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The Demonization of ‘Diet’ Is Nothing New
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’...
... In contrast to veganism, O'Keefe and colleagues recommended a 'plant-forward omnivorous whole-foods diet'. 1 Although we agree fully that the inclusion of both animal and plant sources are essential to a nutritionally adequate diet and health, the concept of 'whole-foods' lacks a scientific foundation 10,11 -and the position that the 'American diet' is unhealthy and nutrient-depleted lacks valid evidence. [9][10][11][12][13][14] For example, in the early 20th century, nutritional diseases such as pellagra, beriberi, rickets, and goiter were severe public health challenges. In the US, pellagra (a disease of niacin deficiency) claimed more than 100,000 lives and afflicted more than 3 million. ...
... Moreover, the concept of 'whole-foods' and the presumed detriments of 'processing' have no scientific basis. 10,11 Since the 1950s, most infants in industrialized nations were raised on infant formulaa 100% synthetic, highly-processed sugar-sweetened beverage with added salt, added fats, and~40% of the calories from 'added' sugar. Yet contrary to anti-sugar and anti-processing rhetoric, nations with the highest rates of sugar-sweetened beverage (formula) consumption by infants and children also have the lowest rates of obesity, type-2 diabetes mellitus (T2DM), and cardiovascular disease (CVD; e.g., Japan and Norway). ...
... Yet contrary to anti-sugar and anti-processing rhetoric, nations with the highest rates of sugar-sweetened beverage (formula) consumption by infants and children also have the lowest rates of obesity, type-2 diabetes mellitus (T2DM), and cardiovascular disease (CVD; e.g., Japan and Norway). 10,11 Furthermore, 'diet-centrism' -as embodied by the belief that consuming 'too much' of the 'wrong' foods, beverages, or nutrients causes obesity and metabolic disordersis based almost entirely on epidemiologic data that were shown to be physiologically implausible and pseudo-scientific (non-falsifiable). 9,12-14 Yet more importantly, dietcentrism inverts the role of foods and beverages in health and disease. ...
... … the subject of nutrition seems to have a special appeal to the credulous, the social zealot and, in the commercial field, the unscrupulous. Ancel Keys (Keys 1946) The pursuit of power and profit via the demonization of dietary factors such as alcohol and sugar dates to at least the seventeenth century (Levenstein 2012;Levinovitz 2015;Archer 2018a). Thus, as the public's fear of fat and cholesterol waned and the lipid-heart disease hypothesis began to lose empirical support (Ravnskov 2008;Ravnskov et al. 2014;Teicholz 2014Teicholz , 2015de Souza et al. 2015;Harcombe et al. 2015;Ramsden et al. 2016;Hamley 2017;Harcombe 2017;Malhotra, Redberg, and Meier 2017), it was only a matter of time before media attention, political grandstanding, and research funding were once again directed at dietary sugars (e.g., see Lustig, Schmidt, and Brindis 2012;Ax 2013;Boseley 2013;Chung et al. 2016;Tybor et al. 2018). ...
... Given this reality, the purpose of this analytic review and commentary is to present evidence to show that anti-sugar rhetoric is divorced from established scientific facts and has led to politically expedient but physiologically ill-informed policies reminiscent of those enacted about alcohol a century ago. We contend that current policy recommendations on 'added' sugars and sugar-sweetened beverages are not only unscientific, but also regressive and unjust because they harm the most vulnerable members of our society while providing no personal or public health benefits (Marlow and Shiers 2010;Archer, Marlow, and Williams 2017;Marlow and Abdukadirov 2018;Archer 2018aArcher , 2018cMarlow 2019). in humans. As such, the failure to consume or synthesize sufficient glucose results in rapid death (Sokoloff 1989;Cryer 2007;Wasserman 2009;Archer 2018c). ...
... Skepticism is the chastity of the intellect, and it is shameful to surrender it too soon … (Santayana 1923, p. 69) It is an empirical fact that sugar molecules, whether naturally occurring in foods and beverages (i.e., 'intrinsic') or 'added' to foods and beverages during processing are chemically equivalent and have identical physiologic effects (Glinsmann, Irausquin, and Park 1986;Raatz, Johnson, and Picklo 2015;Archer 2018a). This means that the glucose molecules in breast milk are the same as the glucose molecules in infant formula and other sugar-sweetened beverages (Archer 2018a(Archer , 2018c; and the fructose molecules in fruits and vegetables are identical to those in honey, high fructose corn-syrup, and sucrose (table sugar) (Raatz, Johnson, and Picklo 2015). ...
