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Abstract

Highlights 1. Current confusion over ‘what to eat’ and controversies on the putative health effects of dietary sugar, fat, salt, and cholesterol are not driven by legitimates differences in scientific inference from valid data, but were engendered by five-decades of deeply flawed, demonstrably misleading, and largely pseudoscientific epidemiologic reports based on memory-based (self-reported) dietary assessment methods (M-BMs). 2. The use of M-BMs is founded upon two logical fallacies: a ‘category error’ and reification (i.e., the fallacy of misplaced concreteness). 3. M-BMs do not measure dietary intake; these methods collect reported memories of perceptions of dietary intake. These data are irrelevant to the physiologic effects of consumed foods and beverages and diet-disease relations. 4. Statistical analyses of impermissibly transformed (i.e., reified) perceptions of dietary intake led to a fictional dietary discourse with significant public health consequences. 5. M-BMs are pseudo-scientific and should not be used to inform public policy or establish the Dietary Guidelines for Americans.

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... By the mid-twentieth century, as diet-related diseases (e.g., scurvy, pellagra) and protein-energy malnutrition became increasingly rare in industrialized nations, a small but influential group of investigators began speculating that complex chronic non-communicable diseases (NCDs) were somehow causally related to diet [e.g., see (10)(11)(12)(13)(14)] The evidence ostensibly supporting these conjectures was inferred from epidemiologic studies based on the naïve notion that a person's usual dietary intake (i.e., consumed foods and beverages) could be estimated simply by asking what he or she remembered eating and drinking (9,(15)(16)(17). Despite the fact that the data collected by these memory-based dietary assessment methods (M-BMs) were nonfalsifiable anecdotes (i.e., verbal or textual self-reports) and were repeatedly demonstrated to lack validity and reliability as far back as the 1950s (18,19), studies employing M-BMs came to dominate the empiric, policy, and media landscapes (15)(16)(17)20). ...
... By the mid-twentieth century, as diet-related diseases (e.g., scurvy, pellagra) and protein-energy malnutrition became increasingly rare in industrialized nations, a small but influential group of investigators began speculating that complex chronic non-communicable diseases (NCDs) were somehow causally related to diet [e.g., see (10)(11)(12)(13)(14)] The evidence ostensibly supporting these conjectures was inferred from epidemiologic studies based on the naïve notion that a person's usual dietary intake (i.e., consumed foods and beverages) could be estimated simply by asking what he or she remembered eating and drinking (9,(15)(16)(17). Despite the fact that the data collected by these memory-based dietary assessment methods (M-BMs) were nonfalsifiable anecdotes (i.e., verbal or textual self-reports) and were repeatedly demonstrated to lack validity and reliability as far back as the 1950s (18,19), studies employing M-BMs came to dominate the empiric, policy, and media landscapes (15)(16)(17)20). By the 1980s, tens of thousands of research reports based on M-BMs were published and some of these publications became the most highly-cited and widely publicized articles in the biomedical literature. ...
... Nevertheless, six decades of rigorous and highly-replicated research demonstrated unequivocally that M-BMs data were physiologically implausible (i.e., meaningless numbers) (9,(15)(16)(17)(21)(22)(23)(24)(25), often "incompatible with life, " (26) and had trivial relations to actual nutrient and caloric consumption (9, 15-17, 21-23, 26-44). For example, in 2013 we used multiple methods to show that from 1971 to 2010, no human being could survive on the average reported caloric intake in the National Health and Nutrition Examination Survey (NHANES) (21). ...
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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.
... Some studies have shown that individuals can be inaccurate and may alter dietary patterns when asked to report their dietary intake [27,28]. In our experience, Italian males with fertility problems usually report almost full adherence to a Mediterranean diet even when their BMI index and clinical parameters strongly suggest unhealthy diet habits [unpublished data]. ...
... 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]. ...
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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.
... Genome wide association and linkage studies have added more than 600 genetic variants and chromosomal regions to the repertoire of genetic factors associated with obesity, body weight, body mass index, body fat composition and distribution, energy expenditure and fuel oxidation and various other phenotypic features linked with nutrition (67)(68)(69)(70)(71)(72)(73)(74)(75)(76)(77)(78)(79)(80)(81)(82)(83). One of the first genetic variants associated with obesity was a single nucleotide polymorphism in the FTO gene. ...
... This method involves extensive and vigorous exercise or physical activity. On the other hand, intake of low calories with a more satiating diet may also result in weight loss in association with physical activity (67,81,83). Several genes have been reported to be linked with weight loss in response to hypocaloric diet coupled with physical activity. ...
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Owing to the fields of nutrigenetics and nutrigenomics today we can think of devising approaches to optimize health, delay onset of diseases and reduce its severity according to our genetic blue print. However this requires a deep understanding of nutritional impact on expression of genes that may result in a specific phenotype. The extensive research and observational studies during last two decades reporting interactions between genes, diet and physical activity suggest a cross talk between various genetic and environmental fac-tors and lifestyle interventions. Although considerable efforts have been made in unraveling the mechanisms of gene-diet interactions the scientific evidences behind developing commercial genetic tests for providing personalized nutrition recommendations are still scarce. In this scenario the current mini-review aims to provide useful insights into salient feature of nutrition based genetic research and its commercial application and the ethical issue and concerns related to its outcome.
... For observational research on LES specifically, the validity of certain associations must however be questioned when they are repeatedly disconfirmed by evidence from intervention trials, combined with a susceptibility to confounding that undermines the assignment of a causal interpretation [27,29,42,43]. It is perhaps useful here to consider the "white swan" metaphor [44]: given the chequered history of claims based on nutritional epidemiology, the practice of continuously propping up a particular observation ("all swans are white") with further observational research is fundamentally undermined when controlled studies reveal something different (i.e., the presence of "black swans"). ...
