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Secular differences in the association between caloric intake, macronutrient intake, and physical activity with obesity
Abstract
Background:
To determine whether the relationship between caloric intake, macronutrient intake, and physical activity with obesity has changed over time.
Methods:
Dietary data from 36,377 U.S. adults from the National Health and Nutrition Survey (NHANES) between 1971 and 2008 was used. Physical activity frequency data was only available in 14,419 adults between 1988 and 2006. Generalised linear models were used to examine if the association between total caloric intake, percent dietary macronutrient intake and physical activity with body mass index (BMI) was different over time.
Results:
Between 1971 and 2008, BMI, total caloric intake and carbohydrate intake increased 10-14%, and fat and protein intake decreased 5-9%. Between 1988 and 2006, frequency of leisure time physical activity increased 47-120%. However, for a given amount of caloric intake, macronutrient intake or leisure time physical activity, the predicted BMI was up to 2.3kg/m(2) higher in 2006 that in 1988 in the mutually adjusted model (P<0.05).
Conclusions:
Factors other than diet and physical activity may be contributing to the increase in BMI over time. Further research is necessary to identify these factors and to determine the mechanisms through which they affect body weight.
... Traditionally, obesity has been attributed to overnutrition and a sedentary lifestyle; however, over the past decade, it has become clear that additional factors are involved [5]. Between 1998 and 2006, BMI increased by 2.3 kg/m 2 on average in the USA when controlling for dietary intake and exercise levels [6]. In addition, Brown et al. [6] found that leisure time spent on exercise in fact increased between 1988 and 2006, indicating that other causes should be investigated [6]. ...
... Between 1998 and 2006, BMI increased by 2.3 kg/m 2 on average in the USA when controlling for dietary intake and exercise levels [6]. In addition, Brown et al. [6] found that leisure time spent on exercise in fact increased between 1988 and 2006, indicating that other causes should be investigated [6]. Other potential direct causes of obesity proposed include changes in the gut microbiome [7], effects of air conditioning on thermogenesis [8], chronic sleep deprivation [9], and certain pharmaceutical drugs inducing weight gain [5]. ...
... Between 1998 and 2006, BMI increased by 2.3 kg/m 2 on average in the USA when controlling for dietary intake and exercise levels [6]. In addition, Brown et al. [6] found that leisure time spent on exercise in fact increased between 1988 and 2006, indicating that other causes should be investigated [6]. Other potential direct causes of obesity proposed include changes in the gut microbiome [7], effects of air conditioning on thermogenesis [8], chronic sleep deprivation [9], and certain pharmaceutical drugs inducing weight gain [5]. ...
The prevalence of obesity and associated diseases has reached pandemic levels. Obesity is often associated with overnutrition and a sedentary lifestyle, but clearly other factors also increase the susceptibility of metabolic disease states. Ancestral and direct exposures to environmental toxicants and altered nutrition have been shown to increase susceptibility for obesity and metabolic dysregulation. Environmental insults can reprogram the epigenome of the germline (sperm and eggs), which transmits the susceptibility for disease to future generations through epigenetic transgenerational inheritance. In this review, we discuss current evidence and molecular mechanisms for epigenetic transgenerational inheritance of obesity susceptibility. Understanding ancestral environmental insults and epigenetic transgenerational impacts on future generations will be critical to fully understand the etiology of obesity and to develop preventative therapy options.
... 19 Penelitian yang dilakukan Brown dkk terhadap dewasa di Kanada menemukan bahwa tidak ada hubungan langsung antara asupan kalori dengan indeks massa tubuh seseorang meskipun terjadi peningkatan asupan kalori dan bersamaan dengan peningkatan obesitas. 21 Seseorang yang obesitas cenderung tidak puas dengan berat badannya dan ketidakbahagiaan terhadap citra tubuh sehingga lebih lanjut berupaya mencapai penurunan berat badan melalui pembatasan asupan kalori yang dikonsumsi. 22 Selain itu, individu obesitas cenderung lebih sedikit melaporkan asupan makanannya dibandingkan individu IMT normal karena rasa malu terhadap konsumsi makanan berlebih. ...
Latar Belakang: Kejadian obesitas terus meningkat dari tahun ke tahun termasuk pada kategori pekerjaan petugas kesehatan. Salah satu faktor penyebab obesitas adalah adanya peningkatan asupan nutrisi dan penurunan aktivitas fisik. Objektif: Penelitian ini bertujuan untuk mengetahui gambaran asupan makronutrien pada petugas kesehatan RSUP Dr. M. Djamil Padang dengan IMT obesitas. Metode: Penelitian ini menggunakan metode deskriptif dengan desain penelitian cross sectional study pada data sekunder penelitian pengembangan diet terhadap petugas kesehatan RSUP Dr. M. Djamil Padang yang obesitas dengan subjek penelitian 40 responden yang diambil dengan teknik total sampling. Data IMT diukur dengan metode antropometrik dan data asupan makronutrien menggunakan food recall 2x24 jam. Analisis data menggunakan analisis univariat. Hasil: Hasil penelitian didapatkan rerata asupan energi, karbohidrat, protein, dan lemak petugas kesehatan RSUP Dr.M. Djamil Padang dengan kategori obesitas 1 secara berurutan adalah 1796,6 kkal/hari, 158,4 gr/hari, 58,44 gr/hari, dan 58,50 g/hari. Untuk rerata asupan asupan energi, karbohidrat, protein, dan lemak pada kategori obesitas 2 secara berurutan adalah 1473,92 kkal/hari, 224,35 gr/hari, 64,12 gr/hari, dan 60,60 g/hari. Kesimpulan: Kesimpulan penelitian ini adalah gambaran asupan energi dan makronutrien (karbohidrat, protein dan lemak) pada kategori obesitas 2 lebih tinggi dibandingkan kategori obesitas 1. Kata kunci: Asupan energi, asupan makronutrien, obesitas 1, obesitas 2, petugas kesehatan
... Indeed, a growing volume of literature suggests that lifestyle changes in the last 50 years are insufficient to explain the prominent surge in obesity over the same period. Between 1988 and 2006, average adult BMI increased by 2.3 kg/m 2 despite equivalent caloric intake and physical activity [2]. A substantial volume of evidence supports the existence of a metabolic set point for body weight [3], which is established by several biological factors including heritable epigenetic modifications. ...
Purpose of review
To present recent evidence that strengthens the concept that exogenous pollutants contribute to adipose dysfunction and increased rates of disease and to highlight the ineffective regulation of this risk as industry switches to related but similarly toxic variants.
Recent findings
Substitutes for common phthalates and the highly regulated bisphenol A (BPA) show similar deleterious effects on adipocytes. The well tolerated limit for BPA exposure has been reduced in Europe to below the level detected in recent population studies. Additionally, the role for BPA-induced inflammation mediated by interleukin 17a has been described in animal and human studies.
Summary
Despite experimental and associative evidence that supports plastics and plastic associated chemicals deleteriously influencing adipose homeostatasis and contributing to metabolic diseases, structurally related alternate chemicals are being substituted by manufacturers to circumvent trailing regulatory actions.
... NHANES data compared BMI between US adults in 1988 and 2006 and found a 2.3 kg/m 2 increase in adult BMI in 2006 compared with 1988 even with the same amount of caloric intake (macronutrient specific) and energy spent. 16 Current evidence indicates that gene variants can only explain about 2.7% of the individual variation in BMI. 17 Environmental chemicals, dubbed "obesogens," due to their promotion of adiposity, have been documented to contribute to these changes over the last 15 years. These chemicals impact metabolism through a variety of mechanisms such as microbiome disruption, effect on adipocytes, PPAR agonist activity, hormonal alterations of sex hormones or thyroid hormones, and promotion of insulin resistance. ...
The emerging field of Environmental Medicine- the clinical side to body burden of toxicants in people causing health issues.
... NHANES data compared BMI between US adults in 1988 and 2006 and found a 2.3 kg/m 2 increase in adult BMI in 2006 compared with 1988 even with the same amount of caloric intake (macronutrient specific) and energy spent. 16 Current evidence indicates that gene variants can only explain about 2.7% of the individual variation in BMI. 17 Environmental chemicals, dubbed "obesogens," due to their promotion of adiposity, have been documented to contribute to these changes over the last 15 years. These chemicals impact metabolism through a variety of mechanisms such as microbiome disruption, effect on adipocytes, PPAR agonist activity, hormonal alterations of sex hormones or thyroid hormones, and promotion of insulin resistance. ...
Environmental toxicant exposure, according to many researchers in the field, is the leading cause of chronic disease and premature death globally. For the purposes of this review, we will use obesity and type 2 diabetes as examples of toxicant-induced chronic diseases. Endocrine Disrupting chemicals (EDCs) such as phthalates and bisphenols, per- and polyfluoroalkyl substances (PFAS), and persistent organic pollutants (POPs) have been linked to increased risk for obesity and type 2 diabetes in both animal and large epidemiologic studies. These two conditions are well-documented examples of evidence for mechanisms of both adipose metabolism disruption and pancreatic cell dysfunction. The implications for health care directives to both identify, prevent, and treat these exposures are reviewed.
... Fat bodies are not necessarily indicative of poor diet, little exercise, or poorer health (Brown et al. 2016;Kuk et al. 2018). Decades of research have found that improving eating and physical activity produces only small impacts on weight in most people (Wadden et al. 2014). ...
This chapter in the Seasonal Sociology reader offers a sociological analysis of new year's resolutions. We situate these resolutions through a historical sociological lens, as a ritual that promotes social solidarity. We then explore why why, among all the possibilities for self-improvement, the most common resolutions in many Western countries are about changing eating and/or physical activity habits. To do so, we apply ideas from sociology of food, and sociology of the body.
... Evidence also suggests increasing variation in BMI distribution within and across countries (3). Given the size of the population affected by overweight and obesity, as well as the well-known health impairments associated with overweight and obesity (4,5), researchers have focused on identifying various modifiable risk factors ranging from global food supply system (6), societal norms (7), socioeconomic and physical environments (8,9), and individual health behaviors (10). ...
In light of recent findings on the small proportion of variance in body mass index (BMI) explained by shared environment, and growing interests in the role of genetic susceptibility, we assess the relative contribution of socioeconomic status (SES) and genome-wide polygenic score for BMI to explaining variation in BMI. Our final analytic sample included 4,918 white and 1,546 black individuals from the US National Longitudinal Study of Adolescent to Adult Health Wave IV (2007-2008) who had complete measures on BMI, demographics, SES, genetic data, and health behaviors. We employed ordinary least-squares regression to assess variation in log(BMI) as a function of the aforementioned predictors, independently and mutually adjusted. All analyses were stratified by race/ethnicity and further by sex. The age-adjusted variation in log(BMI) was 0.055 among whites and 0.066 among blacks. The contribution of SES and polygenic score ranged from <1%-6% and 2-8%, respectively, and majority of the variation (87-96%) in log(BMI) remained unexplained. Differential distribution of socioeconomic resources, stressors and buffers may interact to produce systematically larger variation in vulnerable populations. Further understanding on the contribution of biological, genetic and environmental factors as well as stochastic elements in diverse phenotypic variance is needed in population health sciences.
... Further, they are independent predictor of health risks. [12][13][14][15] Thus, failing to account for differences in WC and these lifestyle factors over time, may in part explain the differences in how BMI relates in health risks over time. ...
To examine the trends in chronic conditions after accounting for temporal differences in body mass index (BMI) and waist circumference (WC). Pooled cycles (1999‐2014) of the U.S. National Health and Nutrition Examination Survey (NHANES) were analysed (n = 36 959). The models were adjusted for caloric intake, smoking, medications use and physical activity. The prevalence of diabetes increased in women with general or abdominal obesity (BMI*time; WC*time, P < .05), but there were no differences in men. For hypertension, independent of BMI, the prevalence was not different over time in both sexes (P > .05), whereas for a given WC, there was a decrease in the prevalence over time in women (WC*time, P = .05). For dyslipidemia, independent of BMI, the prevalence decreased in men, whereas for a given WC, there was a decrease in the prevalence in both sexes (P < .05). Over the same time frame, blood pressure, low‐density lipoprotein and triglycerides decreased, while plasma glucose increased independent of general and abdominal obesity (P < .001). The relationship between obesity and chronic conditions has changed over time. There may be other changes that have altered how obesity is related with metabolic health markers over time. Further investigation is needed to better understand the current causes of chronic conditions.
... Obesity is often associated with overnutrition and a sedentary lifestyle, however, this does not fully account for the dramatic changes in prevalence. Even after controlling for exercise levels and caloric intake, body mass index (BMI) increased by 2.3 kg/m 2 between 1998-2006 within the United States population, suggesting an increased disease susceptibility and other factors should be considered [8]. Human epidemiological studies have suggested that obesity may have early life developmental origins [9,10]. ...
The incidence of obesity has increased dramatically over the past two decades with a prevalence of approximately 40% of the adult population within the United States. The current study examines the potential for transgenerational adipocyte (fat cell) epigenetic alterations. Adipocytes were isolated from the gonadal fat pad of the great-grand offspring F3 generation 1-year old rats ancestrally exposed to DDT (dichlorodiphenyltrichloroethane), atrazine, or vehicle control in order to obtain adipocytes for DNA methylation analysis. Observations indicate that there were differential DNA methylated regions (DMRs) in the adipocytes with the lean or obese phenotypes compared to control normal (non-obese or lean) populations. The comparison of epigenetic alterations indicated that there were substantial overlaps between the different treatment lineage groups for both the lean and obese phenotypes. Novel correlated genes and gene pathways associated with DNA methylation were identified, and may aid in the discovery of potential therapeutic targets for metabolic diseases such as obesity. Observations indicate that ancestral exposures during critical windows of development can induce the epigenetic transgenerational inheritance of DNA methylation changes in adipocytes that ultimately may contribute to an altered metabolic phenotype.