Sugar, tobacco, and alcohol have been demonized since the seventeenth century. Yet unlike tobacco and alcohol, there is indisputable scientific evidence that dietary sugars were essential for human evolution and are essential for human health and development. Therefore, the purpose of this analytic review and commentary is to demonstrate that anti-sugar rhetoric is divorced from established scientific facts and has led to politically expedient but ill-informed policies reminiscent of those enacted about alcohol a century ago in the United States. Herein, we present a large body of interdisciplinary research to illuminate several misconceptions, falsehoods, and facts about dietary sugars. We argue that anti-sugar policies and recommendations are not merely unscientific but are regressive and unjust because they harm the most vulnerable members of our society while providing no personal or public health benefits.
... This fictional discourse was widely disseminated by the popular press and exacerbated by governmental and non-governmental health organizations, and commercial interests (e.g., weight-loss industries and manufacturers of "heart-healthy" foods). The wide-spread publication of spurious diet-related speculations had significant adverse public health consequences (15,20) that included public confusion (15,52), regressive and misdirected public policy (20,53,54), the misallocation of research resources (9), scientifically illiterate recommendations on sugar (15,55), and potentially harmful recommendations on salt (20,(56)(57)(58)(59)(60) that may have led to "deaths due to hyponatremia" (20) p. 22. ...
... Furthermore, 80% of the studies in the US Department of Agriculture's National Evidence Library (107) used by the 2015 DGAC to establish the DGA employed M-BMs. We contend that the unremitting use of this large body of refuted evidence in concert with the failure to cite or even acknowledge contrary evidence exacerbated the fictional discourse and led to the "Disease-Mongering of the American Diet" (108) and the "demonization" of dietary sugar (15,55). For example, despite biochemical analyses demonstrating that the vast majority of Americans were not at risk of vitamin and mineral deficiencies (7), the 2015 DGAC report stated that "several nutrients are underconsumed"18(PartA,p20) (i.e., vitamins A, C, D, E, and folate) and that for women of childbearing age, "iron also is a shortfall nutrient."18(PartA,p2). ...
... Thus, by failing to acknowledge the existence of contrary biochemical data and reporting only the implausible NHANES M-BM data, the 2015 DGAC presented a false and alarmist perspective on the nutritional status of Americans. This misleading presentation was an exemplar of "disease-mongering" (15,108) because it distorted the scientific record and misled both the public and policy makers by erroneously suggesting that Americans were at risk for nutritional deficiencies when objective evidence demonstrated they were not (15,55). ...
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.
... In this critical hypothesis, diet is an essential component of health, however it may be a trivial risk factor in the case of chronic diseases [65,66], suggesting that macronutrients can have metabolic effects dependent of the individual physiologic context (e.g., physical activity level) [65]. In addition, the role of diet in chronic diseases has been highly controversial [66]. ...
... In this critical hypothesis, diet is an essential component of health, however it may be a trivial risk factor in the case of chronic diseases [65,66], suggesting that macronutrients can have metabolic effects dependent of the individual physiologic context (e.g., physical activity level) [65]. In addition, the role of diet in chronic diseases has been highly controversial [66]. Some of this controversy was prompted by the publication of epidemiologic reports supporting memory-based methods to measure dietary intake [27,28,65,67] even though these methods can produce inaccurate dietary data collection, resulting in spurious associations and effects [27]. ...
Nutrition is a modifiable key factor that is able to interact with both the genome and epigenome to influence human health and fertility. In particular, specific genetic variants can influence the response to dietary components and nutrient requirements, and conversely, the diet itself is able to modulate gene expression. In this context and the era of precision medicine, nutrigenetic and nutrigenomic studies offer significant opportunities to improve the prevention of metabolic disturbances, such as Type 2 diabetes, gestational diabetes, hypertension, and cardiovascular diseases, even with transgenerational effects. The present review takes into account the interactions between diet, genes and human health, and provides an overview of the role of nutrigenetics, nutrigenomics and epigenetics in the prevention of non-communicable diseases. Moreover, we focus our attention on the mechanism of intergenerational or transgenerational transmission of the susceptibility to metabolic disturbances, and underline that the reversibility of epigenetic modifications through dietary intervention could counteract perturbations induced by lifestyle and environmental factors.
