ArticleLiterature Review

Causes of Obesity

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Abstract

The prevalence of obesity has been rising steadily over the last several decades and is currently at unprecedented levels: more than 68% of US adults are considered overweight, and 35% are obese (Flegal et al., JAMA 303:235-241, 2010). This increase has occurred across every age, sex, race, and smoking status, and data indicate that segments of individuals in the highest weight categories (i.e., BMI > 40 kg/m(2)) have increased proportionately more than those in lower BMI categories (BMI < 35 kg/m(2)). The dramatic rise in obesity has also occurred in many other countries, and the causes of this increase are not fully understood (Hill and Melanson, Med Sci Sports Exerc 31:S515-S521, 1999).

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... Obesity is usually due to an imbalance between energy consumption and energy expenditure, but it can also be caused by genetic, environmental, psychological and economic factors [14]. The genetic etiology of obesity is a deeply researched topic, and the genetic analysis of obese patients has shown that rare polymorphisms should also be considered for understanding molecular etiology [15][16][17][18][19]. Due to genetic heterogeneity, it can be difficult to identify genetic defects in patients with obesity. ...
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Improved human material living standards have resulted in a continuous increase in the rate of obesity caused by excessive sugar intake. Consequently, the number of diabetic patients has skyrocketed, not only resulting in a global health problem but also causing huge medical pressure on the government. Limiting sugar intake is a serious problem in many countries worldwide. To this end, the market for sugar substitute products, such as artificial sweeteners and natural sugar substitutes (NSS), has begun to rapidly grow. In contrast to controversial artificial sweeteners, NSS, which are linked to health concepts, have received particular attention. This review focuses on the extraction technology and biomedical function of NSS, with a view of generating insights to improve extraction for its large-scale application. Further, we highlight research progress in the use of NSS as food for special medical purpose (FSMP) for patients.
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There are fundamental sex differences in the regulation of energy homeostasis. Better understanding of the underlying mechanisms of energy balance that account for this asymmetry will assist in developing sex-specific therapies for sexually dimorphic diseases such as obesity. Multiple organs, including the hypothalamus and adipose tissue, play vital roles in the regulation of energy homeostasis, which are regulated differently in males and females. Various neuronal populations, particularly within the hypothalamus, such as arcuate nucleus (ARC), can sense nutrient content of the body by the help of peripheral hormones such leptin, derived from adipocytes, to regulate energy homeostasis. This review summarizes how adipose tissue crosstalk with homeostatic network control systems in the brain, which includes energy regulatory regions and the hypothalamic–pituitary axis, contribute to energy regulation in a sex-specific manner. Moreover, development of obesity is contingent upon diet and environmental factors. Substances from diet and environmental contaminants can exert insidious effects on energy metabolism, acting peripherally through the aryl hydrocarbon receptor (AhR). Developmental AhR activation can impart permanent alterations of neuronal development that can manifest a number of sex-specific physiological changes, which sometimes become evident only in adulthood. AhR is currently being investigated as a potential target for treating obesity. The consensus is that impaired function of the receptor protects from obesity in mice. AhR also modulates sex steroid receptors, and hence, one of the objectives of this review is to explain why investigating sex differences while examining this receptor is crucial. Overall, this review summarizes sex differences in the regulation of energy homeostasis imparted by the adipose–hypothalamic axis and examines how this axis can be affected by xenobiotics that signal through AhR.
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The global prevalence of obesity is alarmingly high and is impacting both developed and underdeveloped countries, beyond the borders of ethnicity, sex, and age. On the other hand, the global interest in dieting has increased, and people are obsessed with certain fad diets, assuming them as a magic bullet for their long-term problems. A fad diet is a popular dietary pattern known to be a quick fix for obesity. These diets are quite appealing due to the proposed claims, but the lack of scientific evidence is a big question mark. Such diets are often marketed with specific claims that defy the basic principles of biochemistry and nutritional adequacy. These diets may have protective effects against obesity and certain chronic diseases like cardiovascular diseases, metabolic syndrome, and certain cancers. Limited evidence exists to support the proposed claims; rather certain studies suggest the negative health consequences of long-term adherence to such dietary patterns. Many fad diets have emerged in the previous few decades. This review article will explore the current evidence related to the health impacts of some most popular diets: Atkins diet, ketogenic diet, Paleolithic diet, Mediterranean diet, vegetarian diet, intermittent fasting and detox diet.
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To combat the immense toll on global public health induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), new vaccines were developed. While these vaccines have protected the populations who received them from severe SARS-CoV-2 infection, the effectiveness and durability of these vaccines in individuals with obesity are not fully understood. Our uncertainty of the ability of these novel vaccines to induce protective immunity in humans with obesity stems from historical data that revealed obesity-associated immune defects to influenza vaccines. This review analyzes the efficacy of SARS-CoV-2 vaccines in humans with obesity. According to the vaccine safety and efficacy information for the Pfizer, Moderna, and Johnson & Johnson formulations, these vaccines showed a similar efficacy in both individuals with and without obesity. However, clinical trials that assess BMI and central obesity showed that induced antibody titers are lower in individuals with obesity when compared to healthy weight subjects, highlighting a potential early waning of vaccine-induced antibodies linked to obesity rates. Thus, the desired protective effects of SARS-CoV-2 vaccination were potentially diminished in humans with obesity when compared to the healthy weight population, but further studies outlining functional implications of the link between obesity and lower antibody titers need to be conducted to understand the full impact of this immune phenomenon. Further, additional research must be completed to truly understand the immune responses mounted against SARS-CoV-2 in patients with obesity, and whether these responses differ from those elicited by previously studied influenza viruses.