This study examines the in vitro effects of a soluble protein hydrolysate (SPH) derived from Atlantic salmon (Salmo salar) on incretin receptor activity and pancreatic islet cell protection to explore the mechanisms underlying SPH’s observed benefits on weight loss and metabolic health in overweight individuals. SPH demonstrated a dose-dependent enhancement of glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP) receptor activity, with significant increases of 2.4-fold (p < 0.05) and 2.6-fold (p < 0.01) at 10 mg/mL, respectively, compared to the control. Pancreatic islet cell assays showed a substantial proliferation effect, with up to a 57% increase at 50 µL/well, indicating potential protective properties against inflammation-induced cell loss. Notably, the smallest SPH peptide fraction (<1000 Da) exhibited GLP-1 agonist activity comparable to semaglutide, a widely used therapeutic agent, underscoring SPH’s potential efficacy in modulating metabolic pathways. These results suggest that SPH not only enhances key incretin signaling but also promotes islet cell health, positioning it as a promising dietary intervention to improve age-related metabolic health, including the weight gain and underlying adverse metabolic changes frequently encountered through the menopause.
Food sampling at retail stores and restaurants (e.g., amuse bouche) is a widespread practice. These food samples vary considerably in healthfulness levels. Prior research has primarily focused on the effects of sampling on evaluations and sales of the sampled item. However, can there be unintended consequences of sampling a healthy versus an unhealthy item on subsequent purchases of other food items? Also, would the degree of dissimilarity between the sampled item and subsequent options moderate the effects? The results from a series of experiments, including four studies conducted in field settings, show that sampling a healthy (vs. unhealthy) item paradoxically leads to greater subsequent purchase/choice of unhealthy foods – but only when consumers perceive a relatively high level of dissimilarity between the sampled item and subsequent options. This effect reverses when the sampled food and subsequent options are perceived as being relatively low on dissimilarity (i.e., high on similarity).
A high-fat diet can cause health problems, such as hyperlipidemia, obesity, cardiovascular disease, and metabolic disorders. Dietary supplementation with beneficial microbes might reduce the detrimental effects of a high-fat diet by modulating the gut microbiome, metabolic pathways and metabolites. This study assessed the effects of Limosilactobacillus fermentum HNU312 (L. fermentum HNU312) on blood lipid levels, fat accumulation, inflammation and the gut microbiome in mice on a high-fat diet. The results indicate that L. fermentum HNU312 supplementation to high-fat diet-fed mice led to decreases of 7.52% in the final body weight, 22.30% in total triglyceride, 24.87% in total cholesterol, and 27.3% in low-density lipoprotein cholesterol. Furthermore, the addition of L. fermentum HNU312 significantly reduced the fat accumulation in the liver and adipose tissue by 18.99% and 32.55%, respectively, and decreased chronic inflammation induced by a high-fat diet. Further analysis of the gut microbiome revealed that on the one hand, L. fermentum HNU312 changed the structure of the intestinal microbiota, increased the abundance of beneficial intestinal bacteria related to lipid metabolism, and reversed the enrichment of lipid-related metabolic pathways. On the other hand, L. fermentum HNU312 increased the production of short-chain fatty acids, which can reduce liver inflammation and chronic inflammation induced by a high-fat diet. In summary, by regulating gut microbiota, L. fermentum HNU312 improved lipid metabolism pathways and increased short-chain fatty acids, which reduced body weight, blood lipids, fat accumulation and chronic inflammation caused by high-fat diets. Therefore, L. fermentum HNU312 could be a good candidate probiotic for ameliorating metabolic syndrome.
Objectives: To determine secular trends in body height, fat-mass, fat-free mass, and external skeletal robustness in young adults and examine possible relationship between them. Methods: Anthropometric data (body height, body mass; skinfold thickness (SFT) – triceps, abdominal, thigh; circumferences (C) – waist, upper arm, thigh; width – elbow, knee) of young adults aged 20-25 years (N = 5303; males 1985, females 3318) were used from the Slovenian (data)Base of Anthropometric Measurements from 1960 to 2023. Multiple linear regressions were performed. Results: The most significant positive secular trends (p < 0.000) were observed in males for abdominal SFT (B = 0.151, R2 = 0.169) and thigh SFT (B = 0.131, R2 = 0.142). In females, similar trend was observed in waist C (B = 0.151; R2 = 0.169). The most significant negative secular trend (p < 0.001) was observed in muscle area of lower limbs in both sexes (males: B = - 0.427, R2 = 0.000; females: B = - 0.875, R2 = 0.300). Body height and overall body mass were the most important factors influencing the observed decline in external skeletal robustness assessed with frame index according to elbow and knee width according to multiple linear regression. Conclusion: Over the last 60 years, a positive secular trend was observed in body height and body fat, while a negative trend was noted in muscle mass. Increases in body height and overall body mass had the most significant impact on the observed decrease in assessed external skeletal robustness over time.
In recent years, the worldwide epidemic of metabolic diseases, namely obesity, metabolic syndrome, diabetes and metabolic-associated fatty liver disease (MAFLD) has been strongly associated with constant exposure to endocrine-disruptive chemicals (EDCs), in particular, the ones able to disrupt various metabolic pathways. EDCs have a negative impact on several human tissues/systems, including metabolically active organs, such as the liver and pancreas. Among their deleterious effects, EDCs induce mitochondrial dysfunction and oxidative stress, which are also the major pathophysiological mechanisms underlying metabolic diseases. In this narrative review, we delve into the current literature on EDC toxicity effects on the liver and pancreatic tissues in terms of impaired mitochondrial function and redox homeostasis.
Introduction
Historical maps of racialized evaluation of mortgage lending risk (i.e., redlined neighborhoods) have been linked to adverse health outcomes. Little research has examined whether living in historically redlined neighborhoods is associated with obesity, differentially by race or gender.
Methods
This is a cross-sectional study to examine whether living in historically redlined neighborhoods is associated with BMI and waist circumference among Black and White adults in 1985–1986. Participants’ addresses were linked to the 1930s Home Owners’ Loan Corporation maps that evaluated mortgage lending risk across neighborhoods. The authors used multilevel linear regression models clustered on Census tract, adjusted for confounders to estimate main effects, and stratified, and interaction models by (1) race, (2) gender, and (3) race by gender with redlining differentially for Black versus White adults and men versus women. To better understand strata differences, they compared Census tract–level median household income across race and gender groups within Home Owners’ Loan Corporation grade.
Results
Black adults (n=2,103) were more likely than White adults (n=1,767) to live in historically rated hazardous areas and to have higher BMI and waist circumference. Redlining and race and redlining and gender interactions for BMI and waist circumference were statistically significant (p<0.10). However, in stratified analyses, the only statistically significant associations were among White participants. White participants living in historically rated hazardous areas had lower BMI (β=−0.63 [95% CI= −1.11, −0.15]) and lower waist circumference (β=−1.50 [95% CI= −2.62, −0.38]) than those living in declining areas. Within each Home Owners’ Loan Corporation grade, residents in White participants’ neighborhoods had higher incomes than those living in Black participants’ neighborhoods (p<0.0001). The difference was largest within historically redlined areas. Covariate associations differed for men, women, Black, and White adults, explaining the difference between the interaction and the stratified models. Race by redlining interaction did not vary by gender.
Conclusions
White adults may have benefitted from historical redlining, which may have reinforced neighborhood processes that generated racial inequality in BMI and waist circumference 50 years later.
Despite varied treatment, mitigation, and prevention efforts, the global prevalence and severity of obesity continue to worsen. Here we propose a combined model of obesity, a unifying paradigm that links four general models: the energy balance model (EBM), based on calories as the driver of weight gain; the carbohydrate-insulin model (CIM), based on insulin as a driver of energy storage; the oxidation-reduction model (REDOX), based on reactive oxygen species (ROS) as a driver of altered metabolic signaling; and the obesogens model (OBS), which proposes that environmental chemicals interfere with hormonal signaling leading to adiposity. We propose a combined OBS/REDOX model in which environmental chemicals (in air, food, food packaging, and household products) generate false autocrine and endocrine metabolic signals, including ROS, that subvert standard regulatory energy mechanisms, increase basal and stimulated insulin secretion, disrupt energy efficiency, and influence appetite and energy expenditure leading to weight gain. This combined model incorporates the data supporting the EBM and CIM models, thus creating one integrated model that covers significant aspects of all the mechanisms potentially contributing to the obesity pandemic. Importantly, the OBS/REDOX model provides a rationale and approach for future preventative efforts based on environmental chemical exposure reduction.
Microplastics (MPs) are recognized as environmental pollutants with potential implications for human health. Considering the rapid increase in obesity rates despite stable caloric intake, there is a growing concern about the link between obesity and exposure to environmental pollutants, including MPs. In this study, we conducted a comprehensive investigation utilizing in silico, in vitro, and in vivo approaches to explore the brain distribution and physiological effects of MPs. Molecular docking simulations were performed to assess the binding affinity of three plastic polymers (ethylene, propylene, and styrene) to immune cells (macrophages, CD4⁺, and CD8⁺ lymphocytes). The results revealed that styrene exhibited the highest binding affinity for macrophages. Furthermore, in vitro experiments employing fluorescence-labeled PS-MPs (fPS-MPs) of 1 μm at various concentrations demonstrated a dose-dependent binding of fPS-MPs to BV2 murine microglial cells. Subsequent oral administration of fPS-MPs to high-fat diet-induced obese mice led to the co-existence of fPS-MPs with immune cells in the blood, exacerbating impaired glucose metabolism and insulin resistance and promoting systemic inflammation. Additionally, fPS-MPs were detected throughout the brain, with increased activation of microglia in the hypothalamus. These findings suggest that PS-MPs significantly contribute to the exacerbation of systemic inflammation in high-fat diet-induced obesity by activating peripheral and central inflammatory immune cells.
The main goal of the current research was to perform ADMET and molecular docking studies for a synthetic genistein derivative that can imitate Estrogen and function as an endocrine disruptor, activating the ER receptor on beta-cells in the pancreas to release insulin. The created molecule was molecularly docked using the online molecular docking research tool Dockthor. NGL viewer, an online program for viewing Dockthor data, displayed the docking experiment results. The 2D legend-protein interactions were estimated with BIOVIA Discovery Studio Visualizer. Estrogen-Receptor Alpha was the targeted target, while Compound-A was employed as the legend. In this study, we created a synthetic derivative of genistein, an analogue of Estrogen in terms of ER-α receptor binding. We used molecular docking to evaluate the affinity of compound-A binding to the ER-α and its 2D interactions and Ramachandran plots. We then ran ADMET experiments on the molecule, which revealed a substantial relationship with the molecule's Estrogen Receptor binding capabilities, as well as scores for absorption, distribution, metabolism, excretion, and toxicity.
Adipose tissues represent an important energy storage organ in animals and are the largest endocrine organ. It plays an important regulatory role in the pathogenesis of insulin resistance, cardiovascular disease, and metabolic syndrome. Adipose development is a complex biological process involving multiple key genes, signaling pathways, and non-coding RNAs, including microRNAs and circular RNAs. In this study, we characterized circITGB1 and named its host gene ITGB1, which is differentially expressed in sheep of different months based on sequencing data. We collated and analyzed the sequencing data to select miRNA-23a with strong binding to ARRB1. We found that miRNA-23a regulates the development and differentiation of sheep adipocytes by targeting ARRB1. As a competing endogenous RNA, circITGB1 overexpression effectively alleviated the inhibitory effect of miR-23a on ARRB1. Conclusively, we provide evidence that circITGB1 regulates the proliferation and differentiation of sheep adipocytes via the miR-23a/ARRB1 pathway. This study provides a scientific basis for further studies on adipose tissue development at the circRNA level.
We previously synthesized two retinoid X receptor (RXR) agonists, 4′-hydroxy-3′-propyl-[1,1′-biphenyl]-3-propanoic acid ethyl ester (4′OHE) and 6-hydroxy-3′-propyl-[1,1′-biphenyl]-3-propanoic acid ethyl ester (6OHE), based on the structure of magnaldehyde B, a natural product obtained from Magnolia obovata. 4′OHE and 6OHE exhibited different selectivities for peroxisome proliferator-activated receptor (PPAR)/RXR heterodimers. To examine the regulatory effects of these compounds in adipogenesis, 3T3–L1 mouse preadipocytes were treated with a differentiation cocktail with or without test compounds to induce differentiation, and subsequently treated with test compounds in insulin-containing medium every alternate day. Lipid droplets were stained with Oil Red O to examine lipid accumulation. In addition, adipogenesis-related gene expression was measured using RT–qPCR and immunoblotting. The results showed that a PPARγ agonist, 4′OHE, which exerts agonistic effects on PPARγ and RXRα, enhanced adipogenesis similar to rosiglitazone. However, unlike GW501516, a PPARδ agonist, 6OHE and its hydrolysis product (6OHA), which exert agonistic effects on PPARδ and RXRα, suppressed adipogenesis. In a manner similar to 6OHE and 6OHA, bexarotene, an RXR agonist, suppressed adipocyte differentiation, and its anti-adipogenic effect was reversed by an RXR antagonist. Furthermore, 6OHA and bexarotene inhibited the increase in Pparγ2 and Cebpa mRNA levels 2 days after the induction of differentiation. We demonstrated the adipogenic effect of 4′OHE and anti-adipogenic effects of 6OHE and 6OHA in 3T3–L1 cells. Previously, RXR agonists have been reported to positively regulate the differentiation of mesenchymal stem cells into adipocytes, but our current data showed that they inhibited the differentiation of preadipocytes, at least 3T3–L1 cells, into adipocytes.Graphical abstract
Rates of human obesity, type 2 diabetes, and non-alcoholic fatty liver disease (NAFLD) have risen faster than anticipated and cannot solely be explained by excessive caloric intake or physical inactivity. Importantly, this effect is also observed in many other domesticated and non-domesticated mammals, which has led to the hypothesis that synthetic environmental pollutants may be contributing to disease development. While the impact of these chemicals on appetite and adipogenesis has been extensively studied, their potential role in reducing energy expenditure is less studied. An important component of whole-body energy expenditure is adaptive and diet-induced thermogenesis in human brown adipose tissue (BAT). This review summarizes recent evidence that environmental pollutants such as the pesticide chlorpyrifos inhibit BAT function, diet-induced thermogenesis and the potential signaling pathways mediating these effects. Lastly, we discuss the importance of housing experimental mice at thermoneutrality, rather than room temperature, to maximize the translation of findings to humans.