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This perspective considers evidence of a common academic bias against low-energy sweeteners (LES). The core proposition is that this bias is manifested in research and reporting focused on generating and placing a negative spin on LESs, largely through selective citation, interpretation and reporting. The evidence centres on three inter-related points, which together may generate a misleading impression of the balance of evidence: (1) basic and mechanistic research on LES perpetuates “explanations” for unsubstantiated adverse effects of LES; (2) the literature on LES—particularly narrative reviews and commentaries—continually reprises hypotheses of adverse effects without acknowledging where these hypotheses have been rigorously tested and rejected; and (3) negative interpretations of the effects of LES largely rely upon selectively emphasising lower-quality research whilst ignoring or dismissing higher-quality evidence. The expert community should consider these issues in assuring scientific integrity and balance in the academic discourse on LES, and how this is translated into messages for public health and consumers.
... Further studies are needed to elucidate whether genetic variants may influence the outcomes of the nutritional intervention. To date, it should be emphasized that there are discrepancies in previous weight loss clinical studies due to: (i) the types of interventions, including energyrestricted diets, duration of the intervention, and physical activity interventions; (ii) the participants' heterogeneity in what concerns age (adults, older adults), ancestry, nutritional status (overweight, obese, severely obese), pathologic situation/status (prediabetic, diabetic); (iii) the dietary assessment method that can produce inaccurate dietary data collection [74]. Therefore, with regard to the analysis of gene-diet interactions, all the aspects mentioned above make comparisons between findings difficult and should be considered in order to achieve comparability across different studies. ...
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Aims Nutritional and lifestyle interventions can contribute to prevent and treat obesity and its complications; however, genetic background may influence the success of a therapy. The aim of this pilot study is to evaluate the effects of the interaction between nutrigenetic variants and nutritional intervention, as well as the changes in clinical parameters and the adherence to Mediterranean diet (MedDiet) and to physical activity, of 18 overweight or obese subjects affected by T2D or dysglycemia included in a nutritional program. Methods The subjects’ clinical parameters as well as their PREDIMED score and physical activity levels were recorded and compared at baseline, at 6 months and at the end of the intervention. Rs9939609 in FTO , rs17782313 near MC4R , rs326 in LPL , rs16147 in NPY , rs2943641 near IRS-1 were genotyped. Results The subjects carrying the A allele in FTO lost less weight ( p = 0.022) and had a lower BMI decrease from baseline to 12 months ( p -interaction = 0.047) than TT carriers. In addition, there was a significant PREDIMED score modification over time, according to genotypes for FTO rs9939609 ( p = 0.025) and NPY rs16147 ( p = 0.039), respectively. Conclusions These preliminary findings show a significant interaction between genetic variants and the PREDIMED score, suggesting that individuals carrying the FTO variant may lose less weight than non-carriers through diet/lifestyle intervention.
... Large prospective cohort studies are necessary to distinguish a causal relation. In addition, all data derived from FFQs might be invalid and physiologically implausible because memory and recall are not valid tools to collect scientific data (61). Since the number of lean participants was low in our sample (n = 114, 3.4%), we had to include these individuals in the category of normal-weight participants. ...
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Background: The association between meat consumption and mental disorders is less investigated in Iranian population. We examined the association between meat consumption and prevalence of symptoms of depression, anxiety, and psychological distress in Iranian adults. Methods: This cross-sectional study included 3,362 participants aged 18–55 years old. A dish-based 106-item semiquantitative food frequency questionnaire (FFQ) was used to assess usual dietary intake of study population. Hospital Anxiety and Depression Scale (HADS) and General Health Questionnaire (GHQ), all validated in Iranian population, were applied to collect data on symptoms of anxiety, depression, and psychological distress, respectively. Results: The prevalence of symptoms of depression, anxiety, and psychological distress in the study population was 28.6, 13.6, and 22.6%, respectively. After considering potential confounders, individuals in the top quartile of red meat intake had 43% increased risk of depression symptoms [odds ratio (OR) = 1.43; 95% CI: 1.09–1.89] compared to those in the first quartile. No significant relation was observed between red meat intake and anxiety or psychological distress symptoms. White meat consumption was not associated with mental disorders. Stratified analysis by sex showed that male participants in the highest quartile of red meat intake had 92% greater risk of depression symptoms (95% CI: 1.17–3.15) than those individuals in the lowest category. Red and white meat intake was not associated with mental disorders in women. In overweight or obese individuals, despite lack of any association between red meat intake and mental disorders, high intake of white meat was associated with a lower odds of psychological distress symptoms (OR = 0.64; 95% CI: 0.42–0.99) and a lower risk of depression symptoms (OR = 0.68; 95% CI: 0.45–1.00). In normal-weight participants, those in the highest quartile of red meat intake had greater odds for depression symptoms than those in the lowest quartile (OR = 1.66; 95% CI: 1.14–2.42). Conclusions: We found that red meat consumption was associated with increased risk of depression symptoms, especially in men, and normal-weight participants. In overweight or obese participants, white meat intake was inversely associated with psychological distress symptoms.
... 40 All self-reported data have limitations, and we are unable to quantify the effect that both intentional and nonintentional factors at participant level may have had on the accuracy of UK Biobank's self-reported data. 41,42 For example, the dietary variables used here are categorical, and we are unable exclude potential outliers or implausible values owing to the nature of the data. Therefore, our results may have been influenced by unknown inaccuracies in the self-reported data. ...