... Moreover, we assert that distinguishing between etiology and treatment is critical for discussions revolving around the roles of PA, genes, diet, and exercise. For example, we contend that although specific macro-nutrients are not causal to obesity and other disease states, except as a source of calories (for details please see [69,[73][74][75][76]), we argue strongly that caloric restriction with further reductions in carbohydrates are essential protocols for reducing body and fat mass and the treatment of acquired obesity and T2DM. ...
The etiology of obesity is complex and idiosyncratic—with inherited, behavioral, and environmental factors determining the age and rate at which excessive adiposity develops. Moreover, the etiologic status of an obese phenotype (how and when it developed initially) strongly influences both the short-term response to intervention and long-term health trajectories. Nevertheless, current management strategies tend to be ‘one-size-fits-all’ protocols that fail to anticipate the heterogeneity of response generated by the etiologic status of each individual’s phenotype. As a result, the efficacy of current lifestyle approaches varies from ineffective and potentially detrimental, to clinically successful; therefore, we posit that effective management strategies necessitate a personalized approach that incorporates the subtyping of obese phenotypes. Research shows that there are two broad etiologic subtypes: ‘acquired’ and ‘inherited’. Acquired obesity denotes the development of excessive adiposity after puberty—and because the genesis of this subtype is behavioral, it is amenable to interventions based on diet and exercise. Conversely, inherited obesity subsumes all forms of excessive adiposity that are present at birth and develop prior to pubescence (pediatric and childhood). As the inherited phenotype is engendered in utero, this subtype has irreversible structural (anatomic) and physiologic (metabolic) perturbations that are not susceptible to intervention. As such, the most realizable outcome for many individuals with an inherited subtype will be a ‘fit but fat’ phenotype. Given that etiologic subtype strongly influences the effects of intervention and successful health management, the purpose of this ‘perspective’ article is to provide a concise overview of the differential development of acquired versus inherited obesity and offer insight into subtype-specific management.
... Other potential confounders Clearly, diet is not the only determinant of psychological health (Archer 2018a(Archer , 2018b. Nevertheless, a number of the studies failed to include important potential confounders and effect modifiers. ...
Objective: To examine the relation between the consumption or avoidance of meat and psychological health and well-being.
Methods: A systematic search of online databases (PubMed, PsycINFO, CINAHL Plus, Medline, and Cochrane Library) was conducted for primary research examining psychological health in meat-consumers and meat-abstainers. Inclusion criteria were the provision of a clear distinction between meat-consumers and meat-abstainers, and data on factors related to psychological health. Studies examining meat consumption as a continuous or multi-level variable were excluded. Summary data were compiled, and qualitative analyses of methodologic rigor were conducted. The main outcome was the disparity in the prevalence of depression, anxiety, and related conditions in meat-consumers versus meat-abstainers. Secondary outcomes included mood and self-harm behaviors.
Results: Eighteen studies met the inclusion/exclusion criteria; representing 160,257 participants (85,843 females and 73,232 males) with 149,559 meat-consumers and 8584 meat-abstainers (11 to 96 years) from multiple geographic regions. Analysis of methodologic rigor revealed that the studies ranged from low to severe risk of bias with high to very low confidence in results. Eleven of the 18 studies demonstrated that meat-abstention was associated with poorer psychological health, four studies were equivocal, and three showed that meat-abstainers had better outcomes. The most rigorous studies demonstrated that the prevalence or risk of depression and/or anxiety were significantly greater in participants who avoided meat consumption.
Conclusion: Studies examining the relation between the consumption or avoidance of meat and psychological health varied substantially in methodologic rigor, validity of interpretation, and confidence in results. The majority of studies, and especially the higher quality studies, showed that those who avoided meat consumption had significantly higher rates or risk of depression, anxiety, and/or self-harm behaviors. There was mixed evidence for temporal relations, but study designs and a lack of rigor precluded inferences of causal relations. Our study does not support meat avoidance as a strategy to benefit psychological health.
This paper presents two inter-dependent frameworks for understanding the etiology of obesity and the regain of body and fat mass after weight loss. The ‘Invisible Hand of Metabolism’ illustrates how physiologic states such as body and fat mass and blood glucose levels arise from the unregulated, uncontrolled, yet competitive behavior of trillions of semi-autonomous cells. The ‘Competition Model of Metabolism’ is an explanatory (mechanistic) framework that details how organismal and cell-specific behaviors generate the apparent stability of physiologic states despite metabolic perturbations (e.g., weight-loss and exercise). Together, these frameworks show that body and fat mass and blood glucose levels are not regulated, controlled, or defended but emerge from the complexity and functional plasticity of competitive cellular relations. Therefore, we argue that the use of abstract constructs such as ‘regulation’, ‘control’, ‘glucostats’, ‘adipostats’, and ‘set−/settling-points’ hinders the understanding of obesity and cardiometabolic diseases in human and nonhuman mammals.