Chronically elevated oxidative stress causes and/or exacerbates disease in all body systems. These include, metabolic, respiratory, neurological, endocrine, cardiovascular, gastrointestinal, musculoskeletal, urinary tract, kidney, liver, skin, immunological and autoimmunological, eye, periodontal, pathogenic and carcinogenic diseases. Oxidative stress, the driving force for these, can be seen from the presence of common biomarkers, the most widely examined of these being serum malondialdehyde. It is total oxidative stress, no matter what the sources, that determines the likelihood of disease onset. Studies that demonstrate this relationship include total oxidative stress resulting from different chemical, chemical-radiation and chemical-disease combinations. Disease prevention strategies based on oxidative stress reduction are presented.
Obesity is a multifactorial disease with both genetic and environmental components. The prevailing view is that obesity results from an imbalance between energy intake and expenditure caused by overeating and insufficient exercise. We describe another environmental element that can alter the balance between energy intake and energy expenditure: obesogens. Obesogens are a subset of environmental chemicals that act as endocrine disruptors affecting metabolic endpoints. The obesogen hypothesis posits that exposure to endocrine disruptors and other chemicals can alter the development and function of the adipose tissue, liver, pancreas, gastrointestinal tract, and brain, thus changing the set point for control of metabolism. Obesogens can determine how much food is needed to maintain homeostasis and thereby increase the susceptibility to obesity. The most sensitive time for obesogen action is in utero and early childhood, in part via epigenetic programming that can be transmitted to future generations. This review explores the evidence supporting the obesogen hypothesis and highlights knowledge gaps that have prevented widespread acceptance as a contributor to the obesity pandemic. Critically, the obesogen hypothesis changes the narrative from curing obesity to preventing obesity.
Childhood obesity and metabolic disorders are of concern and are public health problems globally. Environmental endocrine disruptors, including phthalates, are well known as “obesogens” and "metabolic disruptors". Several studies have investigated the relationships between prenatal phthalate exposure and childhood obesity with inconsistent conclusions. Given the child growth trajectory/pattern as a possible early marker of metabolic disorders, we aimed to assess the effect of prenatal phthalate exposure on offspring growth trajectory. A systematic literature search was conducted using MEDLINE (accessed through PubMed), Web of Science, and CNKI (Chinese National Knowledge Infrastructure) until July 2021. We evaluated the risk of bias for adherence to the prespecified criteria. Fourteen eligible articles were finally included in this systematic review according to the defined PECOS statement. The risk of bias of the included studies was “low” or “probably low”, and few were “probably high” and “high”. These studies were mostly carried out in the United States (N = 6); others were conducted in China (N = 2), Mexico (N = 2), France (N = 1), Spain (N = 1), Greece (N = 1), and Australia (N = 1) and published from 2015 to 2021. The combined subjects of the 14 studies were 10,396 mother-child pairs. Except for 3 studies not reporting the sex ratio, at least 4001 boys and 3366 girls were included. For the association of prenatal phthalate exposure with an absolute adiposity marker (at a specific visit timepoint), only a few studies were using the same obesity marker as the outcome endpoint and using the same statistical method to explore their associations. However, MEP appeared to be positively associated with several obesity markers, such as the absolute BMI z score, weight-for-age z score, waist circumference, and overweight status. For the association of prenatal phthalate exposure with a repeated measurement of the adiposity marker over the age range, neither associations of adiposity markers with a specific phthalate metabolite nor relationships of a specific adiposity marker with prenatal phthalate exposure were of a consistent result. All four articles reported that phthalate metabolite exposure during pregnancy was associated with children’s growth trajectory. Three suggested a sex-specific association between prenatal phthalate exposure and obesity trajectory. In conclusion, the current articles did not show any relationship between prenatal phthalate exposure and children's age-specific outcomes, except for positive associations of prenatal MEP exposure with absolute adiposity markers. However, epidemiological data supported a weak relationship between prenatal phthalate exposure and children's obesity trajectory in a sex-specific manner.
Bisphenols and phthalates, chemicals frequently used in plastic products, promote obesity in cell and animal models. However, these well-known metabolism-disrupting chemicals (MDCs) represent only a minute fraction of all compounds found in plastics. To gain a comprehensive understanding of plastics as a source of exposure to MDCs, we characterized the chemicals present in 34 everyday products using nontarget high-resolution mass spectrometry and analyzed their joint adipogenic activities by high-content imaging. We detected 55,300 chemical features and tentatively identified 629 unique compounds, including 11 known MDCs. Importantly, the chemicals extracted from one-third of the products caused murine 3T3-L1 preadipocytes to proliferate, and differentiate into adipocytes, which were larger and contained more triglycerides than those treated with the reference compound rosiglitazone. Because the majority of plastic extracts did not activate the peroxisome proliferator-activated receptor γ and the glucocorticoid receptor, the adipogenic effects are mediated via other mechanisms and, thus, likely to be caused by unknown MDCs. Our study demonstrates that daily-use plastics contain potent mixtures of MDCs and can, therefore, be a relevant yet underestimated environmental factor contributing to obesity.
Adult and childhood obesity have reached pandemic level proportions. The idea that caloric excess and insufficient levels of physical activity leads to obesity is a commonly accepted answer for unwanted weight gain. This paradigm offers an inconclusive explanation as the world continually moves towards an unhealthier and heavier existence irrespective of energy balance. Endocrine disrupting chemicals (EDCs) are chemicals that resemble natural hormones and disrupt endocrine function by interfering with the body’s endogenous hormones. A subset of EDCs called obesogens have been found to cause metabolic disruptions such as increased fat storage, in vivo. Obesogens act on the metabolic system through multiple avenues and have been found to affect the homeostasis of a variety of systems such as the gut microbiome and adipose tissue functioning. Obesogenic compounds have been shown to cause metabolic disturbances later in life that can even pass into multiple future generations, post exposure. The rising rates of obesity and related metabolic disease are demanding increasing attention on chemical screening efforts and worldwide preventative strategies to keep the public and future generations safe. This review addresses the most current findings on known obesogens and their effects on the metabolic system, the mechanisms of action through which they act upon, and the screening efforts through which they were identified with. The interplay between obesogens, brown adipose tissue, and the gut microbiome are major topics that will be covered.
The ubiquitous exposure of humans to microplastics (MPs) through inhalation of particles in air and ingestion in dust, water, and diet is well established. Humans are estimated to ingest tens of thousands to millions of MP particles annually, or on the order of several milligrams daily. Available information suggests that inhalation of indoor air and ingestion of drinking water bottled in plastic are the major sources of MP exposure. Little is known on the occurrence of MPs in human diet. Evidence is accumulating that feeding bottles and medical devices can contribute to MP exposure in newborns and infants. Biomonitoring studies of human stool, fetus, and placenta provide direct evidence of MP exposure in infants and children. MPs <20 µm were reported to cross biological membranes. Although plastics were once perceived as inert materials, MP exposure in laboratory animals is linked to various forms of inflammation, immunological response, endocrine disruption, alteration of lipid and energy metabolism, and other disorders. Whereas exposure to MPs itself is a concern, MPs can also be sources of exposure to plastic additives and other toxicants. Exposure of human cell lines to MP additives such as phthalates, bisphenols, and organotins causes adverse effects through the activation of nuclear receptors, peroxisome proliferator-activated receptors (PPARs) α, β, and γ, and retinoid X receptor (RXR), leading to oxidative stress, cytotoxicity, immunotoxicity, thyroid hormone disruption, and altered adipogenesis and energy production. The size, shape, chemical composition, surface charge, and hydrophobicity of MPs influence their toxicity. Maternal transfer of MPs to the developing fetus has been demonstrated in exposed laboratory animals and through the analysis of human placenta. In laboratory animal studies, maternal exposure to MPs altered energy and lipid metabolism in offspring and subsequent generations. Moreover, concomitant with the global increase in plastics production, the prevalence of overweight and obesity in human populations has increased over the past five decades, and there is evidence to support the hypothesis that MPs and their additives are potential obesogens. Even though MP exposures are ubiquitous and toxic effects from such exposures are a concern, systematic studies on this topic remain urgently needed.
Obesity is known to cause physical and metabolic diseases. It is often assumed by people (including the healthcare workers) that the person with obesity lacks self-control in matters of diet and physical exercise, and is therefore responsible for his or her weight. Persons with obesity have to face sarcasm, barbs, and discrimination due to their condition. They often have difficulty in getting jobs or have to accept lower than standard pay for their work. Although weight gain requires calorie intake in excess of calorie expenditure, it is sometimes not easy for the person to restrict calories due to the underlying causes of obesity. The body resists losing weight, and attempts to hoard calories by reducing the metabolic rate. In this chapter we have explained and classified the causes of obesity into endogenous and exogenous. The endogenous causes include genetic and epigenetic causes, maternal factors, and hormonal causes, while exogenous causes include obesogenic environment, lifestyle, and weight-gain promoting medicines. It must be realized that losing weight and keeping it off is not easy for a person with obesity.
Longitudinal research suggests that living in a cognitively enriched home environment, in which access to activities including hobbies and books are plentiful, can prevent excess weight gain and obesity in children. In order for the enriched home environment to influence weight it should influence energy and macronutrient intake and/or energy expenditure. To test this hypothesis, we used a cross sectional design to study aspects of the child’s enriched home environment along with energy and macronutrient intake. A sample of 158 6-9-year-old children measured between February 2017 – April 2019 in Buffalo, NY were selected from a larger study based on criteria for accurate reporting of energy intake using the Block Kid’s Food Frequency Questionnaire. Results showed that the Home Observation for Measurement of the Environment (HOME) subscales enriched environment, parental warmth and an integrated family structure were negatively related to child percent overBMI. Hierarchical regression showed that each of these factors improved variance in child percent overBMI accounted for beyond dietary intake or macronutrients, specifically accounting for a total of 18.2% variance in models controlling for total energy intake. These results provide the first demonstration that characteristics of a child’s home environment are associated with lower energy intake and independently associated with percent overBMI beyond knowledge of diet. Enriching a child’s home environment by providing alternative activities to eating, improving parental warmth and providing opportunities for parents to interact positively with their children may be novel ways to reduce childhood obesity that should be experimentally tested in future research.
Increasing evidence from epidemiological, animal and in vitro studies suggests that the increased production of synthetic chemicals that interfere with the proper functioning of the hormonal system, so-called endocrine-disrupting compounds (EDCs), might be involved in the development and rapid spread of obesity, coined the obesity epidemic. Recent findings have demonstrated that EDCs may interfere with hormonal receptors that regulate adipogenesis and metabolic pathways. Furthermore, prenatal exposure to EDCs has been shown to influence the metabolism of the developing embryo through epigenetic mechanisms and to promote obesity in subsequent generations. In this Review, we discuss the potential impact of bisphenol A (BPA) and phthalate-based plasticizers on obesity and obesity-related metabolic disorders. Special emphasis is given to the obesogenic effects of prenatal exposure and strategies for identifying, regulating, and replacing EDCs.
Background:
Obesity prevalence has become one of the most prominent issues in global public health. Physical activity has been recognized as a key player in the obesity epidemic.
Objectives:
The objectives of this study are to (1) examine the relationship between physical activity and weight status and (2) assess the performance and predictive power of a set of popular machine learning and traditional statistical methods.
Methods:
National Health and Nutrition Examination Survey (NHANES, 2003 to 2006) data were used. A total of 7162 participants met our inclusion criteria (3682 males and 3480 females), with average age ranging from 48.6 (normal weight) to 52.1 years old (overweight). Eleven classifying algorithms-including logistic regression, naïve Bayes, Radial Basis Function (RBF), local k-nearest neighbors (k-NN), classification via regression (CVR), random subspace, decision table, multiobjective evolutionary fuzzy classifier, random tree, J48, and multilayer perceptron-were implemented and evaluated, and they were compared with traditional logistic regression model estimates.
Results:
With physical activity and basic demographic status, of all methods analyzed, the random subspace classifier algorithm achieved the highest overall accuracy and area under the receiver operating characteristic (ROC) curve (AUC). The duration of vigorous-intensity activity in one week and the duration of moderate-intensity activity in one week were important attributes. In general, most algorithms showed similar performance. Logistic regression was middle-ranking in terms of overall accuracy, sensitivity, specificity, and AUC among all methods.
