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Obesity research: Moving from bench to bedside to population

* E-mail: [email protected]

Affiliation Diabetes Research Program, Department of Medicine, New York University Grossman School of Medicine, New York, New York, United States of America

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  • Ann Marie Schmidt


Published: December 4, 2023

  • https://doi.org/10.1371/journal.pbio.3002448
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Fig 1

Globally, obesity is on the rise. Research over the past 20 years has highlighted the far-reaching multisystem complications of obesity, but a better understanding of its complex pathogenesis is needed to identify safe and lasting solutions.

Citation: Schmidt AM (2023) Obesity research: Moving from bench to bedside to population. PLoS Biol 21(12): e3002448. https://doi.org/10.1371/journal.pbio.3002448

Copyright: © 2023 Ann Marie Schmidt. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: AMS received funding from U.S. Public Health Service (grants 2P01HL131481 and P01HL146367). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The author has declared that no competing interests exist.

Abbreviations: EDC, endocrine disruptor chemical; GIP, gastric inhibitory polypeptide; GLP1, glucagon-like peptide 1; HFCS, high-fructose corn syrup

This article is part of the PLOS Biology 20th anniversary collection.

Obesity is a multifaceted disorder, affecting individuals across their life span, with increased prevalence in persons from underrepresented groups. The complexity of obesity is underscored by the multiple hypotheses proposed to pinpoint its seminal mechanisms, such as the “energy balance” hypothesis and the “carbohydrate–insulin” model. It is generally accepted that host (including genetic factors)–environment interactions have critical roles in this disease. The recently framed “fructose survival hypothesis” proposes that high-fructose corn syrup (HFCS), through reduction in the cellular content of ATP, stimulates glycolysis and reduces mitochondrial oxidative phosphorylation, processes that stimulate hunger, foraging, weight gain, and fat accumulation [ 1 ]. The marked upswing in the use of HFCS in beverages and foods, beginning in the 1980s, has coincided with the rising prevalence of obesity.

The past few decades of scientific progress have dramatically transformed our understanding of pathogenic mechanisms of obesity ( Fig 1 ). Fundamental roles for inflammation were unveiled by the discovery that tumor necrosis factor-α contributed to insulin resistance and the risk for type 2 diabetes in obesity [ 2 ]. Recent work has ascribed contributory roles for multiple immune cell types, such as monocytes/macrophages, neutrophils, T cells, B cells, dendritic cells, and mast cells, in disturbances in glucose and insulin homeostasis in obesity. In the central nervous system, microglia and their interactions with hypothalamic neurons affect food intake, energy expenditure, and insulin sensitivity. In addition to cell-specific contributions of central and peripheral immune cells in obesity, roles for interorgan communication have been described. Extracellular vesicles emitted from immune cells and from adipocytes, as examples, are potent transmitters of obesogenic species that transfer diverse cargo, including microRNAs, proteins, metabolites, lipids, and organelles (such as mitochondria) to distant organs, affecting functions such as insulin sensitivity and, strikingly, cognition, through connections to the brain [ 3 ].


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Basic, clinical/translational, and epidemiological research has made great strides in the past few decades in uncovering novel components of cell-intrinsic, intercellular, and interorgan communications that contribute to the pathogenesis of obesity. Both endogenous and exogenous (environmental) stressors contribute to the myriad of metabolic perturbations that impact energy intake and expenditure; mediate innate disturbances in the multiple cell types affected in obesity in metabolic organelles and organs, including in immune cells; and impair beneficial interkingdom interactions of the mammalian host with the gut microbiome. The past few decades have also witnessed remarkable efforts to successfully treat obesity, such as the use of the incretin agonists and bariatric surgery. Yet, these and other strategies may be accompanied by resistance to weight loss, weight regain, adverse effects of interventions, and the challenges of lifelong implementation. Hence, through leveraging novel discoveries from the bench to the bedside to the population, additional strategies to prevent obesity and weight regain post-weight loss, such as the use of “wearables,” with potential for implementation of immediate and personalized behavior modifications, may hold great promise as complementary strategies to prevent and identify lasting treatments for obesity. Figure created with BioRender.


Beyond intercellular communication mediated by extracellular vesicles, the discovery of interactions between the host and the gut microbiome has suggested important roles for this interkingdom axis in obesity. Although disturbances in commensal gut microbiota species and their causal links to obesity are still debated, transplantation studies have demonstrated relationships between Firmicutes/Bacteroidetes ratios and obesity [ 4 ]. Evidence supports the concept that modulation of gut microbiota phyla modulates fundamental activities, such as thermogenesis and bile acid and lipid metabolism. Furthermore, compelling discoveries during the past few decades have illustrated specific mechanisms within adipocytes that exert profound effects on organismal homeostasis, such as adipose creatine metabolism, transforming growth factor/SMAD signaling, fibrosis [ 5 ], hypoxia and angiogenesis, mitochondrial dysfunction, cellular senescence, impairments in autophagy, and modulation of the circadian rhythm. Collectively, these recent discoveries set the stage for the identification of potential new therapeutic approaches in obesity.

Although the above discoveries focus largely on perturbations in energy metabolism (energy intake and expenditure) as drivers of obesity, a recently published study suggests that revisiting the timeline of obesogenic forces in 20th and 21st century society may be required. The authors tracked 320,962 Danish schoolchildren (born during 1930 to 1976) and 205,153 Danish male military conscripts (born during 1939 to 1959). Although the overall trend of the percentiles of the distributions of body mass index were linear across the years of birth, with percentiles below the 75th being nearly stable, those above the 75th percentile demonstrated a steadily steeper rise the more extreme the percentile; this was noted in the schoolchildren and the military conscripts [ 6 ]. The authors concluded that the emergence of the obesity epidemic might have preceded the appearance of the factors typically ascribed to mediating the obesogenic transformation of society by several decades. What are these underlying factors and their yet-to-be-discovered mechanisms?

First, in terms of endogenous factors relevant to individuals, stressors such as insufficient sleep and psychosocial stress may impact substrate metabolism, circulating appetite hormones, hunger, satiety, and weight gain [ 7 ]. Reduced access to healthy foods rich in vegetables and fruits but easy access to ultraprocessed ingredients in “food deserts” and “food swamps” caused excessive caloric intake and weight gain in clinical studies [ 8 ]. Second, exogenous environmental stresses have been associated with obesity. For example, air pollution has been directly linked to adipose tissue dysfunction [ 9 ], and ubiquitous endocrine disruptor chemicals (EDCs) such as bisphenols and phthalates (found in many items of daily life including plastics, food, clothing, cosmetics, and paper) are linked to metabolic dysfunction and the development of obesity [ 10 ]. Hence, factors specific to individuals and their environment may exacerbate their predisposition to obesity.

In addition to the effects of exposure to endogenous and exogenous stressors on the risk of obesity, transgenerational (passed through generations without direct exposure of stimulant) and intergenerational (direct exposure across generations) transmission of these stressors has also been demonstrated. A leading proposed mechanism is through epigenetic modulation of the genome, which then predisposes affected offspring to exacerbated responses to obesogenic conditions such as diet. A recent study suggested that transmission of disease risk might be mediated through transfer of maternal oocyte-derived dysfunctional mitochondria from mothers with obesity [ 11 ]. Additional mechanisms imparting obesogenic “memory” may be evoked through “trained immunity.”

Strikingly, the work of the past few decades has resulted in profound triumphs in the treatment of obesity. Multiple approved glucagon-like peptide 1 (GLP1) and gastric inhibitory polypeptide (GIP) agonists [ 12 ] (alone or in combinations) induce highly significant weight loss in persons with obesity [ 13 ]. However, adverse effects of these agents, such as pancreatitis and biliary disorders, have been reported [ 14 ]. Therefore, the long-term safety and tolerability of these drugs is yet to be determined. In addition to pharmacological agents, bariatric surgery has led to significant weight loss as well. However, efforts to induce weight loss through reduction in caloric intake and increased physical activity, pharmacological approaches, and bariatric surgery may not mediate long-term cures in obesity on account of resistance to weight loss, weight regain, adverse effects of interventions, and the challenges of lifelong implementation of these measures.

Where might efforts in combating obesity lie in the next decades? At the level of basic and translational science, the heterogeneity of metabolic organs could be uncovered through state-of-the-art spatial “omics” and single-cell RNA sequencing approaches. For example, analogous to the deepening understanding of the great diversity in immune cell subsets in homeostasis and disease, adipocyte heterogeneity has also been suggested, which may reflect nuances in pathogenesis and treatment approaches. Further, approaches to bolster brown fat and thermogenesis may offer promise to combat evolutionary forces to hoard and store fat. A better understanding of which interorgan communications may drive obesity will require intensive profiling of extracellular vesicles shed from multiple metabolic organs to identify their cargo and, critically, their destinations. In the three-dimensional space, the generation of organs-on-a-chip may facilitate the discovery of intermetabolic organ communications and their perturbations in the pathogenesis of obesity and the screening of new therapies.

Looking to prevention, recent epidemiological studies suggest that efforts to tackle obesity require intervention at multiple levels. The institution of public health policies to reduce air pollution and the vast employment of EDCs in common household products could impact the obesity epidemic. Where possible, the availability of fresh, healthy foods in lieu of highly processed foods may be of benefit. At the individual level, focused attention on day-to-day behaviors may yield long-term benefit in stemming the tide of obesity. “Wearable” devices that continuously monitor the quantity, timing, and patterns of food intake, physical activity, sleep duration and quality, and glycemic variability might stimulate on-the-spot and personalized behavior modulation to contribute to the prevention of obesity or of maintenance of the weight-reduced state.

Given the involvement of experts with wide-ranging expertise in the science of obesity, from basic science, through clinical/translational research to epidemiology and public health, it is reasonable to anticipate that the work of the next 2 decades will integrate burgeoning multidisciplinary discoveries to drive improved efforts to treat and prevent obesity.


The author is grateful to Ms. Latoya Woods of the Diabetes Research Program for assistance with the preparation of the manuscript and to Ms. Kristen Dancel-Manning for preparation of the Figure accompanying the manuscript.

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Introduction to Obesity

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  • Imran Alam MBBS,BSc,FRCS(Glas),FRCSEd,MD 2 &
  • Sanjay Agrawal MS, FRCSEd, FRCSGlasg, FRCS 3 , 4  

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Obesity is defined as an abnormal or excessive accumulation of fat that may impair health. According to World Health Organization (WHO), any individual with a body mass index (BMI) greater than or equal to 30 kg/m 2 is obese and severe or class III obesity is defined as a BMI equal to or greater than 40 kg/m 2 ; this term is also used for individuals with a BMI between 30 and 39.9 kg/m 2 who have significant comorbidities. National Institute of Clinical Excellence (NICE) has recommended bariatric surgery for such individuals. The prevalence of severe obesity has increased significantly in the last two to three decades. Mexico and United States of America have highest prevalence in the world and United Kingdom is leading in Europe. BMI is used as a surrogate for adiposity. There are other methods like bioimpedance analysis, dual-energy x-ray absorptiometry (DEXA), hydrometry, computed tomography (CT), magnetic resonance imaging (MRI) and others but for all clinical and interventional purposes, BMI is used as a measure of obesity.

Fat is the main source of stored energy and it also secretes number of hormones and cytokines. Excess central fat deposition is associated with increased risk of morbidity and mortality. Overweight (BMI of 25 kg/m 2 to 29.9 kg/m 2 ) is associated with increased risk of comorbidities such as type 2 diabetes mellitus, cardiovascular diseases, respiratory disorders, infertility, certain forms of cancers, psychological and social problems; and the risk of these comorbidities increases significantly with further increase in BMI. The cost of treating obesity and associated comorbidity is causing significant burden on the health system. Conservative treatment has a high failure rate. Bariatric surgery performed primarily for weight reduction also causes resolution/remission of associated comorbidities.

  • Severe Obesity
  • Body Mass Index
  • Waist and Hip Circumference
  • Adipose Tissue

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Imran Alam MBBS,BSc,FRCS(Glas),FRCSEd,MD

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Sanjay Agrawal MS, FRCSEd, FRCSGlasg, FRCS ( Consultant Surgeon Honorary Senior Lecturer )

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Alam, I., Agrawal, S. (2016). Introduction to Obesity. In: Agrawal, S. (eds) Obesity, Bariatric and Metabolic Surgery. Springer, Cham. https://doi.org/10.1007/978-3-319-04343-2_1

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A systematic literature review on obesity: Understanding the causes & consequences of obesity and reviewing various machine learning approaches used to predict obesity


  • 1 Centre for Software Technology and Management, Faculty of Information Science and Technology, Universiti Kebangsaan Malaysia (UKM), Bangi, 43600, Selangor, Malaysia.
  • 2 Centre for Software Technology and Management, Faculty of Information Science and Technology, Universiti Kebangsaan Malaysia (UKM), Bangi, 43600, Selangor, Malaysia. Electronic address: [email protected].
  • 3 RIADI Laboratory, University of Manouba, Manouba, Tunisia; College of Computer Science and Engineering, Taibah University, Medina, Saudi Arabia.
  • 4 Center for Artificial Intelligence Technology, Faculty of Information Science and Technology, Universiti Kebangsaan Malaysia (UKM), Bangi, 43600, Selangor, Malaysia.
  • PMID: 34426171
  • DOI: 10.1016/j.compbiomed.2021.104754

Obesity is considered a principal public health concern and ranked as the fifth foremost reason for death globally. Overweight and obesity are one of the main lifestyle illnesses that leads to further health concerns and contributes to numerous chronic diseases, including cancers, diabetes, metabolic syndrome, and cardiovascular diseases. The World Health Organization also predicted that 30% of death in the world will be initiated with lifestyle diseases in 2030 and can be stopped through the suitable identification and addressing of associated risk factors and behavioral involvement policies. Thus, detecting and diagnosing obesity as early as possible is crucial. Therefore, the machine learning approach is a promising solution to early predictions of obesity and the risk of overweight because it can offer quick, immediate, and accurate identification of risk factors and condition likelihoods. The present study conducted a systematic literature review to examine obesity research and machine learning techniques for the prevention and treatment of obesity from 2010 to 2020. Accordingly, 93 papers are identified from the review articles as primary studies from an initial pool of over 700 papers addressing obesity. Consequently, this study initially recognized the significant potential factors that influence and cause adult obesity. Next, the main diseases and health consequences of obesity and overweight are investigated. Ultimately, this study recognized the machine learning methods that can be used for the prediction of obesity. Finally, this study seeks to support decision-makers looking to understand the impact of obesity on health in the general population and identify outcomes that can be used to guide health authorities and public health to further mitigate threats and effectively guide obese people globally.

Keywords: Diseases; Machine learning; Obesity; Overweight; Risk factors.

Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.

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Effectiveness of weight management interventions for adults delivered in primary care: systematic review and meta-analysis of randomised controlled trials

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  • Peer review
  • Claire D Madigan , senior research associate 1 ,
  • Henrietta E Graham , doctoral candidate 1 ,
  • Elizabeth Sturgiss , NHMRC investigator 2 ,
  • Victoria E Kettle , research associate 1 ,
  • Kajal Gokal , senior research associate 1 ,
  • Greg Biddle , research associate 1 ,
  • Gemma M J Taylor , reader 3 ,
  • Amanda J Daley , professor of behavioural medicine 1
  • 1 Centre for Lifestyle Medicine and Behaviour (CLiMB), The School of Sport, Exercise and Health Sciences, Loughborough University, Loughborough LE11 3TU, UK
  • 2 School of Primary and Allied Health Care, Monash University, Melbourne, Australia
  • 3 Department of Psychology, Addiction and Mental Health Group, University of Bath, Bath, UK
  • Correspondence to: C D Madigan c.madigan{at}lboro.ac.uk (or @claire_wm and @lboroclimb on Twitter)
  • Accepted 26 April 2022

Objective To examine the effectiveness of behavioural weight management interventions for adults with obesity delivered in primary care.