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The macroeconomic effect of the obesity epidemic on environmental degradation was examined for panel data from thirty-one European countries from 1991 to 2016. The quantile via moments model (QVM) was used to realize our empirical investigation. The empirical results indicate that the obesity epidemic, electricity consumption, and urbanisation encourage environmental degradation by increasing CO2 emissions, while economic growth decreases them. Moreover, we identify that the obesity epidemic raises the environmental degradation problem in three ways. First, the obesity epidemic is caused by the increased consumption of processed foods from multinational food corporations. The increase in food production will positively impact energy consumption from non-renewable energy sources. Second, obesity reduces physical and outdoor activities, increasing the intensive use of home appliances and motorized transportation and screen-viewing leisure activities, consequently increasing energy consumption from non-renewable energy sources. A third possible way can be related indirectly to economic growth, globalization, and urbanisation. This empirical investigation will contribute to the literature and for policymakers and governments. Therefore, this investigation will encourage the development of initiatives to mitigate the obesity problem in European countries and accelerate the energy transition process. Finally, this investigation will open a new topic in the literature regarding the correlation between the obesity epidemic and environmental degradation
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Background: Previous studies have shown that the C allele of melanocortin 4 receptor (MC4R) rs17782313 and Alternative Healthy Eating Index (AHEI) are separately associated with obesity. However, no study has assessed the aim of this study which is to investigate the interaction between MC4R rs17782313 variants and AHEI and their association with central and general obesity indices. Methods: A total of 291 women with BMI ≥25 and aged 18-48 years enrolled in this cross-sectional study. All participants were assessed for body composition, anthropometric measures, dietary intake, and blood parameters. After obtaining data of dietary intake from the 147-item food frequency questionnaire (FFQ) the AHEI was calculated. MC4R rs17782313 SNPs were assessed using the restriction fragment length polymorphism (PCR-RFLP) method. Results: After adjustment for age, energy intake, physical activity, marital and economic status, the interaction between MC4R rs17782313 and AHEI was associated with hip circumference (HC) (β=-0.41, 95%CI: -0.77 to -0.05, P=0.02), body mass index (BMI) (β=-0.15, 95%CI: -0.29 to -0.02, P=0.02), fat mass (kg) (β=-0.28, 95%CI: -0.56 to -0.01, P=0.03), Visceral fat area (VFA) (β=-5.68, 95%CI: -9.55 to -1.80, P=0.004). The other measures that seem to be suggestively related to this interaction (0.05< P <0.07) are waist circumference (WC), waist-to-height ratio (WHtR), trunk fat (TF) (%), TF (kg), fat mass (%), and fat mass index (FMI). Conclusion: Interaction between MC4R rs17782313 and AHEI can be related to some central and general obesity indices in overweight/obese women. This article is protected by copyright. All rights reserved.
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A wide and interacting range of individual, environmental and socioeconomic factors contribute to obesity. As a consequence, weight management strategies almost always comprise a mixture of several parallel approaches, each with its challenges and unique goals. Broadly, weight management strategies comprise of two main strands. The non-pharmacotherapy approach includes various lifestyle modifications in terms of dietary therapy, exercise and behavioral modifications, including the prevention of possible relapses. Pharmacotherapy, on the other hand, involves several anti-obesity medications, employed as single or combination therapy. Generally, the goals of weight management should be realistic and individualized to patient’s experiences, abilties, and risks in order to maximize the likelihood of success. This chapter tackles these weight management strategies in turn, explaining each as well as highlighting their distinctive features and challenges, effectiveness and safety, requisites, and where appropriate, indications and contraindications. Keywords: Obesity, weight management, dietary therapy, behavioral therapy, physical activity, exercise, anti-obesity medications, pharmacotherapy Citation: Elhag W & El Ansari W. (2022) Medical Weight Management: A Multidisciplinary Approach. In: Weight Management - Challenges and Opportunities, Hassan M. Heshmati (Ed.). Intech Open. ISBN 978-1-80355-187-6
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Objective: To investigate the influence of body mass index (BMI) on perioperative outcomes, postoperative Patient-Reported Outcome Measures (PROMs), and minimal clinically important difference (MCID) achievement among Workers' Compensation (WC) claimants undergoing minimally invasive lumbar decompression (MIS-LD). Methods: WC patients diagnosed with herniated nucleus pulposus (HNP) undergoing single-level MIS-LD were identified. Patients were divided into three groups: Non-Obese (<30 kg/m2), Obese I (≥30 and <35 kg/m2), and Obese II/III (≥35 kg/m2).1 PROMs were collected preoperatively and at 6-weeks/12-weeks/6-months/1-year/2-years postoperatively. The predictive influence of BMI grouping on mean PROM scores was computed using simple linear regression. To compare PROMs between groups, post-hoc pairwise comparisons of adjusted means were utilized. MCID achievement was compared between groups with chi-squared analysis. Results: 81 patients were in the non-obese cohort, and 43 and 45 in the Obese I and Obese II/III cohorts, respectively. VAS leg, ODI, and SF-12 PCS were worse in the Obese I cohort at 12-weeks, and SF-12 PCS was lower in the Obese I vs. Obese II/III subgroup analysis (p≤0.045, all). MCID achievement rates for ODI were higher for the Non-Obese group at 12-weeks and for overall (p≤0.049, both). MCID attainment for VAS back was higher among the Non-Obese cohort at 6-weeks (p=0.022). Conclusion: Patients with higher levels of obesity were more likely to experience longer LOS and delayed discharge following MIS-LD. Increasing BMI was generally not a significant predictor of postoperative pain, disability, or physical health PROMs at most timepoints. MCID achievement rates for disability relief were significantly higher for non-obese patients.
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Objective Obesity is a highly prevalent, non-communicable, disease associated with numerous comorbid complications, such as cardiovascular disease. Following a healthy diet is known to help reduce the risk of both obesity and cardiovascular disease. This study was conducted to evaluate the association of recommended food score (RFS) and none recommended food score (NRFS) with cardiovascular risk factors in overweight and obese women. Methods This cross-sectional study was performed on 379 overweight and obese (BMI ≥25 kg/m²) women aged 18-48 years. Anthropometric measurements and body composition analysis were assessed in all participants. Dietary intake was assessed by a valid and reliable food frequency questionnaire (FFQ) containing 147 items, and RFS and NRFS was calculated. Biochemical assessments including TC, HDL, LDL, TG, FBS, insulin, HOMA-IR, and hs-CRP were quantified by ELISA. Results The mean age and BMI of participants were 36.73 ± 9.21 (y) and 31.17 ± 4.22 (kg/m²), respectively. Binary logistic regression showed that participants in the highest tertile of the RFS compared to the lowest tertile had 57% lower odds for hypertriglyceridemia [OR = 0.43, 95%CI = 0.20-0.92, P = 0.03]. Subjects with high adherence to the NRFS had lower HDL [OR = 2.11, 95%CI = 1.08-4.12, P = 0.02] and higher odds for hypertriglyceridemia [OR = 2.95, 95%CI = 1.47-5.94, P = 0.002] compared to low adherence. Conclusions There was an inverse significant association between adherence to RFS and odds of hypertriglyceridemia. There was a significant association between NRFS and hypertriglyceridemia, in addition to an inverse association between NRFS and HDL. We recommend that people increase their consumption of fruits, vegetables, whole grains, lean meats or meat alternates, and low-fat dairy and avoid red meat, processed meat, chips, high-fat dairy, solid oil, refined grains, and variety of sweetened foods to prevent cardiovascular disease.