Conclusions:
Physical activity was an important factor in predicting weight status, with gender, age, and race/ethnicity being less but still essential factors associated with weight outcomes. Tailored intervention policies and programs should target the differences rooted in these demographic factors to curb the increase in the prevalence of obesity and reduce disparities among sub-demographic populations.
Background:
Obesity is a complex multifactorial disorder affecting a growing proportion of the population. While therapeutic lifestyle change (TLC) is foundational, results of interventional programs are often inconsistent. Factors related to systemic inflammation, toxin load and endotoxemia have been postulated to play a contributory role. This pilot study sought to evaluate the role of TLC with enhanced laboratory evaluation and interventions to address these emerging therapeutic targets.
Methods:
Twelve participants with a body mass index (BMI) greater than 30 (or 27 with metabolic co-morbidities) were recruited from an outpatient clinic for participation with a primary outcome of pre/post changes in body composition. Participants completed a 12-week program involving weekly group and individualized dietary, exercise, and behavioral support, supplemented with a commercial, 30-day dietary detoxification intervention and ongoing nutritional counseling. All participants completed baseline and post-intervention evaluation including metabolic, toxin load, endotoxin, body composition and functional fitness profiles.
Results:
After 12-weeks, participants as a group significantly improved body composition parameters including BMI, body fat, fat mass, and waist and hip circumference (P < .01). Significant improvement in several secondary outcomes including levels of lipopolysaccharide, zonulin and leptin were noted. Additionally, results demonstrate substantial improvements in pain, pain interference and functional fitness. Upon completion, all participants rated the program favorably with a high likelihood of continuing or recommending participation to others.
Conclusions:
Obesity remains a challenging and often refractory clinical scenario with emerging evidence indicating the potential role of systemic inflammation, toxin load and endotoxemia. A group therapeutic lifestyle change program enhanced with a detoxification component is feasible and may provide a promising intervention for achieving weight loss while also addressing functional and pain related co-morbidities. Future randomized trials evaluating the components of such a program are needed to better delineate the role of specific interventions in the complex setting of obesity.
Obesity is now a worldwide pandemic. The usual explanation given for the prevalence of obesity is that it results from consumption of a calorie dense diet coupled with physical inactivity. However, this model inadequately explains rising obesity in adults and in children over the past few decades, indicating that other factors must be important contributors. An Endocrine-Disrupting Chemical (EDC) is an exogenous chemical, or mixture that interferes with any aspect of hormone action. EDCs have become pervasive in our environment, allowing humans to be exposed daily through ingestion, inhalation, and direct dermal contact. Exposure to EDCs has been causally linked with obesity in model organisms and associated with obesity occurrence in humans. Obesogens are chemicals, including some EDCs that promote adipogenesis and obesity, in vivo, by a variety of mechanisms. The environmental obesogen model holds that exposure to obesogens elicits a predisposition to obesity and that such exposures may be an important yet overlooked factor in the obesity pandemic. Effects produced by EDCs and obesogen exposure may be passed to subsequent, unexposed generations. This “generational toxicology” is not currently factored into risk assessment by regulators but may be another important factor in the obesity pandemic as well as in the worldwide increases in the incidence of noncommunicable diseases that plague populations everywhere. This review addresses the current evidence on how obesogens affect body mass, discusses long-known chemicals that have been more recently identified as obesogens, and how the accumulated knowledge can help identify EDCs hazards.
Exposure to endocrine-disrupting chemicals such as Bisphenol-A (BPA) is associated with an increase in obesity prevalence. Diet is the primary cause of human exposure to this contaminant. BPA promotes obesity by inducing adipocyte dysfunction and altering adipogenesis. Contradictory evidence and unanswered questions are reported in the literature concerning the BPA effects on adipogenesis. To clarify this issue, we tested the effects of prolonged low-dose BPA exposure on different phases of adipogenesis in committed 3T3L1 and uncommitted NIH3T3 preadipocytes. Our findings show that BPA effects on the adipogenesis are mediated by epigenetic mechanisms by reducing peroxisome proliferator-activated receptor gamma (Pparγ) promoter methylation in preadipocytes. Nevertheless, in BPA-exposed 3T3L1, Pparγ expression only transiently increases as lipid accumulation at day 4 of differentiation, without altering the adipogenic potential of the precursor cells. In the absence of differentiation mix, BPA does not make the 3T3L1 an in vitro model of spontaneous adipogenesis and the effects on the Pparγ expression are still limited at day 4 of differentiation. Furthermore, BPA exposure does not commit the NIH3T3 to the adipocyte lineage, although Pparγ overexpression is more evident both in preadipocytes and during the adipocyte differentiation. Interestingly, termination of the BPA exposure restores the Pparγ promoter methylation and inflammatory profile of the 3T3L1 cells. This study shows that BPA induces epigenetic changes in a key adipogenic gene. These modifications are reversible and do not affect preadipocyte commitment and/or differentiation. We identify an alternative transcriptional mechanism by which BPA affects gene expression and demonstrate how the challenge of preventing exposure is fundamental for human health.
Methyl- and propyl- parabens are generally regarded as safe by the U.S Food and Drug Administration and as such are commonly used in personal care products. These parabens have been associated with increased white adipogenesis in vitro and methyl paraben also increased the white adipose mass of mice. Given brown adipose also plays a role in energy balance, we sought to evaluate whether the effects of methyl- and propyl- parabens on white adipocytes extended to brown adipocytes. We challenged white and brown pre-adipocytes at low doses of both parabens (up to 1 < mu > M) during the differentiation process and examined adipogenesis with the ORO assay. The impact of each paraben on glucose uptake and lipolytic activity of adipocytes were measured with a fluorescent glucose analog and enzymatically, respectively. Methyl- and propyl- parabens increased adipogenesis of 3T3-L1 white adipocytes but not brown adipocytes. In white adipocytes, methyl paraben increased glucose uptake and both parabens reduced basal lipolysis. However, in brown adipocytes, parabens had no effect on basal lipolysis and instead attenuated isoproterenol induced lipolysis. These data indicate that methyl- and propyl- parabens target the differentiation and metabolic processes of multiple types of adipocytes in a cell autonomous manner.
Protein-rich diets are surging in popularity for weight loss. An increase in diet-induced thermogenesis, better preservation of fat-free mass, and enhanced satiety with greater dietary protein intakes may lead to increased energy expenditure and decreased energy intake; and thus promote a more negative energy balance that facilitates weight loss. Results from large randomized trials and meta-analyses of many smaller trials indicate that high-protein diets typically induce significantly greater amounts of weight loss than conventional low-fat or high-carbohydrate diets during the early, rapid weight loss phase (3–6 months), but differences between diets are attenuated and no longer significant during the late, slow weight loss phase (12–24 months). Gradually decreasing adherence may be responsible for this observation; in fact, dietary adherence, rather than macronutrient composition, is likely the major predictor of long-term weight loss success. Recently, some randomized trials evaluated the efficacy of high-protein (vs. normal-protein) diets consumed ad libitum during weight loss maintenance, i.e. after clinically significant weight loss. Weight regain may be smaller with high-protein diets in the short-term (3–12 months), but longer studies are needed to confirm this. Given the lack of conclusive evidence in favor of high-protein diets, or any other dietary pattern, it is reasonable to conclude that no individual nutrient is a friend or a foe when it comes to weight loss and its maintenance. Therefore, any diet that best suits one’s dietary habits and food preferences is likely to be better adhered to, and thus lead to more successful long-term weight loss.
Abstract There is increasing evidence for the role of environmental endocrine disrupting contaminants, coined obesogens, in exacerbating the rising obesity epidemic. Obesogens can be found in everyday items ranging from pesticides to food packaging. Although research shows that obesogens can have effects on adipocyte size, phenotype, metabolic activity, and hormone levels, much remains unknown about these chemicals. This review will discuss what is currently known about the mechanisms of obesogens, including expression of the PPARs, hormone interference, and inflammation. Strategies for identifying obesogenic chemicals and their mechanisms through chemical characteristics and model systems will also be discussed. Ultimately, research should focus on improving models to discern precise mechanisms of obesogenic action and to test therapeutics targeting these mechanisms.
The aim of this study was to evaluate the distribution of energy intake and macronutrients consumption throughout the day, and how its effect on nutritional status can be modulated by the presence of the rs3749474 polymorphism of the CLOCK gene in the Cantoblanco Platform for Nutritional Genomics (“GENYAL Platform”). This cross-sectional study was carried out on 898 volunteers between 18 and 69 years old (65.5% women). Anthropometric measurements, social issues and health, dietary, biochemical, genetic, and physical activity data were collected. Subsequently, 21 statistical interaction models were designed to predict the body mass index (BMI) considering seven dietary variables analyzed by three genetic models (adjusted by age, sex, and physical activity). The average BMI was 26.9 ± 4.65 kg/m2, 62.14% presented an excess weight (BMI > 25 kg/m2). A significant interaction was observed between the presence of the rs3749474 polymorphism and the evening carbohydrate intake (% of the total daily energy intake [%TEI]) (adjusted p = 0.046), when predicting the BMI. Participants carrying TT/CT genotype showed a positive association between the evening carbohydrate intake (%TEI) and BMI (β = 0.3379, 95% CI = (0.1689,0.5080)) and (β = 0.1529, 95% CI = (−0.0164,0.3227)), respectively, whereas the wild type allele (CC) showed a negative association (β = −0.0321, 95% CI = (−0.1505,0.0862)). No significant interaction with the remaining model variables was identified. New dietary strategies may be implemented to schedule the circadian distribution of macronutrients according to the genotype. Clinical Trial number: NCT04067921.
Background & Aims
A Western-style diet, which is high in fat and sugar, can cause significant dyslipidemia and non-alcoholic fatty liver disease; the diet has an especially strong effect in women, regardless of total calorie intake. Dietary supplementation with beneficial microbes might reduce the detrimental effects of a Western-style diet. We assessed the effects of Lactococcus lactis subsp. cremoris on weight gain, liver fat, serum cholesterol, and insulin resistance in female mice on a high-fat, high-carbohydrate diet.
Methods
Female C57BL/6 mice were fed either a high-fat, high-carbohydrate (Western-style) diet that contained 40% fat, (mostly milk fat) and 43% carbohydrate (mostly sucrose) or calorie-matched per gram control diet. The diets of mice were supplemented with 1x 10⁹ CFU of L lactis subsp. cremoris ATCC 19257 or Lactobacillus rhamnosus GG ATCC 53103 (control bacteria), 3 times per week for 16 weeks. Body weights were measured, and fecal, blood, and liver tissues were collected and analyzed. Livers were analyzed for fat accumulation and inflammation and blood samples were analyzed for cholesterol and glucose levels. Mice were housed within CLAMS-HC monitoring systems and respiratory exchange ratio and activity measured. Hepatic lipid profiles of L lactis subsp. cremoris-supplemented mice were characterized by lipidomic mass spectrometry analysis.
Results
Mice fed L lactis subsp. cremoris while on the Western-style diet gained less weight, developed less hepatic steatosis and inflammation, and had a lower mean serum level of cholesterol and body mass index than mice fed the control bacteria. Mice fed the L lactis subsp. cremoris had increased glucose intolerance while on the Western-style diet, compared to mice fed control bacteria, and had alterations in hepatic lipids, including oxylipins.
Conclusions
Dietary supplementation with L lactis subsp. cremoris in female mice on a high-fat, high-carbohydrate (Western-style) diet caused them to gain less weight, develop less liver fat an inflammation, reduce serum cholesterol levels, and increase glucose tolerance, compared with mice on the same diet fed control bacteria. L lactis subsp. cremoris is safe for oral ingestion and might be developed for persons with metabolic and liver disorders caused by a Western-style diet.
The incidence of obesity has reached an all-time high and this increase is observed worldwide. There is a growing need to understand all of the factors that contribute to obesity in order to effectively treat and prevent it and associated comorbidities. The obesogen hypothesis proposes that there are chemicals in our environment termed “obesogens” that can impact individual susceptibility to obesity and thus help explain the recent large increases in obesity. This review discusses current advances in our understanding of how obesogens act to impact health and obesity susceptibility. Newly discovered obesogens, and potential obesogens are discussed, together with future directions for research that may help to reduce the impact of these pervasive chemicals.
There is a global obesity pandemic. The prevailing theory is that obesity is the result of overeating and lack of exercise. However, the imbalance of calorie consumption and exercise per se cannot explain the reasons for the obesity epidemic. The susceptibility to obesity, like many noncommunicable diseases, has been shown to start during development due to poor nutrition, stress, or exposure to environmental chemicals. The subclass of environmental chemicals that can increase the susceptibility to obesity following exposure in utero or early life are called obesogens. There are now significant animal and human data indicating a role for obesogens in the obesity pandemic. This review presents an overview of the importance of exposure to obesogens in the etiology of obesity. The possibility of reducing exposures to obesogens during development could lead to a focus on prevention of obesity.