Article
Objective To inform potential guideline development, we investigated nonlinear associations between television viewing time (TV time) and adverse health outcomes. Methods From 2006 to 2010, 490,966 UK Biobank participants, aged 37 to 73 years, were recruited. They were followed from 2006 to 2018. Nonlinear associations between self-reported TV time (hours per day) and outcomes explored using penalized cubic splines in Cox proportional hazards adjusted for demographics and lifestyle. Population-attributable and potential impact fractions were calculated to contextualize population-level health outcomes associated with different TV time levels. Nonlinear isotemporal substitution analyses were used to investigate substituting TV time with alternative activities. Primary outcomes were mortality: all-cause, cardiovascular disease (CVD) and cancer; incidence: CVD and cancer; secondary outcomes were incident myocardial infarction, stroke, and heart failure and colon, lung, breast, and prostate cancer. Results Those with noncommunicable disease (109,867 [22.4%]), CVD (32,243 [6.6%]), and cancer (37,81 [7.7%]) at baseline were excluded from all-cause mortality, CVD, and cancer analyses, respectively. After 7.0 years (mortality) and 6.2 years (disease incidence) mean follow-up, there were 10,306 (2.7%) deaths, 24,388 (5.3%) CVD events, and 39,121 (8.7%) cancer events. Associations between TV time and all-cause and CVD mortality were curvilinear (Pnon-linear ≤.003), with lowest risk observed <2 hours per day. Theoretically, 8.64% (95% confidence interval [CI], 6.60-10.73) of CVD mortality is attributable to TV time. Limiting TV time to 2 hours per day might have prevented, or at least delayed, 7.97% (95% CI, 5.54-10.70) of CVD deaths. Substituting TV time with sleeping, walking, or moderate or vigorous physical activity was associated with reduced risk for all outcomes when baseline levels of substitute activities were low. Conclusion TV time is associated with numerous adverse health outcomes. Future guidelines could suggest limiting TV time to less than 2 hours per day to reduce most of the associated adverse health events.
... First, the included prospective cohort studies were observational in nature, and so one cannot discount the possibility of measured and unmeasured residual confounding. In addition, the validity of self-reported dietary consumption is limited, [63][64][65] as it is argued that it represents only a collection of memories of perception of dietary intake, leading to its possible implausibility due to misestimations. [66][67][68] Estimates of sugar dose in our paper are based upon self-reported dietary recall and should be inferred in light of this limitation. ...
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Objective: To determine the association of total and added fructose-containing sugars on cardiovascular (CVD) incidence and mortality. Methods: MEDLINE, EMBASE and Cochrane Library were searched from January 1, 1980, to July 31, 2018. Prospective cohort studies assessing the association of reported intakes of total, sucrose, fructose and added sugars with CVD incidence and mortality in individuals free from disease at baseline were included. Risk estimates were pooled using the inverse variance method, and dose-response analysis was modeled. Results: Eligibility criteria were met by 24 prospective cohort comparisons (624,128 unique individuals; 11,856 CVD incidence cases and 12,224 CVD mortality cases). Total sugars, sucrose, and fructose were not associated with CVD incidence. Total sugars (risk ratio, 1.09 [95% confidence interval, 1.02 to 1.17]) and fructose (1.08 [1.01 to 1.15]) showed a harmful association for CVD mortality, there was no association for added sugars and a beneficial association for sucrose (0.94 [0.89 to 0.99]). Dose-response analyses showed a beneficial linear dose-response gradient for sucrose and nonlinear dose-response thresholds for harm for total sugars (133 grams, 26% energy), fructose (58 grams, 11% energy) and added sugars (65 grams, 13% energy) in relation to CVD mortality (P<.05). The certainty of the evidence using GRADE was very low for CVD incidence and low for CVD mortality for all sugar types. Conclusion: Current evidence supports a threshold of harm for intakes of total sugars, added sugars, and fructose at higher exposures and lack of harm for sucrose independent of food form for CVD mortality. Further research of different food sources of sugars is needed to define better the relationship between sugars and CVD.
... Two commentaries extend the fascinating controversy and debate covered by four recent articles [5][6][7][8] in the December 2018 issue on the merits or flaws in memory based methods for assessing dietary intake. Barnes tackles this by partitioning each argument into two principal components: data and claim. ...
... Twenty-four-hour recalls (24HRs) and food frequency questionnaires (FFQs) are common instruments to collect self-reported dietary intakes [3]. However, the validity of self-reported data obtained via such memory-based dietary assessment methods, and hence the whole value of nutrition epidemiology, is being challenged based on their purported inability to correctly reflect true food and nutrient consumption [4][5][6][7]. However, others have argued that despite recognized limitations, relying on self-reported dietary intake data in epidemiological studies has been instrumental in developing impactful dietary guidelines and recommendations over the years [1,2,[7][8][9][10]. ...
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Traditional food frequency questionnaires (FFQs) are influenced by systematic error, but web-based FFQ (WEB-FFQs) may mitigate this source of error. The objective of this study was to compare the accuracy of interview-based and web-based FFQs to assess energy requirements (mERs). The mER was measured in a series of controlled feeding trials in which participants daily received all foods and caloric drinks to maintain stable body weight over 4 to 6 weeks. FFQs assessing dietary intakes and hence mean energy intake were either interviewer-administered by a registered dietitian (IA-FFQ, n = 127; control method) or self-administered using a web-based platform (WEB-FFQ, n = 200; test method), on a single occasion. Comparison between self-reported energy intake and mER revealed significant under-reporting with the IA-FFQ (−9.5%; 95% CI, −12.7 to −6.1) and with the WEB-FFQ (−11.0%; 95% CI, −15.4 to −6.4), but to a similar extent between FFQs (p = 0.62). However, a greater proportion of individuals were considered as accurate reporters of energy intake using the IA-FFQ compared with the WEB-FFQ (67.7% vs. 48.0%, respectively), while the prevalence of over-reporting was lower with the IA-FFQ than with the WEB-FFQ (6.3% vs. 17.5%, respectively). These results suggest less accurate prediction of true energy intake by a self-administered WEB-FFQ than with an IA-FFQ.
