threatens to obscure well-established evidence. We posit that the failure to distinguish between causal factors and mere statistical associations engendered the proliferation of misleading and demonstrably false research programs and failed public health initiatives. Nevertheless, scientific progress necessitates the elimination of unsupported speculation via critical examinations of contrary evidence. Thus, the purpose of this review is to present a concise survey of potentially falsifying evidence for the major presumptive etiologic factors inclusive of 'diet', 'genes', physical activity, and non-physiologic factors from the social sciences. Herein, we advance two 'Fundamental Questions of Obesity' that provide a conceptually clear but challenging constraint on conjecture. First, why would an individual (i.e., human or non-human animal) habitually consume more calories than s/he expends? And second, why would the excess calories be stored predominantly as 'fat' rather than as lean tissue? We posit that the conceptual constraint presented by these questions in concert with the parallel trends in body-mass, adiposity, and metabolic diseases in both human and non-human mammals offer a unique opportunity to refute the oversimplification, causal reductionism, and unrestrained speculation that impede progress. We conclude this review with an attempt at consilience and present two novel paradigms, the 'Metabolic Tipping Point' and the 'Maternal Resources Hypothesis', that offer interdisciplinary explanatory narratives on the etiology of obesity and metabolic diseases across mammalian species.
  • Article
    Sugars are foundational to biological life and played essential roles in human evolution and dietary patterns for most of recorded history. The simple sugar glucose is so central to human health that it is one of the World Health Organization's Essential Medicines. Given these facts, it defies both logic and a large body of scientific evidence to claim that sugars and other nutrients that played fundamental roles in the substantial improvements in life- and health-spans over the past century are now suddenly responsible for increments in the prevalence of obesity and chronic non-communicable diseases. Thus, the purpose of this review is to provide a rigorous, evidence-based challenge to 'diet-centrism' and the disease-mongering of dietary sugar. The term 'diet-centrism' describes the naïve tendency of both researchers and the public to attribute a wide-range of negative health outcomes exclusively to dietary factors while neglecting the essential and well-established role of individual differences in nutrient-metabolism. The explicit conflation of dietary intake with both nutritional status and health inherent in 'diet-centrism' contravenes the fact that the human body is a complex biologic system in which the effects of dietary factors are dependent on the current state of that system. Thus, macronutrients cannot have health or metabolic effects independent of the physiologic context of the consuming individual (e.g., physical activity level). Therefore, given the unscientific hyperbole surrounding dietary sugars, I take an adversarial position and present highly-replicated evidence from multiple domains to show that 'diet' is a necessary but trivial factor in metabolic health, and that anti-sugar rhetoric is simply diet-centric disease-mongering engendered by physiologic illiteracy. My position is that dietary sugars are not responsible for obesity or metabolic diseases and that the consumption of simple sugars and sugar-polymers (e.g., starches) up to 75% of total daily caloric intake is innocuous in healthy individuals.
  • Article
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  • Article
    Full-text available
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  • Article
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  • Article
    Full-text available
    The Scientific Report of the 2015 Dietary Guidelines Advisory Committee was primarily informed by memory-based dietary assessment methods (M-BMs) (eg, interviews and surveys). The reliance on M-BMs to inform dietary policy continues despite decades of unequivocal evidence that M-BM data bear little relation to actual energy and nutrient consumption. Data from M-BMs are defended as valid and valuable despite no empirical support and no examination of the foundational assumptions regarding the validity of human memory and retrospective recall in dietary assessment. We assert that uncritical faith in the validity and value of M-BMs has wasted substantial resources and constitutes the greatest impediment to scientific progress in obesity and nutrition research. Herein, we present evidence that M-BMs are fundamentally and fatally flawed owing to well-established scientific facts and analytic truths. First, the assumption that human memory can provide accurate or precise reproductions of past ingestive behavior is indisputably false. Second, M-BMs require participants to submit to protocols that mimic procedures known to induce false recall. Third, the subjective (ie, not publicly accessible) mental phenomena (ie, memories) from which M-BM data are derived cannot be independently observed, quantified, or falsified; as such, these data are pseudoscientific and inadmissible in scientific research. Fourth, the failure to objectively measure physical activity in analyses renders inferences regarding diet-health relationships equivocal. Given the overwhelming evidence in support of our position, we conclude that M-BM data cannot be used to inform national dietary guidelines and that the continued funding of M-BMs constitutes an unscientific and major misuse of research resources. Copyright © 2015 Mayo Foundation for Medical Education and Research. Published by Elsevier Inc. All rights reserved.
  • Fetal and early postnatal programming and its influence on adult health
    • E Archer
    • S M Mcdonald
    Archer E, McDonald SM. The maternal resources hypothesis and childhood obesity. In: Patel MS, Nielsen JS, eds. Fetal and early postnatal programming and its influence on adult health. New York: CRC Press; Taylor and Francis Group; 2017. p. 17-32.
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    Don't blame gluttony or genes for obesity. It's our sedentary habits echoing down the generations, says Edward Archer.