Metabolically healthy obesity refers to an obesity phenotype with no or little evidence of metabolic dysfunction. Lower liver fat content and visceral adipose tissue, greater insulin sensitivity and secretion, greater cardiorespiratory fitness, and a predominantly lower body (i.e., leg) fat deposition are key physiological traits of a metabolically healthy phenotype. About 35% of all subjects with obesity are metabolically healthy. These individuals have approximately half the risk of developing type 2 diabetes and cardiovascular disease compared with metabolically unhealthy subjects with obesity, but they still have a significantly greater risk (by 50-300%) compared with metabolically healthy lean subjects. Therefore, absence of metabolic risk factors in people with obesity should not be a contraindication for weight-loss treatment. Metabolically healthy obesity needs to be treated, and this need is reinforced by the fact that this phenotype is not stable over time, as ∼50% of these subjects will cease being metabolically healthy within ∼10 y. Intervening early is therefore important. Weight loss dose-dependently decreases visceral adipose tissue and liver fat content, and it improves multiorgan insulin sensitivity and β-cell function (i.e., it beneficially affects many of the physiological traits of a metabolically healthy phenotype); however, weight loss is very difficult to maintain. This typically results in disappointment among patients and hinders adherence, which is likely critical for the limited success of most weight-loss treatments in the long term. On the other hand, using ≥1 metabolic health targets in a non-weight-loss-centered treatment paradigm that includes prudent dietary changes and increased physical activity can serve as an appropriate first goal that can help motivate patients toward the long-term goals of obesity treatment.
Purpose of Review
This review summarises the issues related to the measurement and interpretation of dietary intake in individuals with overweight and obesity, as well as identifies future research priorities.
Recent Findings
Some aspects of the assessment of dietary intake have improved through the application of technology-based methods and the use of dietary biomarkers. In populations with overweight and obesity, misreporting bias related to social desirability is a prominent issue. Future efforts should focus on combining technology-based dietary methods with the use of dietary biomarkers to help reduce and account for the impact of these biases.
Summary
Future research will be important in terms of strengthening methods used in the assessment and interpretation of dietary intake data in the context of overweight and obesity.
Endocrine disrupting chemicals (EDCs), a heterogeneous group of exogenous chemicals that can interfere with any aspect of endogenous hormones, represent an emerging global threat for human metabolism. There is now considerable evidence that the observed upsurge of metabolic disease cannot be fully attributed to increased caloric intake, physical inactivity, sleep deficit, and ageing. Among environmental factors implicated in the global deterioration of metabolic health, EDCs have drawn the biggest attention of scientific community, and not unjustifiably. EDCs unleash a coordinated attack toward multiple components of human metabolism, including crucial, metabolically-active organs such as hypothalamus, adipose tissue, pancreatic beta cells, skeletal muscle, and liver. Specifically, EDCs' impact during critical developmental windows can promote the disruption of individual or multiple systems involved in metabolism, via inducing epigenetic changes that can permanently alter the epigenome in the germline, enabling changes to be transmitted to the subsequent generations. The clear effect of this multifaceted attack is the manifestation of metabolic disease, clinically expressed as obesity, metabolic syndrome, diabetes mellitus, and non-alcoholic fatty liver disease. Although limitations of EDCs research do exist, there is no doubt that EDCs constitute a crucial parameter of the global deterioration of metabolic health we currently encounter.
Obesity and associated disorders are now a global pandemic. The prevailing clinical model for obesity is overconsumption of calorie‐dense food and diminished physical activity (the calories in ‐ calories out model). However, this explanation does not account for numerous recent research findings demonstrating that a variety of environmental factors can be superimposed on diet and exercise to influence the development of obesity. The environmental obesogen model proposes that exposure to chemical obesogens during in utero and/or early life can strongly influence later predisposition to obesity. Obesogens are chemicals that inappropriately stimulate adipogenesis and fat storage, in vivo either directly or indirectly. Numerous obesogens have been identified in recent years and some of these elicit transgenerational effects on obesity as well as a variety of health endpoints after exposure of pregnant F0 females. Prenatal exposure to environmental obesogens can produce lasting effects on the exposed animals and their offspring to at least the F4 generation. Recent results show that some of these transgenerational effects of obesogen exposure can be carried across the generations via alterations in chromatin structure and accessibility. That some chemicals can have permanent effects on the offspring of exposed animals suggests increased caution in the debate about whether and to what extent exposure to endocrine disrupting chemicals and obesogens should be regulated.
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DE JONGE, LILIAN, GEORGE BRAY. The thermic effect of food and obesity: A critical review.
This review has examined the factors that influence the thermic effect of food (TEF) by evaluating 49 studies that have compared subjects who are obese with those who are lean. Meal size, meal composition, the nature of the previous diet, insulin resistance, physical activity, and ageing influence TEF. In the studies of individuals who are obese or lean, of those who used intravenous glucose infusions, all but one found an impaired thermic response. A total of 29 out of 49 studies of individuals of normal weight or with obesity were identified where there was no difference in age between the groups, and where the subjects who were “overweight” were clearly obese. Of these 29, 22 reported a statistically significant reduction in TEF, 3 studies were not designed to look primarily at the effect of obesity on TEF, and the other 4 may not have had sufficiently palatable meals. From this review, we conclude that the reduction of TEF in obesity is related to the degree of insulin resistance, which may be influenced by a low level of sympathetic activity.
More than one-third of adults and 17% of youth in the United States are obese, although the prevalence remained stable between 2003-2004 and 2009-2010.
To provide the most recent national estimates of childhood obesity, analyze trends in childhood obesity between 2003 and 2012, and provide detailed obesity trend analyses among adults.
Weight and height or recumbent length were measured in 9120 participants in the 2011-2012 nationally representative National Health and Nutrition Examination Survey.
In infants and toddlers from birth to 2 years, high weight for recumbent length was defined as weight for length at or above the 95th percentile of the sex-specific Centers for Disease Control and Prevention (CDC) growth charts. In children and adolescents aged 2 to 19 years, obesity was defined as a body mass index (BMI) at or above the 95th percentile of the sex-specific CDC BMI-for-age growth charts. In adults, obesity was defined as a BMI greater than or equal to 30. Analyses of trends in high weight for recumbent length or obesity prevalence were conducted overall and separately by age across 5 periods (2003-2004, 2005-2006, 2007-2008, 2009-2010, and 2011-2012).
In 2011-2012, 8.1% (95% CI, 5.8%-11.1%) of infants and toddlers had high weight for recumbent length, and 16.9% (95% CI, 14.9%-19.2%) of 2- to 19-year-olds and 34.9% (95% CI, 32.0%-37.9%) of adults (age-adjusted) aged 20 years or older were obese. Overall, there was no significant change from 2003-2004 through 2011-2012 in high weight for recumbent length among infants and toddlers, obesity in 2- to 19-year-olds, or obesity in adults. Tests for an interaction between survey period and age found an interaction in children (P = .03) and women (P = .02). There was a significant decrease in obesity among 2- to 5-year-old children (from 13.9% to 8.4%; P = .03) and a significant increase in obesity among women aged 60 years and older (from 31.5% to 38.1%; P = .006).
Overall, there have been no significant changes in obesity prevalence in youth or adults between 2003-2004 and 2011-2012. Obesity prevalence remains high and thus it is important to continue surveillance.
Intestinal microbes regulate metabolic function and energy balance; an altered microbial ecology is believed to contribute to development of several metabolic diseases. Relative species abundance and metabolic characteristics of the intestinal microbiota change substantially in individuals who are obese or have other metabolic disorders, and in response to ingested nutrients or therapeutic agents. The mechanisms through which the intestinal microbiota and its metabolites affect host homeostasis are just beginning to be understood. We review the relationships between the intestinal microbiota and host metabolism, including energy intake, energy use, and expenditure in relation to glucose and lipid metabolism. These associations, along with interactions among the intestinal microbiota, mucus layer, bile acids, and mucosal immune responses reveal potential mechanisms by which the microbiota affect metabolism. We discuss how controlled studies, involving direct perturbations of microbial communities in human and animal models, are required to identify effective therapeutic targets in the microbiota.
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.
Background
The aims of this study were to examine temporal trends in the prevalence of sufficient moderate-to-vigorous intensity physical activity (MVPA), high levels of screen time, combined measures of these behaviors and overweight or obesity in Australian adults during the period 2002–2008. Trends over this time period in overweight or obesity within each behavior group (sufficient/insufficient MVPA, high/low screen time and combined behaviors) were also examined.
Methods
Data were collected via annually conducted cross-sectional computer-assisted-telephone-interviews (CATI) of adults (n=7908) living in Central Queensland, Australia (2002–2008). Self-reported MVPA, screen time (TV viewing and computer use), and BMI were used to create dichotomous classifications of physical activity (Sufficient MVPA (S-MVPA), Insufficient Physical Activity (I-MVPA)), screen time (High Screen Time (HST), Low Screen Time (LST)), combined behavior categories (S-MVPA/LST, I-MVPA/LST, S-MVPA/HST, I-MVPA/HST) and BMI (Overweight or Obese, Healthy Weight) respectively.
Results
The prevalence of S-MVPA, HST, and overweight or obesity increased at approximately the same rate over the study period in the overall sample and females (p≤0.05). In the overall sample and in females, the prevalence of overweight and obesity increased over the study period in those individuals classified as I-MVPA/HST (p≤0.05).
Conclusion
Results provide evidence that while the prevalence of S-MVPA appears to be modestly increasing, the proportion of the population engaging in HST and classified as overweight or obese are increasing at approximately the same rate. These observations highlight the need to increase levels of total physical activity (including light intensity physical activity) and decrease sedentary behavior including screen time.
Western lifestyles differ markedly from those of our hunter-gatherer ancestors, and these differences in diet and activity level are often implicated in the global obesity pandemic. However, few physiological data for hunter-gatherer populations are available to test these models of obesity. In this study, we used the doubly-labeled water method to measure total daily energy expenditure (kCal/day) in Hadza hunter-gatherers to test whether foragers expend more energy each day than their Western counterparts. As expected, physical activity level, PAL, was greater among Hadza foragers than among Westerners. Nonetheless, average daily energy expenditure of traditional Hadza foragers was no different than that of Westerners after controlling for body size. The metabolic cost of walking (kcal kg(-1) m(-1)) and resting (kcal kg(-1) s(-1)) were also similar among Hadza and Western groups. The similarity in metabolic rates across a broad range of cultures challenges current models of obesity suggesting that Western lifestyles lead to decreased energy expenditure. We hypothesize that human daily energy expenditure may be an evolved physiological trait largely independent of cultural differences.
Obesity interventions can result in weight loss, but accurate prediction of the bodyweight time course requires properly accounting for dynamic energy imbalances. In this report, we describe a mathematical modelling approach to adult human metabolism that simulates energy expenditure adaptations during weight loss. We also present a web-based simulator for prediction of weight change dynamics. We show that the bodyweight response to a change of energy intake is slow, with half times of about 1 year. Furthermore, adults with greater adiposity have a larger expected weight loss for the same change of energy intake, and to reach their steady-state weight will take longer than it would for those with less initial body fat. Using a population-averaged model, we calculated the energy-balance dynamics corresponding to the development of the US adult obesity epidemic. A small persistent average daily energy imbalance gap between intake and expenditure of about 30 kJ per day underlies the observed average weight gain. However, energy intake must have risen to keep pace with increased expenditure associated with increased weight. The average increase of energy intake needed to sustain the increased weight (the maintenance energy gap) has amounted to about 0·9 MJ per day and quantifies the public health challenge to reverse the obesity epidemic.
The prevalence of obesity in the United States has increased dramatically.
The aim of this study was to determine trends in carbohydrate, fat, and protein intakes in adults and their association with energy intake by using data from the National Health and Nutrition Examination Survey (NHANES)-a representative sample of the US population.
Data on adults aged 20-74 y from the first NHANES (NHANES I, 1971-1975; n = 13,106) were compared with data from NHANES 2005-2006 (n = 4381). Normal weight was defined as a body mass index (BMI; in kg/m(2)) of 19 to <25, overweight as a BMI of 25 to <30, and obese as a BMI of ≥30. Carbohydrate, fat, and protein intakes were obtained by dietary recall. Regression analyses were adjusted for potential confounders.
The prevalence of obesity increased from 11.9% to 33.4% in men and from 16.6% to 36.5% in women. The percentage of energy from carbohydrates increased from 44.0% to 48.7%, the percentage of energy from fat decreased from 36.6% to 33.7%, and the percentage of energy from protein decreased from 16.5% to 15.7%. Trends were identical across normal-weight, overweight, and obese groups. Energy intake increased substantially in all 3 BMI groups. In NHANES 2005-2006, a 1% increase in the percentage of energy from protein was associated with a decrease in energy intake of 32 kcal (substituted for carbohydrates) or 51 kcal (substituted for fat). Similar findings were seen across all BMI categories, in men and women, and in NHANES I.
Energy intake and the prevalence of obesity have increased dramatically. Dietary interventions should focus on decreasing energy intake and potentially by substituting protein for fat or carbohydrates.
There is debate over the casual factors for the rise in body weight in the UK. The present study investigates whether increases between 1986 and 2000 for men and women were a result of increases in mean total energy intake, decreases in mean physical activity levels or both. Estimates of mean total energy intake in 1986 and 2000 were derived from food availability data adjusted for wastage. Estimates of mean body weight for adults aged 19-64 years were derived from nationally representative dietary surveys conducted in 1986-7 and 2000-1. Predicted body weight in 1986 and 2000 was calculated using an equation relating body weight to total energy intake and sex. Differences in predicted mean body weight and actual mean body weight between the two time points were compared. Monte Carlo simulation methods were used to assess the stability of the estimates. The predicted increase in mean body weight due to changes in total energy intake between 1986 and 2000 was 4·7 (95 % credible interval 4·2, 5·3) kg for men and 6·4 (95 % credible interval 5·9, 7·1) kg for women. Actual mean body weight increased by 7·7 kg for men and 5·4 kg for women between the two time points. We conclude that increases in mean total energy intake are sufficient to explain the increase in mean body weight for women between 1986 and 2000, but for men, the increase in mean body weight is likely to be due to a combination of increased total energy intake and reduced physical activity levels.