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Purpose Obesity is a growing, global health problem and previous cross-sectional studies have demonstrated an association between obesity and chronic rhinosinusitis (CRS). There is, however, a lack of prospective studies regarding the impact of obesity on developing (new-onset) CRS. Methods Questionnaire-based data (n = 5769) relating to new-onset CRS and Body Mass Index (BMI) were collected in 2013 and 2018 from the Telemark population study in Telemark, Norway. Odds ratios for the risk of new-onset CRS in 2018 in relation to BMI in 2013 were calculated, adjusted for smoking habits, asthma, gender and age. Results When comparing the group with normal weight (18.5 ≤ BMI < 25) with the obese group (BMI ≥ 30), the odds of new-onset CRS was 53% higher [OR 1.53 (1.11, 2.10)] in the obese group. Conclusion CRS is a multifactorial disease with different phenotypes and it is important to consider obesity when assessing patients with CRS in a clinical setting.
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The increasing prevalence of obesity and overweight is a significant public concern throughout the world. Obesity is a complex disorder involving an excessive amount of body fat. It is not just a cosmetic concern. It is a medical challenge that increases the risk of other diseases and health circumstances, such as diabetes, heart disease, high blood pressure and certain cancers. Environmental and genetic factors are involved in obesity as a significant metabolic disorder along with diabetes. Gut microbiota (GM) has a high potential for energy harvesting from the diet. In the current review, we aim to consider the role of GM, gut dysbiosis and significant therapies to treat obesity. Dietary modifications, probiotics, prebiotics, synbiotics compounds, using faecal microbiota transplant, and other microbial-based therapies are the strategies to intervene in obesity reducing improvement. Each of these factors serves through various mechanisms including a variety of receptors and compounds to control body weight. Trial and animal investigations have indicated that GM can affect both sides of the energy-balancing equation; first, as an influencing factor for energy utilisation from the diet and also as an influencing factor that regulates the host genes and energy storage and expenditure. All the investigated articles declare the clear and inevitable role of GM in obesity. Overall, obesity and obesity-relevant metabolic disorders are characterised by specific modifications in the human microbiota’s composition and functions. The emerging therapeutic methods display positive and promising effects; however, further research must be done to update and complete existing knowledge.
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Introduction: The role of genetic factors in obesity has long been recognized, but their involved specific genes remained unidentified. The relationship between p53 gene single nucleotide polymorphisms and the risk of obesity has been investigated in recent years. Therefore, this study aimed to investigate the association of p53 Arg72Pro C>G (rs1042522) polymorphism with the risk of obesity in our study. Methods: This study included 52 patients with obesity (26 were females and 26 were males) and 52 normal-weight healthy controls. Genomic DNA isolation was performed from the blood samples of all participants. p53 Arg72Pro C>G (rs1042522) polymorphism was detected by real-time quantitative polymerase chain reaction from genomic DNA samples. Results: No significant associations were identified between Arg72Pro (rs1042522) p53 polymorphism and obesity risk. Glucose levels are significantly different between the obese and control groups with the CC and CG genotypes, but without difference in the GG homozygous genotype. Conclusion: Our study is one of the first to investigate the relationship between p53 codon 72 polymorphisms and obesity risk but revealed no correlation between them. The relatively small number of participants may limit our study. Further research is needed in a large cohort to associate the p53 gene Arg72Pro C>G (rs1042522) variant with obesity risk.
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Obesity is a major health problem that is caused by body fat accumulation and that can lead to metabolic diseases. Owing to several side effects of the currently used antiobesity drugs, natural plants have risen as safe and potential candidates to alleviate obesity. We have previously reported the antiobesity effect of Hydrangea serrata (Thunb.) Ser. leaves extract (WHS) and its underlying mechanisms. As an extension of our preclinical studies, this study aimed to investigate the effect of WHS on body weight and body fat reduction in overweight or obese humans. A total of 93 healthy overweight or obese males and females, aged 19–65 years, with body mass indexes (BMIs) ≥ 25 and <32 kg/m2, were recruited and received either an oral administration of 600 mg of WHS, or placebo tablets for 12 weeks. Daily supplementation with WHS decreased body weights, body fat masses, and BMIs compared with the placebo-treated group. The hip circumferences, visceral fat areas, abdominal fat areas, and visceral-to-subcutaneous ratios decreased after WHS supplementation. No significant side effects were observed during or after the 12 weeks of WHS intake. In conclusion, WHS, which has beneficial effects on body weight and body fat reduction, could be a promising antiobesity supplement that does not produce any side effects.
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Galacto-oligosaccharides (GOS) are commonly used as prebiotic with a variety of known metabolic benefits; however, whether GOS plays a protective role in obesity remains unknown. Here, we demonstrate that GOS prevented obesity in a rat model of obesity induced by a high-fat diet. Our results showed that GOS effectively slowed weight gain in diet-induced obese rats without affecting energy intake. GOS significantly suppressed the hypertrophy and hyperplasia of white adipose tissue and markedly reduced the ratio of the fat/body. Consistently, GOS significantly improved serum total cholesterol, triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol levels, indicating the weight loss activity of GOS. Interestingly, GOS also significantly increased the expression levels of browning proteins, including uncoupling protein 1, peroxisome proliferator-activated receptor-γ, peroxisome proliferator-activated receptor-γ coactivator 1α, and PR domain 16, in both white and brown adipose tissue. Furthermore, we found that GOS markedly increased the expression levels of liver X receptor α, peroxisome proliferation-activated receptor-α, low-density lipoprotein receptor, and cholesterol 7α-hydroxylase proteins in the liver of obese rats. Taken together, we concluded that GOS inhibits obesity by accelerating the browning of white fat cells and the thermogenesis of brown fat cells and that GOS improves host lipid homeostasis by promoting cholesterol catabolism.
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Background: Obesity is a prevalent disease in modern society. Despite the various interventions available in conventional medicine, their success rates are not satisfactory because of the complex mechanisms involved in obesity. Cupping therapy is a traditional Chinese medicinal intervention, and it has become widely used in various clinical settings for the treatment of obesity. This systematic review and meta-analysis will investigate the effects of cupping on obesity. Methods: Three Korean databases (KoreaMed, Oriental Medicine Advanced Searching Integrated System, and ScienceON), 1 Japanese database (Citation Information by the National Institute of Informatics), 1 Chinese database (Chinese National Knowledge Infrastructure), MEDLINE/PubMed, EMBASE, and The Cochrane Central Register of Controlled Trials will be searched for studies published until March 2021. The primary outcome is body weight. The secondary outcomes will be body mass index, waist-hip ratio, waist circumference, hip circumference, body fat mass, body fat percentage, and adverse events. Results: This systematic review and meta-analysis will evaluate the effects of cupping therapy for obesity. Conclusion: The results of this systematic review and meta-analysis will then be discussed in a related journal for clinicians working with obese patients to apply the interventions in this article. Trial registration number: DOI 10.17605/OSF.IO/P8JVM (https://osf.io/p8jvm).