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  • Article
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  • Article
    The field of sugar metabolism, and fructose metabolism in particular, has experienced a resurgence of interest in the past decade. The "fructose hypothesis" alleges that the fructose component common to all major caloric sweeteners (sucrose, high-fructose corn syrup, honey, and fruit juice concentrates) plays a unique and causative role in the increasing rates of cardiovascular disease, hypertension, diabetes, cancer, and nonalcoholic fatty liver disease. This review challenges the fructose hypothesis by comparing normal U.S. levels and patterns of fructose intake with contemporary experimental models and looking for substantive cause-and-effect evidence from real-world diets. It is concluded that 1) fructose intake at normal population levels and patterns does not cause biochemical outcomes substantially different from other dietary sugars and 2) extreme experimental models that feature hyperdosing or significantly alter the usual dietary glucose-to-fructose ratio are not predictive of typical human outcomes or useful to public health policymakers. It is recommended that granting agencies and journal editors require more physiologically relevant experimental designs and clinically important outcomes for fructose research.
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    Relationships between socio-environmental factors and obesity are poorly understood due to a dearth of longitudinal population-level research. The objective of this analysis was to examine 45-year trends in time-use, household management (HM) and energy expenditure in women. Using national time-use data from women 19-64 years of age, we quantified time allocation and household management energy expenditure (HMEE) from 1965 to 2010. HM was defined as the sum of time spent in food preparation, post-meal cleaning activities (e.g., dish-washing), clothing maintenance (e.g., laundry), and general housework. HMEE was calculated using body weights from national surveys and metabolic equivalents. The time allocated to HM by women (19-64 yrs) decreased from 25.7 hr/week in 1965 to 13.3 hr/week in 2010 (P<0.001), with non-employed women decreasing by 16.6 hr/week and employed women by 6.7 hr/week (P<0.001). HMEE for non-employed women decreased 42% from 25.1 Mj/week (6004 kilocalories per week) in 1965 to 14.6 Mj/week (3486 kcal/week) in 2010, a decrement of 10.5 Mj/week or 1.5 Mj/day (2518 kcal/week; 360 kcal/day) (P<0.001), whereas employed women demonstrated a 30% decrement of 3.9 Mj/week, 0.55 Mj/day (923 kcal/week, 132 kcal/day) (P<0.001). The time women spent in screen-based media use increased from 8.3 hr/week in 1965 to 16.5 hr/week in 2010 (P<0.001), with non-employed women increasing 9.6 hr/week and employed women 7.5 hr/week (P<0.001). From 1965 to 2010, there was a large and significant decrease in the time allocated to HM. By 2010, women allocated 25% more time to screen-based media use than HM (i.e., cooking, cleaning, and laundry combined). The reallocation of time from active pursuits (i.e., housework) to sedentary pastimes (e.g., watching TV) has important health consequences. These results suggest that the decrement in HMEE may have contributed to the increasing prevalence of obesity in women during the last five decades.
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    The historical evolution of infant feeding includes wet nursing, the feeding bottle, and formula use. Before the invention of bottles and formula, wet nursing was the safest and most common alternative to the natural mother's breastmilk. Society's negative view of wet nursing, combined with improvements of the feeding bottle, the availability of animal's milk, and advances in formula development, gradually led to the substitution of artificial feeding for wet nursing. In addition, the advertising and safety of formula products increased their popularity and use among society. Currently, infant formula-feeding is widely practiced in the United States and appears to contribute to the development of several common childhood illnesses, including atopy, diabetes mellitus, and childhood obesity.
  • Article
    To learn more about the metabolic effects of dietary fructose and sucrose, 12 type I and 12 type II diabetic subjects were fed three isocaloric (or isoenergic) diets for eight days each according to a randomized, crossover design. The three diets provided, respectively, 21% of the energy as fructose, 23% of the energy as sucrose, and almost all carbohydrate energy as starch. The fructose diet resulted in significantly lower one- and two-hour postprandial plasma glucose levels, overall mean plasma glucose levels, and urinary glucose excretion in both type I and type II subjects than did the starch diet. There were no significant differences between the sucrose and starch diets in any of the measures of glycemic control in either subject group. The fructose and sucrose diets did not significantly increase serum triglyceride values when compared with the starch diet, but both increased postprandial serum lactate levels. We conclude that short-term replacement of other carbohydrate sources in the diabetic diet with fructose will improve glycemic control, whereas replacement with sucrose will not aggravate glycemic control.