Design Systematic review and meta-analysis of randomised controlled trials.

Eligibility criteria for selection of studies Randomised controlled trials of behavioural weight management interventions for adults with a body mass index ≥25 delivered in primary care compared with no treatment, attention control, or minimal intervention and weight change at ≥12 months follow-up.

Data sources Trials from a previous systematic review were extracted and the search completed using the Cochrane Central Register of Controlled Trials, Medline, PubMed, and PsychINFO from 1 January 2018 to 19 August 2021.

Data extraction and synthesis Two reviewers independently identified eligible studies, extracted data, and assessed risk of bias using the Cochrane risk of bias tool. Meta-analyses were conducted with random effects models, and a pooled mean difference for both weight (kg) and waist circumference (cm) were calculated.

Main outcome measures Primary outcome was weight change from baseline to 12 months. Secondary outcome was weight change from baseline to ≥24 months. Change in waist circumference was assessed at 12 months.

Results 34 trials were included: 14 were additional, from a previous review. 27 trials (n=8000) were included in the primary outcome of weight change at 12 month follow-up. The mean difference between the intervention and comparator groups at 12 months was −2.3 kg (95% confidence interval −3.0 to −1.6 kg, I 2 =88%, P<0.001), favouring the intervention group. At ≥24 months (13 trials, n=5011) the mean difference in weight change was −1.8 kg (−2.8 to −0.8 kg, I 2 =88%, P<0.001) favouring the intervention. The mean difference in waist circumference (18 trials, n=5288) was −2.5 cm (−3.2 to −1.8 cm, I 2 =69%, P<0.001) in favour of the intervention at 12 months.

Conclusions Behavioural weight management interventions for adults with obesity delivered in primary care are effective for weight loss and could be offered to members of the public.

Systematic review registration PROSPERO CRD42021275529.


Obesity is associated with an increased risk of diseases such as cancer, type 2 diabetes, and heart disease, leading to early mortality. 1 2 3 More recently, obesity is a risk factor for worse outcomes with covid-19. 4 5 Because of this increased risk, health agencies and governments worldwide are focused on finding effective ways to help people lose weight. 6

Primary care is an ideal setting for delivering weight management services, and international guidelines recommend that doctors should opportunistically screen and encourage patients to lose weight. 7 8 On average, most people consult a primary care doctor four times yearly, providing opportunities for weight management interventions. 9 10 A systematic review of randomised controlled trials by LeBlanc et al identified behavioural interventions that could potentially be delivered in primary care, or involved referral of patients by primary care professionals, were effective for weight loss at 12-18 months follow-up (−2.4 kg, 95% confidence interval −2.9 to−1.9 kg). 11 However, this review included trials with interventions that the review authors considered directly transferrable to primary care, but not all interventions involved primary care practitioners. The review included interventions that were entirely delivered by university research employees, meaning implementation of these interventions might differ if offered in primary care, as has been the case in other implementation research of weight management interventions, where effects were smaller. 12 As many similar trials have been published after this review, an updated review would be useful to guide health policy.

We examined the effectiveness of weight loss interventions delivered in primary care on measures of body composition (weight and waist circumference). We also identified characteristics of effective weight management programmes for policy makers to consider.

This systematic review was registered on PROSPERO and is reported according to the preferred reporting items for systematic reviews and meta-analyses (PRISMA) statement. 13 14

Eligibility criteria

We considered studies to be eligible for inclusion if they were randomised controlled trials, comprised adult participants (≥18 years), and evaluated behavioural weight management interventions delivered in primary care that focused on weight loss. A primary care setting was broadly defined as the first point of contact with the healthcare system, providing accessible, continued, comprehensive, and coordinated care, focused on long term health. 15 Delivery in primary care was defined as the majority of the intervention being delivered by medical and non-medical clinicians within the primary care setting. Table 1 lists the inclusion and exclusion criteria.

Study inclusion and exclusion criteria

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We extracted studies from the systematic review by LeBlanc et al that met our inclusion criteria. 11 We also searched the exclusions in this review because the researchers excluded interventions specifically for diabetes management, low quality trials, and only included studies from an Organisation for Economic Co-operation and Development country, limiting the scope of the findings.

We searched for studies in the Cochrane Central Register of Controlled Trials, Medline, PubMed, and PsychINFO from 1 January 2018 to 19 August 2021 (see supplementary file 1). Reference lists of previous reviews 16 17 18 19 20 21 and included trials were hand searched.

Data extraction

Results were uploaded to Covidence, 22 a software platform used for screening, and duplicates removed. Two independent reviewers screened study titles, abstracts, and full texts. Disagreements were discussed and resolved by a third reviewer. All decisions were recorded in Covidence, and reviewers were blinded to each other’s decisions. Covidence calculates proportionate agreement as a measure of inter-rater reliability, and data are reported separately by title or abstract screening and full text screening. One reviewer extracted data on study characteristics (see supplementary table 1) and two authors independently extracted data on weight outcomes. We contacted the authors of four included trials (from the updated search) for further information. 23 24 25 26

Outcomes, summary measures, and synthesis of results

The primary outcome was weight change from baseline to 12 months. Secondary outcomes were weight change from baseline to ≥24 months and from baseline to last follow-up (to include as many trials as possible), and waist circumference from baseline to 12 months. Supplementary file 2 details the prespecified subgroup analysis that we were unable to complete. The prespecified subgroup analyses that could be completed were type of healthcare professional who delivered the intervention, country, intensity of the intervention, and risk of bias rating.

Healthcare professional delivering intervention —From the data we were able to compare subgroups by type of healthcare professional: nurses, 24 26 27 28 general practitioners, 23 29 30 31 and non-medical practitioners (eg, health coaches). 32 33 34 35 36 37 38 39 Some of the interventions delivered by non-medical practitioners were supported, but not predominantly delivered, by GPs. Other interventions were delivered by a combination of several different practitioners—for example, it was not possible to determine whether a nurse or dietitian delivered the intervention. In the subgroup analysis of practitioner delivery, we refer to this group as “other.”

Country —We explored the effectiveness of interventions by country. Only countries with three or more trials were included in subgroup analyses (United Kingdom, United States, and Spain).

Intensity of interventions —As the median number of contacts was 12, we categorised intervention groups according to whether ≤11 or ≥12 contacts were required.

Risk of bias rating —Studies were classified as being at low, unclear, and high risk of bias. Risk of bias was explored as a potential influence on the results.


Meta-analyses were conducted using Review Manager 5.4. 40 As we expected the treatment effects to differ because of the diversity of intervention components and comparator conditions, we used random effects models. A pooled mean difference was calculated for each analysis, and variance in heterogeneity between studies was compared using the I 2 and τ 2 statistics. We generated funnel plots to evaluate small study effects. If more than two intervention groups existed, we divided the number of participants in the comparator group by the number of intervention groups and analysed each individually. Nine trials were cluster randomised controlled trials. The trials had adjusted their results for clustering, or adjustment had been made in the previous systematic review by LeBlanc et al. 11 One trial did not report change in weight by group. 26 We calculated the mean weight change and standard deviation using a standard formula, which imputes a correlation for the baseline and follow-up weights. 41 42 In a non-prespecified analysis, we conducted univariate and multivariable metaregression (in Stata) using a random effects model to examine the association between number of sessions and type of interventionalist on study effect estimates.

Risk of bias

Two authors independently assessed the risk of bias using the Cochrane risk of bias tool v2. 43 For incomplete outcome data we defined a high risk of bias as ≥20% attrition. Disagreements were resolved by discussion or consultation with a third author.

Patient and public involvement

The study idea was discussed with patients and members of the public. They were not, however, included in discussions about the design or conduct of the study.

The search identified 11 609 unique study titles or abstracts after duplicates were removed ( fig 1 ). After screening, 97 full text articles were assessed for eligibility. The proportionate agreement ranged from 0.94 to 1.0 for screening of titles or abstracts and was 0.84 for full text screening. Fourteen new trials met the inclusion criteria. Twenty one studies from the review by LeBlanc et al met our eligibility criteria and one study from another systematic review was considered eligible and included. 44 Some studies had follow-up studies (ie, two publications) that were found in both the second and the first search; hence the total number of trials was 34 and not 36. Of the 34 trials, 27 (n=8000 participants) were included in the primary outcome meta-analysis of weight change from baseline to 12 months, 13 (n=5011) in the secondary outcome from baseline to ≥24 months, and 30 (n=8938) in the secondary outcome for weight change from baseline to last follow-up. Baseline weight was accounted for in 18 of these trials, but in 14 24 26 29 30 31 32 44 45 46 47 48 49 50 51 it was unclear or the trials did not consider baseline weight. Eighteen trials (n=5288) were included in the analysis of change in waist circumference at 12 months.

Fig 1

Studies included in systematic review of effectiveness of behavioural weight management interventions in primary care. *Studies were merged in Covidence if they were from same trial

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Study characteristics

Included trials (see supplementary table 1) were individual randomised controlled trials (n=25) 24 25 26 27 28 29 32 33 34 35 38 39 41 44 45 46 47 50 51 52 53 54 55 56 59 or cluster randomised controlled trials (n=9). 23 30 31 36 37 48 49 57 58 Most were conducted in the US (n=14), 29 30 31 32 33 34 35 36 37 45 48 51 54 55 UK (n=7), 27 28 38 41 47 57 58 and Spain (n=4). 25 44 46 49 The median number of participants was 276 (range 50-864).

Four trials included only women (average 65.9% of women). 31 48 51 59 The mean BMI at baseline was 35.2 (SD 4.2) and mean age was 48 (SD 9.7) years. The interventions lasted between one session (with participants subsequently following the programme unassisted for three months) and several sessions over three years (median 12 months). The follow-up period ranged from 12 months to three years (median 12 months). Most trials excluded participants who had lost weight in the past six months and were taking drugs that affected weight.


Overall, 27 trials were included in the primary meta-analysis of weight change from baseline to 12 months. Three trials could not be included in the primary analysis as data on weight were only available at two and three years and not 12 months follow-up, but we included these trials in the secondary analyses of last follow-up and ≥24 months follow-up. 26 44 50 Four trials could not be included in the meta-analysis as they did not present data in a way that could be synthesised (ie, measures of dispersion). 25 52 53 58 The mean difference was −2.3 kg (95% confidence interval −3.0 to −1.6 kg, I 2 =88%, τ 2 =3.38; P<0.001) in favour of the intervention group ( fig 2 ). We found no evidence of publication bias (see supplementary fig 1). Absolute weight change was −3.7 (SD 6.1) kg in the intervention group and −1.4 (SD 5.5) kg in the comparator group.

Fig 2

Mean difference in weight at 12 months by weight management programme in primary care (intervention) or no treatment, different content, or minimal intervention (control). SD=standard deviation

Supplementary file 2 provides a summary of the main subgroup analyses.

Weight change

The mean difference in weight change at the last follow-up was −1.9 kg (95% confidence interval −2.5 to −1.3 kg, I 2 =81%, τ 2 =2.15; P<0.001). Absolute weight change was −3.2 (SD 6.4) kg in the intervention group and −1.2 (SD 6.0) kg in the comparator group (see supplementary figs 2 and 3).

At the 24 month follow-up the mean difference in weight change was −1.8 kg (−2.8 to −0.8 kg, I 2 =88%, τ 2 =3.13; P<0.001) (see supplementary fig 4). As the weight change data did not differ between the last follow-up and ≥24 months, we used the weight data from the last follow-up in subgroup analyses.

In subgroup analyses of type of interventionalist, differences were significant (P=0.005) between non-medical practitioners, GPs, nurses, and other people who delivered interventions (see supplementary fig 2).

Participants who had ≥12 contacts during interventions lost significantly more weight than those with fewer contacts (see supplementary fig 6). The association remained after adjustment for type of interventionalist.

Waist circumference

The mean difference in waist circumference was −2.5 cm (95% confidence interval −3.2 to −1.8 cm, I 2 =69%, τ 2 =1.73; P<0.001) in favour of the intervention at 12 months ( fig 3 ). Absolute changes were −3.7 cm (SD 7.8 cm) in the intervention group and −1.3 cm (SD 7.3) in the comparator group.

Fig 3

Mean difference in waist circumference at 12 months. SD=standard deviation

Risk of bias was considered to be low in nine trials, 24 33 34 35 39 41 47 55 56 unclear in 12 trials, 25 27 28 29 32 45 46 50 51 52 54 59 and high in 13 trials 23 26 30 31 36 37 38 44 48 49 53 57 58 ( fig 4 ). No significant (P=0.65) differences were found in subgroup analyses according to level of risk of bias from baseline to 12 months (see supplementary fig 7).

Fig 4

Risk of bias in included studies

Worldwide, governments are trying to find the most effective services to help people lose weight to improve the health of populations. We found weight management interventions delivered by primary care practitioners result in effective weight loss and reduction in waist circumference and these interventions should be considered part of the services offered to help people manage their weight. A greater number of contacts between patients and healthcare professionals led to more weight loss, and interventions should be designed to include at least 12 contacts (face-to-face or by telephone, or both). Evidence suggests that interventions delivered by non-medical practitioners were as effective as those delivered by GPs (both showed statistically significant weight loss). It is also possible that more contacts were made with non-medical interventionalists, which might partially explain this result, although the metaregression analysis suggested the effect remained after adjustment for type of interventionalist. Because most comparator groups had fewer contacts than intervention groups, it is not known whether the effects of the interventions are related to contact with interventionalists or to the content of the intervention itself.

Although we did not determine the costs of the programme, it is likely that interventions delivered by non-medical practitioners would be cheaper than GP and nurse led programmes. 41 Most of the interventions delivered by non-medical practitioners involved endorsement and supervision from GPs (ie, a recommendation or checking in to see how patients were progressing), and these should be considered when implementing these types of weight management interventions in primary care settings. Our findings suggest that a combination of practitioners would be most effective because GPs might not have the time for 12 consultations to support weight management.

Although the 2.3 kg greater weight loss in the intervention group may seem modest, just 2-5% in weight loss is associated with improvements in systolic blood pressure and glucose and triglyceride levels. 60 The confidence intervals suggest a potential range of weight loss and that these interventions might not provide as much benefit to those with a higher BMI. Patients might not find an average weight loss of 3.7 kg attractive, as many would prefer to lose more weight; explaining to patients the benefits of small weight losses to health would be important.

Strengths and limitations of this review

Our conclusions are based on a large sample of about 8000 participants, and 12 of these trials were published since 2018. It was occasionally difficult to distinguish who delivered the interventions and how they were implemented. We therefore made some assumptions at the screening stage about whether the interventionalists were primary care practitioners or if most of the interventions were delivered in primary care. These discussions were resolved by consensus. All included trials measured weight, and we excluded those that used self-reported data. Dropout rates are important in weight management interventions as those who do less well are less likely to be followed-up. We found that participants in trials with an attrition rate of 20% or more lost less weight and we are confident that those with high attrition rates have not inflated the results. Trials were mainly conducted in socially economic developed countries, so our findings might not be applicable to all countries. The meta-analyses showed statistically significant heterogeneity, and our prespecified subgroups analysis explained some, but not all, of the variance.