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In this meta-analysis, we examined the quantitative relation between meat consumption or avoidance, depression, and anxiety. In June 2020, we searched five online databases for primary studies examining differences in depression and anxiety between meat abstainers and meat consumers that offered a clear (dichotomous) distinction between these groups. Twenty studies met the selection criteria representing 171,802 participants with 157,778 meat consumers and 13,259 meat abstainers. We calculated the magnitude of the effect between meat consumers and meat abstainers with bias correction (Hedges's g effect size) where higher and positive scores reflect better outcomes for meat consumers. Meat consumption was associated with lower depression (Hedges's g = 0.216, 95% CI [0.14 to 0.30], p < .001) and lower anxiety (g = 0.17, 95% CI [0.03 to 0.31], p = .02) compared to meat abstention. Compared to vegans, meat consumers experienced both lower depression (g = 0.26, 95% CI [0.01 to 0.51], p = .041) and anxiety (g = 0.15, 95% CI [-0.40 to 0.69], p = .598). Sex did not modify these relations. Study quality explained 58% and 76% of between-studies heterogeneity in depression and anxiety, respectively. The analysis also showed that the more rigorous the study, the more positive and consistent the relation between meat consumption and better mental health. The current body of evidence precludes causal and temporal inferences.
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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.
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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.
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The mammalian body is a complex physiologic ‘ecosystem’ in which cells compete for calories (i.e., nutrient-energy). Axiomatically, cell-types with competitive advantages acquire a greater number of consumed calories, and when possible, increase in size and/or number. Thus, it is logical and parsimonious to posit that obesity is the competitive advantages of fat-cells (adipocytes) driving a disproportionate acquisition and storage of nutrient-energy. Accordingly, we introduce two conceptual frameworks. Asymmetric Nutrient-Energy Partitioning describes the context-dependent, cell-specific competition for calories that determines the partitioning of nutrient-energy to oxidation, anabolism, and/or storage; and Effective Caloric Intake which describes the number of calories available to constrain energy-intake via the inhibition of the sensorimotor appetitive cells in the liver and brain that govern ingestive behaviors. Inherent in these frameworks is the independence and dissociation of the energetic demands of metabolism and the neuro-muscular pathways that initiate ingestive behaviors and energy intake. As we demonstrate, if the sensorimotor cells suffer relative caloric deprivation via asymmetric competition from other cell-types (e.g., fat-cells), energy-intake is increased to compensate for both real or merely apparent deficits in energy-homeostasis (i.e., true and false signals, respectively). Thus, we posit that the chronic positive energy balance (i.e., over-nutrition) that leads to obesity and metabolic diseases is engendered by apparent deficits (i.e., false signals) driven by the asymmetric inter-cellular competition for calories and concomitant differential partitioning of nutrient-energy to storage. These frameworks, in concert with our previous theoretic work, the Maternal Resources Hypothesis, provide a parsimonious and rigorous explanation for the rapid rise in the global prevalence of increased body and fat mass, and associated metabolic dysfunctions in humans and other mammals inclusive of companion, domesticated, laboratory, and feral animals.
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This paper describes the Observing Protein and Energy Nutrition (OPEN) Study, conducted from September 1999 to March 2000. The purpose of the study was to assess dietary measurement error using two self-reported dietary instruments-the food frequency questionnaire (FFQ) and the 24-hour dietary recall (24HR)-and unbiased biomarkers of energy and protein intakes: doubly labeled water and urinary nitrogen. Participants were 484 men and women aged 40-69 years from Montgomery County, Maryland. Nine percent of men and 7% of women were defined as underreporters of both energy and protein intake on 24HRs; for FFQs, the comparable values were 35% for men and 23% for women. On average, men underreported energy intake compared with total energy expenditure by 12-14% on 24HRs and 31-36% on FFQs and underreported protein intake compared with a protein biomarker by 11-12% on 24HRs and 30-34% on FFQs. Women underreported energy intake on 24HRs by 16-20% and on FFQs by 34-38% and underreported protein intake by 11-15% on 24HRs and 27-32% on FFQs. There was little underreporting of the percentage of energy from protein for men or women. These findings have important implications for nutritional epidemiology and dietary surveillance.
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NHANES is the cornerstone for national nutrition monitoring to inform nutrition and health policy. Nutritional assessment in NHANES is described with a focus on dietary data collection, analysis, and uses in nutrition monitoring. NHANES has been collecting thorough data on diet, nutritional status, and chronic disease in cross-sectional surveys with nationally representative samples since the early 1970s. Continuous data collection began in 1999 with public data release in 2-y cycles on ∼10,000 participants. In 2002, the Continuing Survey of Food Intakes by Individuals and the NHANES dietary component were merged, forming a consolidated dietary data collection known as What We Eat in America; since then, 24-h recalls have been collected on 2 d using the USDA's Automated Multiple-Pass Method. Detailed and targeted food-frequency questionnaires have been collected in some NHANES cycles. Dietary supplement use data have been collected (in detail since 2007) so that total nutrient intakes can be described for the population. The continuous NHANES can adapt its content to address emerging public health needs and reflect federal priorities. Changes in data collection methods are made after expert input and validation/crossover studies. NHANES dietary data are used to describe intake of foods, nutrients, food groups, and dietary patterns by the US population and large sociodemographic groups to plan and evaluate nutrition programs and policies. Usual dietary intake distributions can be estimated after adjusting for day-to-day variation. NHANES remains open and flexible to incorporate improvements while maintaining data quality and providing timely data to track the nation's nutrition and health status. In summary, NHANES collects dietary data in the context of its broad, multipurpose goals; the strengths and limitations of these data are also discussed in this review.
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Recent reports have asserted that, because of energy underreporting, dietary self-report data suffer from measurement error so great that findings that rely on them are of no value. This commentary considers the amassed evidence that shows that self-report dietary intake data can successfully be used to inform dietary guidance and public health policy. Topics discussed include what is known and what can be done about the measurement error inherent in data collected by using self-report dietary assessment instruments and the extent and magnitude of underreporting energy vs. other nutrients and food groups. Also discussed is the overall impact of energy underreporting on dietary surveillance and nutritional epidemiology. In conclusion, 7 specific recommendations for collecting, analyzing, and interpreting self-report dietary data are provided: 1) continue to collect self-report dietary intake data because they contain valuable, rich, and critical information about foods and beverages consumed by populations that can be used to inform nutrition policy and assess diet-disease associations; 2) do not use self-reported energy intake as a measure of true energy intake; 3) do use self-reported energy intake for energy adjustment of other self-reported dietary constituents to improve risk estimation in studies of diet-health associations; 4) acknowledge the limitations of self-report dietary data and analyze and interpret them appropriately; 5) design studies and conduct analyses that allow adjustment for measurement error; 6) design new epidemiologic studies to collect dietary data from both short-term (recalls or food records) and long-term (food-frequency questionnaires) instruments on the entire study population to allow for maximizing the strengths of each instrument; and 7) continue to develop, evaluate, and further expand methods of dietary assessment, including dietary biomarkers and methods using new technologies.