The obesity epidemic is a global issue and shows no signs of abating, while the cause of this epidemic remains unclear. Marketing practices of energy-dense foods and institutionally-driven declines in physical activity are the alleged perpetrators for the epidemic, despite a lack of solid evidence to demonstrate their causal role. While both may contribute to obesity, we call attention to their unquestioned dominance in program funding and public efforts to reduce obesity, and propose several alternative putative contributors that would benefit from equal consideration and attention. Evidence for microorganisms, epigenetics, increasing maternal age, greater fecundity among people with higher adiposity, assortative mating, sleep debt, endocrine disruptors, pharmaceutical iatrogenesis, reduction in variability of ambient temperatures, and intrauterine and intergenerational effects as contributing factors to the obesity epidemic are reviewed herein. While the evidence is strong for some contributors such as pharmaceutical-induced weight gain, it is still emerging for other reviewed factors. Considering the role of such putative etiological factors of obesity may lead to comprehensive, cause specific, and effective strategies for prevention and treatment of this global epidemic.
Social desirability (the tendency to respond in such a way as to avoid criticism) and social approval (the tendency to seek praise) are two prominent response set biases evident in answers on structured questionnaires. These biases were tested by comparing nutrient intakes as estimated from a single 24-hour diet recall interview (24HR) and a 7-day dietary recall (7DDR). Data were collected as part of the Worcester Area Trial for Counseling in Hyperlipidemia, a randomized, physician-delivered nutrition intervention trial for hypercholesterolemic patients conducted in Worcester, Massachusetts, from 1991 to 1995. Of the 1,278 total study subjects, 759 had complete data for analysis. Men overestimated their fat and energy intakes on the 7DDR as compared with the 24HR according to social approval: One unit increase in the social approval score was associated with an overestimate of 21.5 kcal/day in total energy intake and 1.2 g/day in total fat intake. Women, however, underestimated their dietary intakes on the 7DDR relative to the 24HR according to social desirability: One unit increase in the social desirability score was associated with an underestimate of 19.2 kcal/day in energy intake and 0.8 g/day in total fat. The results from the present study indicate that social desirability and social approval biases appear to vary by gender. Such biases may lead to misclassification of dietary exposure estimates resulting in a distortion in the perceived relation between health-related outcomes and exposure to specific foods or nutrients. Because these biases may vary according to the perceived demands of research subjects, it is important that they be assessed in a variety of potential research study populations. Am J Epidemiol 1997;146:1046–55.
Self-report of dietary intake could be biased by social desirability or social approval thus affecting risk estimates in epidemiological studies. These constructs produce response set biases, which are evident when testing in domains characterized by easily recognizable correct or desirable responses. Given the social and psychological value ascribed to diet, assessment methodologies used most commonly in epidemiological studies are particularly vulnerable to these biases.
Social desirability and social approval biases were tested by comparing nutrient scores derived from multiple 24-hour diet recalls (24HR) on seven randomly assigned days with those from two 7-day diet recalls (7DDR) (similar in some respects to commonly used food frequency questionnaires), one administered at the beginning of the test period (pre) and one at the end (post). Statistical analysis included correlation and multiple linear regression.
Cross-sectionally, no relationships between social approval score and the nutritional variables existed. Social desirability score was negatively correlated with most nutritional variables. In linear regression analysis, social desirability score produced a large downward bias in nutrient estimation in the 7DDR relative to the 24HR. For total energy, this bias equalled about 50 kcal/point on the social desirability scale or about 450 kcal over its interquartile range. The bias was approximately twice as large for women as for men and only about half as large in the post measures. Individuals having the highest 24HR-derived fat and total energy intake scores had the largest downward bias due to social desirability.
We observed a large downward bias in reporting food intake related to social desirability score. These results are consistent with the theoretical constructs on which the hypothesis is based. The effect of social desirability bias is discussed in terms of its influence on epidemiological estimates of effect. Suggestions are made for future work aimed at improving dietary assessment methodologies and adjusting risk estimates for this bias.
This review has examined the factors that influence the thermic effect of food (TEF) by evaluating 49 studies that have compared subjects who are obese with those who are lean. Meal size, meal composition, the nature of the previous diet, insulin resistance, physical activity, and ageing influence TEF. In the studies of individuals who are obese or lean, of those who used intravenous glucose infusions, all but one found an impaired thermic response. A total of 29 out of 49 studies of individuals of normal weight or with obesity were identified where there was no difference in age between the groups, and where the subjects who were "overweight" were clearly obese. Of these 29, 22 reported a statistically significant reduction in TEF, 3 studies were not designed to look primarily at the effect of obesity on TEF, and the other 4 may not have had sufficiently palatable meals. From this review, we conclude that the reduction of TEF in obesity is related to the degree of insulin resistance, which may be influenced by a low level of sympathetic activity.
Diverging trends of decreasing energy intake and increasing prevalence of obesity suggest that physical inactivity and sedentary lifestyle may be one of the key determinants of the growing rates of overweight/obesity in Western populations information about the impact of physical inactivity and sedentary lifestyles on the prevalence of obesity among the general adult population in the European Union is sparse.
To estimate the association of leisure-time sedentary and non-sedentary activities with body mass index (BMI, kg/m2) and with the prevalence of obesity (BMI>30 kg/m2) in a sample of the 15 member states of the European Union.
Professional interviewers administered standardized in-home questionnaires to 15,239 men and women aged 15 years upwards, selected by a multi-stage stratified cluster sampling with quotas applied to ensure national and European representativeness. Energy expenditure during leisure time was calculated based on data on frequency of and amount of time participating in various physical activities, assigning metabolic equivalents (METS) to each activity. Sedentary lifestyle was assessed by means of self-reported hours spent sitting down during leisure time. Multiple linear regression models with BMI as the dependent variable, and logistic regression models with obesity (BMI>30 kg/m2) as the outcome, were fitted.
Independent associations of leisure-time physical activity (inverse) and amount of time spent sitting down (direct) with BMI were found. The adjusted prevalence odds ratio (OR) for obesity was 0.52 [95% confidence interval (CI): 0.43-0.64, P<0.001] for the upper quintile of physical activity (>30 METS) compared with the most physically inactive quintile (<1.75 METS). A positive independent association was also evident for the time spent sitting down, with an adjusted OR= 1.61(95% CI: 1.33-1.95, P<0.001) for those who spent more than 35 h of their leisure time sitting down compared with those who spent less than 15 h. Conclusions: Obesity and higher body weight are strongly associated with a sedentary lifestyle and lack of physical activity in the adult population of the European Union. These results, however, need to be interpreted with caution due to the cross-sectional design. Nonetheless, they are consistent with the view that a reduction in energy expenditure during leisure time may be the main determinant of the current epidemic of obesity.
To examine secular trends in diet reporting error.
Dietary information was obtained from 228 Danish men and women in 1987-88, and from 122 men and women in 1993-94.
Bias in dietary reporting of energy and protein intake was assessed by comparing reported intake with intake data, estimated from 24 h nitrogen output, validated by administering P-aminobenzoic acid, and estimated 24 h energy expenditure. Total energy was under-reported more than energy from protein at both surveys, suggesting that energy from other nutrients, like fat and/or carbohydrate, must have been under-reported too. There was a greater under-reporting for energy than for protein in 1993-94 (29%) than in 1987-88 (15%). Obesity was positively associated with under-reporting, both in 1987-88 and in 1993-94.
The higher macro-nutrient specific error in 1993-94 compared to 1987-88 may reflect a trend to increasingly omitting fat and/or carbohydrate-rich foods in dietary reporting. This may be a consequence of increased awareness of diet intake, which, in turn, may be related to intensified public health campaigns to reduce intake of fat and/or simple carbohydrate. These results may have consequences for our understanding of the apparent decline in dietary fat and associated health benefits.
We provide an updated version of the Compendium of Physical Activities, a coding scheme that classifies specific physical activity (PA) by rate of energy expenditure. It was developed to enhance the comparability of results across studies using self-reports of PA. The Compendium coding scheme links a five-digit code that describes physical activities by major headings (e.g., occupation, transportation, etc.) and specific activities within each major heading with its intensity, defined as the ratio of work metabolic rate to a standard resting metabolic rate (MET). Energy expenditure in MET-minutes, MET-hours, kcal, or kcal per kilogram body weight can be estimated for specific activities by type or MET intensity. Additions to the Compendium were obtained from studies describing daily PA patterns of adults and studies measuring the energy cost of specific physical activities in field settings. The updated version includes two new major headings of volunteer and religious activities, extends the number of specific activities from 477 to 605, and provides updated MET intensity levels for selected activities.
To examine the relationship between secular trends in energy supply and body mass index (BMI) among several countries.
Aggregate level analyses of annually reported country food data against anthropometric data collected in independent cross-sectional samples from 34 populations in 21 countries from the early 1980s to the mid-1990s.
Population randomly selected participants aged 35-64 y.
BMI data were obtained from the WHO MONICA Project. Food energy supply data were derived from the Food Balance Sheet of the Food and Agriculture Organization of the United Nations.
Mean BMI as well as the prevalence of overweight (BMI > or =25 kg/m2) increased in virtually all Western European countries, Australia, the USA, and China. Decreasing trends in BMI were seen in Central and Eastern European countries. Increasing trends in total energy supply per capita were found in most high-income countries and China while decreasing trends existed in Eastern European countries. Between country differences in temporal trends of total energy supply per capita explained 41% of the variation of trends in mean BMI; the effect was similar upon the prevalence of overweight and obesity. Trends in percent of energy supply from total fat per capita had a slight effect on the trends in mean BMI (+7% increment in R2) when the total energy supply per capita was adjusted for, while energy supply from total sweeteners per capita had no additional effect.
Increasing energy supply is closely associated with the increase of overweight and obesity in western countries. This emphasizes the importance of dietary issues when coping with the obesity epidemic.
To investigate plausible contributors to the obesity epidemic beyond the two most commonly suggested factors, reduced physical activity and food marketing practices.
A narrative review of data and published materials that provide evidence of the role of additional putative factors in contributing to the increasing prevalence of obesity.
Information was drawn from ecological and epidemiological studies of humans, animal studies and studies addressing physiological mechanisms, when available.
For at least 10 putative additional explanations for the increased prevalence of obesity over the recent decades, we found supportive (although not conclusive) evidence that in many cases is as compelling as the evidence for more commonly discussed putative explanations.
Undue attention has been devoted to reduced physical activity and food marketing practices as postulated causes for increases in the prevalence of obesity, leading to neglect of other plausible mechanisms and well-intentioned, but potentially ill-founded proposals for reducing obesity rates.
Under-reporting (UR) of energy intake (EI) by self-reported dietary methods is well-documented but the methods used to estimate UR in population-based studies commonly assume a sedentary lifestyle. We compared estimated UR using individualised estimates of energy requirements with a population cut-off based on minimum energy needs. UR was estimated for 1551 adults aged 19-64 years enrolled in the National Diet and Nutrition Survey. Physical activity diaries and 7 d weighed dietary records were completed concurrently. Mean daily EI (kJ/d) was calculated from the dietary records. Reported physical activity was used to assign each subject's activity level, and then to calculate estimated energy requirements (EER) from published equations. UR was calculated both as EER - EI with an adjustment for daily EER and EI variation, and also by a population method. By the individual method UR was approximately 27 % of energy needs in men and 29 % in women, with 75 % of men and 77 % of women classified as under-reporters; by the population method 80 and 88 % were classified as under-reporters respectively. When subjects who reported their eating being affected by dieting or illness during dietary recording were excluded, UR was 25 % of energy needs in both sexes. UR was higher in overweight and obese men and women compared with their lean counterparts (P < 0.001). UR of EI must be considered in dietary surveys. The EER method allows UR to be quantified and takes into account an individual's activity level. Measures of physical activity and questions to identify under-eating during dietary recording may help to evaluate secular trends in UR.
This study examined the relationships among body fat, diet composition, energy intake, and exercise in adults. Male (n = 107) and female (n = 109) adults aged 18-71 y (36.6 +/- 1.0 y, means +/- SEM) were hydrostatically weighed to determine body fat (5.7-49.0% of total weight). Diet and exercise behaviors were determined by use of a questionnaire. As body fat increased, percent of energy intake derived from fat increased (p less than 0.001) whereas the percent from carbohydrate decreased (p less than 0.001). There was no relationship between energy intake and adiposity although leanness and exercise were related (p less than 0.001). When subgroups of lean and obese subjects were compared, the lean subjects derived approximately 29% of their energy from fat and 53% from carbohydrate vs 35% and 46%, respectively, for the obese subjects. No differences were found between groups for energy intake but the lean individuals exercised more often than did the obese individuals. These data suggest that diet composition may play as important a role in fat deposition as do energy intake and lack of exercise.
Background:
Energy intake is a key determinant of weight.
Objective:
Our objective was to examine trends in energy intake in adults in the United States from 1971-1975 to 2009-2010.
Design:
The study was a trend analysis of 9 national surveys in the United States that included data from 63,761 adults aged 20-74 y.
Results:
Adjusted mean energy intake increased from 1955 kcal/d during 1971-1975 to 2269 kcal/d during 2003-2004 and then declined to 2195 kcal/d during 2009-2010 (P-linear trend < 0.001, P-nonlinear trend < 0.001). During the period from 1999-2000 to 2009-2010, no significant linear trend in energy intake was observed (P = 0.058), but a significant nonlinear trend was noted (P = 0.042), indicating a downward trend in energy intake. Significant decreases in energy intake from 1999-2000 to 2009-2010 were noted for participants aged 20-39 y, men, women, and participants with a BMI (in kg/m(2)) of 18.5 to <25 and ≥30.