Comparison with other studies

The mean difference of −2.3 kg in favour of the intervention group at 12 months is similar to the findings in the review by LeBlanc et al, who reported a reduction of −2.4 kg in participants who received a weight management intervention in a range of settings, including primary care, universities, and the community. 11 61 This is important because the review by LeBlanc et al included interventions that were not exclusively conducted in primary care or by primary care practitioners. Trials conducted in university or hospital settings are not typically representative of primary care populations and are often more intensive than trials conducted in primary care as a result of less constraints on time. Thus, our review provides encouraging findings for the implementation of weight management interventions delivered in primary care. The findings are of a similar magnitude to those found in a trial by Ahern et al that tested primary care referral to a commercial programme, with a difference of −2.7 kg (95% confidence interval −3.9 to −1.5 kg) reported at 12 month follow-up. 62 The trial by Ahern et al also found a difference in waist circumference of −4.1 cm (95% confidence interval −5.5 to −2.3 cm) in favour of the intervention group at 12 months. Our finding was smaller at −2.5 cm (95% confidence interval −3.2 to −1.8 cm). Some evidence suggests clinical benefits from a reduction of 3 cm in waist circumference, particularly in decreased glucose levels, and the intervention groups showed a 3.7 cm absolute change in waist circumference. 63

Policy implications and conclusions

Weight management interventions delivered in primary care are effective and should be part of services offered to members of the public to help them manage weight. As about 39% of the world’s population is living with obesity, helping people to manage their weight is an enormous task. 64 Primary care offers good reach into the community as the first point of contact in the healthcare system and the remit to provide whole person care across the life course. 65 When developing weight management interventions, it is important to reflect on resource availability within primary care settings to ensure patients’ needs can be met within existing healthcare systems. 66

We did not examine the equity of interventions, but primary care interventions may offer an additional service and potentially help those who would not attend a programme delivered outside of primary care. Interventions should consist of 12 or more contacts, and these findings are based on a mixture of telephone and face-to-face sessions. Previous evidence suggests that GPs find it difficult to raise the issue of weight with patients and are pessimistic about the success of weight loss interventions. 67 Therefore, interventions should be implemented with appropriate training for primary care practitioners so that they feel confident about helping patients to manage their weight. 68

Unanswered questions and future research

A range of effective interventions are available in primary care settings to help people manage their weight, but we found substantial heterogeneity. It was beyond the scope of this systematic review to examine the specific components of the interventions that may be associated with greater weight loss, but this could be investigated by future research. We do not know whether these interventions are universally suitable and will decrease or increase health inequalities. As the data are most likely collected in trials, an individual patient meta-analysis is now needed to explore characteristics or factors that might explain the variance. Most of the interventions excluded people prescribed drugs that affect weight gain, such as antipsychotics, glucocorticoids, and some antidepressants. This population might benefit from help with managing their weight owing to the side effects of these drug classes on weight gain, although we do not know whether the weight management interventions we investigated would be effective in this population. 69

What is already known on this topic

Referral by primary care to behavioural weight management programmes is effective, but the effectiveness of weight management interventions delivered by primary care is not known

Systematic reviews have provided evidence for weight management interventions, but the latest review of primary care delivered interventions was published in 2014

Factors such as intensity and delivery mechanisms have not been investigated and could influence the effectiveness of weight management interventions delivered by primary care

What this study adds

Weight management interventions delivered by primary care are effective and can help patients to better manage their weight

At least 12 contacts (telephone or face to face) are needed to deliver weight management programmes in primary care

Some evidence suggests that weight loss after weight management interventions delivered by non-medical practitioners in primary care (often endorsed and supervised by doctors) is similar to that delivered by clinician led programmes

Ethics statements

Ethical approval.

Not required.

Data availability statement

Additional data are available in the supplementary files.

Contributors: CDM and AJD conceived the study, with support from ES. CDM conducted the search with support from HEG. CDM, AJD, ES, HEG, KG, GB, and VEK completed the screening and full text identification. CDM and VEK completed the risk of bias assessment. CDM extracted data for the primary outcome and study characteristics. HEJ, GB, and KG extracted primary outcome data. CDM completed the analysis in RevMan, and GMJT completed the metaregression analysis in Stata. CDM drafted the paper with AJD. All authors provided comments on the paper. CDM acts as guarantor. The corresponding author attests that all listed authors meet authorship criteria and that no others meeting the criteria have been omitted.

Funding: AJD is supported by a National Institute for Health and Care Research (NIHR) research professorship award. This research was supported by the NIHR Leicester Biomedical Research Centre. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR, or the Department of Health and Social Care. ES’s salary is supported by an investigator grant (National Health and Medical Research Council, Australia). GT is supported by a Cancer Research UK fellowship. The funders had no role in considering the study design or in the collection, analysis, interpretation of data, writing of the report, or decision to submit the article for publication.

Competing interests: All authors have completed the ICMJE uniform disclosure form at www.icmje.org/disclosure-of-interest/ and declare: This research was supported by the National Institute for Health and Care Research Leicester Biomedical Research Centre; no financial relationships with any organisations that might have an interest in the submitted work in the previous three years, no other relationships or activities that could appear to have influenced the submitted work.

The lead author (CDM) affirms that the manuscript is an honest, accurate, and transparent account of the study being reported, and that no important aspects of the study have been omitted.

Dissemination to participants and related patient and public communities: We plan to disseminate these research findings to a wider community through press releases, featuring on the Centre for Lifestyle Medicine and Behaviour website ( www.lboro.ac.uk/research/climb/ ) via our policy networks, through social media platforms, and presentation at conferences.

Provenance and peer review: Not commissioned; externally peer reviewed.

This is an Open Access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 4.0) license, which permits others to distribute, remix, adapt and build upon this work, for commercial use, provided the original work is properly cited. See: http://creativecommons.org/licenses/by/4.0/ .

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obesity introduction research paper

  • Introduction
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Hazard ratio for obesity was modeled according to mean daily step counts and 25th, 50th, and 75th percentile PRS for body mass index. Shaded regions represent 95% CIs. Model is adjusted for age, sex, mean baseline step counts, cancer status, coronary artery disease status, systolic blood pressure, alcohol use, educational level, and a PRS × mean steps interaction term.

Mean daily steps and polygenic risk score (PRS) for higher body mass index are independently associated with hazard for obesity. Hazard ratios model the difference between the 75th and 25th percentiles for continuous variables. CAD indicate coronary artery disease; and SBP, systolic blood pressure.

Each point estimate is indexed to a hazard ratio for obesity of 1.00 (BMI [calculated as weight in kilograms divided by height in meters squared] ≥30). Error bars represent 95% CIs.

eTable. Cumulative Incidence Estimates of Obesity Based on Polygenic Risk Score for Body Mass Index and Mean Daily Steps at 1, 3, and 5 Years

eFigure 1. CONSORT Diagram

eFigure 2. Risk of Incident Obesity Modeled by Mean Daily Step Count and Polygenic Risk Scores Adjusted for Baseline Body Mass Index

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Brittain EL , Han L , Annis J, et al. Physical Activity and Incident Obesity Across the Spectrum of Genetic Risk for Obesity. JAMA Netw Open. 2024;7(3):e243821. doi:10.1001/jamanetworkopen.2024.3821

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Physical Activity and Incident Obesity Across the Spectrum of Genetic Risk for Obesity

  • 1 Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee
  • 2 Center for Digital Genomic Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee
  • 3 Division of Genetic Medicine, Vanderbilt Genetics Institute, Vanderbilt University Medical Center, Nashville, Tennessee
  • 4 Vanderbilt Institute of Clinical and Translational Research, Vanderbilt University Medical Center, Nashville, Tennessee
  • 5 Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee
  • 6 Department of Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee
  • 7 Department of Biomedical Informatics, Vanderbilt University Medical Center, Nashville, Tennessee
  • 8 Department of Biomedical Engineering, Vanderbilt University Medical Center, Nashville, Tennessee
  • 9 Department of Biostatistics, Vanderbilt University Medical Center, Nashville, Tennessee
  • 10 Department of Psychiatry and Behavioral Sciences, Vanderbilt University Medical Center, Nashville, Tennessee

Question   Does the degree of physical activity associated with incident obesity vary by genetic risk?

Findings   In this cohort study of 3124 adults, individuals at high genetic risk of obesity needed higher daily step counts to reduce the risk of obesity than those at moderate or low genetic risk.

Meaning   These findings suggest that individualized physical activity recommendations that incorporate genetic background may reduce obesity risk.

Importance   Despite consistent public health recommendations, obesity rates in the US continue to increase. Physical activity recommendations do not account for individual genetic variability, increasing risk of obesity.

Objective   To use activity, clinical, and genetic data from the All of Us Research Program (AoURP) to explore the association of genetic risk of higher body mass index (BMI) with the level of physical activity needed to reduce incident obesity.

Design, Setting, and Participants   In this US population–based retrospective cohort study, participants were enrolled in the AoURP between May 1, 2018, and July 1, 2022. Enrollees in the AoURP who were of European ancestry, owned a personal activity tracking device, and did not have obesity up to 6 months into activity tracking were included in the analysis.

Exposure   Physical activity expressed as daily step counts and a polygenic risk score (PRS) for BMI, calculated as weight in kilograms divided by height in meters squared.

Main Outcome and Measures   Incident obesity (BMI ≥30).

Results   A total of 3124 participants met inclusion criteria. Among 3051 participants with available data, 2216 (73%) were women, and the median age was 52.7 (IQR, 36.4-62.8) years. The total cohort of 3124 participants walked a median of 8326 (IQR, 6499-10 389) steps/d over a median of 5.4 (IQR, 3.4-7.0) years of personal activity tracking. The incidence of obesity over the study period increased from 13% (101 of 781) to 43% (335 of 781) in the lowest and highest PRS quartiles, respectively ( P  = 1.0 × 10 −20 ). The BMI PRS demonstrated an 81% increase in obesity risk ( P  = 3.57 × 10 −20 ) while mean step count demonstrated a 43% reduction ( P  = 5.30 × 10 −12 ) when comparing the 75th and 25th percentiles, respectively. Individuals with a PRS in the 75th percentile would need to walk a mean of 2280 (95% CI, 1680-3310) more steps per day (11 020 total) than those at the 50th percentile to have a comparable risk of obesity. To have a comparable risk of obesity to individuals at the 25th percentile of PRS, those at the 75th percentile with a baseline BMI of 22 would need to walk an additional 3460 steps/d; with a baseline BMI of 24, an additional 4430 steps/d; with a baseline BMI of 26, an additional 5380 steps/d; and with a baseline BMI of 28, an additional 6350 steps/d.

Conclusions and Relevance   In this cohort study, the association between daily step count and obesity risk across genetic background and baseline BMI were quantified. Population-based recommendations may underestimate physical activity needed to prevent obesity among those at high genetic risk.

In 2000, the World Health Organization declared obesity the greatest threat to the health of Westernized nations. 1 In the US, obesity accounts for over 400 000 deaths per year and affects nearly 40% of the adult population. Despite the modifiable nature of obesity through diet, exercise, and pharmacotherapy, rates have continued to increase.

Physical activity recommendations are a crucial component of public health guidelines for maintaining a healthy weight, with increased physical activity being associated with a reduced risk of obesity. 2 - 4 Fitness trackers and wearable devices have provided an objective means to capture physical activity, and their use may be associated with weight loss. 5 Prior work leveraging these devices has suggested that taking around 8000 steps/d substantially mitigates risk of obesity. 3 , 4 However, current recommendations around physical activity do not take into account other contributors such as caloric intake, energy expenditure, or genetic background, likely leading to less effective prevention of obesity for many people. 6

Obesity has a substantial genetic contribution, with heritability estimates ranging from 40% to 70%. 7 , 8 Prior studies 9 - 11 have shown an inverse association between genetic risk and physical activity with obesity, whereby increasing physical activity can help mitigate higher genetic risk for obesity. These results have implications for physical activity recommendations on an individual level. Most of the prior work 9 - 11 focused on a narrow set of obesity-associated variants or genes and relied on self-reported physical activity, and more recent work using wearable devices has been limited to 7 days of physical activity measurements. 12 Longer-term capture in large populations will be required to accurately estimate differences in physical activity needed to prevent incident obesity.

We used longitudinal activity monitoring and genome sequencing data from the All of Us Research Program (AoURP) to quantify the combined association of genetic risk for body mass index (BMI; calculated as weight in kilograms divided by height in meters squared) and physical activity with the risk of incident obesity. Activity monitoring was quantified as daily step counts obtained from fitness tracking devices. Genetic risk was quantified by using a polygenic risk score (PRS) from a large-scale genomewide association study (GWAS) of BMI. 13 We quantified the mean daily step count needed to overcome genetic risk for increased BMI. These findings represent an initial step toward personalized exercise recommendations that integrate genetic information.

Details on the design and execution of the AoURP have been published previously. 14 The present study used AoURP Controlled Tier dataset, version 7 (C2022Q4R9), with data from participants enrolled between May 1, 2018, and July 1, 2022. Participants who provided informed consent could share data from their own activity tracking devices from the time their accounts were first created, which may precede the enrollment date in AoURP. We followed the Strengthening the Reporting of Observational Studies in Epidemiology ( STROBE ) reporting guideline. In this study, only the authorized authors who completed All of Us Responsible Conduct of Research training accessed the deidentified data from the Researcher Workbench (a secured cloud-based platform). Since the authors were not directly involved with the participants, institutional review board review was exempted in compliance with AoURP policy.

Activity tracking data for this study came from the Bring Your Own Device program that allowed individuals who already owned a tracking device (Fitbit, Inc) to consent to link their activity data with other data in the AoURP. By registering their personal device on the AoURP patient portal, patients could share all activity data collected since the creation of their personal device account. For many participants, this allowed us to examine fitness activity data collected prior to enrollment in the AoURP. Activity data in AoURP are reported as daily step counts. We excluded days with fewer than 10 hours of wear time to enrich our cohort for individuals with consistently high wear time. The initial personal activity device cohort consisted of 12 766 individuals. Consistent with our prior data curation approach, days with less than 10 hours of wear time, less than 100 steps, or greater than 45 000 steps or for which the participant was younger than 18 years were removed. For time-varying analyses, mean daily steps were calculated on a monthly basis for each participant. Months with fewer than 15 valid days of monitoring were removed.

The analytic cohort included only individuals with a BMI of less than 30 at the time activity monitoring began. The primary outcome was incident obesity, defined as a BMI of 30 or greater documented in the medical record at least 6 months after initiation of activity monitoring. The latter stipulation reduced the likelihood that having obesity predated the beginning of monitoring but had not yet been clinically documented. We extracted BMI values and clinical characteristics from longitudinal electronic health records (EHRs) for the consenting participants who were associated with a health care provider organization funded by the AoURP. The EHR data have been standardized using the Observational Medical Outcomes Partnership Common Data Model. 15 In the AoURP, upon consent, participants are asked to complete the Basics survey, in which they may self-report demographic characteristics such as race, ethnicity, and sex at birth.

We filtered the data to include only biallelic, autosomal single-nucleotide variants (SNVs) that had passed AoURP initial quality control. 16 We then removed duplicate-position SNVs and kept only individual genotypes with a genotype quality greater than 20. We further filtered the SNVs based on their Hardy-Weinberg equilibrium P value (>1.0 × 10 −15 ) and missing rate (<5%) across all samples. Next, we divided the samples into 6 groups (Admixed American, African, East Asian, European, Middle Eastern, and South Asian) based on their estimated ancestral populations 16 , 17 and further filtered the SNVs within each population based on minor allele frequency (MAF) (>0.01), missing rate (<0.02), and Hardy-Weinberg equilibrium P value (>1.0 × 10 −6 ). The SNVs were mapped from Genome Reference Consortium Human Build 38 with coordinates to Build 37. Because the existing PRS models have limited transferability across ancestry groups and to ensure appropriate power of the subsequent PRS analysis, we limited our analysis to the populations who had a sample size of greater than 500, resulting in 5964 participants of European ancestry with 5 515 802 common SNVs for analysis.

To generate principal components, we excluded the regions with high linkage disequilibrium, including chr5:44-51.5 megabase (Mb), chr6:25-33.5 Mb, chr8:8-12 Mb, and chr11:45-57 Mb. We then pruned the remaining SNVs using PLINK, version 1.9 (Harvard University), pairwise independence function with 1-kilobase window shifted by 50 base pairs and requiring r 2 < 0.05 between any pair, resulting in 100 983 SNPs for further analysis. 18 Principal component analysis was run using PLINK, version 1.9. The European ancestry linkage disequilibrium reference panel from the 1000 Genomes Project phase 3 was downloaded, and nonambiguous SNPs with MAF greater than 0.01 were kept in the largest European ancestry GWAS summary statistics of BMI. 13 We manually harmonized the strand-flipping SNPs among the SNP information file, GWAS summary statistics files, and the European ancestry PLINK extended map files (.bim).