Background:
Poor lifestyle behaviors are leading causes of preventable diseases globally. Added sugars contribute to a diet that is energy dense but nutrient poor and increase risk of developing obesity, cardiovascular disease, hypertension, obesity-related cancers, and dental caries.
Methods and results:
For this American Heart Association scientific statement, the writing group reviewed and graded the current scientific evidence for studies examining the cardiovascular health effects of added sugars on children. The available literature was subdivided into 5 broad subareas: effects on blood pressure, lipids, insulin resistance and diabetes mellitus, nonalcoholic fatty liver disease, and obesity.
Conclusions:
Associations between added sugars and increased cardiovascular disease risk factors among US children are present at levels far below current consumption levels. Strong evidence supports the association of added sugars with increased cardiovascular disease risk in children through increased energy intake, increased adiposity, and dyslipidemia. The committee found that it is reasonable to recommend that children consume ≤25 g (100 cal or ≈6 teaspoons) of added sugars per day and to avoid added sugars for children <2 years of age. Although added sugars most likely can be safely consumed in low amounts as part of a healthy diet, few children achieve such levels, making this an important public health target.
Excess sugar consumption may promote adverse changes in hepatic and total body insulin resistance. Debate continues over the effects of sugars at more typically consumed levels and whether the identity of the sugar consumed is important. In the present study participants (20-60 years old) were randomly assigned to one of five groups, three that consumed low fat milk with added fructose containing sugars in amounts equivalent to the 50th percentile of fructose consumption (US), one which consumed low-fat milk sweetened with glucose, and one unsweetened low-fat milk control group. The intervention lasted ten weeks. In the entire study population there was less than 1 kg increase in weight (73.6 ±13.0 vs. 74.5 ± 13.3 kg, p < 0.001), but the change in weight was comparable among groups (p > 0.05). There were no changes in fasting glucose (49 ± 0.4 vs. 5.0 ± 0.5 mmol/L), insulin (56.9 ± 38.9 vs. 61.8 ± 50.0 pmol/L), or insulin resistance, as measured by the Homeostasis Model Assessment method (1.8 ± 1.3 vs. 2.0 ± 1.5, all p > 0.05). These data suggest that added sugar consumed at the median American intake level does not produce changes in measures of insulin sensitivity or glucose tolerance and that no sugar has more deleterious effects than others.
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.
Over the past century, socioenvironmental evolution (eg, reduced pathogenic load, decreased physical activity, and improved nutrition) led to cumulative increments in maternal energy resources (ie, body mass and adiposity) and decrements in energy expenditure and metabolic control. These decrements reduced the competition between maternal and fetal energy demands and increased the availability of energy substrates to the intrauterine milieu. This perturbation of mother-conceptus energy partitioning stimulated fetal pancreatic β-cell and adipocyte hyperplasia, thereby inducing an enduring competitive dominance of adipocytes over other tissues in the acquisition and sequestering of nutrient energy via intensified insulin secretion and hyperplastic adiposity. At menarche, the competitive dominance of adipocytes was further amplified via hormone-induced adipocyte hyperplasia and weight-induced decrements in physical activity. These metabolic and behavioral effects were propagated progressively when obese, inactive, metabolically compromised women produced progressively larger, more inactive, metabolically compromised children. Consequently, the evolution of human energy metabolism was markedly altered. This phenotypic evolution was exacerbated by increments in the use of cesarean sections, which allowed both the larger fetuses and the metabolically compromised mothers who produced them to survive and reproduce. Thus, natural selection was iatrogenically rendered artificial selection, and the frequency of obese, inactive, metabolically compromised phenotypes increased in the global population. By the late 20th century, a metabolic tipping point was reached at which the postprandial insulin response was so intense, the relative number of adipocytes so large, and inactivity so pervasive that the competitive dominance of adipocytes in the sequestering of nutrient energy was inevitable and obesity was unavoidable.
Methodological limitations compromise the validity of U.S. nutritional surveillance data and the empirical foundation for formulating dietary guidelines and public health policies.
Evaluate the validity of the National Health and Nutrition Examination Survey (NHANES) caloric intake data throughout its history, and examine trends in the validity of caloric intake estimates as the NHANES dietary measurement protocols evolved.