Conclusion:
After decades of increases, mean energy intake has decreased significantly since 2003-2004.
Objective:
To examine whether the recent increasing prevalence of obesity was accompanied by variations in energy and macronutrient intakes by weight status.
Design:
Time series of cross-sectional surveys.
Setting:
National Health and Nutrition Examination Surveys (NHANES) in the USA.
Subjects:
Adult participants of NHANES I (1971-1974), II (1976-1980), III (1988-1994) and continuous (1999-2004).
Results:
Daily energy intake increased over time for men (9832 to 11 652 kJ, P < 0·01) and women (6418 to 8142 kJ, P < 0·01) in all BMI classes. Percentage of energy intake from carbohydrate increased over time (men: 42·7% to 48·0%, P < 0·01; women: 45·4% to 50·6%, P < 0·01), whereas percentage of energy intake from fat (men: 36·7% to 33·1%, P < 0·01; women: 36·1% to 33·8%, P < 0·01) and protein (men: 16·4% to 15·1%, P < 0·01; women: 16·9% to 14·7%, P < 0·01) decreased. With surveys combined, daily energy intake varied among BMI classes for women (underweight/normal weight: 7460 kJ; overweight: 6799 kJ; obese I: 7033 kJ; obese II/III: 7401 kJ; P < 0·01) but not men. Percentage of energy intake from carbohydrate decreased with increasing BMI class (men: 46·6% to 45·5%, P < 0·01; women: 49·0% to 48·6%, P < 0·01) whereas percentage of energy intake from fat (men: 34·3% to 36·5%, P < 0·01; women: 34·4% to 35·4%, P < 0·01) and protein (men: 15·3% to 16·5%, P < 0·01; women: 15·2% to 16·0%, P < 0·01) increased. Interactions of survey period and BMI class were not statistically significant.
Conclusions:
Time trends in energy and macronutrient intakes were similar across BMI classes. Research examining how individuals respond differently to varying dietary compositions may provide greater insight about contributors to the rise in obesity.
We compare consumer valuations of beef ribeye steaks from cattle produced without growth hormones or genetically modified
corn in France, Germany, the United Kingdom, and the United States. Results suggest that French consumers place a higher value
on beef from cattle that have not been administered added growth hormones than U.S. consumers; however, valuations of non-hormone-treated
beef are statistically indistinguishable across Germany, the United Kingdom, and the United States. Results also suggest that
European consumers place a much higher value on beef from cattle that have not been fed genetically modified corn than U.S.
consumers.
Aim:
Diet is considered an important modifiable factor in the overweight. The role of macronutrients in obesity has been examined in general in selected populations, but the results of these studies are mixed, depending on the potential confounders and adjustments for other macronutrients. For this reason, we examined the association between macronutrient intake patterns and being overweight in a population-based representative sample of middle-aged (55.1+/-6.1 years) men (n=966), using various adjustment modalities.
Methods:
The study subjects kept 3-day food-intake records, and the standard cardiovascular risk factors were assessed. Weight, height and waist circumference (WC) were also measured.
Results:
Carbohydrate intake was negatively associated and fat intake was positively associated with body mass index (BMI) and WC in regression models adjusted for energy intake and other factors, including age, smoking and physical activity. However, with mutual adjustments for other energy-yielding nutrients, the negative association of carbohydrate intake with WC remained significant, whereas the associations between fat intake and measures of obesity did not. Adjusted odds ratios (95% confidence interval) comparing the highest and lowest quartiles of carbohydrate intake were 0.50 (0.25-0.97) for obesity (BMI>29.9) and 0.41 (0.23-0.73) for abdominal obesity (WC>101.9 cm).
Conclusion:
Consistent negative associations between carbohydrate intake and BMI and WC were seen in this random representative sample of the general male population. The associations between fat intake and these measures of being overweight were attenuated on adjusting for carbohydrate intake. Thus, the balance of carbohydrate-to-fat intake is an important element in obesity in a general male population, and should be highlighted in dietary guidelines.
The prevalence of obesity is increasing rapidly worldwide, which is cause for concern because obesity increases the risk of cardiovascular disease and diabetes, reduces life expectancy, and impairs quality of life. A better understanding of the risk factors for obesity is therefore a critical global health concern, and human biologists can play an important role in identifying these risk factors in various populations. The objective of this review is to present the evidence that inadequate sleep may be a novel risk factor associated with increased vulnerability to obesity and associated cardiometabolic disease. Experimental studies have found that short-term sleep restriction is associated with impaired glucose metabolism, dysregulation of appetite, and increased blood pressure. Observational studies have observed cross-sectional associations between short sleep duration (generally <6 h per night) and increased body mass index or obesity, prevalent diabetes, and prevalent hypertension. Some studies also reported an association between self-reported long sleep duration (generally >8 h per night) and cardiometabolic disease. A few prospective studies have found a significant increased risk of weight gain, incident diabetes, and incident hypertension associated with inadequate sleep. Given the potential link between inadequate sleep and obesity, a critical next step is to identify the social, cultural, and environmental determinants of sleep, which would help to identify vulnerable populations. Future human biology research should consider variation in sleep characteristics among different populations and determine whether the associations between sleep and obesity observed in Western populations persist elsewhere.
To describe the physical activity patterns across levels of obesity among US adults.
The frequency, intensity, and duration of physical activities were compared across obesity status in 7695 adults from NHANES, 1999-2006.
Significantly more normal-weight adults engaged in moderate- and vigorous- intensity activities and for a longer duration than did their overweight or obese counterparts. Lower intensity, longer duration walking contributed to nearly half of all moderate activity among obese subjects.
Significant differences exist in intensity, frequency, and duration of physical activity by weight status. This information suggests a targeted approach to current physical activity interventions be explored.
In Canada, data show adults had a lower energy intake in 2004 than in 1972. Data also show adults expended more energy through leisure-time physical activity in 2000 than in 1981. On the other hand, the prevalence of overweight and obesity (combined) rose from 49.2% to 59.1% between 1978 and 2004.
This study aimed to chart trends in leisure-, transport-, and work-related physical activity in Canada between 1994 and 2005.
We used nationally representative data from the three National Population Health Surveys (1994, 1996, and 1998) and the three Canadian Community Health Surveys (2000, 2003, and 2005) (a repeated cross-sectional design). Sample sizes ranged from n=17626 (in 1994) to n=132,221 (in 2005).
Between 1994 and 2005, men became less inactive during leisure time (-9.94% [9.89%-9.98%]), less inactive during transports (-15.31% [15.26%-15.35%]), and more inactive at work (+5.18% [5.14%-5.22%]). Similar results were found for women.
Declining levels of physical activity at work may help explain the rising prevalence of overweight and obesity in Canada.
Characteristics of weight cyclers have not been fully assessed. The objective of this study was to determine the anthropometric, metabolic, psychosocial, and dietary profile of postmenopausal women according to weight-cycling history, defined as the frequency of going on a diet and losing >10 kg: never (0 times), low (1 time), moderate (2 to 3 times), or frequent (> or = 4 times). The sample of this cross-sectional study consisted of 121 overweight/obese postmenopausal women enrolled in a 6-month randomized weight-loss intervention between 2003 and 2006. Measures at baseline were used to evaluate body composition (fat mass by dual-energy x-ray absorptiometry and visceral fat by computed tomography); resting metabolic rate by indirect calorimetry; insulin sensitivity by hyperinsulinemic-euglycemic clamp; fasting plasma levels of glucose, lipids, leptin, ghrelin, and adiponectin; blood pressure; psychosocial profile (eg, body-esteem, self-esteem, stress, perceived risks, perceived benefits, self-efficacy, quality of life, dietary restraint, disinhibition, hunger); and dietary profile (3-day food record). Differences among groups of weight cyclers were determined using analyses of variance. Among the 121 women, 15.7%, 24.8%, 33.9%, and 25.6% were non-, low, moderate, and frequent cyclers, respectively. Frequent cyclers were characterized by higher body mass index (calculated as kg/m(2)) (current and at 25 years of age) and percent body fat mass, larger waist circumference, and lower resting metabolic rate/kg body weight than noncyclers (P<0.05); and moderate cyclers had lower plasma adiponectin values than noncyclers (P<0.05). For psychosocial measures, frequent cyclers were characterized by greater disinhibition and lower body esteem after controlling for body mass index (P<0.05). In conclusion, weight cycling was found to be associated with some unfavorable metabolic and psychosocial parameters.
Hypothetical bias is a persistent problem in stated preference studies. We propose and test a method for reducing hypothetical bias based on the cognitive dissonance literature in social psychology. A central element of this literature is that people prefer not to take inconsistent stands and will change their attitudes and behavior to make them consistent. We find that participants in a stated preference willingness-to-pay study, when told that a nonhypothetical study of similar goods would follow, state significantly lower willingness to pay than participants not so informed. In other words, participants adjust their stated willingness to pay to avoid cognitive dissonance from taking inconsistent stands on their willingness to pay for the good being offered. (09-WP 486)
The measurement of dietary intake by self-report has played a central role in nutritional science for decades. Despite its important role, however, little is known about the accuracy of self-reported intake. Recently, the doubly-labeled water method has been validated for the measurement of total energy expenditure in free-living subjects, and this method can serve as a reference for validating the accuracy of self-reported energy intake. Such comparisons have been made in nine recent studies, and considerable inaccuracy in self-reports of energy intake has been documented. Reported intakes tend to be lower than expenditure and thus are often underestimates of true habitual energy intake. Because the degree of underreporting increases with intake, it is speculated that individuals tend to report intakes that are closer to perceived norms than to actual intake.
The Harris Benedict equations (HBE) were derived from indirect calorimetric data obtained in 239 normal subjects. Using these data and additional data published by Benedict, which were obtained from subjects spanning a wider age range (n = 98), the present study evaluated the relationship between measured resting energy expenditure and age, sex, and predicted body cell mass (BCM). When the additional subjects from the subsequently published series are included, the regression equations, standard error of the estimate, and 95% confidence limits are similar to the original equations. The HBE estimate resting energy expenditure of a normal subject with a precision of 14%. Resting energy expenditure is directly related to the size of the BCM and is independent of age and sex. The variables of height, weight, age, and sex in the HBE reflect the relationship between body weight and the BCM. Indirect calorimetry and body composition measurements were performed in both normally nourished and malnourished patients (n = 74) to assess the accuracy of the HBE in malnourished patients. Malnutrition is associated with an increase in resting oxygen consumption (VO2) which becomes apparent only when VO2 is expressed as a function of the BCM. There is no difference in resting VO2 between the sexes when expressed as a function of BCM. A regression equation was derived from the Harris Benedict data to predict resting VO2 from age, height, weight, and sex. Predicted VO2 was not significantly different from measured VO2 for the normally nourished patients (n = 33) whereas in the malnourished (n = 41) predicted VO2 underestimated the measured value. The HBE accurately predict resting energy expenditure in normally nourished individuals with a precision of +/- 14%, but are unreliable in the malnourished patient.
The role of energy expenditure in energy regulation remains a subject of continuing controversy. New data have emerged from studies conducted over the last decade demonstrating that energy expenditure is a critical factor contributing to successful energy regulation in normal individuals, as well as to the disregulation of energy balance that characterizes obesity. Reduced energy expenditure appears to facilitate weight gain in individuals susceptible to obesity and also appears to reduce the extent of body energy loss during undereating in both lean and obese individuals. The magnitude of the reduction in energy expenditure during, and perhaps after, weight loss is greater than expected on the basis of the reduction in body weight and appears to occur in response to undefined underlying determinants of energy regulation. In addition, exercise intervention studies and cross-sectional investigations of the relationship between energy expenditure for physical activity and body composition demonstrate an apparent equilibration between physical activity and body fat content. This equilibration is suggestive of a direct influence of physical activity on the underlying metabolic determinants of energy balance.
The therapeutic effectiveness of diet, exercise, and diet plus exercise for weight loss in obesity was determined.
All human research reported in English, published in peer-reviewed scientific journals within the past 25 y was reviewed.
Acceptance criteria (n = 493 from > 700 studies) were that a therapeutic intervention of diet, exercise or diet plus exercise was employed, specifically for weight reduction in obese adult humans and that weight change was reported numerically. Only aerobic exercise studies were included, while drug, hormone and surgical treatments were excluded.
All data were extracted by the same investigator from the original research report. Except for gender and program type, all extracted data were numerical.
ANOVA, with a Newman-Keuls post hoc test, was used to determine differences among programs (P < 0.05). One analysis was performed on the group mean data and one based on effect sizes. Analyses were repeated using initial body weight, initial percent body fat and program length, as covariates.
Primarily, subjects aged 40 y have been studied (39.5 +/- 0.4 y, mean +/- s.e.m.) who are only moderately obese (92.7 +/- 0.9 kg, 33.2 +/- 0.5 body mass index (BMI), 33.4 +/- 0.7% body fat); for short durations (15.6 +/- 0.6 weeks). Exercise studies were of a shorter duration, used younger subjects who weighed less, had lower BMI and percentage body fat values, than diet or diet plus exercise studies. Despite these differences, weight lost through diet, exercise and diet plus exercise was 10.7 +/- 0.5, 2.9 +/- 0.4* and 11.0 +/- 0.6 kg, respectively. However, at one-year follow-up, diet plus exercise tended to be the superior program. Effect size and covariate analyses revealed similar program differences.