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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.
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Dietary assessment has long been known to be challenged by measurement error. A substantial amount of literature on methods for determining the effects of error on causal inference has accumulated over the past decades. These methods have unrealized potential for improving the validity of data collected for research studies and national nutritional surveillance, primarily through the NHANES. Recently, the validity of dietary data has been called into question. Arguments against using dietary data to assess diet–health relations or to inform the nutrition policy debate are subject to flaws that fall into 2 broad areas: 1) ignorance or isunderstanding of methodologic issues; and 2) faulty logic in drawing inferences. Nine specific issues are identified in these arguments, indicating insufficient grasp of themethods used for assessing diet and designing nutritional epidemiologic studies. These include a narrow operationalization of validity, failure to properly account for sources of error, and large, unsubstantiated jumps to policy implications. Recent attacks on the inadequacy of 24-h recall–derived data from the NHANES are uninformative regarding effects on estimating risk of health outcomes and on inferences to inform the diet-related health policy debate. Despite errors, for many purposes and inmany contexts, these dietary data have proven to be useful in addressing important research and policy questions. Similarly, structured instruments, such as the food frequency questionnaire, which is the mainstay of epidemiologic literature, can provide useful data when errors are measured and considered in analyses. Adv. Nutr. 5: 447–455, 2014.
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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.
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A recent decision in the United States by the New Jersey Supreme Court has led to improved jury instructions that incorporate psychological research showing that memory does not operate like a video recording. Here we consider how cognitive neuroscience could contribute to addressing memory in the courtroom. We discuss conditions in which neuroimaging can distinguish true and false memories in the laboratory and note reasons to be skeptical about its use in courtroom cases. We also discuss neuroscience research concerning false and imagined memories, misinformation effects and reconsolidation phenomena that may enhance understanding of why memory does not operate like a video recording.
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The evidence of informant inaccuracy ought not to lead to complaints or despair among researchers. It ought instead to lead to a rich, relatively unexplored arena of inquiry. Informants are not to blame for being wrong. People everywhere get along quite well without being able to dredge up accurately the sort of information that social scientists ask of them. If the latter have a great deal of inaccurate data, then they have only themselves to blame. The instruments of their craft have been used too uncritically. - J.Sheail
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Two experiments (modeled after J. Deese's 1959 study) revealed remarkable levels of false recall and false recognition in a list learning paradigm. In Exp 1, Ss studied lists of 12 words (e.g., bed, rest, awake); each list was composed of associates of 1 nonpresented word (e.g., sleep). On immediate free recall tests, the nonpresented associates were recalled 40% of the time and were later recognized with high confidence. In Exp 2, a false recall rate of 55% was obtained with an expanded set of lists, and on a later recognition test, Ss produced false alarms to these items at a rate comparable to the hit rate. The act of recall enhanced later remembering of both studied and nonstudied material. The results reveal a powerful illusion of memory: People remember events that never happened. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
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Human memory is not a literal reproduction of the past, but instead relies on constructive processes that are sometimes prone to error and distortion. Understanding of constructive memory has accelerated during recent years as a result of research that has linked together its cognitive and neural bases. This article focuses on three aspects of constructive memory that have been the target of recent research: (i) the idea that certain kinds of memory distortions reflect the operation of adaptive cognitive processes that contribute to the efficient functioning of memory; (ii) the role of a constructive memory system in imagining or simulating possible future events; and (iii) differences between true and false memories that have been revealed by functional neuroimaging techniques. The article delineates the theoretical implications of relevant research, and also considers some clinical and applied implications.
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Prevalence estimates of illicit drug use by teens are typically generated from confidential or anonymous self-report. While data comparing teen self-report with biological measures are limited, adult studies identify varying degrees of under-reporting. Hair analyses for cocaine, opiates and marijuana were compared to confidential teen self- and parent-reported teen drug use in a longitudinal cohort of >400 high-risk urban teens and parents. Both teens and parents substantially underreported recent teen cocaine and opiate use. However, compared with parents, teens were more likely to deny biomarker-verified cocaine use. Teen specimens (hair) were 52 times more likely to identify cocaine use compared with self-report. Parent hair analyses for cocaine and opiate use were 6.5 times and 5.5 times, respectively, more likely to indicate drug use than were parental self-report. The lack of concordance between self-report and bioassay occurred despite participant's knowledge that a "certificate of confidentiality" protected both teen and adult participants, and that the biological specimens would be tested for drugs. These findings confirm prior reports of adult under-reporting of their own drug use while extending our understanding of teen's self-admitted drug use. The lack of concordance between teen self- or parent-reported teen drug use and biomarkers confirm our concerns that both teen- and parent-reported teen drug use is limited, at least for youth in high-risk urban settings. Methods of ascertainment other than self- or parent-report must be considered when health care providers, researchers and public health agencies attempt to estimate teen drug-use prevalence.