We used PRS–continuous shrinkage to infer posterior SNP effect sizes under continuous shrinkage priors with a scaling parameter set to 0.01, reflecting the polygenic architecture of BMI. GWAS summary statistics of BMI measured in 681 275 individuals of European ancestry was used to estimate the SNP weights. 19 The scoring command in PLINK, version 1.9, was used to produce the genomewide scores of the AoURP European individuals with their quality-controlled SNP genotype data and these derived SNP weights. 20 Finally, by using the genomewide scores as the dependent variable and the 10 principal components as the independent variable, we performed linear regression, and the obtained residuals were kept for the subsequent analysis. To check the performance of the PRS estimate, we first fit a generalized regression model with obesity status as the dependent variable and the PRS as the independent variable with age, sex, and the top 10 principal components of genetic ancestry as covariates. We then built a subset logistic regression model, which only uses the same set of covariates. By comparing the full model with the subset model, we measured the incremental Nagelkerke R 2 value to quantify how much variance in obesity status was explained by the PRS.

Differences in clinical characteristics across PRS quartiles were assessed using the Wilcoxon rank sum or Kruskal-Wallis test for continuous variables and the Pearson χ 2 test for categorical variables. Cox proportional hazards regression models were used to examine the association among daily step count (considered as a time-varying variable), PRS, and the time to event for obesity, adjusting for age, sex, mean baseline step counts, cancer status, coronary artery disease status, systolic blood pressure, alcohol use, educational level, and interaction term of PRS × mean steps. We presented these results stratified by baseline BMI and provided a model including baseline BMI in eFigure 2 in Supplement 1 as a secondary analysis due to collinearity between BMI and PRS.

Cox proportional hazards regression models were fit on a multiply imputed dataset. Multiple imputation was performed for baseline BMI, alcohol use, educational status, systolic blood pressure, and smoking status using bootstrap and predictive mean matching with the aregImpute function in the Hmisc package of R, version 4.2.2 (R Project for Statistical Computing). Continuous variables were modeled as restricted cubic splines with 3 knots, unless the nonlinear term was not significant, in which case it was modeled as a linear term. Fits and predictions of the Cox proportional hazards regression models were obtained using the rms package in R, version 4.2.2. The Cox proportional hazards regression assumptions were checked using the cox.zph function from the survival package in R, version 4.2.2.

To identify the combinations of PRS and mean daily step counts associated with a hazard ratio (HR) of 1.00, we used a 100-knot spline function to fit the Cox proportional hazards regression ratio model estimations across a range of mean daily step counts for each PRS percentile. We then computed the inverse of the fitted spline function to determine the mean daily step count where the HR equals 1.00 for each PRS percentile. We repeated this process for multiple PRS percentiles to generate a plot of mean daily step counts as a function of PRS percentiles where the HR was 1.00. To estimate the uncertainty around these estimations, we applied a similar spline function to the upper and lower estimated 95% CIs of the Cox proportional hazards regression model to find the 95% CIs for the estimated mean daily step counts at each PRS percentile. Two-sided P < .05 indicated statistical significance.

We identified 3124 participants of European ancestry without obesity at baseline who agreed to link their personal activity data and EHR data and had available genome sequencing. Among those with available data, 2216 of 3051 (73%) were women and 835 of 3051 (27%) were men, and the median age was 52.7 (IQR, 36.4-62.8) years. In terms of race and ethnicity, 2958 participants (95%) were White compared with 141 participants (5%) who were of other race or ethnicity (which may include Asian, Black or African American, Middle Eastern or North African, Native Hawaiian or Other Pacific Islander, multiple races or ethnicities, and unknown race or ethnicity) ( Table ). The analytic sample was restricted to individuals assigned European ancestry based on the All of Us Genomic Research Data Quality Report. 16 A study flowchart detailing the creation of the analytic dataset is provided in eFigure 1 in Supplement 1 . The BMI-based PRS explained 8.3% of the phenotypic variation in obesity (β = 1.76; P  = 2 × 10 −16 ). The median follow-up time was 5.4 (IQR, 3.4-7.0) years and participants walked a median of 8326 (IQR, 6499-10 389) steps/d. The incidence of obesity over the study period was 13% (101 of 781 participants) in the lowest PRS quartile and 43% (335 of 781 participants) in the highest PRS quartile ( P  = 1.0 × 10 −20 ). We observed a decrease in median daily steps when moving from lowest (8599 [IQR, 6751-10 768]) to highest (8115 [IQR, 6340-10 187]) PRS quartile ( P  = .01).

We next modeled obesity risk stratified by PRS percentile with the 50th percentile indexed to an HR for obesity of 1.00 ( Figure 1 ). The association between PRS and incident obesity was direct ( P  = .001) and linear (chunk test for nonlinearity was nonsignificant [ P  = .07]). The PRS and mean daily step count were both independently associated with obesity risk ( Figure 2 ). The 75th percentile BMI PRS demonstrated an 81% increase in obesity risk (HR, 1.81 [95% CI, 1.59-2.05]; P  = 3.57 × 10 −20 ) when compared with the 25th percentile BMI PRS, whereas the 75th percentile median step count demonstrated a 43% reduction in obesity risk (HR, 0.57 [95% CI, 0.49-0.67]; P  = 5.30 × 10 −12 ) when compared with the 25th percentile step count. The PRS × mean steps interaction term was not significant (χ 2 = 1.98; P  = .37).

Individuals with a PRS at the 75th percentile would need to walk a mean of 2280 (95% CI, 1680-3310) more steps per day (11 020 total) than those at the 50th percentile to reduce the HR for obesity to 1.00 ( Figure 1 ). Conversely, those in the 25th percentile PRS could reach an HR of 1.00 by walking a mean of 3660 (95% CI, 2180-8740) fewer steps than those at the 50th percentile PRS. When assuming a median daily step count of 8740 (cohort median), those in the 75th percentile PRS had an HR for obesity of 1.33 (95% CI, 1.25-1.41), whereas those at the 25th percentile PRS had an obesity HR of 0.74 (95% CI, 0.69-0.79).

The mean daily step count required to achieve an HR for obesity of 1.00 across the full PRS spectrum and stratified by baseline BMI is shown in Figure 3 . To reach an HR of 1.00 for obesity, when stratified by baseline BMI of 22, individuals at the 50th percentile PRS would need to achieve a mean daily step count of 3290 (additional 3460 steps/d); for a baseline BMI of 24, a mean daily step count of 7590 (additional 4430 steps/d); for a baseline BMI of 26, a mean daily step count of 11 890 (additional 5380 steps/d); and for a baseline BMI of 28, a mean daily step count of 16 190 (additional 6350 steps/d).

When adding baseline BMI to the full Cox proportional hazards regression model, daily step count and BMI PRS both remain associated with obesity risk. When comparing individuals at the 75th percentile with those at the 25th percentile, the BMI PRS is associated with a 61% increased risk of obesity (HR, 1.61 [95% CI, 1.45-1.78]). Similarly, when comparing the 75th with the 25th percentiles, daily step count was associated with a 38% lower risk of obesity (HR, 0.62 [95% CI, 0.53-0.72]) (eFigure 2 in Supplement 1 ).

The cumulative incidence of obesity increases over time and with fewer daily steps and higher PRS. The cumulative incidence of obesity would be 2.9% at the 25th percentile, 3.9% at the 50th percentile, and 5.2% at the 75th percentile for PRS in year 1; 10.5% at the 25th percentile, 14.0% at the 50th percentile, and 18.2% at the 75th percentile for PRS in year 3; and 18.5% at the 25th percentile, 24.3% at the 50th percentile, and 30.9% at the 75th percentile for PRS in year 5 ( Figure 4 ). The eTable in Supplement 1 models the expected cumulative incidence of obesity at 1, 3, and 5 years based on PRS and assumed mean daily steps of 7500, 10 000, and 12 500.

We examined the combined association of daily step counts and genetic risk for increased BMI with the incidence of obesity in a large national sample with genome sequencing and long-term activity monitoring data. Lower daily step counts and higher BMI PRS were both independently associated with increased risk of obesity. As the PRS increased, the number of daily steps associated with lower risk of obesity also increased. By combining these data sources, we derived an estimate of the daily step count needed to reduce the risk of obesity based on an individual’s genetic background. Importantly, our findings suggest that genetic risk for obesity is not deterministic but can be overcome by increasing physical activity.

Our findings align with those of prior literature 9 indicating that engaging in physical activity can mitigate genetic obesity risk and highlight the importance of genetic background for individual health and wellness. Using the data from a large population-based sample, Li et al 9 characterized obesity risk by genotyping 12 susceptibility loci and found that higher self-reported physical activity was associated with a 40% reduction in genetic predisposition to obesity. Our study extends these results in 2 important ways. First, we leveraged objectively measured longitudinal activity data from commercial devices to focus on physical activity prior to and leading up to a diagnosis of obesity. Second, we used a more comprehensive genomewide risk assessment in the form of a PRS. Our results indicate that daily step count recommendations to reduce obesity risk may be personalized based on an individual’s genetic background. For instance, individuals with higher genetic risk (ie, 75th percentile PRS) would need to walk a mean of 2280 more steps per day than those at the 50th percentile of genetic risk to have a comparable risk of obesity.

These results suggest that population-based recommendations that do not account for genetic background may not accurately represent the amount of physical activity needed to reduce the risk of obesity. Population-based exercise recommendations may overestimate or underestimate physical activity needs, depending on one’s genetic background. Underestimation of physical activity required to reduce obesity risk has the potential to be particularly detrimental to public health efforts to reduce weight-related morbidity. As such, integration of activity and genetic data could facilitate personalized activity recommendations that account for an individual’s genetic profile. The widespread use of wearable devices and the increasing demand for genetic information from both clinical and direct-to-consumer sources may soon permit testing the value of personalized activity recommendations. Efforts to integrate wearable devices and genomic data into the EHR further support the potential future clinical utility of merging these data sources to personalize lifestyle recommendations. Thus, our findings support the need for a prospective trial investigating the impact of tailoring step counts by genetic risk on chronic disease outcomes.

The most important limitation of this work is the lack of diversity and inclusion only of individuals with European ancestry. These findings will need validation in a more diverse population. Our cohort only included individuals who already owned a fitness tracking device and agreed to link their activity data to the AoURP dataset, which may not be generalizable to other populations. We cannot account for unmeasured confounding, and the potential for reverse causation still exists. We attempted to diminish the latter concern by excluding prevalent obesity and incident cases within the first 6 months of monitoring. Genetic risk was simplified to be specific to increased BMI; however, genetic risk for other cardiometabolic conditions could also inform obesity risk. Nongenetic factors that contribute to obesity risk such as dietary patterns were not available, reducing the explanatory power of the model. It is unlikely that the widespread use of drug classes targeting weight loss affects the generalizability of our results, because such drugs are rarely prescribed for obesity prevention, and our study focused on individuals who were not obese at baseline. Indeed, less than 0.5% of our cohort was exposed to a medication class targeting weight loss (phentermine, orlistat, or glucagonlike peptide-1 receptor agonists) prior to incident obesity or censoring. Finally, some fitness activity tracking devices may not capture nonambulatory activity as well as triaxial accelerometers.

This cohort study used longitudinal activity data from commercial wearable devices, genome sequencing, and clinical data to support the notion that higher daily step counts can mitigate genetic risk for obesity. These results have important clinical and public health implications and may offer a novel strategy for addressing the obesity epidemic by informing activity recommendations that incorporate genetic information.

Accepted for Publication: January 30, 2024.

Published: March 27, 2024. doi:10.1001/jamanetworkopen.2024.3821

Open Access: This is an open access article distributed under the terms of the CC-BY License . © 2024 Brittain EL et al. JAMA Network Open .

Corresponding Author: Evan L. Brittain, MD, MSc ( [email protected] ) and Douglas M. Ruderfer, PhD ( [email protected] ), Vanderbilt University Medical Center, 2525 West End Ave, Suite 300A, Nashville, TN 37203.

Author Contributions: Drs Brittain and Ruderfer had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Concept and design: Brittain, Annis, Master, Roden, Ruderfer.

Acquisition, analysis, or interpretation of data: Brittain, Han, Annis, Master, Hughes, Harris, Ruderfer.

Drafting of the manuscript: Brittain, Han, Annis, Master, Ruderfer.

Critical review of the manuscript for important intellectual content: All authors.

Statistical analysis: Brittain, Han, Annis, Master.

Obtained funding: Brittain, Harris.

Administrative, technical, or material support: Brittain, Annis, Master, Roden.

Supervision: Brittain, Ruderfer.

Conflict of Interest Disclosures: Dr Brittain reported receiving a gift from Google LLC during the conduct of the study. Dr Ruderfer reported serving on the advisory board of Illumina Inc and Alkermes PLC and receiving grant funding from PTC Therapeutics outside the submitted work. No other disclosures were reported.

Funding/Support: The All of Us Research Program is supported by grants 1 OT2 OD026549, 1 OT2 OD026554, 1 OT2 OD026557, 1 OT2 OD026556, 1 OT2 OD026550, 1 OT2 OD 026552, 1 OT2 OD026553, 1 OT2 OD026548, 1 OT2 OD026551, 1 OT2 OD026555, IAA AOD21037, AOD22003, AOD16037, and AOD21041 (regional medical centers); grant HHSN 263201600085U (federally qualified health centers); grant U2C OD023196 (data and research center); 1 U24 OD023121 (Biobank); U24 OD023176 (participant center); U24 OD023163 (participant technology systems center); grants 3 OT2 OD023205 and 3 OT2 OD023206 (communications and engagement); and grants 1 OT2 OD025277, 3 OT2 OD025315, 1 OT2 OD025337, and 1 OT2 OD025276 (community partners) from the National Institutes of Health (NIH). This study is also supported by grants R01 HL146588 (Dr Brittain), R61 HL158941 (Dr Brittain), and R21 HL172038 (Drs Brittain and Ruderfer) from the NIH.

Role of the Funder/Sponsor: The NIH had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.

Data Sharing Statement: See Supplement 2 .

Additional Contributions: The All of Us Research Program would not be possible without the partnership of its participants.

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Obesity Research Paper

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Obesity has increasingly been identified as a critical global public health concern. This focus on obesity as a health priority raises complex bioethical issues. These include how obesity is defined and categorized, the implications of the centrality of personal responsibility in medical and public health approaches, how competing ethical frames impact social justice concerns, and the growing “moral panic” concerning obesity. A critical examination of how obesity is defined as a medical problem suggests that ethical approaches could be more productive if obesity were addressed as a social problem with medical consequences, rather than emphasizing it as a medical problem with social consequences.

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There has been a dramatic rise in the prevalence of obesity globally in the last three decades, and the World Health Organization (WHO) estimates around 11 % of the world’s total population is obese (WHO 2012). Obesity is seen as a major public health concern because it is widely recognized as a precipitating factor in the parallel emergence of chronic diseases as a primary cause of death in many countries. Obesity is often reported as a major drain on medical systems, and the growing obesity rates in developing countries are often cited as especially worrying in this regard. From a bioethics perspective, the focus on obesity as a health priority raises complex issues. This entry highlights inter-related and key bioethical dimensions of contemporary concerns around and approaches to obesity, including the means by which people are categorized as obese or not, the medicalization of obesity as a disease that needs to be treated, implications of the centrality of individual responsibility in medical and public health approaches, obesity as a social justice issue, and media and growing “moral panic.”

Obesity is most simply defined as an excess of adipose (fat) tissue, usually with negative health effects. However, this definition is problematic. Medically, as discussed below, the science of obesity is increasingly suggesting that many people can be both obese and healthy. However, “obese” and “obesity” are terms that have also entered everyday media and other public discourses in ways that are mostly negative and imply ill-health and disease. The growing assumption that obesity is defined as a negative characteristic is historically and culturally particular, in marked contrast to cross-cultural records that describe plump bodies as powerful, sexy, social, abundant, fertile, and certainly healthy (Brewis 2011a).