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The past few decades have shown a worrisome increase in the prevalence of obesity and its related illnesses. This increasing burden has a noteworthy impact on overall worldwide mortality and morbidity, with significant economic implications as well. The same trend is apparent regarding pediatric obesity. This is a particularly concerning aspect when considering the well-established link between cardiovascular disease and obesity, and the fact that childhood obesity frequently leads to adult obesity. Moreover, most obese adults have a history of excess weight starting in childhood. In addition, given the cumulative character of both time and severity of exposure to obesity as a risk factor for associated diseases, the repercussions of obesity prevalence and related morbidity could be exponential in time. The purpose of this review is to outline key aspects regarding the current knowledge on childhood and adolescent obesity as a cardiometabolic risk factor, as well as the most common etiological pathways involved in the development of weight excess and associated cardiovascular and metabolic diseases.
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A large amount of waste is generated within the different steps of the food supply chain, representing a significant loss of natural resources, plant material, and economic value for producers and consumers. During harvesting and processing, many parts of edible plants are not sold for consumption and end up as massive waste, adding environmental hazards to the list of concerns regarding food wastage. An example is Brassica oleracea var. Italica (broccoli) by-products, which represent 75% of the plant mass-generated. A growing concern in the Western world is obesity, which results from incorrect lifestyles and comprises an extensive array of co-morbidities. Several studies have linked these co-morbidities to increased oxidative stress, thus, naturally occurring and readily available antioxidant compounds are an attractive way to mitigate metabolic diseases. The idea of by-products selected for their biomedical value is not novel. However, there is innovation underlying the use of Brassica by-products in the context of obesity. For this reason, Brassica by-products are prime candidates suggested to be used in the treatment of obesity due to its bioactive compounds, such as sulforaphane, with antioxidant activity. Here, we review the economic and health potential of Brassica bioactive compounds in the context of obesity.
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Objective: To review the scientific literature on the influence of verified nutrition, food and diet interventions on occupational health. Method: This study involved a critical analysis of articles retrieved from MEDLINE (via PubMed), Embase, Cochrane Library, PsycINFO, Scopus, Web of Science, Latin American and Caribbean Health Sciences Literature (LILACS) and Medicina en Español (MEDES) using the descriptors "Diet, Food, and Nutrition" and "Occupational Health" and applying the filters "Clinical Trial", "Humans" and "Adult: 19+ years"; the search was conducted on 29 May 2021. Results: A total of 401 references were retrieved from the bibliographic databases, with an additional 16 identified through a secondary search; among the studies retrieved, 34 clinical trials were selected after applying the inclusion and exclusion criteria. The interventions were grouped into seven categories: (1) dietary interventions associated with exercise or educational programs; (2) individual environmental interventions or other educational actions; (3) educational interventions oriented toward lifestyle, dietetics, physical activity and stress management; (4) economic incentives; (5) multicomponent interventions (combination of mindfulness, e-coaching and the addition of fruits and vegetables); or dietary interventions (facilitating greater food supply in cafeterias); or interventions focused on physical exercise. Conclusions: Given that most people spend a large part of their time in the workplace and, therefore, eat at least one of their daily meals there, well-planned interventions-preferably including several strategies-have been demonstrated, in general, as useful for combating overweight and obesity. From the meta-regression study, it was observed that the interventions give better results in people who presented high Body Mass Index (BMI) values (obesity). In contrast, intervention 2 (interventions related to workplace environment) would not give the expected results (it would increase the BMI).
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Objective Cognitive interventions may be effective in weight loss. The purpose of this study was to assess if cognitive reappraisal (CR; reframing the meaning of a stimulus in order to change the resulting emotional response), can reduce food attentional bias (FAB) using the Visual Dot Probe (VDP) paradigm. Method 126 participants (age 27 ± 5.8) were randomly assigned either to a CR or to a control (CN) group. After assessing baseline VDP levels for FAB, participants either wrote sentences that discourage eating fattening food or neutral sentences. Next, all participants performed the VDP post intervention. Participants also self-reported on disordered eating behaviors and their height and weight were charted. We hypothesized that CR would reduce FAB and that disordered eating would moderate the association between group and FAB. Results FAB decreased post intervention, specifically in the CR group. The bulimia sub-scale showed an interaction between bulimic eating, time and group. Among those who were high on the bulimia scale, the CR group showed lower FAB post-intervention compared to the CN group. Discussion This study suggests that CR may decrease the attentional bias toward high-calorie food compared to other strategies in the general population and among people with high bulimia measures, in particular. Plain English summary Obesity has a negative impact on many aspects of life and much research is dedicated to trying to better understand behaviors concerning obesity. People are prone to focus their attention on things that are of importance to them, such as food. When people focus their attention on food, we call this Food Attention Bias (FAB). Cognitive reappraisal (CR) interventions involve the person's conscious cognitive change of the meaning of the situation aiming to consequently change the emotional response to it, such as saying to yourself “I shouldn’t eat this because I don’t want to get fat”. CR has been found to be helpful in lowering FAB using brain imagining techniques but has not yet been studied in cognitive processes. Our study used a Visual dot probe paradigm (VDP) to assess the efficacy of CR on lowering FAB. Two groups, one using CR and a control group were assessed twice on FAB, using the VDP paradigm. Compared to the normal condition, the CR intervention helped reduce FAB. This reduction was especially significant for people with a higher tendency for bulimic behavior. The VDP paradigm, utilizing CR. can be expanded to help build an intervention aimed at reducing FAB over time. This, in turn might bring to weight reduction. People with bulimic tendencies might especially benefit from CR interventions when dealing with weight loss.