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There is an escalating debate over the value and validity of memory-based dietary assessment methods (M-BMs). Proponents argue that despite limitations, M-BMs such as food frequency questionnaires (FFQs), provide valid and valuable information about consumed foods and beverages, and therefore can be used to assess diet-disease relations and inform public policy. In fact, over the past 60 years thousands of research reports using these methods were published and used to populate the United States Department of Agriculture's National Evidence Library, inform public policy, and establish the Dietary Guidelines for Americans. Despite this impressive history, our position is that FFQs and other M-BMs are invalid and inadmissible for scientific research and cannot be employed in evidence-based policy making. Herein, we present the empirical evidence, and theoretic and philosophic perspectives that render M-BMs data both fatally flawed and pseudo-scientific. First, the use of M-BMs is founded upon two inter-related logical fallacies: a category error and reification. Second, human memory and recall are not valid instruments for scientific data collection. Third, in standard epidemiologic contexts, the measurement errors associated with self-reported data are non-falsifiable (i.e., pseudo-scientific) because there is no way to ascertain if the reported foods and beverages match the respondent's actual intake. Fourth, the assignment of nutrient and energy values to self-reported intake (i.e., the pseudo-quantification of qualitative/anecdotal data) is impermissible and violates the foundational tenets of measurement theory. Fifth, the proxy-estimates created via pseudo-quantification are physiologically implausible (i.e. meaningless numbers) and have little relation to actual nutrient and energy consumption. Finally, investigators engendered a fictional discourse on the health effects of dietary sugar, salt, fat and cholesterol when they failed to cite contrary evidence or address decades of research demonstrating the fatal measurement, analytic, and inferential flaws presented herein.
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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.
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Background: Underreporting of food intake is common in obese subjects. Objective: One aim of this study was to assess to what extent underreporting by obese men is explained by underrecording (failure to record in a food diary everything that is consumed) or undereating. Another aim of the study was to find out whether there was an indication for selective underreporting. Design: Subjects were 30 obese men with a mean (±SD) body mass index (in kg/m²) of 34 ± 4. Total food intake was measured over 1 wk. Energy expenditure (EE) was measured with the doubly labeled water method, and water loss was estimated with deuterium-labeled water. Energy balance was checked for by measuring body weight at the start and end of the food-recording week and 1 wk after the recording week. Results: Mean energy intake and EE were 10.4 ± 2.5 and 16.7 ± 2.4 MJ/d, respectively; underreporting was 37 ± 16%. The mean body mass loss of 1.0 ± 1.3 kg over the recording week was significantly different (P < 0.05) from the change in body mass over the nonrecording week, and indicated 26% undereating. Water intake (reported + metabolic water) and water loss were significantly different from each other and indicated 12% underrecording. The reported percentage of energy from fat was a function of the level of underreporting: percentage of energy from fat = 46 – 0.2 × percentage of underreporting (r² = 0.28, P = 0.003). Conclusions: Total underreporting by the obese men was explained by underrecording and undereating. The obese men selectively underreported fat intake.
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Aims: To estimate the prevalence and predictors of failed biochemical verification of self-reported abstinence among participants enrolled in trials of hospital-initiated smoking cessation interventions. Design: Comparison of characteristics between participants who verified and those who failed to verify self-reported abstinence. Settings: Multi-site randomized clinical trials conducted between 2010 and 2014 in hospitals throughout the United States. Participants: Recently hospitalized smokers who reported tobacco abstinence 6 months post-randomization and provided a saliva sample for verification purposes (n = 822). Measurements: Outcomes were salivary cotinine-verified smoking abstinence at 10 and 15 ng/ml cut-points. Predictors and correlates included participant demographics and tobacco use; hospital diagnoses and treatment; and study characteristics collected via surveys and electronic medical records. Findings: Usable samples were returned by 69.8% of the 1178 eligible trial participants who reported 7-day point prevalence abstinence. The proportion of participants verified as quit was 57.8% [95% confidence interval (CI) = 54.4, 61.2; 10 ng/ml cut-off] or 60.6% (95% CI = 57.2, 63.9; 15 ng/ml). Factors associated independently with verification at 10 ng/ml were education beyond high school education [odds ratio (OR) = 1.51; 95% CI = 1.07, 2.11], continuous abstinence since hospitalization (OR = 2.82; 95% CI = 2.02, 3.94), mailed versus in-person sample (OR = 3.20; 95% CI = 1.96, 5.21) and race. African American participants were less likely to verify abstinence than white participants (OR = 0.64; 95% CI = 0.44, 0.93). Findings were similar for verification at 15 ng/ml. Verification rates did not differ by treatment group. Conclusions: In the United States, high rates (40%) of recently hospitalized smokers enrolled in smoking cessation trials fail biochemical verification of their self-reported abstinence.
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Calibrating dietary self-report instruments is recommended as a way to adjust for measurement error when estimating diet-disease associations. Because biomarkers available for calibration are limited, most investigators use self-reports (e.g., 24-hour recalls (24HRs)) as the reference instrument. We evaluated the performance of 24HRs as reference instruments for calibrating food frequency questionnaires (FFQs), using data from the Validation Studies Pooling Project, comprising 5 large validation studies using recovery biomarkers. Using 24HRs as reference instruments, we estimated attenuation factors, correlations with truth, and calibration equations for FFQ-reported intakes of energy and for protein, potassium, and sodium and their densities, and we compared them with values derived using biomarkers. Based on 24HRs, FFQ attenuation factors were substantially overestimated for energy and sodium intakes, less for protein and potassium, and minimally for nutrient densities. FFQ correlations with truth, based on 24HRs, were substantially overestimated for all dietary components. Calibration equations did not capture dependencies on body mass index. We also compared predicted bias in estimated relative risks adjusted using 24HRs as reference instruments with bias when making no adjustment. In disease models with energy and 1 or more nutrient intakes, predicted bias in estimated nutrient relative risks was reduced on average, but bias in the energy risk coefficient was unchanged.