Ethical Dimensions

The Categorization of Obesity. A definition of obesity based upon the notion of excess body fat requires measurement against a standard of what constitutes “normal.” Given that human bodies are highly ecologically flexible and vary in averages across populations, the imposition of a single standard for classification as obese raises some complex bioethical issues. The most widely employed means to classify people as obese, and then assess variation in population levels of obesity, is through use of body mass index (BMI).

BMI does not directly measure body fat; rather, it is a proxy measure using the ratio of mass (weight) relative to height. Using statistical methods and prescriptive and risk models, four basic categories of weight (underweight, normal, overweight, obese) have been identified and are now widely applied, from the doctor’s office to large public health interventions. These standard categories are arbitrarily defined through cutoff points related to morbidity and mortality rates found in large-scale epidemiological studies, with obesity normally set at a BMI of 30 or higher.

While BMI as a measure of obesity is sometimes useful, particularly in clinical studies, because of both individual and population variation, this mapping of weight to health risk is not precise or even especially predictive. For example, there is growing evidence that many people clinically defined as obese prove to be metabolically healthy even as they are advised by doctors they need to lose weight, and that the level of obesity at which conditions like diabetes and heart disease become more prevalent differs across populations. Moreover, BMI does not discriminate between muscle mass, bone, connective tissue, and amount types of adipose tissue, obscuring accurate measurement of total body fat. As a result, people with highly-developed musculature are labeled obese by the measure, even when they have low levels of actual body fat. Further, some populations have greater bone density on average or shorter leg bone length resulting in falsely high BMI scores (Hruschka et al. 2013). For example, for decades there has been a public health concern focused on very high obesity risk in Pacific Island populations, but more recent studies have shown that the disease correlates of obesity emerge at higher levels of adiposity in comparison to other groups. Hence, the common standard for categorizing obesity probably misassigns a significant number of people and accordingly implies health risks where none may exist (and vice versa). Additionally, women have a higher percentage of body fat than men, and weight tends to increase in both genders as individuals age. Attempts to address the weaknesses in BMI classifications have resulted in alternative methods that more accurately measure the amount and distribution of body fat, but these use technologies or expertise that are difficult to implement in real-world settings.

Defining Obesity as a Disease. Defining obesity against a set standard of what is a normal or healthy level of body fat leads to an emphasis on prevention and cure, and underscores obesity as (1) a problem, with (2) an identifiable cause (diagnosis), and that (3) requires evaluation, intervention, management, and control. The central bioethical issue is this: regardless of how people are classified into an obese category, once so categorized it is generally assumed that labeling a person as unhealthy is warranted and medical or other intervention is necessary. Certainly, obesity has become increasingly identified as a major factor and index of ill-health over the last two decades. This culminated in the formal recognition of obesity as a disease by the American Medical Association in 2013, even in the absence of other risk factors or clinical symptoms. The growing medicalization of obesity as a condition explains why highly invasive and often risky medical treatments for obesity, such as bariatric surgery, are on the rise. The emphasis on excess weight as a health problem also negatively impacts how people view and relate to their own and others’ bodies and in ways that create emotional and social distress related to failing to meet social prescriptions for an ideal or acceptable body size.

Levels of Analyses and Ultimate Causation. Current scientific evidence on the causes of obesity can be analyzed at different levels, often working iteratively and in feedback with each other. At the genetic level, some individuals have a predisposition toward higher weights, weight gain, and difficulty in weight loss, related to genetic variants in appetite, metabolism, and activity. At the individual level, obesity is the result of excess calorie intake over calories expended through physical activity, but individual-level factors such as income, education level, ethnicity, age, and gender also predict differential risks of being obese, as does use of certain medications or comorbidities such as depression. Institutional factors such as health care access also matter.

At the community, neighborhood, or regional level, obesity risk accrues differently based solely on where people live. One factor in this pattern is the rapid urbanization of the world’s population: urbanization is associated with higher rates of obesity, and an increasing majority of humans live in cities. This correlation is due, in part, to the low cost of high density foods, changes in activity with the move to urban settings and structural and economic barriers to healthier lifestyles (Metzl and Hansen 2014). Further, within those cities, specific locales and their inhabitants’ lifestyles vary based upon social, spatial, and economic factors. The built environment of a particular locale is one example of how the physical expression of social, spatial, and economic factors relates to obesity prevalence: walkability, public transportation, access to fresh foods, safety, parks, light and shade, access to healthcare, and density all help shape obesity risk. For example, barriers in transportation and distance may make it difficult for residents to access healthy foods, while the perception by residents that the place they live in is unsafe or of poor quality may limit opportunities to be physically active. Social and economic factors also influence residential effects, including social exclusion, discrimination, and diminished economic infrastructure. Efforts to address residential effects often evoke stakeholder objections, as these efforts may inhibit personal choice, stigmatize neighborhood residents, or create changes that conflict with personal lifestyles and cultural values (ten Have et al. 2011).

Education and wealth, and most especially poverty, are also implicated in obesity risk. The relationship between income and obesity is complex and varies depending on the economic development of the resident country. Most nations, even the poorest, demonstrate some level of obesity, even in the presence of food shortages and undernutrition. The combination of under and over nutrition increases the likelihood of obesity and has significant implications in terms of health risks and negative health effects. As poorer nations become increasingly urbanized and industrialized, these problems are exacerbated, particularly as low income countries have fewer healthcare resources to meet the challenges posed by chronic conditions associated with obesity. This “dual burden” is also evident in middle-income countries: as economic changes at both the household and national level occur, families with a dual burden of having overweight and underweight individuals become increasingly prevalent.

Evidence suggests that income and obesity also rise together as inexpensive food becomes easily accessible. However, this trend reverses at the point where the apparent social costs of obesity outweigh the advantages. In middle to high-income countries, obesity tends to be inversely correlated with socioeconomic status, meaning that the highest obesity rates are found in those populations with the lowest incomes and with the lowest levels of educational achievement (Brewis 2011a). At a national level, BMI appears to rise in the early and accelerated phases of economic development due to a complex set of factors including urban migration, a shift from traditional occupations, and increased technology. At the individual level, poverty is contextual, demonstrating a complex residential pattern, with both rural and urban poverty linked to lower education and higher obesity.

While there have been some efforts to develop community-level interventions in line with increasing recognition of these upstream causes of obesity risk, medical and public health interventions continue to give the most attention to individual behavior change. The standard treatment model, often shared by clinicians and patients alike, is that the individual must lose excess weight by eating less and/or exercising more. This is despite decades of evidence that most such behavioral change strategies eventually fail to result in weight lost, and often serve to promote weight regain (Brewis 2011a).

Obesity and Social Justice Considerations. The role of proximate and ultimate factors discussed above means that obesity can be framed as a social justice issue, not solely a medical one. This suggests a very different course, emphasis, and pathway for public health interventions. Policies that seek to restrict behavior (passively or actively) can disproportionately affect the poor, the rural, and the malnourished. Of critical importance is who designs, implements, and evaluates these efforts. How do these interventions ethically impact personal physical health while promoting equality and maintaining individual autonomy? If population-level interventions are not necessarily individually beneficial and may in fact have psychosocial and cultural costs with their own negative health consequences, should public health entities intervene at all? These are some of the ethical issues that arise when the focus moves away from considering obesity fundamentally a medical problem to thinking about obesity at the aggregate level.

The challenge is to consider both the ultimate (structural) as well as the proximate factors (nutrition, activity, and medical conditions) that shape obesity risk when developing obesity policy and interventions. Identifying the causes of obesity, when coupled with how it is defined, becomes important in the ethical frame used to intervene. To date, there have been multiple framings in approaches to combat the rise of obesity. These ethical frames are not mutually exclusive and often coexist within a particular approach. Understanding the ethical platform from which programs spring will enable better understanding of the consequences (intentional or unintentional), successes, and failures. Identifying obesity as a health problem is more than defining disease, biomedical risk, and treatment; assigning responsibility – individual or otherwise – becomes part of the equation. The increasing prevalence of obesity on a global scale is accompanied by concerns that society is harmed in some way. This sense of harm in turn is linked to the notion of blame. How responsibility and blame are assigned varies with different ethical frames.

Framing Obesity Solutions

Emphasis on Individual Responsibility. The notion of individual responsibility has dominated the discourse surrounding the obesity crisis and efforts to contain the problem. Individual responsibility is rooted in notions of individual autonomy based within a moralistic theory of personal determination. Morality frames emphasize the threat to social values and economic stability by focusing on personal choice and the impact these choices have on society (Boero 2012). A morality frame advances notions of normal, ideal, virtue, right, and wrong. In this frame, obesity is related to personal failings – a lack of self-discipline, restraint, rationality, and moral failings attributed to poor life choices (gluttony, sloth, and a lack of adherence to personal improvement). Obesity, therefore, is self-induced and harm is self-inflicted. Because the individual is responsible for their health and body, blame is personal and can take the form of value imperatives about who is obese or overweight and who is responsible. Interventions and public health campaigns using this frame focus on problem awareness, promote better individual health behaviors, and encourage personal responsibility. Interventions range from educational efforts to weight loss programs, “fat taxes” (on calorie or fat dense foods), and increased insurance rates for individuals with high BMIs. This type of framing, when used in conjunction with a medical definition of obesity, places the focus of the intervention on achieving a physical ideal body weight and ignores the psychosocial dimensions of health, even as it places responsibility upon the individual (as psychologically weak or morally lax). Stigmatization, discrimination, and negative self-image are the result, which have their own negative health consequences (Sagay 2013; Puhl and Heuer 2010).

Biomedical and Public Health Frames. The biomedical frame uses the language of risk to intervene and regulate the body in order to promote health or, more usually, decrease illness or disease. Obesity in this frame is seen as pathologic – a biological condition to be monitored, treated, and cured. The body is understood to be the recipient of treatment, a somewhat passive vessel that needs management by healthcare professionals (Sagay 2013). De-emphasizing personal responsibility can be helpful in decreasing stigma, but medicalization also promotes stigmatization by labeling obese bodies as sick. Framing obesity in terms of mortality and morbidity imparts urgency and authority to the issue. The locus for intervention is on proximate factors and responsibility remains with the individual-aspatient, though the medical system is a crucial partner in terms of defining the problem and determining and managing treatment. Generally individual and small-scale interventions focused on dietary choice, activity, and medical/surgical interventions are utilized in this context. However, the biomedical frame informs larger policy issues resulting in industry and governmental regulations generally rooted in economic analyses, such as differential insurance rates for individuals based upon weight, corporate programs to incentivize weight reduction or dietary choice, bans or taxes on sugar-sweetened beverages, and regulation of nutritional information on food products.

A public health frame assigns responsibility to the government (local, state, and federal). Public health entities are most often located within governments and are charged with setting standards, regulating and protecting public safety and promoting health, and minimizing or preventing public harm while at the same time ensuring individual liberty, privacy, and public access to needed resources. This equation differs internationally as notions of individual and public health are culturally constituted. In general, obesity is seen as a threat to public health and the approach taken is to reduce the threat, generally combining individual and systemic approaches to address the issue. Ethical approaches in this frame deal with the differential distribution of obesity across groups and subpopulations as prevalence and risk manifest variably within cultural groups, gender, socioeconomic status, etc. Financial triggers (incentives & disincentives), built environment changes that alter lifestyle options (slowing elevators, car-free zoning, food banning), and informational campaigns are often used or suggested within a public health intervention. Issues of justice and fairness can be particularly problematic in this framing as the dual focus of public health creates a tension between liberty and protection. Obesity at the individual level includes social and economic disparities as well as discrimination and psychological stress from weight bias. Addressing these issues within the systemic frames of government, business, and infrastructure (including larger social forces) can contribute to stigmatization, discrimination, and differential opportunities and access.

Thus, in practice, there is a smorgasbord of antiobesity efforts, structured within multiple framings – moralistic, biomedical, and public health – that tend to be disconnected from each other. Even assuming a universal definition of obesity and its determinants exists, the ethics of policy interventions still needs to be addressed. At the heart of the ethics, debate is concerned over individual choice, autonomy, and the exacerbation of stigma and discrimination. Rephrasing the two previous ethical questions might then ask: What are the individual’s essential rights and responsibilities concerning weight? Secondly, what is the responsibility of the government in providing healthy, safe environments for its citizens?

This tension between rights and responsibilities (individual, societal, and governmental) plays out differently globally. The body (and body size) is understood as a “domain of liberty and autonomy” (Tirosh 2014, p. 1801), but the expression of these values is differentially understood across societies. When seen as a lifestyle issue, obesity remains focused at the individual and local levels, to be dealt with through small-scale interventions in select populations to encourage individuals to control their weight and make healthier choices (moralistic frame). These types of interventions tend to ignore the complexity of factors (and responsibilities) underlying obesity and keep responsibility (and blame) with the individual. Growing public discourse has revolved around policy changes to combat the “rising epidemic” of obesity. Public health officials have supported this groundswell of opinion through campaigns to promote the adoption of a healthy lifestyle, emphasizing a diet high in fruits, vegetables, complex carbohydrates, and lean proteins and sufficient exercise – efforts that highlight personal choice and responsibility. Much of the work on prevention and intervention at this level has had mixed results. Even among public health practitioners who seek to address structural components underlying obesity, the political weight of the morality frame leads them to use “code language” such as “make the healthy choice, the easy choice.” Essentially structural changes are presented as changes enabling personal choice.

At a governmental level, rising healthcare costs in conjunction with rising obesity rates globally and concerns over the efficacy of individual-level interventions are frequently cited as an impetus for governmental strategies and policies to guide widespread interventions, primarily through legislation. Governmental interventions are influenced by the culture, political system, economics, and traditions of the nations involved, resulting in a spectrum of policies and programs globally. Efforts range from health education to restrictive taxes on unhealthy foods and beverages, with a goal of shaping behavior by restricting or coercing individual choice. In the European Union (EU), a concerted effort is being made to encourage voluntary action on the part of industry partners to alter nutrition and activity environments. Voluntary efforts to support decision-making through evidence-based information, self-regulation of product claims (labeling, advertisements) through the proposed establishment of an industry code of conduct, food redistribution (surplus fruits/vegetables) focused on children 4–12 years old, reformulation of foods to decrease sugar, fat, and salt, and sustainable urban transportation facilities to promote physical activity/ public infrastructure (Commission of the European Communities 2007) are examples of this type of intervention. In the USA, taxation of SSBs and calorie-dense foods has been implemented (or attempted), most notably in New York City and the Navajo Nation. China, Britain, and Mexico have all passed or attempted to enact legislation that aims to regulate behavior with an eye to reducing the economic burden of healthcare. Often, particular populations are targeted for interventions, as evidence indicates that obesity is more prevalent in these groups. Unfortunately, these efforts can take the form of value imperatives about who is obese or overweight and who is responsible, encouraging the spread of stigmatization and victimization (Puhl and Heuer 2010).

Some initiatives have sought to create structural or environmental changes to address the inequities, disparities, and deficits implicated in obesity (public health framing with social justice focus). Policies attempting to reduce the unequal distribution of resources, barriers to healthy foods and activities, and social and economic inequities can be found in new regulations requiring enhanced visibility and simplified nutritional labeling; limitations on commercial advertising of high density, low-nutrient foods to children; venue-specific banning of “unhealthy items” such as high-fat items in restaurants or SSBs in school vending machines; and limiting the proximity of fast-food restaurants to schools (Kass et al. 2014; ten Have et al. 2011). These types of initiatives still impact personal choice and liberty and have resulted in public debates regarding the role of government in regulating health. Impacting broader economic and social structures is more challenging from the local level, though increasingly tools like health impact assessments and health in all policies are being used to provide more equity in land use decisions, and have even been used to evaluate local minimum wage, affordable housing, and supplemental nutrition policies. Criticisms of obesity policies have ranged from concerns over the inhibition of individual autonomy, the expansion of the paternalistic “nanny” state (and subsequent economic burden), and the inequitable treatment and stigmatization of low-income populations.