Weight loss research over the past 25 y has been very narrowly focused on a middle age population that is only moderately obese, while the interventions lasted for only short periods of time. The data shows, however, that a 15-week diet or diet plus exercise program, produces a weight loss of about 11 kg, with a 6.6 +/- 0.5 and 8.6 +/- 0.8 kg maintained loss after one year, respectively.
Regular physical activity has profound effects on body composition and the utilisation of nutrients and help to maintain and increase skeletal muscle mass, with increased resting metabolic rate and enhanced capacity for lipid oxidation during rest and exercise. Regular exercise may also prevent or limit the loss of lean tissue (fat-free mass, FFM) during slimming regimens. Increased physical activity induces a number of favourable changes in the metabolism of lipoproteins: serum triglycerides are lowered by the increased lipolytic activity, the HDL concentration increases and the concentration of small dense LDL decreases. In addition, the enhanced metabolic capacity of skeletal muscle (metabolic fitness) will favorably influence risk factors such as insulin resistance and hypertension. Because regular physical activity has favorable effects on several of the comorbid conditions of obesity, particularly cardiovascular disease and type 2 diabetes, it is not surprising that the mortality rates seem to be lower in the overweight and moderately obese individuals who are physically fit compared with the unfit. The treatment of overweight and obese persons should perhaps be more focused on the level of regular physical activity than on body weight per se. For most of those who wish to reduce their body weight, it is recommended that they combine regular physical activity with a somewhat reduced energy intake, in particular of food rich in fat. Emphasis should be on promoting relatively low-intensity, long-duration physical activity which can be conveniently incorporated into daily life.
Diets high in fat have been proposed as one cause of obesity, primarily because fat is more energy-dense than other macronutrients. However, the literature on fat consumption and human obesity is inconclusive. This research examines associations between dietary fat intake and obesity in men participating in the Prostate Cancer Prevention Trial.
Data in this cross-sectional study are from 15,266 men (55-79 years) who completed questionnaires on usual diet, physical activity, and health-related characteristics. Height and weight were collected by clinic personnel. Obesity was defined as body mass index (BMI) greater than or equal to 30 kg/m2.
In this healthy cohort, 23.3% were obese. Younger age, a sedentary lifestyle, lower education, and black race were positively associated with obesity (all P < 0.001). Using two statistical approaches, both total energy and energy from fat, but not total energy from other macronutrients, increased linearly and significantly with increasing BMI. Mean fat intake increased from 691 kcal (31.4% energy) among normal-BMI men to 797 kcal (34.3% energy) among the obese (P for trend <0.001). After controlling for demographic and health-related characteristics in regression models, BMI increased by 0.53 and 0.14 kg/m(2) for every 500 kcal of fat and total energy consumed, respectively. Energy underreporting, based on estimated basal metabolic rate and physical activity, was fourfold higher among obese compared to normal-weight men.
In this large cohort of healthy older men, energy from fat was associated with obesity, suggesting that high-fat dietary patterns are contributing to the high rates of obesity in U.S. men.
The number of obese people worldwide has escalated recently, revealing a complex picture of significant variations among nations and different profiles among adults and children, regions, and occupations. The commonly held causes of obesity-overeating and inactivity-do not explain the current obesity epidemic. There is evidence of a general decrease in food consumption by humans and a significant decline in their overall levels of physical activity. There is also more evidence to indicate that the body's natural weight-control mechanisms are not functioning properly in obesity. Because the obesity epidemic occurred relatively quickly, it has been suggested that environmental causes instead of genetic factors maybe largely responsible. What has, up to now, been overlooked is that the earth's environment has changed significantly during the last few decades because of the exponential production and usage of synthetic organic and inorganic chemicals. Many of these chemicals are better known for causing weight loss at high levels of exposure but much lower concentrations of these same chemicals have powerful weight-promoting actions. This property has already been widely exploited commercially to produce growth hormones that fatten livestock and pharmaceuticals that induce weight gain in grossly underweight patients. This paper presents a hypothesis that the current level of human exposure to these chemicals may have damaged many of the body's natural weight-control mechanisms. Furthermore, it is posited here that these effects, together with a wide range of additional, possibly synergistic, factors may play a significant role in the worldwide obesity epidemic.
Studies have yielded discrepant results concerning whether the thermic effect of food (TEF) is reduced in obesity. Methodological variations among published studies make understanding the discrepant results very difficult. Although methodological differences are often noted as contributing to the discrepant results, little work has been done to address these differences and standardize experimental protocols. This paper reviews 50 studies that have investigated TEF in obesity and focuses on factors related to experimental protocol and subject control that reportedly affect measurements of resting energy expenditure, postprandial energy expenditure, and the calculation of TEF.
Untested alternative weight loss diets, such as very low carbohydrate diets, have unsubstantiated efficacy and the potential to adversely affect cardiovascular risk factors. Therefore, we designed a randomized, controlled trial to determine the effects of a very low carbohydrate diet on body composition and cardiovascular risk factors. Subjects were randomized to 6 months of either an ad libitum very low carbohydrate diet or a calorie-restricted diet with 30% of the calories as fat. Anthropometric and metabolic measures were assessed at baseline, 3 months, and 6 months. Fifty-three healthy, obese female volunteers (mean body mass index, 33.6 +/- 0.3 kg/m(2)) were randomized; 42 (79%) completed the trial. Women on both diets reduced calorie consumption by comparable amounts at 3 and 6 months. The very low carbohydrate diet group lost more weight (8.5 +/- 1.0 vs. 3.9 +/- 1.0 kg; P < 0.001) and more body fat (4.8 +/- 0.67 vs. 2.0 +/- 0.75 kg; P < 0.01) than the low fat diet group. Mean levels of blood pressure, lipids, fasting glucose, and insulin were within normal ranges in both groups at baseline. Although all of these parameters improved over the course of the study, there were no differences observed between the two diet groups at 3 or 6 months. beta- Hydroxybutyrate increased significantly in the very low carbohydrate group at 3 months (P = 0.001). Based on these data, a very low carbohydrate diet is more effective than a low fat diet for short-term weight loss and, over 6 months, is not associated with deleterious effects on important cardiovascular risk factors in healthy women.
This review focuses on dietary intake and dietary supplement use among the U.S. population age 1-74 based on four National Health and Nutrition Examination Surveys conducted in 1971-74, 1976-80, 1988-94, and 1999-2000. Secular trends in intake of energy, macronutrients, cholesterol, sodium, calcium, iron, folate, zinc, vitamins A and C, fruits, vegetables, and grain products are summarized. During the 30-year period, mean energy intake increased among adults, and changed little among children age 1-19, except for an increase among adolescent females. Factors contributing to increases in energy intake include increases in the percentage of the population eating away from home (particularly at fast-food restaurants), larger portion sizes of foods and beverages, increased consumption of sweetened beverages, changes in snacking habits, and improved dietary methodology. Dietary supplement use increased among adult men and women, decreased among children age 1-5, and was stable for children age 6-11 and adolescents.
To determine the relation between the average daily physical activity level (PAL) and the trajectory of weight change in men at risk for weight gain.
Clinic-based cohort study over an average of 5 y.
Healthy men (N=2501) ages 20-55 y participating in the Aerobics Center Longitudinal Study who had received at least four medical examinations at the Cooper Clinic between 1970 and 1998.
Daily leisure-time physical activity was reported and body weight was measured at all four examinations. The average daily PAL (METs 24 h(-1)) was estimated from all activities, as well as from other incidental active and passive activities. Weight change over four examinations was regressed on the change in PAL between the first and third examinations.
Random coefficient regression modeling indicated a curvilinear slope for weight gain over the follow-up among those maintaining the same PAL between the first and third examinations. Weight gain was further accelerated among men who decreased their activity. A shift from a low PAL (<1.45 METs 24 h(-1)) to a moderate (1.45-1.60 METs 24 h(-1)) or high (>1.60 METs 24 h(-1)) PAL was necessary for weight loss over time. Men with initially the lowest PAL had the greatest benefit from increasing activity.
Daily PAL was inversely related to weight gain in this cohort. Increasing to or maintaining a daily PAL at least 60% above the resting metabolic rate (ie, PAL >1.60 METs 24 h(-1)) may be necessary to maintain body weight in middle-age and can be achieved by incorporating 45-60 min of brisk walking, gardening/yardwork, or cycling into the daily routine.
Sleep deprivation has been hypothesized to contribute toward obesity by decreasing leptin, increasing ghrelin, and compromising insulin sensitivity. This study examines cross-sectional and longitudinal data from a large United States sample to determine whether sleep duration is associated with obesity and weight gain.
Longitudinal analyses of the 1982-1984, 1987, and 1992 NHANES I Followup Studies and cross-sectional analysis of the 1982-1984 study.
Probability sample of the civilian noninstitutionalized population of the United States.
Sample sizes of 9,588 for the cross-sectional analyses, 8,073 for the 1987, and 6,981 for the 1992 longitudinal analyses.
Measured weight in 1982-1984 and self-reported weights in 1987 and 1992. Subjects between the ages of 32 and 49 years with self-reported sleep durations at baseline less than 7 hours had higher average body mass indexes and were more likely to be obese than subjects with sleep durations of 7 hours. Sleep durations over 7 hours were not consistently associated with either an increased or decreased likelihood of obesity in the cross-sectional and longitudinal results. Each additional hour of sleep at baseline was negatively associated with change in body mass index over the follow-up period, but this association was small and statistically insignificant.
These findings support the hypothesis that sleep duration is associated with obesity in a large longitudinally monitored United States sample. These observations support earlier experimental sleep studies and provide a basis for future studies on weight control interventions that increase the quantity and quality of sleep.
Approximately $50 billion a year is spent by Americans on weight-loss products and services. Despite the high cost, few national studies have described specific weight-loss and weight-maintenance practices among U.S. adults. This analysis describes the use of specific practices by U.S. adults who tried to lose weight or tried only not to gain weight during the previous 12 months.
Data were analyzed from the 2001-2002 National Health and Nutrition Examination Survey (NHANES) conducted on a nationally representative sample of the U.S. population. This study focused on adults aged 20 years or older who were both interviewed and examined (n =5027).
Fifty-one percent of U.S. adults tried to control their weight in the previous 12 months, including those who tried to lose weight (34% of men, 48% of women) and those who tried only not to gain weight (11% vs 10%, respectively). Among 2051 adults who tried to control their weight, the top four practices were the same: ate less food (65% among those who tried to lose weight, 52% among those who tried only not to gain weight); exercised (61% vs 46%, respectively); ate less fat (46% vs 42%); and switched to foods with lower calories (37% vs 36%). Less than one fourth combined caloric restriction with the higher levels of physical activity (300 or more minutes per week) recommended in the 2005 dietary guidelines by the U.S. Department of Health and Human Services and U.S. Department of Agriculture.
Although weight control is a common concern, most people who try do not use recommended combinations of caloric restriction and adequate levels of physical activity.
Twenty-year trends in lifestyle (leisure, household, and transportation related) physical activity and leisure-time physical activity (LTPA) were evaluated in the Minnesota Heart Survey (MHS), a population-based surveillance study to monitor trends in cardiovascular risk factor levels among residents of the Minneapolis-St. Paul metropolitan area.
The Minnesota LTPA questionnaire was administered to adult participants in one of five cross-sectional MHS surveys conducted in 1980 (N = 1626), 1985 (N = 2292), 1990 (N = 2552), 1995 (N = 2432), and 2000 (N = 3089). Occupational activity was queried in 1980, 1995, and 2000. Age-adjusted, gender-specific geometric means of lifestyle physical activity and LTPA and of light-, moderate-, and vigorous-intensity activities were calculated for each survey. The proportion of adults participating in regular physical activity for 30 and 60 min x d(-1) was reported.
Male gender, younger age, higher educational status, and employment were characteristic of greater participation in physical activity. Daily energy expenditure from lifestyle physical activity and LTPA increased between 1980 and 2000 in both genders, and workplace activity decreased. Using direct questions, the prevalence of men and women participating in 30 or more minutes of physical activity at least five times per week ranged from 8 to 12%, with no time trend. Only 1% of participants participated 60 min daily. Overall, BMI was 1-2 kg x m(-2) lower among individuals who participated regularly in physical activity.
Although energy expenditure was lower than national recommendations, greater physical activity was associated with lower body mass. Public health strategies are needed to facilitate participation in physical activity, especially for women, elderly, and less educated individuals.
To describe physical activity levels of children (6-11 yr), adolescents (12-19 yr), and adults (20+ yr), using objective data obtained with accelerometers from a representative sample of the U.S. population.
These results were obtained from the 2003-2004 National Health and Nutritional Examination Survey (NHANES), a cross-sectional study of a complex, multistage probability sample of the civilian, noninstitutionalized U.S. population in the United States. Data are described from 6329 participants who provided at least 1 d of accelerometer data and from 4867 participants who provided four or more days of accelerometer data.
Males are more physically active than females. Physical activity declines dramatically across age groups between childhood and adolescence and continues to decline with age. For example, 42% of children ages 6-11 yr obtain the recommended 60 min x d(-1) of physical activity, whereas only 8% of adolescents achieve this goal. Among adults, adherence to the recommendation to obtain 30 min x d(-1) of physical activity is less than 5%.
Objective and subjective measures of physical activity give qualitatively similar results regarding gender and age patterns of activity. However, adherence to physical activity recommendations according to accelerometer-measured activity is substantially lower than according to self-report. Great care must be taken when interpreting self-reported physical activity in clinical practice, public health program design and evaluation, and epidemiological research.