Validity of data from 28,993 men and 34,369 women, aged 20 to 74 years from NHANES I (1971-1974) through NHANES 2009-2010 was assessed by: calculating physiologically credible energy intake values as the ratio of reported energy intake (rEI) to estimated basal metabolic rate (BMR), and subtracting estimated total energy expenditure (TEE) from NHANES rEI to create 'disparity values'.
1) Physiologically credible values expressed as the ratio rEI/BMR and 2) disparity values (rEI-TEE).
The historical rEI/BMR values for men and women were 1.31 and 1.19, (95% CI: 1.30-1.32 and 1.18-1.20), respectively. The historical disparity values for men and women were -281 and -365 kilocalorie-per-day, (95% CI: -299, -264 and -378, -351), respectively. These results are indicative of significant under-reporting. The greatest mean disparity values were -716 kcal/day and -856 kcal/day for obese (i.e., ≥30 kg/m2) men and women, respectively.
Across the 39-year history of the NHANES, EI data on the majority of respondents (67.3% of women and 58.7% of men) were not physiologically plausible. Improvements in measurement protocols after NHANES II led to small decreases in underreporting, artifactual increases in rEI, but only trivial increases in validity in subsequent surveys. The confluence of these results and other methodological limitations suggest that the ability to estimate population trends in caloric intake and generate empirically supported public policy relevant to diet-health relationships from U.S. nutritional surveillance is extremely limited.
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.
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.
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.
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...
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.
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.
The purpose of this study was to examine the validity of the 1971-2010 United States Department of Agriculture's (USDA's) loss-adjusted food availability (LAFA) per capita caloric consumption estimates. Estimated total daily energy expenditure (TEE) was calculated for nationally representative samples of US adults, 20-74 years, using the Institute of Medicine's predictive equations with “low-active” (TEE L-ACT) and “sedentary” (TEE SED) physical activity values. TEE estimates were subtracted from LAFA estimates to create disparity values (kcal/d). A validated mathematical model was applied to calculate expected weight change in reference individuals resulting from the disparity. From 1971-2010, the disparity between LAFA and TEE L-ACT varied by 394 kcal/d—(P < 0.001), from −205 kcal/d (95% CI: −214, −196) to +189 kcal/d (95% CI: 168, 209). The disparity between LAFA and TEE SED varied by 412 kcal/d (P < 0.001), from −84 kcal/d (95% CI: −93, −76) to +328 kcal/d (95% CI: 309, 348). Our model suggests that if LAFA estimates were actually consumed, reference individuals would have lost ~1-4 kg/y from 1971-1980 (an accumulated loss of ~12 to ~36 kg), and gained ~3-7 kg/y from 1988-2010 (an accumulated gain of ~42 to ~98 kg). These estimates differed from the actual measured increments of 10 kg and 9 kg in reference men and women, respectively, over the 39-year period. The USDA LAFA data provided inconsistent, divergent estimates of per capita caloric consumption over its 39-year history. The large, variable misestimation suggests that the USDA LAFA per capita caloric intake estimates lack validity and should not be used to inform public policy.
http://www.mayoclinicproceedings.org/article/S0025-6196(15)00797-1/fulltext
Public health recommendations call for a reduction in added sugars; however, controversy exits over whether all nutritive sweeteners produce similar metabolic effects.
The aim was to compare the effects of the chronic consumption of 3 nutritive sweeteners [honey, sucrose, and high-fructose corn syrup containing 55% fructose (HFCS55)] on circulating glucose, insulin, lipids, and inflammatory markers; body weight; and blood pressure in individuals with normal glucose tolerance (GT) and those with impaired glucose tolerance (IGT).
In a crossover design, participants consumed daily, in random order, 50 g carbohydrate from assigned sweeteners for 2 wk with a 2- to 4-wk washout period between treatments. Participants included 28 GT and 27 IGT volunteers with a mean age of 38.9 ± 3.6 y and 52.1 ± 2.7 y, respectively, and a body mass index (in kg/m(2)) of 26 ± 0.8 and 31.5 ± 1.0, respectively. Body weight, blood pressure (BP), serum inflammatory markers, lipids, fasting glucose and insulin, and oral-glucose-tolerance tests (OGTTs) were completed pre- and post-treatment. The OGTT incremental areas under the curve (iAUCs) for glucose and insulin were determined and homeostasis model assessment of insulin resistance (HOMA-IR) scores were calculated.