Ethical discussions concerning interventions that limit choice or coerce behavior tend to be centered on arguments about legitimacy and utility. Legitimacy focuses on the value to society in instituting a particular policy or practice. Generally, the discussion revolves around the role of paternalism (soft or hard) in promoting the general welfare of the individual. Paternalism is best viewed as a sliding scale that ranges from promoting informed choice (information campaigns) through implementation of incentives (free or reduced costs, tax benefits, etc.) and ultimately various forms of coercion (bans, taxation). Utility looks at the cost-benefit ratio: is a policy or intervention likely to succeed and does it offer enough benefit to offset the reduction in choice, liberty, or privacy. Because there is little cohesion in how data is collected internationally, making evidence based comparisons of the effectiveness of different types of interventions is difficult. In general, arguments made for coercive policies are rooted in the premise that obesity is associated with higher morbidity and attendant higher costs of treatment. As previously noted, this is by no means a validated conclusion and therefore the utility of such efforts is suspect.

An example of this trade-off is the call for school districts to restrict soft drinks on school campuses. This type of intervention may have the unintended consequence of reducing the school’s revenue stream, resulting in less money available for student education or extra-curricular activities. Obesity prevalence is associated with poverty and disadvantage, disproportionately impacting precisely those communities whose schools need funding the most. Reduced funding may lead to a reduction in programming and healthy food options, elimination of physical education or play equipment, poor food quality to reduce costs, increased sedentism, and reduced educational opportunities (Crooks 2003). The result may be an environmental trade-off of biological costs for social benefits – poorer nutritional quality in order to provide education for all students and thus hopefully propel the students out of poverty.

Another example is the call to use social pressure tactics, similar to antismoking campaigns, to leverage public opinion toward acceptance of stringent governmental regulations. The trade-off here is to focus on increased legitimacy at the expense of utility. This type of intervention operates at the individual, acute, and proximate level and does not address any of the underlying structural conditions. Couched as “stigmatization lite” the argument is that overweight and obese individuals do not recognize their “problem” and need to be awakened to reality. Unfortunately increasing stigmatization of the individual has not been demonstrated to positively impact behavior change; rather, it produces the opposite impact. Discrimination is implicated in stress induced physiological responses associated with obesity that not only negatively impact health but also discourage potential participation in health-related activities. Beyond this, how is the level of stigma “titrated?” Increasing antiobesity thinking may contribute to the moral panic over the rise in obesity rates (Campos et al. 2006).

Stigmatization And Moral Panic

Obesity and Weight-related Stigma. Any discussion on bioethics needs to address the issue of stigmatization (and resulting victimization and discrimination) of obese individuals. Placing the responsibility for one’s weight on the individual has led to sanctioned discrimination in the form of diminished access to goods, services, and employment opportunities and higher healthcare costs for obese individuals. Obesity has even been used as evidence in child abuse cases and other legal interventions. Despite multiple framings of obesity as a medical and public health problem, the persistent focus on individual responsibility and autonomy continues to direct the understanding of obesity through the lens of morality – a platform for value imperatives and subsequent stigmatization.

Obesity stigma must be addressed within the social and structural conditions that produce it. That is, there must be recognition that even a focus on ultimate factors (zoning laws, bans, taxation, urban renewal) can have unintended consequences resulting in increased discrimination. In the past, public health concerns were often the result of an external agent (bacterial or viral agent, poor sanitation, cigarettes, etc.), allowing the focus of interventions to remain external to the body/self. However, weight (and excess weight) is rooted in the body itself – it is a domain of the self. Eating and movement are necessary components of life and are seen as highly personal, as one chooses what, when, and how to eat, move, and function bodily within personal environments. Because these activities are necessary (one cannot stop eating, for example), efforts have focused on changing personal decisions related to eating and activity. Attempts to alter these bodily functions with an external agent (medication, surgery) have had mixed results, but as long as eating and activity are categorized as personal choices, stigmatization will remain a factor.

Media and Corporate Roles. The “moral panic” that has resulted from the framing of obesity as an epidemic has produced a media onslaught. This begs the question of whether the media is reflecting this panic or creating it. Popular media promotes a thin ideal body size (particularly for women), while continuing to also promote the sale of obesogenic products. Fast food and junk food advertisements, product placement in movies, casting of thin ideal body types, and disparaging characterizations of obese characters are prevalent throughout multiple media formats. Visual representations of obese bodies that employ “de-evolution tropes” (which portray the human species as degenerating from more fit ancestors) are common. Media use (screen time) is certainly associated with increased snacking and requests for caloriedense foods and decreased activity and altered sleep patterns (American Academy of Pediatrics 2011).

The increasing documentation of these negative social and physical impacts of media treatment of obesity has led to a mishmash of corporate efforts and legislative calls to action. For example, the Disney Corporation has announced that it will no longer advertise “junk foods” on its television channel. However, Disney continues to promote thin body ideals in its movie and cartoon heroines. McDonald’s has been criticized for targeting children with “toy” gifts in their high fat and sugar Happy Meals. Several European Union countries have instituted restrictions on food advertising aimed at very young children. The impacts of the media on obesity risk and stigma bring to the fore the ongoing ethical conundrum concerning the extent to which governments should have control over media that promote unhealthy behaviors or stigmatization. Issues of free speech, government regulation, and equal access to opportunity and goods have all been cited as deterrents to government regulation of advertising and media. Combining this with a moralistic frame that castigates large bodies as personal failures and the bioethical landscape is messy indeed.

Obesity arises through individual behaviors shaped within varied epigenetic, cognitive, sociocultural, physical, material, political, and other institutional structures and environments. Bioethically, based on the discussion above, this entry suggests that obesity is perhaps more productively addressed as a social problem with medical consequences rather than a medical problem with social consequences. Competing frames of obesity, whether medically or otherwise problematized or not (moralistic, medical/ healthcare, public health, governmental), are rooted in concerns about the ethical behavior of members within the group, not about the larger social, economic, and political domains. Social justice models for obesity intervention rightly focus on the role of the built environment, but rarely tackle the ultimate determinants like poverty, education, and discrimination. Many complex bioethical questions remain: Is it possible to account for acute and chronic dimensions as well as proximate and ultimate factors and mitigate some of the unintended, negative consequences of interventions? How can health policies and interventions ethical approaches be constructed to take into account the very real social dimensions of weight and the body? If health is a public good, what are the ethical implications of not intervening?

Ultimately, being obese is both a private and public matter. While an individual’s weight is the result of multiple individual and biosocial components, the individual’s body is subject to public scrutiny and – increasingly – public regulation. The consequences of public efforts, both intended and unintended, need to be critically examined within the context of how obesity is defined as a problem, the frame used to address the problem as defined, and then how, with whom, and at what level various prevention and intervention efforts are implemented.

Bibliography :

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Childhood and Adolescent Obesity: A Review

Alvina r. kansra.

1 Division of Endocrinology, Diabetes and Metabolism, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, United States

Sinduja Lakkunarajah

2 Division of Adolescent Medicine, Department of Pediatrics, Medical College of Wisconsin Affiliated Hospitals, Milwaukee, WI, United States

M. Susan Jay

3 Division of Adolescent Medicine, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, United States

Obesity is a complex condition that interweaves biological, developmental, environmental, behavioral, and genetic factors; it is a significant public health problem. The most common cause of obesity throughout childhood and adolescence is an inequity in energy balance; that is, excess caloric intake without appropriate caloric expenditure. Adiposity rebound (AR) in early childhood is a risk factor for obesity in adolescence and adulthood. The increasing prevalence of childhood and adolescent obesity is associated with a rise in comorbidities previously identified in the adult population, such as Type 2 Diabetes Mellitus, Hypertension, Non-alcoholic Fatty Liver disease (NAFLD), Obstructive Sleep Apnea (OSA), and Dyslipidemia. Due to the lack of a single treatment option to address obesity, clinicians have generally relied on counseling dietary changes and exercise. Due to psychosocial issues that may accompany adolescence regarding body habitus, this approach can have negative results. Teens can develop unhealthy eating habits that result in Bulimia Nervosa (BN), Binge- Eating Disorder (BED), or Night eating syndrome (NES). Others can develop Anorexia Nervosa (AN) as they attempt to restrict their diet and overshoot their goal of “being healthy.” To date, lifestyle interventions have shown only modest effects on weight loss. Emerging findings from basic science as well as interventional drug trials utilizing GLP-1 agonists have demonstrated success in effective weight loss in obese adults, adolescents, and pediatric patients. However, there is limited data on the efficacy and safety of other weight-loss medications in children and adolescents. Nearly 6% of adolescents in the United States are severely obese and bariatric surgery as a treatment consideration will be discussed. In summary, this paper will overview the pathophysiology, clinical, and psychological implications, and treatment options available for obese pediatric and adolescent patients.


Obesity is a complex issue that affects children across all age groups ( 1 – 3 ). One-third of children and adolescents in the United States are classified as either overweight or obese. There is no single element causing this epidemic, but obesity is due to complex interactions between biological, developmental, behavioral, genetic, and environmental factors ( 4 ). The role of epigenetics and the gut microbiome, as well as intrauterine and intergenerational effects, have recently emerged as contributing factors to the obesity epidemic ( 5 , 6 ). Other factors including small for gestational age (SGA) status at birth, formula rather than breast feeding in infancy, and early introduction of protein in infant's dietary intake have been reportedly associated with weight gain that can persist later in life ( 6 – 8 ). The rising prevalence of childhood obesity poses a significant public health challenge by increasing the burden of chronic non-communicable diseases ( 1 , 9 ).

Obesity increases the risk of developing early puberty in children ( 10 ), menstrual irregularities in adolescent girls ( 1 , 11 ), sleep disorders such as obstructive sleep apnea (OSA) ( 1 , 12 ), cardiovascular risk factors that include Prediabetes, Type 2 Diabetes, High Cholesterol levels, Hypertension, NAFLD, and Metabolic syndrome ( 1 , 2 ). Additionally, obese children and adolescents can suffer from psychological issues such as depression, anxiety, poor self-esteem, body image and peer relationships, and eating disorders ( 13 , 14 ).

So far, interventions for overweight/obesity prevention have mainly focused on behavioral changes in an individual such as increasing daily physical exercise or improving quality of diet with restricting excess calorie intake ( 1 , 15 , 16 ). However, these efforts have had limited results. In addition to behavioral and dietary recommendations, changes in the community-based environment such as promotion of healthy food choices by taxing unhealthy foods ( 17 ), improving lunch food quality and increasing daily physical activity at school and childcare centers, are extra measures that are needed ( 16 ). These interventions may include a ban on unhealthy food advertisements aimed at children as well as access to playgrounds and green spaces where families can feel their children can safely recreate. Also, this will limit screen time for adolescents as well as younger children.

However, even with the above changes, pharmacotherapy and/or bariatric surgery will likely remain a necessary option for those youth with morbid obesity ( 1 ). This review summarizes our current understanding of the factors associated with obesity, the physiological and psychological effects of obesity on children and adolescents, and intervention strategies that may prevent future concomitant issues.

Definition of Childhood Obesity

Body mass index (BMI) is an inexpensive method to assess body fat and is derived from a formula derived from height and weight in children over 2 years of age ( 1 , 18 , 19 ). Although more sophisticated methods exist that can determine body fat directly, they are costly and not readily available. These methods include measuring skinfold thickness with a caliper, Bioelectrical impedance, Hydro densitometry, Dual-energy X-ray Absorptiometry (DEXA), and Air Displacement Plethysmography ( 2 ).

BMI provides a reasonable estimate of body fat indirectly in the healthy pediatric population and studies have shown that BMI correlates with body fat and future health risks ( 18 ). Unlike in adults, Z-scores or percentiles are used to represent BMI in children and vary with the age and sex of the child. BMI Z-score cut off points of >1.0, >2.0, and >3.0 are recommended by the World Health Organization (WHO) to define at risk of overweight, overweight and obesity, respectively ( 19 ). However, in terms of percentiles, overweight is applied when BMI is >85th percentile <95th percentile, whereas obesity is BMI > 95th percentile ( 20 – 22 ). Although BMI Z-scores can be converted to BMI percentiles, the percentiles need to be rounded and can misclassify some normal-weight children in the under or overweight category ( 19 ). Therefore, to prevent these inaccuracies and for easier understanding, it is recommended that the BMI Z-scores in children should be used in research whereas BMI percentiles are best used in the clinical settings ( 20 ).

As BMI does not directly measure body fat, it is an excellent screening method, but should not be used solely for diagnostic purposes ( 23 ). Using 85th percentile as a cut off point for healthy weight may miss an opportunity to obtain crucial information on diet, physical activity, and family history. Once this information is obtained, it may allow the provider an opportunity to offer appropriate anticipatory guidance to the families.

Pathophysiology of Obesity

The pathophysiology of obesity is complex that results from a combination of individual and societal factors. At the individual level, biological, and physiological factors in the presence of ones' own genetic risk influence eating behaviors and tendency to gain weight ( 1 ). Societal factors include influence of the family, community and socio-economic resources that further shape these behaviors ( Figure 1 ) ( 3 , 24 ).

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Multidimensional factors contributing to child and adolescent obesity.

Biological Factors

There is a complex architecture of neural and hormonal regulatory control, the Gut-Brain axis, which plays a significant role in hunger and satiety ( Figure 2 ). Sensory stimulation (smell, sight, and taste), gastrointestinal signals (peptides, neural signals), and circulating hormones further contribute to food intake ( 25 – 27 ).

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Pictorial representation of the Hunger-Satiety pathway a and the various hormones b involved in the pathway. a, Y1/Y5R and MC3/4 are second order neuro receptors which are responsible in either the hunger or satiety pathway. Neurons in the ARC include: NPY, Neuropeptide Y; AgRP, Agouti-Related Peptide; POMC, Pro-Opiomelanocortin; CART, Cocaine-and Amphetamine-regulated Transcript; α-MSH, α-Melanocyte Stimulating Hormone. b, PYY, Peptide YY; PP, Pancreatic Polypeptide; GLP-1, Glucagon-Like Peptide- I; OMX, Oxyntomodulin.

The hypothalamus is the crucial region in the brain that regulates appetite and is controlled by key hormones. Ghrelin, a hunger-stimulating (orexigenic) hormone, is mainly released from the stomach. On the other hand, leptin is primarily secreted from adipose tissue and serves as a signal for the brain regarding the body's energy stores and functions as an appetite -suppressing (anorexigenic) hormone. Several other appetite-suppressing (anorexigenic) hormones are released from the pancreas and gut in response to food intake and reach the hypothalamus through the brain-blood barrier (BBB) ( 28 – 32 ). These anorexigenic and orexigenic hormones regulate energy balance by stimulating hunger and satiety by expression of various signaling pathways in the arcuate nucleus (ARC) of the hypothalamus ( Figure 2 ) ( 28 , 33 ). Dysregulation of appetite due to blunted suppression or loss of caloric sensing signals can result in obesity and its morbidities ( 34 ).

Emotional dysfunction due to psychiatric disorders can cause stress and an abnormal sleep-wake cycles. These modifications in biological rhythms can result in increased appetite, mainly due to ghrelin, and can contribute to emotional eating ( 35 ).