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Intestinal microbiota has been shown to be a potential determining factor in the development of obesity. The objective of this systematic review is to collect and learn, based on the latest available evidence, the effect of the use of probiotics and synbiotics in randomized clinical trials on weight loss in people with overweight and obesity. A search for articles was carried out in PubMed, Web of science and Scopus until September 2021, using search strategies that included the terms "obesity", "overweight", "probiotic", "synbiotic", "Lactobacillus", "Bifidobacterium" and "weight loss". Of the 185 articles found, only 25 complied with the selection criteria and were analyzed in the review, of which 23 observed positive effects on weight loss. The intake of probiotics or synbi-otics could lead to significant weight reductions, either maintaining habitual lifestyle habits or in combination with energy restriction and/or increased physical activity for an average of 12 weeks. Specific strains belonging to the genus Lactobacillus and Bifidobacterium were the most used and those that showed the best results in reducing body weight. Both probiotics and synbiotics have the potential to help in weight loss in overweight and obese populations.
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High-intensity interval training (HIIT) and linseed oil (LO) supplementation are effective strategies to reduce obesity-induced oxidative stress. Our aim was to determine whether the HIIT + LO combination prevents obesity-induced oxidative stress in high fat diet (HFD)-fed rats. HFD-fed 8-week-old, male, Wistar rats were subdivided in four groups: HFD, LO (2% of sunflower oil replaced with 2% of LO in the HFD), HIIT (4 days/week for 12 weeks), and HIIT + LO. Wistar rats fed a low-fat diet (LFD) were used as controls. Epididymal and subcutaneous adipose tissue, gastrocnemius muscle, liver, and plasma samples were collected to measure oxidative stress markers (AOPP, oxLDL), antioxidant (SOD, CAT, and GPx activities) and pro-oxidant (NOx and XO) enzyme activities. Compared with the LFD, the HFD altered the pro/antioxidant status in different tissues (increase of AOPP, oxLDL, SOD and catalase activities in plasma, and SOD activity increase in liver and decrease in adipose tissues) but not in gastrocnemius. LO upregulated CAT activity and decreased NOx in liver. HIIT alleviated HFD negative effects in liver by reducing SOD and NOx activities. Moreover, the HIIT + LO combination potentiated SOD activity upregulation in subcutaneous tissue. HIIT and LO supplementation have independent beneficial effects on the pro/antioxidant balance. Their association promotes SOD activity in subcutaneous adipose tissue.
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Physical inactivity contributes to weight gain in adults, but whether this relationship is true for children of different ethnic groups is not well established. To assess participation in vigorous activity and television watching habits and their relationship to body weight and fatness in US children. Nationally representative cross-sectional survey with an in-person interview and medical examination. SETTING and Between 1988 and 1994, 4063 children aged 8 through 16 years were examined as part of the National Health and Nutrition Examination Survey III. Mexican Americans and non-Hispanic blacks were oversampled to produce reliable estimates for these groups. Episodes of weekly vigorous activity and daily hours of television watched, and their relationship to body mass index and body fatness. Eighty percent of US children reported performing 3 or more bouts of vigorous activity each week. This rate was lower in non-Hispanic black and Mexican American girls (69% and 73%, respectively). Twenty percent of US children participated in 2 or fewer bouts of vigorous activity perweek, and the rate was higher in girls (26%) than in boys (17%). Overall, 26% of US children watched 4 or more hours of television per day and 67% watched at least 2 hours per day. Non-Hispanic black children had the highest rates of watching 4 or more hours of television per day (42%). Boys and girls who watch 4 or more hours of television each day had greater body fat (P<.001) and had a greater body mass index (P<.001) than those who watched less than 2 hours per day. Many US children watch a great deal of television and are inadequately vigorously active. Vigorous activity levels are lowest among girls, non-Hispanic blacks, and Mexican Americans. Intervention strategies to promote lifelong physical activity among US children are needed to stem the adverse health consequences of inactivity.
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For thirty-five years, U.S. agriculture has operated under a "cheap food" policy that spurred production of a few commodity crops, not fruit or vegetables, and thus of the calories from them. A key driver of childhood obesity is the consumption of excess calories, many from inexpensive, nutrient-poor snacks, sweets, and sweetened beverages made with fats and sugars derived from these policy-supported crops. Limiting or eliminating farm subsidies to commodity farmers is wrongly perceived as a quick fix to a complex agricultural system, evolved over decades, that promotes obesity. Yet this paper does set forth a series of policy recommendations that could help, including managing commodity crop oversupply and supporting farmers who produce more fruit and vegetables to build a healthier, more balanced agricultural policy.
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The prevalence of obesity increased in the United States between 1976-1980 and 1988-1994 and again between 1988-1994 and 1999-2000. To examine trends in obesity from 1999 through 2008 and the current prevalence of obesity and overweight for 2007-2008. Analysis of height and weight measurements from 5555 adult men and women aged 20 years or older obtained in 2007-2008 as part of the National Health and Nutrition Examination Survey (NHANES), a nationally representative sample of the US population. Data from the NHANES obtained in 2007-2008 were compared with results obtained from 1999 through 2006. Estimates of the prevalence of overweight and obesity in adults. Overweight was defined as a body mass index (BMI) of 25.0 to 29.9. Obesity was defined as a BMI of 30.0 or higher. In 2007-2008, the age-adjusted prevalence of obesity was 33.8% (95% confidence interval [CI], 31.6%-36.0%) overall, 32.2% (95% CI, 29.5%-35.0%) among men, and 35.5% (95% CI, 33.2%-37.7%) among women. The corresponding prevalence estimates for overweight and obesity combined (BMI > or = 25) were 68.0% (95% CI, 66.3%-69.8%), 72.3% (95% CI, 70.4%-74.1%), and 64.1% (95% CI, 61.3%-66.9%). Obesity prevalence varied by age group and by racial and ethnic group for both men and women. Over the 10-year period, obesity showed no significant trend among women (adjusted odds ratio [AOR] for 2007-2008 vs 1999-2000, 1.12 [95% CI, 0.89-1.32]). For men, there was a significant linear trend (AOR for 2007-2008 vs 1999-2000, 1.32 [95% CI, 1.12-1.58]); however, the 3 most recent data points did not differ significantly from each other. In 2007-2008, the prevalence of obesity was 32.2% among adult men and 35.5% among adult women. The increases in the prevalence of obesity previously observed do not appear to be continuing at the same rate over the past 10 years, particularly for women and possibly for men.
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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.
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The association of sociodemographic and family composition data with obesity was studied in 1213 black and 1166 white girls, ages 9 and 10, enrolled in the National Heart, Lung, and Blood Institute's Growth and Health Study. Obesity was defined as body mass index at or greater than age- and sex-specific 85th percentile as outlined in the Second National Health and Nutrition Examination Survey. The prevalence of obesity was higher for pubertal girls than for prepubertal girls and for girls with older mothers/female guardians. As odds ratio of 1.14 was observed for each 5-year increase in maternal age. Obesity was less common for girls with more siblings; the odds for obesity decreased by 14% for each additional sibling in the household. In blacks, the prevalence of obesity was not related to parental employment or to parental education. In whites, the odds of obesity were higher for girls with no employed parent/guardian in the household and for girls with parents or guardians with lower levels of educational attainment. Examining the associations between sociodemographic factors and risk of childhood obesity provides important clues for understanding racial differences in obesity, a major risk factor for coronary heart disease.