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To investigate the hypothesis that misreporting observed in dietary assessments would be associated with nutrition knowledge and health consciousness, we compared the degree of misreporting between 99 female dietitians and 117 non-dietitians who worked at welfare facilities in Japan. Sodium, potassium, and protein intake were assessed by two 24-h urine collections, four-day semi-weighed dietary records, and two validated diet history questionnaires. Intake of these three nutrients measured by each method was compared. The ratio of self-reported intake to biomarker-based intake was used as an index of reporting accuracy, and compared between dietitians and non-dietitians. Pearson correlation coefficients between biomarker-based and self-reported intakes were also compared between dietary assessment methods within the same group, as well as between the two groups. The dietitians tended to under-report sodium and protein intake more severely than the non-dietitians, and over-reported potassium intake more obviously. However, the degree of misreporting did not significantly differ between the two groups. The correlation coefficients between biomarker-based and self-reported intakes were significantly lower with the two diet history questionnaires than with the diet record, particularly in the dietitians. In conclusion, misreporting was strongly suspected to be more severe among the dietitians, and the validity of the diet history questionnaires differed between the two groups and this result suggests that misreporting might be associated with higher nutrition knowledge and health consciousness.
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It has a big impact on the diet of American citizens, and those of most Western nations, so why does the expert advice underpinning US government dietary guidelines not take account of all the relevant scientific evidence? Nina Teicholz reports
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Comparing reported energy intakes with estimated energy requirements as multiples of basal metabolic rate (Ein:BMR) is an established method of identifying implausible food intake records. The present study aimed to examine the validity of self-reported food intakes believed to be plausible. One hundred and eighty men and women were provided with all food and beverages for two consecutive days in a residential laboratory setting. Subjects self-reported their food and beverage intakes using the weighed food diary method (WDR). Investigators covertly measured subjects' actual consumption over the same period. Subjects also reported intakes over four consecutive days at home. BMR was measured by indirect calorimetry. Average reported energy intakes were significantly lower than actual intakes (11.2 and 11.8 MJ/d, respectively, P<0.001). Two-thirds (121) of the WDR were under-reported to varying degrees. Only five of these were considered as implausible using an Ein:BMR cut-off value of 1.03*BMR. Under-reporting of food and beverage intakes, as measured by the difference between reported and actual intake, was evident at all levels of Ein;BMR. Reported energy intakes were lower still (10.2 MJ/d) while subjects were at home. Under-recording of self-reported food intake records was extensive but very few under-reported food intake records were identified as implausible using energy intake to BMR ratios. Under-recording was evident at all levels of energy intake.European Journal of Clinical Nutrition advance online publication, 29 July 2015; doi:10.1038/ejcn.2015.124.
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We examine the relation between memory and self by considering errors of memory. We draw on the idea that memory's imperfections can be classified into seven basic categories or “sins.” Three of the sins concern different types of forgetting (transience, absent-mindedness, and blocking), three concern different types of distortion (misattribution, suggestibility, and bias), and one concerns intrusive memories (persistence). We focus in particular on two of the distortion-related sins, misattribution and bias. By describing cognitive, neuropsychological, and neuroimaging studies that illuminate these memory sins, we consider how they might bear on the relation between memory and self.
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As under-reporting of dietary intake, particularly by overweight and obese subjects, is common in dietary surveys, biases inherent in the use of self-reported dietary information may distort true diet-obesity relationships or even create spurious ones. However, empirical evidence of this possibility is limited. The present cross-sectional study compared the relationships of 24 h urine-derived and self-reported intakes of Na, K and protein with obesity. A total of 1043 Japanese women aged 18-22 years completed a 24 h urine collection and a self-administered diet history questionnaire. After adjustment for potential confounders, 24 h urine-derived Na intake was associated with a higher risk of general obesity (BMI ≥ 25 kg/m2) and abdominal obesity (waist circumference ≥ 80 cm; both P for trend = 0·04). For 24 h urine-derived protein intake, positive associations with general and abdominal obesity were observed (P for trend = 0·02 and 0·053, respectively). For 24 h urine-derived K intake, there was an inverse association with abdominal obesity (P for trend = 0·01). Conversely, when self-reported dietary information was used, only inverse associations between K intake and general and abdominal obesity were observed (P for trend = 0·04 and 0·02, respectively), with no associations of Na or protein intake. In conclusion, we found positive associations of Na and protein intakes and inverse associations of K intake with obesity when using 24 h urinary excretion for estimating dietary intakes. However, no association was observed based on using self-reported dietary intakes, except for inverse association of K intake, suggesting that the ability of self-reported dietary information using the diet history questionnaire for investigating diet-obesity relationships is limited.
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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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The article’s authors describe recent movement in science communications and research to embrace a broader approach than has been utilized previously in reaching understanding of modern, complex issues facing scientists, policy makers, and the public today, such as obesity and climate change. Referring to what social anthropologists have called “distanciation,” “disembedding,” and “unresolved trust issues,” between scientists and the public, the authors cite recent calls by academicians, policy analysts, and health professionals for a greater scientific inclusionary focus to research and communication. They argue that the physical sciences alone may not describe the food and lifestyle behaviors or the food system that have led to alarming increases in noncommunicable diseases such as diabetes, obesity, and other modern health conditions. They point to increasing participation by experts in the social sciences and humanities in conferences, research, and communications, regarding contemporary critical nutrition and health issues, a move to transdisciplinarity.
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Nutritional epidemiology has recently been criticized on several fronts, including the inability to measure diet accurately, and for its reliance on observational studies to address etiologic questions. In addition, several recent meta-analyses with serious methodologic flaws have arrived at erroneous or misleading conclusions, reigniting controversy over formerly settled debates. All of this has raised questions regarding the ability of nutritional epidemiologic studies to inform policy. These criticisms, to a large degree, stem from a misunderstanding of the methodologic issues of the field and the inappropriate use of the drug trial paradigm in nutrition research. The exposure of interest in nutritional epidemiology is human diet, which is a complex system of interacting components that cumulatively affect health. Consequently, nutritional epidemiology constantly faces a unique set of challenges and continually develops specific methodologies to address these. Misunderstanding these issues can lead to the nonconstructive and sometimes naive criticisms we see today. This article aims to clarify common misunderstandings of nutritional epidemiology, address challenges to the field, and discuss the utility of nutritional science in guiding policy by focusing on 5 broad questions commonly asked of the field. © 2015 American Society for Nutrition.