Recently, the role of changes in the gut microbiome with increased weight gain through several pathways has been described in literature ( 36 , 37 ). The human gut serves as a host to trillions of microorganisms, referred to as gut microbiota. The dominant gut microbial phyla are Firmicutes, Bacteroidetes, Actinobacteria, Proteobacteria, Fusobacteria, and Verrucomicrobia, with Firmicutes and Bacteroidetes representing 90% of human gut microbiota ( 5 , 38 ). The microbes in the gut have a symbiotic relationship within their human host and provide a nutrient-rich environment. Gut microbiota can be affected by various factors that include gestational age at birth, mode of infant delivery, type of neonatal and infant feeding, introduction of solid food, feeding practices and external factors like antibiotic use ( 5 , 38 ). Also, the maturation of the bacterial phyla that occurs from birth to adulthood ( 39 ), is influenced by genetics, environment, diet, lifestyle, and gut physiology and stabilizes in adulthood ( 5 , 39 , 40 ). Gut microbiota is unique to each individual and plays a specific role in maintaining structural integrity, and the mucosal barrier of the gut, nutrient metabolism, immune response, and protection against pathogens ( 5 , 37 , 38 ). In addition, the microbiota ferments the indigestible food and synthesizes other essential micronutrients as well as short chain fatty acids (SCFAs') ( 40 , 41 ). Dysbiosis or imbalance of the gut microbiota, in particularly the role of SCFA has been linked with the patho-physiology of obesity ( 36 , 38 , 41 , 42 ). SCFAs' are produced by anaerobic fermentation of dietary fiber and indigestible starch and play a role in mammalian energy metabolism by influencing gut-brain communication axis. Emerging evidence has shown that increased ratio of Firmicutes to Bacteroidetes causes increased energy extraction of calories from diets and is evidenced by increased production of short chain fatty acids (SCFAs') ( 43 – 45 ). However, this relationship is not affirmed yet, as a negative relationship between SCFA levels and obesity has also been reported ( 46 ). Due to the conflicting data, additional randomized control trials are needed to clarify the role of SCFA's in obese and non-obese individuals.

The gut microbiota also has a bidirectional interaction with the liver, and various additional factors such as diet, genetics, and the environment play a key role in this relationship. The Gut- Liver Axis is interconnected at various levels that include the mucus barrier, epithelial barrier, and gut microbiome and are essential to maintain normal homeostasis ( 47 ). Increased intestinal mucosal permeability can disrupt the gut-liver axis, which releases various inflammatory markers, activates an innate immune response in the liver, and results in a spectrum of liver diseases that include hepatic steatosis, non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC) ( 48 , 49 ).

Other medical conditions, including type 2 Diabetes Mellitus, Metabolic Syndrome, eating disorders as well as psychological conditions such as anxiety and depression are associated with the gut microbiome ( 50 – 53 ).

Genetic Factors

Genetic causes of obesity can either be monogenic or polygenic types. Monogenic obesity is rare, mainly due to mutations in genes within the leptin/melanocortin pathway in the hypothalamus that is essential for the regulation of food intake/satiety, body weight, and energy metabolism ( 54 ). Leptin regulates eating behaviors, the onset of puberty, and T-cell immunity ( 55 ). About 3% of obese children have mutations in the leptin ( LEP ) gene and the leptin receptor (LEPR) and can also present with delayed puberty and immune dysfunction ( 55 , 56 ). Obesity caused by other genetic mutations in the leptin-melanocortin pathway include proopiomelanocortin (POMC) and melanocortin receptor 4 (MC4R), brain-derived neurotrophic factor (BDNF), and the tyrosine kinase receptor B (NTRK2) genes ( 57 , 58 ). Patients with monogenic forms generally present during early childhood (by 2 years old) with severe obesity and abnormal feeding behaviors ( 59 ). Other genetic causes of severe obesity are Prader Willi Syndrome (PWS), Alström syndrome, Bardet Biedl syndrome. Patients with these syndromes present with additional characteristics, including cognitive impairment, dysmorphic features, and organ-specific developmental abnormalities ( 60 ). Individuals who present with obesity, developmental delay, dysmorphic features, and organ dysfunction should receive a genetics referral for further evaluation.

Polygenic obesity is the more common form of obesity, caused by the combined effect of multiple genetic variants. It is the result of the interplay between genetic susceptibility and the environment, also known as the Gene-Environment Interaction (GEI) ( 61 – 64 ). Genome-wide association studies (GWAS) have identified gene variants [single nucleotide polymorphism (SNPs)] for body mass index (BMI) that likely act synergistically to affect body weight ( 65 ). Studies have identified genetic variants in several genes that may contribute to excessive weight gain by increasing hunger and food intake ( 66 – 68 ). When the genotype of an individual confers risk for obesity, exposure to an obesogenic environment may promote a state of energy imbalance due to behaviors that contribute to conserving rather than expending energy ( 69 , 70 ). Research studies have shown that obese individuals have a genetic variation that can influence their actions, such as increased food intake, lack of physical activity, a decreased metabolism, as well as an increased tendency to store body fat ( 63 , 66 , 67 , 69 , 70 ).

Recently the role of epigenetic factors in the development of obesity has emerged ( 71 ). The epigenetic phenomenon may alter gene expression without changing the underlying DNA sequence. In effect, epigenetic changes may result in the addition of chemical tags known as methyl groups, to the individual's chromosomes. This alteration can result in a phenomenon where critical genes are primed to on and off regulate. Complex physiological and psychological adjustment occur during infancy and can thereafter set the stage for health vs. disease. Developmental origins of health and disease (DOHaD) shows that early life environment can impact the risk of chronic diseases later in life due to fetal programming secondary to epigenetic changes ( 72 ). Maternal nutrition during the prenatal or early postnatal period may trigger these epigenetic changes and increase the risk for chronic conditions such as obesity, metabolic and cardiovascular disease due to epigenetic modifications that may persist and cause intergenerational effect on the health children and adults ( 58 , 73 , 74 ). Similarly, adverse childhood experiences (ACE) have been linked to a broad range of negative outcomes through epigenetic mechanisms ( 75 ) and promote unhealthy eating behaviors ( 76 , 77 ). Other factors such as diet, physical activity, environmental and psychosocial stressors can cause epigenetic changes and place an individual at risk for weight gain ( 78 ).

Developmental Factors

Eating behaviors evolve over the first few years of life. Young children learn to eat through their direct experience with food and observing others eating around them ( 79 ). During infancy, feeding defines the relationship of security and trust between a child and the parent. Early childhood eating behaviors shift to more self-directed control due to rapid physical, cognitive, communicative, and social development ( 80 ). Parents or caregivers determine the type of food that is made available to the infant and young child. However, due to economic limitations and parents having decreased time to prepare nutritious meals, consumption of processed and cheaper energy-dense foods have occurred in Western countries. Additionally, feeding practices often include providing large or super-sized portions of palatable foods and encouraging children to finish the complete meal (clean their plate even if they do not choose to), as seen across many cultures ( 81 , 82 ). Also, a segment of parents are overly concerned with dietary intake and may pressurize their child to eat what they perceive as a healthy diet, which can lead to unintended consequences ( 83 ). Parents' excessive restriction of food choices may result in poor self-regulation of energy intake by their child or adolescent. This action may inadvertently promote overconsumption of highly palatable restricted foods when available to the child or adolescent outside of parental control with resultant excessive weight gain ( 84 , 85 ).

During middle childhood, children start achieving greater independence, experience broader social networks, and expand their ability to develop more control over their food choices. Changes that occur in the setting of a new environment such as daycare or school allow exposure to different food options, limited physical activity, and often increased sedentary behaviors associated with school schedules ( 24 ). As the transition to adolescence occurs, physical and psychosocial development significantly affect food choices and eating patterns ( 25 ). During the teenage years, more independence and interaction with peers can impact the selection of fast foods that are calorically dense. Moreover, during the adolescent years, more sedentary behaviors such as video and computer use can limit physical exercise. Adolescence is also a period in development with an enhanced focus on appearance, body weight, and other psychological concerns ( 86 , 87 ).

Environmental Factors

Environmental changes within the past few decades, particularly easy access to high-calorie fast foods, increased consumption of sugary beverages, and sedentary lifestyles, are linked with rising obesity ( 88 ). The easy availability of high caloric fast foods, and super-sized portions, are increasingly common choices as individuals prefer these highly palatable and often less expensive foods over fruits and vegetables ( 89 ). The quality of lunches and snacks served in schools and childcare centers has been an area of debate and concern. Children and adolescents consume one-third to one-half of meals in the above settings. Despite policies in place at schools, encouraging foods, beverages, and snacks that are deemed healthier options, the effectiveness of these policies in improving children's dietary habits or change in obesity rate has not yet been seen ( 90 ). This is likely due to the fact that such policies primarily focus on improving dietary quality but not quantity which can impact the overweight or obese youth ( 91 ). Policies to implement taxes on sugary beverages are in effect in a few states in the US ( 92 ) as sugar and sugary beverages are associated with increased weight gain ( 2 , 3 ). This has resulted in reduction in sales of sugary drinks in these states, but the sales of these types of drinks has risen in neighboring states that did not implement the tax ( 93 ). Due to advancements in technology, children are spending increased time on electronic devices, limiting exercise options. Technology advancement is also disrupting the sleep-wake cycle, causing poor sleeping habits, and altered eating patterns ( 94 ). A study published on Canadian children showed that the access to and night-time use of electronic devices causes decreased sleep duration, resulting in excess body weight, inferior diet quality, and lower physical activity levels ( 95 ).

Infant nutrition has gained significant popularity in relation to causing overweight/obesity and other diseases later in life. Breast feeding is frequently discussed as providing protection against developing overweight/obesity in children ( 8 ). Considerable heterogeneity has been observed in studies and conducting randomized clinical trials between breast feeding vs. formula feeding is not feasible ( 8 ). Children fed with a low protein formula like breast milk are shown to have normal weight gain in early childhood as compared to those that are fed formulas with a high protein load ( 96 ). A recent Canadian childbirth cohort study showed that breast feeding within first year of life was inversely associated with weight gain and increased BMI ( 97 ). The effect was stronger if the child was exclusively breast fed directly vs. expressed breast milk or addition of formula or solid food ( 97 ). Also, due to the concern of poor growth in preterm or SGA infants, additional calories are often given for nutritional support in the form of macronutrient supplements. Most of these infants demonstrate “catch up growth.” In fact, there have been reports that in some children the extra nutritional support can increase the risk for overweight/obesity later in life. The association, however, is inconsistent. Recently a systemic review done on randomized controlled trials comparing the studies done in preterm and SGA infants with feeds with and without macronutrient supplements showed that macronutrient supplements may increase weight and length in toddlers but did not show a significant increase in the BMI during childhood ( 98 ). Increased growth velocity due to early introduction of formula milk and protein in infants' diet, may influence the obesity pathways, and can impact fetal programming for metabolic disease later in life ( 99 ).

General pediatricians caring for children with overweight/obesity, generally recommend endocrine testing as parents often believe that there may be an underlying cause for this condition and urge their primary providers to check for conditions such as thyroid abnormalities. Endocrine etiologies for obesity are rarely identified and patients with underlying endocrine disorders causing excessive weight gain usually are accompanied by attenuated growth patterns, such that a patient continues to gain weight with a decline in linear height ( 100 ). Various endocrine etiologies that one could consider in a patient with excessive weight gain in the setting of slow linear growth: severe hypothyroidism, growth hormone deficiency, and Cushing's disease/syndrome ( 58 , 100 ).

Clinical-Physiology of Pediatric Obesity

It is a well-known fact that early AR(increased BMI) before the age of 5 years is a risk factor for adult obesity, obesity-related comorbidities, and metabolic syndrome ( 101 – 103 ). Typically, body mass index (BMI) declines to a minimum in children before it starts increasing again into adulthood, also known as AR. Usually, AR happens between 5 and 7 years of age, but if it occurs before the age of 5 years is considered early AR. Early AR is a marker for higher risk for obesity-related comorbidities. These obesity-related health comorbidities include cardiovascular risk factors (hypertension, dyslipidemia, prediabetes, and type 2 diabetes), hormonal issues, orthopedic problems, sleep apnea, asthma, and fatty liver disease ( Figure 3 ) ( 9 ).

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Obesity related co-morbidities a in children and adolescents. a, NAFLD, Non-Alcoholic Fatty Liver Disease; SCFE, Slipped Capital Femoral Epiphysis; PCOS, Polycystic Ovary Syndrome; OSA, Obstructive Sleep Apnea.

Clinical Comorbidities of Obesity in Children

Growth and puberty.

Excess weight gain in children can influence growth and pubertal development ( 10 ). Childhood obesity can cause prepubertal acceleration of linear growth velocity and advanced bone age in boys and girls ( 104 ). Hyperinsulinemia is a normal physiological state during puberty, but children with obesity can have abnormally high insulin levels ( 105 ). Leptin resistance also occurs in obese individuals who have higher leptin levels produced by their adipose tissue ( 55 , 106 ). The insulin and leptin levels can act on receptors that impact the growth plates with a resultant bone age advancement ( 55 ).

Adequate nutrition is essential for the typical timing and tempo of pubertal onset. Excessive weight gain can initiate early puberty, due to altered hormonal parameters ( 10 ). Obese children may present with premature adrenarche, thelarche, or precocious puberty (PP) ( 107 ). The association of early pubertal changes with obesity is consistent in girls, and is well-reported; however, data is sparse in boys ( 108 ). One US study conducted in racially diverse boys showed obese boys had delayed puberty, whereas overweight boys had early puberty as compared to normal-weight boys ( 109 ). Obese girls with PP have high leptin levels ( 110 , 111 ). Healthy Lifestyle in Europe by Nutrition in Adolescence (HELENA) is a cross-sectional study and suggested an indirect relationship between elevated leptin levels, early puberty, and cardiometabolic and inflammatory markers in obese girls ( 112 ). Additionally, obese girls with premature adrenarche carry a higher risk for developing polycystic ovary syndrome (PCOS) in the future ( 113 , 114 ).

Sleep Disorders

Obesity is an independent risk factor for obstructive sleep apnea (OSA) in children and adolescents ( 12 , 115 ). Children with OSA have less deleterious consequences in terms of cardiovascular stress of metabolic syndrome when compared to adolescents and adults ( 116 , 117 ). In children, abnormal behaviors and neurocognitive dysfunction are the most critical and frequent end-organ morbidities associated with OSA ( 12 ). However, in adolescents, obesity and OSA can independently cause oxidative systemic stress and inflammation ( 118 , 119 ), and when this occurs concurrently, it can result in more severe metabolic dysfunction and cardiovascular outcomes later in life ( 120 ).

Other Comorbidities

Obesity is related to a clinical spectrum of liver abnormalities such as NAFLD ( 121 ); the most important cause of liver disease in children ( 122 – 124 ). NAFLD includes steatosis (increased liver fat without inflammation) and NASH (increased liver fat with inflammation and hepatic injury). While in some adults NAFLD can progress to an end-stage liver disease requiring liver transplant ( 125 , 126 ), the risk of progression during childhood is less well-defined ( 127 ). NAFLD is closely associated with metabolic syndrome including central obesity, insulin resistance, type 2 diabetes, dyslipidemia, and hypertension ( 128 ).

Obese children are also at risk for slipped capital femoral epiphysis (SCFE) ( 129 ), and sedentary lifestyle behaviors may have a negative influence on the brain structure and executive functioning, although the direction of causality is not clear ( 130 , 131 ).

Clinical Comorbidities of Obesity in Adolescents

Menstrual irregularities and pcos.

At the onset of puberty, physiologically, sex steroids can cause appropriate weight gain and body composition changes that should not affect normal menstruation ( 132 , 133 ). However, excessive weight gain in adolescent girls can result in irregular menstrual cycles and puts them at risk for PCOS due to increased androgen levels. Additionally, they can have excessive body hair (hirsutism), polycystic ovaries, and can suffer from distorted body images ( 134 , 135 ). Adolescent girls with PCOS also have an inherent risk for insulin resistance irrespective of their weight. However, weight gain further exacerbates their existing state of insulin resistance and increases the risk for obesity-related comorbidities such as metabolic syndrome, and type 2 diabetes. Although the diagnosis of PCOS can be challenging at this age due to an overlap with predictable pubertal changes, early intervention (appropriate weight loss and use of hormonal methods) can help restore menstrual cyclicity and future concerns related to childbearing ( 11 ).