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Human adenovirus-36 (Ad-36) increases adiposity and paradoxically lowers serum cholesterol and triglycerides in chickens, mice, and non-human primates. The role of Ad-36 in human obesity is unknown. To determine the prevalence of Ad-36 antibodies in obese and nonobese humans. To evaluate the association of Ad-36 antibodies with body mass index (BMI) and serum lipids. Cohort study. Volunteers from obesity treatment programs, communities, and a research study. Obese and nonobese volunteers at the University of Wisconsin, Madison, WI, and the Bowen Center, Naples, Florida. Obese and thin volunteer research subjects and 89 twin pairs at Columbia University, New York. Study 1: 502 subjects; serum neutralization assay for antibodies to Ad-2, Ad-31, Ad-36, and Ad-37; serum cholesterol and triglycerides assays. Study 2: BMI and %body fat in 28 twin pairs discordant for Ad-36 antibodies. Presence of antibodies to adenoviruses, BMI, serum cholesterol and triglycerides levels. Significant (P < 0.001) association of obesity and positive Ad-36 antibody status, independent of age, sex, and collection site. Ad-36 antibodies in 30% of obese, 11% of nonobese. Lower serum cholesterol and triglycerides (P < 0.003) in Ad-36 antibody-positive vs -negative subjects. Twin pairs: antibody-positive twins had higher BMIs (24.5+/-5.2 vs 23.1+/-4.5 kg/m2, P < 0.03) and %body fat (29.6+/-9.5% vs 27.5+/-9.9%, P < 0.04). No association of Ad-2, Ad-31, or Ad-37 antibodies with BMI or serum lipids. Ad-36 is associated with increased body weight and lower serum lipids in humans. Prospective studies are indicated to determine if Ad-36 plays a role in the etiology of human obesity.
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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.
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Human adenovirus 36 (Ad-36) increases adiposity and reduces serum lipids in chicken, mouse, and non-human primate models, and it is linked to obesity in sero-epidemiological studies in humans. Involvement of the central nervous system (CNS) or adipose tissue in the mechanism of Ad-36-induced adiposity is unknown. The effects of Ad-36 on adiposity and on the neuroendocrine system were investigated in a rat model. Five-week-old male Wistar rats were inoculated intraperitoneally with Ad-36 or medium. Despite similar food intakes, infected rats attained significantly greater body weight and fat pad weight by 30 weeks post-inoculation. Epididymal-inguinal, retroperitoneal, and visceral fat pad weights of the infected group were greater by 60%, 46%, and 86%, respectively (p < 0.00001). The fasting serum insulin level and homeostasis model assessment index indicated greater insulin sensitivity in the infected group. Visceral adipose tissue expression of glycerol 3-phosphate dehydrogenase, peroxisome proliferator-activated receptor gamma, and CCAAT/enhancer-binding protein alpha and beta was markedly increased in the infected animals compared with controls. Ad-36 decreased norepinephrine levels significantly in the paraventricular nucleus in infected vs. control rats (mean +/- standard error, 8.9 +/- 1.1 vs. 12.8 +/- 1.2 pg/microg protein; p < 0.05). Ad-36 markedly decreased serum corticosterone in infected vs. control rats (mean +/- standard error, 97 +/- 41.0 vs. 221 +/- 111 ng/mL; p < 0.005). The results suggest that the pro-adipogenic effect of Ad-36 may involve peripheral as well as central effects. The male Wistar rat is a good model for the elucidation of metabolic and molecular mechanisms of Ad-36-induced adiposity.
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Although we are just beginning to understand how environmental factors such as portion size affect eating behavior, the available data suggest that large portions of energy-dense foods are contributing to the obesity epidemic. Several possible strategies for adjusting portions to bring intake back in line with energy requirements are discussed. The continuing rise in the rates of obesity calls for urgent action.
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The prevalence of obesity has increased substantially over the past 30 years. We performed a quantitative analysis of the nature and extent of the person-to-person spread of obesity as a possible factor contributing to the obesity epidemic. We evaluated a densely interconnected social network of 12,067 people assessed repeatedly from 1971 to 2003 as part of the Framingham Heart Study. The body-mass index was available for all subjects. We used longitudinal statistical models to examine whether weight gain in one person was associated with weight gain in his or her friends, siblings, spouse, and neighbors. Discernible clusters of obese persons (body-mass index [the weight in kilograms divided by the square of the height in meters], > or =30) were present in the network at all time points, and the clusters extended to three degrees of separation. These clusters did not appear to be solely attributable to the selective formation of social ties among obese persons. A person's chances of becoming obese increased by 57% (95% confidence interval [CI], 6 to 123) if he or she had a friend who became obese in a given interval. Among pairs of adult siblings, if one sibling became obese, the chance that the other would become obese increased by 40% (95% CI, 21 to 60). If one spouse became obese, the likelihood that the other spouse would become obese increased by 37% (95% CI, 7 to 73). These effects were not seen among neighbors in the immediate geographic location. Persons of the same sex had relatively greater influence on each other than those of the opposite sex. The spread of smoking cessation did not account for the spread of obesity in the network. Network phenomena appear to be relevant to the biologic and behavioral trait of obesity, and obesity appears to spread through social ties. These findings have implications for clinical and public health interventions.