Body weight and serum glucose, insulin, inflammatory markers, and total and LDL-cholesterol concentrations were significantly higher in the IGT group than in the GT group at baseline. Glucose, insulin, HOMA-IR, and the OGTT iAUC for glucose or insulin did not differ by treatment, but all responses were significantly higher in the IGT group compared with the GT group. Body weight was unchanged by treatment. Systolic BP was unchanged, whereas diastolic BP was significantly lower in response to sugar intake across all treatments. An increase in high-sensitivity C-reactive protein (hsCRP) was observed in the IGT group in response to all sugars. No treatment effect was observed for interleukin 6. HDL cholesterol did not differ as a result of status or treatment. Triglyceride (TG) concentrations increased significantly from pre- to post-treatment in response to all sugars tested.
Daily intake of 50 g carbohydrate from honey, sucrose, or HFCS55 for 14 d resulted in similar effects on measures of glycemia, lipid metabolism, and inflammation. All 3 increased TG concentrations in both GT and IGT individuals and elevated glycemic and inflammatory responses in the latter. This trial was registered at clinicaltrials.gov as NCT01371266.
© 2015 American Society for Nutrition.
Don't blame gluttony or genes for obesity. It's our sedentary habits echoing down the generations, says Edward Archer.
To validate the PAR protocol, a novel method for calculating population-level estimated energy requirements (EERs) and average physical activity ratio (APAR), in a nationally representative sample of US adults.
Estimates of EER and APAR values were calculated via a factorial equation from a nationally representative sample of 2597 adults aged 20 and 74 years (US National Health and Nutrition Examination Survey; data collected between January 1, 2005, and December 31, 2006). Validation of the PAR protocol-derived EER (EERPAR) values was performed via comparison with values from the Institute of Medicine EER equations (EERIOM).
The correlation between EERPAR and EERIOM was high (0.98; P<.001). The difference between EERPAR and EERIOM values ranged from 40 kcal/d (1.2% higher than EERIOM) in obese (body mass index [BMI] ≥30) men to 148 kcal/d (5.7% higher) in obese women. The 2005-2006 EERs for the US population were 2940 kcal/d for men and 2275 kcal/d for women and ranged from 3230 kcal/d in obese (BMI ≥30) men to 2026 kcal/d in normal weight (BMI <25) women. There were significant inverse relationships between APAR and both obesity and age. For men and women, the APAR values were 1.53 and 1.52, respectively. Obese men and women had lower APAR values than normal weight individuals (P=.23 and P=.15, respectively), and younger individuals had higher APAR values than older individuals (P<.001).
The PAR protocol is an accurate method for deriving nationally representative estimates of EER and APAR values. These descriptive data provide novel quantitative baseline values for future investigations into associations of physical activity and health.
To examine 45-year trends in time use and physical activity energy expenditure (PAEE) in a nationally representative sample of US mothers.
We quantified time allocation to physical activity (PA), sedentary behaviors (SED), and PAEE from 1965 to 2010 in mothers with older children (MOC) (>5 to ≤18 years) and mothers with younger children (MYC) (≤5 years). Physical activity was the sum of time allocated to housework, child care, laundry, food preparation, postmeal cleanup, and exercise. Sedentary behavior was the sum of time spent in a vehicle and using screen-based media. Physical activity energy expenditure was calculated using body weights from national surveys and metabolic equivalents.
From 1965 to 2010, the time allocated to PA decreased by 11.1 h/wk (from 32.0 to 20.9 h/wk) in MOC and by 13.9 h/wk (from 43.6 to 29.7 h/wk) in MYC. The time spent in SED increased by 7.0 h/wk in MOC (from 17.7 to 24.7 h/wk) and increased by 5.7 h/wk in MYC (from 17.0 to 22.7 h/wk). Physical activity energy expenditure decreased by 1237.6 kcal/wk (176.8 kcal/d) in MOC (from 5835.3 to 4597.7 kcal/wk), and in MYC, PAEE decreased by 1572.5 kcal/wk (224.6 kcal/d), from 7690.5 to 6118.0 kcal/wk.
There was a significant reallocation of time by mothers from PA (eg, housework) to SED (eg, watching television) between 1965 and 2010. Given the essential role of PA for health and the potential for the intergenerational transmission of obesity and obesogenic behaviors, these results suggest that maternal inactivity may be an important target for the primary prevention of chronic noncommunicable diseases and obesity.
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.
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.
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.
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.
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.
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.
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.
Sedentary behavior and health: concepts, assessment & intervention -Human 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 & intervention -Human 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.