Metabolic Syndrome and Sleep Disorders

Metabolic syndrome (MS) is a group of cardiovascular risk factors characterized by acanthosis nigricans, prediabetes, hypertension, dyslipidemia, and non-alcoholic steatohepatitis (NASH), that occurs from insulin resistance caused by obesity ( 136 ). Diagnosis of MS in adults requires at least three out of the five risk factors: increased central adiposity, hypertension, hyperglycemia, hypertriglyceridemia, or low HDL level. Definitions to diagnose MS are controversial in younger age groups, and many definitions have been proposed ( 136 ). This is due to the complex physiology of growth and development during puberty, which causes significant overlap between MS and features of normal growth. However, childhood obesity is associated with an inflammatory state even before puberty ( 137 ). In obese children and adolescents, hyperinsulinemia during puberty ( 138 , 139 ) and unhealthy sleep behaviors increase MS's risk and severity ( 140 ). Even though there is no consensus on diagnosis regarding MS in this age group, when dealing with obese children and adolescents, clinicians should screen them for MS risk factors and sleep behaviors and provide recommendations for weight management.

Social Psychology of Pediatric Obesity in Children and Adolescents

Obese children and adolescents may experience psychosocial sequelae, including depression, bullying, social isolation, diminished self-esteem, behavioral problems, dissatisfaction with body image, and reduced quality of life ( 13 , 141 ). Compared with normal-weight counterparts, overweight/obesity is one of the most common reasons children and adolescents are bullied at school ( 142 ). The consequence of stigma, bullying, and teasing related to childhood obesity are pervasive and can have severe implications for emotional and physical health and performance that can persist later in life ( 13 ).

In adolescents, psychological outcomes associated with obesity are multifactorial and have a bidirectional relationship ( Figure 4 ). Obese adolescents due to their physique may have a higher likelihood of psychosocial health issues, including depression, body image/dissatisfaction, lower self-esteem, peer victimization/bullying, and interpersonal relationship difficulties. They may also demonstrate reduced resilience to challenging situations compared to their non-obese/overweight counterparts ( 9 , 143 – 146 ). Body image dissatisfaction has been associated with further weight gain but can also be related to the development of a mental health disorder or an eating disorder (ED) or disorder eating habits (DEH). Mental health disorders such as depression are associated with poor eating habits, a sedentary lifestyle, and altered sleep patterns. ED or DEH that include anorexia nervosa (AN), bulimia nervosa (BN), binge-eating disorder (BED) or night eating syndrome (NES) may be related to an individual's overvaluation of their body shape and weight or can result during the treatment for obesity ( 147 – 150 ). The management of obesity can place a patient at risk of AN if there is a rigid focus on caloric intake or if a patient overcorrects and initiates obsessive self-directed dieting. Healthcare providers who primarily care for obese patients, usually give the advice to diet to lose weight and then maintain it. However, strict dieting (hypocaloric diet), which some patients may later engage in can lead to an eating disorder such as anorexia nervosa ( 151 ). This behavior leads to a poor relationship with food, and therefore, adolescents perseverate on their weight and numbers ( 152 ).

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Bidirectional relationship of different psychological outcomes of obesity.

Providers may not recognize DEHs when a morbidly obese patient loses the same weight as a healthy weight individual ( 149 ). It may appear as a positive result with families and others praising the individual without realizing that this youth may be engaging in destructive behaviors related to weight control. Therefore, it is essential to screen regarding the process of how weight loss was achieved ( 144 , 150 ).

Support and attention to underlying psychological concerns can positively affect treatment, overall well-being, and reduce the risk of adult obesity ( 150 ). The diagram above represents the complexity of the different psychological issues which can impact the clinical care of the obese adolescent.

Eating family meals together can improve overall dietary intake due to enhanced food choices mirrored by parents. It has also may serve as a support to individuals with DEHs if there is less attention to weight and a greater focus on appropriate, sustainable eating habits ( 148 ).

Prevention and Anticipatory Guidance

It is essential to recognize and provide preventive measures for obesity during early childhood and adolescence ( 100 , 153 , 154 ). It is well-established that early AR is a risk factor for adult obesity ( 66 – 68 ). Therefore, health care providers caring for the pediatric population need to focus on measures such as BMI but provide anticipatory guidance regarding nutritional counseling without stigmatizing or judging parents for their children's overweight/obesity ( 155 ). Although health care providers continue to pursue effective strategies to address the obesity epidemic; ironically, they frequently exhibit weight bias and stigmatizing behaviors. Research has demonstrated that the language that health care providers use when discussing a patient's body weight can reinforce stigma, reduce motivation for weight loss, and potentially cause avoidance of routine preventive care ( 155 ). In adolescents, rather than motivating positive changes, stigmatizing language regarding weight may negatively impact a teen and result in binge eating, decreased physical activity, social isolation, avoidance of health care services, and increased weight gain ( 156 , 157 ). Effective provider-patient communication using motivational interviewing techniques are useful to encourage positive behavior changes ( 155 , 158 ).

Anticipatory guidance includes educating the families on healthy eating habits and identifying unhealthy eating practices, encouraging increased activity, limiting sedentary activities such as screen time. Lifestyle behaviors in children and adolescents are influenced by many sectors of our society, including the family ( Figure 1 ) ( 3 , 24 ). Therefore, rather than treating obesity in isolation as an individual problem, it is crucial to approach this problem by focusing on the family unit. Family-based multi-component weight loss behavioral treatment is the gold standard for treating childhood obesity, and it is having been found useful in those between 2 and 6 years old ( 150 , 159 ). Additionally, empowering the parents to play an equal role in developing and implementing an intervention for weight management has shown promising results in improving the rate of obesity by decreasing screen time, promoting healthy eating, and increasing support for children's physical activity ( 160 , 161 ).

When dietary/lifestyle modifications have failed, the next option is a structured weight -management program with a multidisciplinary approach ( 15 ). The best outcomes are associated with an interdisciplinary team comprising a physician, dietician, and psychologist generally 1–2 times a week ( 15 , 162 ). However, this treatment approach is not effective in patients with severe obesity ( 122 ). Although healthier lifestyle recommendations for weight loss are the current cornerstone for obesity management, they often fail. As clinicians can attest, these behavioral and dietary changes are hard to achieve, and all too often is not effective in patients with severe obesity. Failure to maintain substantial weight loss over the long term is due to poor adherence to the prescribed lifestyle changes as well as physiological responses that resist weight loss ( 163 ). American TV hosts a reality show called “The Biggest Loser” that centers on overweight and obese contestants attempting to lose weight for a cash prize. Contestants from “The Biggest Loser” competition, had metabolic adaptation (MA) after drastic weight loss, regained more than they lost weight after 6 years due to a significant slow resting metabolic rate ( 164 ). MA is a physiological response which is a reduced basal metabolic rate seen in individuals who are losing or have lost weight. In MA, the body alters how efficient it is at turning the food eaten into energy; it is a natural defense mechanism against starvation and is a response to caloric restriction. Plasma leptin levels decrease substantially during caloric restriction, suggesting a role of this hormone in the drop of energy expenditure ( 165 ).

Pharmacological Management

The role of pharmacological therapy in the treatment of obesity in children and adolescents is limited.

Orlistat is the only FDA approved medication for weight loss in 12-18-year-olds but has unpleasant side effects ( 166 ). Another medicine, Metformin, has been used in children with signs of insulin resistance, may have some impact on weight, but is not FDA approved ( 167 ). The combination of phentermine/topiramate (Qsymia) has been FDA approved for weight loss in obese individuals 18 years and older. In studies, there has been about 9–10% weight loss over 2 years. However, caution must be taken in females as it can lead to congenital disabilities, especially with use in the first trimester of pregnancy ( 167 ).

GLP-1 agonists have demonstrated great success in effective weight loss and are approved by the FDA for adult obesity ( 168 – 170 ). A randomized control clinical trial recently published showed a significant weight loss in those using liraglutide (3.0 mg)/day plus lifestyle therapy group compared to placebo plus lifestyle therapy in children between the ages of 12–18 years ( 171 ).

Recently during the EASL conference, academic researchers and industry partners presented novel interventions targeting different gut- liver axis levels that include intestinal content, intestinal microbiome, intestinal mucosa, and peritoneal cavity ( 47 ). The focus for these therapeutic interventions within the gut-liver axis was broad and ranged anywhere from newer drugs protecting the intestinal mucus lining, restoring the intestinal barriers and improvement in the gut microbiome. One of the treatment options was Hydrogel technology which was shown to be effective toward weight loss in patients with metabolic syndrome. Hydrogel technology include fibers and high viscosity polysaccharides that absorb water in the stomach and increasing the volume, thereby improving satiety ( 47 ). Also, a clinical trial done in obese pregnant mothers using Docosahexaenoic acid (DHA) showed that the mothers' who got DHA had children with lower adiposity at 2 and 4 years of age ( 172 ). Recently the role of probiotics in combating obesity has emerged. Probiotics are shown to alter the gut microbiome that improves intestinal digestive and absorptive functions of the nutrients. Intervention including probiotics may be a possible solution to manage pediatric obesity ( 173 , 174 ). Additionally, the role of Vitamin E for treating the comorbidities of obesity such as diabetes, hyperlipidemia, NASH, and cardiovascular risk, has been recently described ( 175 , 176 ). Vitamin E is a lipid- soluble compound and contains both tocopherols and tocotrienols. Tocopherols have lipid-soluble antioxidants properties that interact with cellular lipids and protects them from oxidation damage ( 177 ). In metabolic disease, certain crucial pathways are influenced by Vitamin E and some studies have summarized the role of Vitamin E regarding the treatment of obesity, metabolic, and cardiovascular disease ( 178 ). Hence, adequate supplementation of Vitamin E as an appropriate strategy to help in the treatment of the prevention of obesity and its associated comorbidities has been suggested. Nonetheless, some clinical trials have shown contradictory results with Vitamin E supplementation ( 177 ). Although Vitamin E has been recognized as an antioxidant that protects from oxidative damage, however, a full understanding of its mechanism of action is still lacking.

Bariatric Surgery

Bariatric surgery has gained popularity since the early 2000s in the management of severe obesity. If performed earlier, there are better outcomes for reducing weight and resolving obesity-related comorbidities in adults ( 179 – 182 ). Currently, the indication for bariatric in adolescents; those who have a BMI >35 with at least one severe comorbidity (Type 2 Diabetes, severe OSA, pseudotumor cerebri or severe steatohepatitis); or BMI of 40 or more with other comorbidities (hypertension, hyperlipidemia, mild OSA, insulin resistance or glucose intolerance or impaired quality of life due to weight). Before considering bariatric surgery, these patients must have completed most of their linear growth and participated in a structured weight-loss program for 6 months ( 159 , 181 , 183 ). The American Society for Metabolic and Bariatric Surgery (AMBS) outlines the multidisciplinary approach that must be taken before a patient undergoing bariatric surgery. In addition to a qualified bariatric surgeon, the patient must have a pediatrician or provider specialized in adolescent medicine, endocrinology, gastroenterology and nutrition, registered dietician, mental health provider, and exercise specialist ( 181 ). A mental health provider is essential as those with depression due to obesity or vice versa may have persistent mental health needs even after weight loss surgery ( 184 ).

Roux-en-Y Gastric Bypass (RYGB), laparoscopic Sleeve Gastrectomy (LSG), and Gastric Banding are the options available. RYGB and LSG currently approved for children under 18 years of age ( 166 , 181 , 185 ). At present, gastric banding is not an FDA recommended procedure in the US for those under 18y/o. One study showed some improvements in BMI and severity of comorbidities but had multiple repeat surgeries and did not believe a suitable option for obese adolescents ( 186 ).

Compared to LSG, RYGB has better outcomes for excess weight loss and resolution of obesity-related comorbidities as shown in studies and clinical trials ( 183 , 184 , 187 ). Overall, LSG is a safer choice and may be advocated for more often ( 179 – 181 ). The effect on the Gut-Brain axis after Bariatric surgery is still inconclusive, especially in adolescents, as the number of procedures performed is lower than in adults. Those who underwent RYGB had increased fasting and post-prandial PYY and GLP-1, which could have contributed to the rapid weight loss ( 185 ); this effect was seen less often in patients with gastric banding ( 185 ). Another study in adult patients showed higher bile acid (BA) subtype levels and suggested a possible BA's role in the surgical weight loss response after LSG ( 188 ). Adolescents have lower surgical complication rates than their adult counterparts, hence considering bariatric surgery earlier rather than waiting until adulthood has been entertained ( 180 ). Complications after surgery include nutritional imbalance in iron, calcium, Vitamin D, and B12 and should be monitored closely ( 180 , 181 , 185 ). Although 5-year data for gastric bypass in very obese teens is promising, lifetime outcome is still unknown, and the psychosocial factors associated with adolescent adherence post-surgery are also challenging and uncertain.

Obesity in childhood and adolescence is not amenable to a single easily modified factor. Biological, cultural, and environmental factors such as readily available high-density food choices impact youth eating behaviors. Media devices and associated screen time make physical activity a less optimal choice for children and adolescents. This review serves as a reminder that the time for action is now. The need for interventions to change the obesogenic environment by instituting policies around the food industry and in the schools needs to be clarified. In clinical trials GLP-1 agonists are shown to be effective in weight loss in children but are not yet FDA approved. Discovery of therapies to modify the gut microbiota as treatment for overweigh/obesity through use of probiotics or fecal transplantation would be revolutionary. For the present, ongoing clinical research efforts in concert with pharmacotherapeutic and multidisciplinary lifestyle programs hold promise.

Author Contributions

AK, SL, and MJ contributed to the conception and design of the study. All authors contributed to the manuscript revision, read, and approved the submitted version.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


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  18. PDF Obesity: An Introduction and Evaluation

    States obesity is estimated to cause an excess 111,909 to 365,000 death per year, while 1 million (7.7%) of deaths in the European Union are attributed to excess weight . [9,10] Classification: Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have an adverse effect on health. [11]

  19. Scoping review of obesity interventions: Research frontiers and

    Introduction. With the acceleration of industrialization and urbanization worldwide, obesity has become the highest incidence of chronic diseases, affecting approximately 650 million individuals. 1 Obesity and overweight are global health problems and have been associated with a variety of diseases such as diabetes, cardiovascular diseases, tumors, skeletal diseases, and digestive system ...

  20. Epidemiology of Obesity in Adults: Latest Trends

    Introduction. Obesity is linked with elevated risk of non-communicable diseases (NCDs) [].An increasing trend in obesity prevalence since the early 1980s has posed a significant population health burden across the globe [] while obesity prevalence varies by region and country [1, 3].Country-specific trends in obesity are generally tracked using longitudinal panel or repeated cross-sectional ...

  21. Childhood Obesity: An Evidence-Based Approach to Family-Centered Advice

    Significant maternal weight gain during pregnancy can increase a child's risk for obesity. 8,9 There is evidence that increases in BMI percentile level or BMI trajectory in children during the first 3 years of life is predictive of obesity. 10 Infants can develop obesity due to being overfed (such as for comfort) and other feeding practices ...

  22. Obesity Research Paper

    View sample obesity research paper. ... Introduction. There has been a dramatic rise in the prevalence of obesity globally in the last three decades, and the World Health Organization (WHO) estimates around 11 % of the world's total population is obese (WHO 2012). Obesity is seen as a major public health concern because it is widely ...

  23. Childhood and Adolescent Obesity in the United States: A Public Health

    Introduction. Childhood and adolescent obesity have reached epidemic levels in the United States, affecting the lives of millions of people. In the past 3 decades, the prevalence of childhood obesity has more than doubled in children and tripled in adolescents. 1 The latest data from the National Health and Nutrition Examination Survey show that the prevalence of obesity among US children and ...

  24. Childhood and Adolescent Obesity: A Review

    Introduction. Obesity is a complex issue that affects children across all age groups (1 ... Research studies have shown that obese individuals have a genetic variation that can influence their actions, ... Prevention of childhood obesity: a position paper of the global federation of international societies of paediatric gastroenterology, ...