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Leptin levels were stable across the daytime period under both sleep conditions, which was consistent with the fact that calories were exclusively delivered in the form of a constant glucose infusion. Average total sleep time was 9 hours and 8 minutes when the men spent 10 hours in bed and 3 hours and 53 minutes when the men spent 4 hours in bed (P < 0.01). When spending 4 hours in bed, the participants had mean leptin levels that were 18% lower (2.1 ng/mL vs. 2.6 ng/mL; P = 0.04) (Figure 1, part A) and mean ghrelin levels that were 28% higher (3.3 ng/mL vs. 2.6 ng/mL; P = 0.04) (Figure 1, part B) than when the participants spent 10 hours in bed. The ratio of the concentrations of orexigenic ghrelin to anorexigenic leptin increased by 71% (CI, 7% to 135%) with 4 hours in bed compared with 10 hours in bed. Sleep restriction relative to sleep extension was associated with a 24% increase in hunger ratings on the 10-cm visual analogue scale (P < 0.01) and a 23% increase in appetite ratings for all food categories combined (P = 0.01) (Figure 1, parts C and D, and Table 1). The increase in appetite tended to be greatest for calorie-dense foods with high carbohydrate content (sweets, salty foods, and starchy foods: increase, 33% to 45%; P = 0.06) (Table 1). The increase in appetite for fruits and vegetables was less consistent and of lesser magnitude (increase, 17% to 21%) (Table 1). Appetite for protein-rich nutrients (meat, poultry, fish, eggs, and dairy foods) was not significantly affected by sleep duration (Table 1). When we considered the changes in ghrelin and leptin in an integrated fashion by calculating the ghrelin-to-leptin ratio, the increase in hunger was proportional to the increase in ghrelin-to-leptin ratio (r = 0.87) (Figure 2). Almost 70% of the variance in increased hunger could be accounted for by the increase in the ghrelin-to-leptin ratio.
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The simultaneous increases in obesity in almost all countries seem to be driven mainly by changes in the global food system, which is producing more processed, affordable, and effectively marketed food than ever before. This passive overconsumption of energy leading to obesity is a predictable outcome of market economies predicated on consumption-based growth. The global food system drivers interact with local environmental factors to create a wide variation in obesity prevalence between populations. Within populations, the interactions between environmental and individual factors, including genetic makeup, explain variability in body size between individuals. However, even with this individual variation, the epidemic has predictable patterns in subpopulations. In low-income countries, obesity mostly affects middle-aged adults (especially women) from wealthy, urban environments; whereas in high-income countries it affects both sexes and all ages, but is disproportionately greater in disadvantaged groups. Unlike other major causes of preventable death and disability, such as tobacco use, injuries, and infectious diseases, there are no exemplar populations in which the obesity epidemic has been reversed by public health measures. This absence increases the urgency for evidence-creating policy action, with a priority on reduction of the supply-side drivers.
Article
The major drivers of the obesity epidemic are much debated and have considerable policy importance for the population-wide prevention of obesity. The objective was to determine the relative contributions of increased energy intake and reduced physical activity to the US obesity epidemic. We predicted the changes in weight from the changes in estimated energy intakes in US children and adults between the 1970s and 2000s. The increased US food energy supply (adjusted for wastage and assumed to be proportional to energy intake) was apportioned to children and adults and inserted into equations that relate energy intake to body weight derived from doubly labeled water studies. The weight increases predicted from the equations were compared with weight increases measured in representative US surveys over the same period. For children, the measured weight gain was 4.0 kg, and the predicted weight gain for the increased energy intake was identical at 4.0 kg. For adults, the measured weight gain was 8.6 kg, whereas the predicted weight gain was somewhat higher (10.8 kg). Increased energy intake appears to be more than sufficient to explain weight gain in the US population. A reversal of the increase in energy intake of approximately 2000 kJ/d (500 kcal/d) for adults and of 1500 kJ/d (350 kcal/d) for children would be needed for a reversal to the mean body weights of the 1970s. Alternatively, large compensatory increases in physical activity (eg, 110-150 min of walking/d), or a combination of both, would achieve the same outcome. Population approaches to reducing obesity should emphasize a reduction in the drivers of increased energy intake.
Article
While global prevalence of obesity continues to increase dramatically, treatment options remain less than optimal. The etiology of obesity is multifactorial, ranging from lifestyle choices such as excess food intake and insufficient physical activity, to use of medications that have weight gain as an undesirable side effect. Economic and political determinants of available foodstuffs and even social networks may also contribute to obesity. Successful management of obesity requires the understanding and acceptance of a new paradigm that identifies obesity as a disease--one defined by waist circumference--that requires treatment. Obesity meets all accepted criteria of a medical disease, including a known etiology, recognized signs and symptoms, and a range of structural and functional changes that culminate in pathologic consequences. Excess adipose tissue acts as an endocrine organ to produce excess free fatty acids, as well as tumor necrosis factor-alpha, interleukin-6, leptin, and plasminogen activator inhibitor-1. These bioactive molecules are associated with hyperinsulinemia, hyperglycemia, insulin resistance, development of diabetes, endothelial damage, and the onset and progression of atherosclerotic lesions. Options for treating obesity include lifestyle modifications (dietary changes, increased physical activity, behavior modification) and, for the morbidly obese, surgery. Lifestyle modification is rarely successful over the long term; therefore, addition of pharmacotherapy should be considered for obese individuals who have difficulty achieving and maintaining weight goals with lifestyle modifications alone. Several weight loss drugs are available for long-term use, with others in various stages of clinical development.
Article
The prezygotic hypothesis considers the possibility that development is subject to environmental influences on the oocyte prior to conception. Such influences may occur in the maternal grandmother's uterus where oogenesis is completed or in the mother before fertilization. According to this hypothesis, the separate eggs from which DZ twins are derived may be sensitive to microenvironmental variations within an ovary. As a first approach, we examined same-sex MZ and DZ twins for maternal age effects on differences between pairs in cognitive and behavioral traits. While no differences between MZ and DZ pairs were found that would indicate a major effect of the prezygotic environment, suggestions are made for further experimental studies of this unexplored question in human development.
Article
The prevalence of obesity has reached epidemic proportions in many countries around the world. However, the genetic and environmental factors contributing to obesity are incompletely understood. We reviewed studies relating to the regulation of energy balance and how these factors may contribute to the development of obesity. Although it is widely believed that genetics contribute significantly to the variability in body fatness, the available data do not support a role for defects in resting metabolic rate, substrate metabolism, dietary induced thermogenesis, or the energy cost of physical activity as significant causes of obesity. Furthermore, it is safe to say that the human genotype has not changed substantially over the past two to three decades. Data from several national surveys indicate that over the past few decades, there has been either a slight increase or a very modest decline in total energy and fat intake. This suggests that decreases in physical activity are a major contributing factor. Participation in leisure time physical activity is low but has remained relatively constant. However, an increased reliance on technology has substantially reduced work-related physical activity and the energy expenditure required for daily living. The most likely environmental factor contributing to the current obesity epidemic is a continued decline in daily energy expenditure that has not been matched by an equivalent reduction in energy intake. Because daily energy expenditure is decreasing, it is difficult for most people to restrict intake to meet energy requirements, and more and more people are becoming obese. Thus, increasing physical activity may be the strategy of choice for public health efforts to prevent obesity.