Article
Misreporting of dietary intake affects the validity of data collected and conclusions drawn in studies exploring diet and health outcomes. One consequence of misreporting is biological implausibility. Little is known regarding how accounting for biological implausibility of reported intake affects nutrient intake estimates in Hispanics, a rapidly growing demographic in the United States. Our study explores the effect of accounting for plausibility on nutrient intake estimates in a sample of Mexican-American women in northern California in 2008. Nutrient intakes are compared with Dietary Reference Intake recommendations, and intakes of Mexican-American women in a national survey are presented as a reference. Eighty-two women provided three 24-hour recalls. Reported energy intakes were classified as biologically plausible or implausible using the reported energy intakes to total energy expenditure cutoff of <0.76 or >1.24, with low-active physical activity levels used to estimate total energy expenditure. Differences in the means of nutrient intakes between implausible (n=36) and plausible (n=46) reporters of energy intake were examined by bivariate linear regression. Estimated energy, protein, cholesterol, dietary fiber, and vitamin E intakes were significantly higher in plausible reporters than implausible. There was a significant difference between the proportions of plausible vs implausible reporters meeting recommendations for several nutrients, with a larger proportion of plausible reporters meeting recommendations. Further research related to misreporting in Hispanic populations is warranted to explore the causes and effects of misreporting in studies measuring dietary intake, as well as actions to be taken to prevent or account for this issue.
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results from the secondary prevention trials should translate equally to the prevention of primary cancers, even regardless of their estrogen receptor (ER) status. Tamoxifen and raloxifene are both geared toward ER-positive cancer cells, but Davidson pointed out that these cells can become ER negative over time. Moreover, tumors are often heterogeneous with respect to their ER-positive or -negative composition. “There is some evidence that chemoprevention can prevent ER-negative tumors, or tumors that become ER negative later,” Davidson said. “But the evidence isn’t strong and we need more work to explain why that might be happening.” Adding oophorectomy to chemoprevention should boost primary cancer prevention even further, because tamoxifen, for instance, does not affect the ovaries, whereas oophorectomy reduces the risk of ovarian cancer by roughly 90% and reduces circulating hormone levels that can promote growth of breast tumors. Narod’s 2000 paper showed that oophorectomy combined with tamoxifen reduced breast cancer risk by 84%, a benefit that, Offit said, approximates that achieved with mastectomy. Later studies have not shown this same degree of combined effect, he said, “but the evidence is clear from these studies that tamoxifen as well as oophorectomy separately confer protection against breast cancer risk in BRCA mutation carriers.”
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Authors of a recent study finding that underreporting of calorie intake by participants in observational studies based on surveillance data focusing on nutrition and obesity may present a problem to governments and scientists who use such flawed data to set health policy or to test hypotheses. But others disagree.People who respond to surveys based on 24-hour dietary recall have a tendency to overstate the amount of the “good” foods or water they consume and to understate the amount of “bad” foods they ingest.
Article
Background: Nutritional epidemiology is a highly prolific field. Debates on associations of nutrients with disease risk are common in the literature and attract attention in public media. Objective: We aimed to examine the conclusions, statistical significance, and reproducibility in the literature on associations between specific foods and cancer risk. Design: We selected 50 common ingredients from random recipes in a cookbook. PubMed queries identified recent studies that evaluated the relation of each ingredient to cancer risk. Information regarding author conclusions and relevant effect estimates were extracted. When >10 articles were found, we focused on the 10 most recent articles. Results: Forty ingredients (80%) had articles reporting on their cancer risk. Of 264 single-study assessments, 191 (72%) concluded that the tested food was associated with an increased (n = 103) or a decreased (n = 88) risk; 75% of the risk estimates had weak (0.05 > P ≥ 0.001) or no statistical (P > 0.05) significance. Statistically significant results were more likely than nonsignificant findings to be published in the study abstract than in only the full text (P < 0.0001). Meta-analyses (n = 36) presented more conservative results; only 13 (26%) reported an increased (n = 4) or a decreased (n = 9) risk (6 had more than weak statistical support). The median RRs (IQRs) for studies that concluded an increased or a decreased risk were 2.20 (1.60, 3.44) and 0.52 (0.39, 0.66), respectively. The RRs from the meta-analyses were on average null (median: 0.96; IQR: 0.85, 1.10). Conclusions: Associations with cancer risk or benefits have been claimed for most food ingredients. Many single studies highlight implausibly large effects, even though evidence is weak. Effect sizes shrink in meta-analyses.
Article
“Any claim coming from an observational study is most likely to be wrong.” Startling, but true. Coffee causes pancreatic cancer. Type A personality causes heart attacks. Trans-fat is a killer. Women who eat breakfast cereal give birth to more boys. All these claims come from observational studies; yet when the studies are carefully examined, the claimed links appear to be incorrect. What is going wrong? Some have suggested that the scientific method is failing, that nature itself is playing tricks on us. But it is our way of studying nature that is broken and that urgently needs mending, say S. Stanley Young and Alan Karr; and they propose a strategy to fix it.
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For centuries knowledge meant proven knowledge — proven either by the power of the intellect or by the evidence of the senses. Wisdom and intellectual integrity demanded that one must desist from unproven utterances and minimize, even in thought, the gap between speculation and established knowledge. The proving power of the intellect or the senses was questioned by the sceptics more than two thousand years ago; but they were browbeaten into confusion by the glory of Newtonian physics. Einstein’s results again turned the tables and now very few philosophers or scientists still think that scientific knowledge is, or can be, proven knowledge. But few realize that with this the whole classical structure of intellectual values falls in ruins and has to be replaced: one cannot simply water down the ideal of proven truth - as some logical empiricists do — to the ideal of’probable truth’1 or — as some sociologists of knowledge do — to ‘truth by [changing] consensus’.2