  • Article
    Exclusion of simple sugars from the diabetic diet is not always followed by patients and may not even be as crucial as was hitherto thought. We tested three types of mixed breakfasts (400 kcal, 50 g HCO) including an isoglucidic amount either of white bread (30 g), honey (20 g) or sucrose (15 g), at the critical morning period i.e. for breakfast, in a group of 21 Type 2 (non-insulin-dependent) diabetic patients (6 well- and 15 badly controlled). Mean plasma glucose and insulin levels were comparable on the three occasions: respectively with bread, sucrose and honey, peak glucose values were 18 mmol/l, 17.7 mmol/l and 17.5 mmol/l in the uncontrolled group versus 13.9 mmol/l, 12.8 mmol/l and 12.7 mmol/l in the well-controlled group. Peak insulin values were 33.6 mU/1,34.0 mU/l and 36.3 mU/l (p greater than 0.05) in uncontrolled patients against 57.5 mU/l, 54.8 mU/l and 52.5 mU/l in well-controlled subjects (p greater than 0.05). The mean increment in peak plasma glucose values for the three breakfasts was as follows: 6.9 mmol/l, 6.3 mmol/l and 6.2 mmol/l for the uncontrolled group against 7.2 mmol/l, 5.9 mmol/l and 6.2 mmol/l in well-controlled subjects; the mean increment in peak plasma insulin levels was 21.8 mU/l,22.0 mU/l and 24.2 mU/l in the controlled group versus 38.2 mU/l, 32.0 mU/l and 34.7 mU/l in the well-controlled subjects, all values being non-significantly different (p greater than 0.05). We conclude that, in acute conditions, simple sugars have no additional hyperglycaemic effect over an isoglucidic amount of bread in well-and in badly controlled Type 2 diabetic patients, even at breakfast.
  • Article
    1. Fasting serum cholesterol and triglyceride, and post prandial insulin secretion and lipaemia were measured in human subjects in a metabolic ward, who were given an ordinary diet (diet 1) in which the sucrose was isocalorically replaced by starch (diet 2) or vice versa. The subjects were nine healthy normolipaemic adult males. In eight of these subjects the effect of sucrose calorie reduction (diet 3) on fasting serum lipids was also studied.2. When starch replaced sucrose, there were no singnificant differences in fasting serum lipid concentrations or immunoreactive insulin or in the insulin response and alimentary lipaemia after a standard mixed breakfast.3. Serum triglyceride concentration fell and cholesterol concentration rose during the period of sucrose (and calorie) restriction.4. After lunch and supper on the first two diets (when different carbohydrates were given) the lipaemic response was larger and the insulin response smaller after meals containing sucrose.5. Thus, there was no difference between concentrations of fasting serum lipids when starch replaced sucrose at 23% total calories, but the concentrations of serum triglycerides were higher after individual mixed meals containing sucrose.6. There were no significant differences in the fatty acid patterns of serum lipids on the different diets.
  • Article
    The hyperglycaemic effect of 20 g sucrose taken at the end of a regular mixed meal by diabetic patients was measured in six adult type 1 diabetics, C-peptide negative, controlled by the artificial pancreas, and twelve adult type 2 diabetics, with fasting plasma glucose levels below 7.2 mmol/l (130 mg/100 ml) and post-prandial plasma glucose levels below 10.0 mmol/l (180 mg/100 ml), treated by diet alone or with glibenclamide and/or metformin. All the patients were given on consecutive days, in random order, two mixed meals of grilled meat, green beans, and cheese, as well as a cake made either of rice, skimmed milk, and saccharine (meal A) or rice, skimmed milk, and 20 g sucrose (meal B). The meals contained equal amounts of calories and of carbohydrate. There was no difference between the meals in plasma glucose curves and plasma insulin or insulin infusion rate variations whether in peak values, peaking times, or areas under the curves, in either group of patients. Sparing use of sucrose taken during mixed meals might help well-controlled diabetic patients to comply with their daily dietary prescription while maintaining good blood glucose control.
  • Article
    To assess in diabetic subjects the effects of dietary sucrose on glycemia and lipemia. Twelve type II diabetic subjects consumed, in random order, two isocaloric, 55% carbohydrate study diets for 28 days. In one diet, 19% of energy was derived from sucrose. In the other diet, < 3% of energy was derived from sucrose, and carbohydrate energy came primarily from starch. Both study diets were composed of common foods. All meals were prepared in a metabolic kitchen where foods were weighed during meal preparation. No significant differences were noted between the study diets at any time point in mean plasma glucose. At day 28, mean plasma glucose values for the sucrose diet were 9.6 +/- 0.5 mM and for the starch diet were 9.4 +/- 0.6 mM (P = 0.63). Also, no significant differences were observed between the study diets in urine glucose, fasting serum total, HDL, or LDL cholesterol; fasting serum TG; or peak postprandial serum TG. A high sucrose diet did not adversely affect glycemia or lipemia in type II diabetic subjects.
  • Article
    The early years of the 20th century were notable for improvements in general sanitation, dairying practices and milk handling. Most infants were breast-fed, often with some formula feeding as well. Availability of the home icebox permitted safe storage of milk and infant formula, and by the 1920s, feeding of orange juice and cod liver oil greatly decreased the incidence of scurvy and rickets. Use of evaporated milk for formula preparation decreased bacterial contamination and curd tension of infant formulas. From 1930 through the 1960s, breast-feeding declined and cow's milk and beikost were introduced into the diet at earlier and earlier ages. Although commercially prepared formulas, including iron-fortified formulas replaced home-prepared formulas, few infants were breast-fed or formula fed after 4-6 mo of age. Iron deficiency was prevalent. From 1970 through 1999, a resurgence of breast-feeding was associated with a prolongation of formula feeding and an increase in usage of iron-fortified formulas. By the end of the century, formula feeding of older infants had largely replaced feeding of fresh cow's milk and the prevalence of iron deficiency had greatly decreased.