Article
Application of a new investigative strategy to assess genetic and environmental influences on relative body weight. Covariance structure analysis of body mass index (BMI) using genetically informative samples. One-hundred and fourteen monozygotic (MZ) twin pairs (age 5.04-22.93 y), 81 dizygotic (DZ) twin pairs (age 6.05-16.52 y), and 98 virtual twin (VT) pairs, ie same-age unrelated siblings (3.68-54.75 y). Height, weight, BMI variously obtained by direct measurement and self-report. In contrast with most previous studies, significant common environmental influence on BMI was observed. Much past research may have underestimated common environmental effects on BMI because the designs lacked the power or ability to detect them.
Article
Organochlorines are fat-soluble chemical compounds resistant to degradation, so they are stored in the adipose tissue of practically every organism on the planet, including humans. Accumulation of these compounds in the body seems to be related to fat mass, obese individuals having a higher plasma organochlorine concentration than lean subjects. During body weight loss, lipid mobilization and a decrease in fat mass result in increased concentrations of organochlorines in plasma and adipose tissue. Organochlorines may have adverse health effects. For example, they have been associated with altered immune and thyroid functions and with some types of cancer. As these compounds may reach their target organs whilst in the circulation, their increase in plasma during weight loss might be associated with some physiological changes occurring during weight loss. Relationships have indeed been reported among weight loss-induced increase in plasma organochlorine concentration and decreased triiodothyronine (T3) concentration, resting metabolic rate, and skeletal muscle markers for fat oxidation. Although further studies are needed to assess the causality of these relationships, they raise concern about some potential undesirable effects of weight loss. Indeed, the effects of organochlorines on energy balance could complicate body weight loss and even favour weight regain. These notions lend support for weight-loss strategies favouring a moderate weight loss, which would reduce risks for cardiovascular diseases, diabetes and hypertension, without resulting in a substantial release of organochlorines.
Article
Although we are just beginning to understand how environmental factors such as portion size affect eating behavior, the available data suggest that large portions of energy-dense foods are contributing to the obesity epidemic. Several possible strategies for adjusting portions to bring intake back in line with energy requirements are discussed. The continuing rise in the rates of obesity calls for urgent action.
Article
Overweight and obesity have become an urgent public health problem in the United States: approximately 61% of the adult population (97 million adults) are overweight or obese, where overweight is defined as a body mass index (BMI) >/= 25 and obesity is defined as a BMI >/= 30. Overweight and obesity increase the risk for developing many serious chronic diseases such as cardiovascular disease, type 2 diabetes, hypertension, dyslipidemia, and certain cancers. Increased morbidity due to obesity-related disorders begins within the normal weight range. Weight gain in adulthood per se, even in individuals who are normal weight, has deleterious health effects. Medications, particularly those commonly used in psychiatry and neurology, are a significant iatrogenic source of overweight and obesity. The weight gain potential of prescription medications should be considered in order to enhance patient compliance and reduce the risk of metabolic sequelae of weight gain. This article provides an overview of the weight-gain potential of several classes of drugs commonly used in psychiatric practice and considerations for clinicians in prescribing these medications.
Article
Cigarette smoking is the single most important preventable cause of death and illness. Smoking cessation is associated with substantial health benefits. Weight gain is cited as a primary reason for not trying to quit smoking. There is a great variability in the amount of weight gain but younger ages, lower socio-economic status and heavier smoking are predictors of higher weight gain. Weight change after smoking cessation appears to be influenced by underlying genetic factors. Besides, weight gain after smoking cessation is largely because of increased body fat and some studies suggest that it mostly occurs in the subcutaneous region of the body. The mechanism of weight gain includes increased energy intake, decreased resting metabolic rate, decreased physical activity and increased lipoprotein lipase activity. Although there is convincing evidence for the association between smoking cessation and weight gain, the molecular mechanisms underlying this relationship are not well understood. This review summarizes current information of the effects of nicotine on peptides involved in feeding behaviour. Smoking was shown to impair glucose tolerance and insulin sensitivity and cross-sectional studies have demonstrated that smokers are insulin-resistant and hyperinsulinaemic, as compared with non-smokers. Smoking cessation seems to improve insulin sensitivity in spite of the weight gain. Nicotine replacement - in particular nicotine gum - appears to be effective in delaying post-cessation weight gain. In a group of women who failed to quit smoking because of weight gain, a dietary intervention (intermittent very-low-calorie diet) plus nicotine gum showed to both increase success rate in terms of smoking cessation and prevent weight gain. On the other hand, body weight gain at the end of treatment was significantly lower in the patients receiving bupropion or bupropion plus nicotine patch, compared with placebo. Studies with new drugs available for the treatment of obesity - sibutramine and orlistat - are warranted.
Article
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.
Article
Cigarette smoking is the single most important preventable cause of death and illness. Smoking cessation is associated with substantial health benefits, but weight gain after smoking cessation is perceived to be a barrier against quitting smoking. The aim of the study was to analyse predictors of weight gain after smoking cessation. The sample included 1067 residents, aged 18-70 years, in a health district of Rome who answered to an anonymous postal questionnaire. Among them 482 were former smokers; 398 provided lifetime histories of both body weight and smoking and were considered in the analysis. 52.5% (49.3% M; 60.5% F) reported weight gain after smoking cessation; among these 25.4% reported a weight gain > or =5 kg. The multivariate logistic regression analysis showed a direct association between female gender (OR 1.9, CI 95% 1.1-3.2), age - 45 years (45-65 years: OR 2.5, CI 95% 1.4-4.4; > 64 years OR 2.1, CI 95% 1.0-4.0), number of cigarettes per day >20/day (OR 3.8, CI 95% 1.3-11.5) and weight gain after smoking cessation. The relevance of weight gain following smoking cessation suggests that health benefits associated with smoking cessation may to some extent be negated by the detrimental effects on health of associated weight gain. Smoking cessation programmes should therefore consider incorporating follow-up support to prevent weight gain; regular measurements of body weight together with dietary indications and increase of physical activity are basic factors to implement in the intervention of smoking cessation.
Prevalence and trends in obesity among US adults
  • K M Flegal
  • M D Carroll
  • C L Ogden
  • KM Flegal
Flegal KM, Carroll MD, Ogden CL et al. (2010) Prevalence and trends in obesity among US adults, 1999–2008. JAMA 303(3):235– 241
Prevalence of overweight and obesity among US children, adolescents, and adults
  • A A Hedley
  • C L Ogden
  • C L Johnson
  • AA Hedley
Prevalence of regular physical activity among adults-United States
  • Centers for Disease Control and Prevention