TY  - JOUR
AB  - BACKGROUND: Early-life exposures might negatively affect fetal and infant development, predisposing children to obesity. This study aimed to systematically identify and evaluate risk factors for childhood obesity in preconception, pregnancy, and infancy, and assess their potential for future prediction and prevention strategies. METHODS: This systematic review (PROSPERO, CRD42022355152) included longitudinal studies from selected electronic databases published between inception and August 17th, 2022, identifying maternal, paternal, or infant risk factors from preconception until infancy for childhood obesity between 2 and 18 years. Screening and data extraction were conducted using standardized forms. We assessed risk factor quality on modifiability and predictive power using a piloted criteria template from ILSI-Europe-Marker-Validation-Initiative. FINDINGS: We identified 172 publications from observational and five publications from intervention studies involving n = 1,879,971 children from 37, predominantly high-income, countries. Average reported childhood obesity prevalence was 11.1%. Pregnancy and infancy risk factors were mostly studied. We identified 59 potential risk factors; 23 were consistently associated. Strongest risk factors were: higher maternal prepregnancy weight (n = 28/31 publications with positive associations), higher gestational weight gain (n = 18/21), maternal smoking during pregnancy (n = 23/29), higher birth weight (n = 20/28), large-size-for-gestational-age-at-birth (n = 17/18), no breastfeeding (n = 20/31), and higher infant weight gain (n = 12/12). Level of evidence was generally moderate due to unreliable exposure measurement, short follow-up/loss to follow-up, and risk of confounding. INTERPRETATION: We identified seven early-life risk factors, which were strongly associated with childhood obesity, and can contribute to future prediction and prevention strategies. These findings support the implementation of prevention strategies targeting these risk factors from a clinical and population perspective, where possible integrated with implementation studies.
AU  - Blaauwendraad, S.M.*
AU  - Kamphuis, A.S.J.*
AU  - Ruiz Ojeda, F.J.
AU  - Brandimonte-Hernández, M.*
AU  - Flores-Ventura, E.*
AU  - Abrahamse-Berkeveld, M.*
AU  - Collado, M.C.*
AU  - van Diepen, J.A.*
AU  - Iozzo, P.*
AU  - Knipping, K.*
AU  - van Loo-Bouwman, C.A.*
AU  - Gil, Á.*
AU  - Gaillard, R.*
C1  - 76088
C2  - 58418
TI  - Risk factors in the first 1000 days of life associated with childhood obesity: A systematic review and risk factor quality assessment.
JO  - Obes. Rev.
PY  - 2025
SN  - 1467-7881
ER  - 

TY  - JOUR
AB  - Obesity, particularly pediatric obesity, has dramatically increased over the last three decades, with a wide range of detrimental health outcomes, including negative consequences for brain neurodevelopment. The present article reviewed magnetic resonance imaging studies between January 2011 and March 2024 examining the brain's role in pediatric obesity, including parental influences and diverse interventions. A literature search identified 97 eligible MRI studies in the pediatric population. Findings suggest that altered brain structures and functions in pediatric obesity are strongly dependent on the developmental stage of children and adolescents. The function and structure of limbic regions, such as the hippocampus, amygdala, and striatum, as well as the prefrontal cortex, seem to be particularly affected by higher body mass index during development. In response to palatable foods, children and adolescents with excess weight have increased activation in reward-related regions and decreased activation in regions involved in interoceptive signal processing, especially during decision processes. In addition, children of mothers with obesity and gestational diabetes mellitus show alterations in brain structure and function independent of their current obesity. Behavioral, exercise, and weight-loss intervention studies showed promising effects on the brain, with increased structural integrity, decreased brain responses to reward, and strengthened inhibitory brain responses in children and adolescents with excess weight after the intervention.
AU  - Zhao, S.
AU  - Semeia, L.
AU  - Veit, R.
AU  - Moser, J.
AU  - Preissl, H.
AU  - Kullmann, S.
C1  - 75308
C2  - 58264
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
TI  - Structural and functional brain changes in children and adolescents with obesity.
JO  - Obes. Rev.
PB  - Wiley
PY  - 2025
SN  - 1467-7881
ER  - 

TY  - JOUR
AB  - The present systematic review and meta-analysis aimed to summarize the associations between gut microbiota composition and non-alcoholic fatty liver disease. To compare the differences between individuals with or without NAFLD, the standardized mean difference and 95% confidence interval were computed for each α-diversity index and relative abundance of gut microbes. The β-diversity indices were summarized in a qualitative manner. A total of 54 studies with 8894 participants were included. Overall, patients with NAFLD had moderate reduction in α-diversity indices including Shannon (SMD = -0.36, 95% CI = [-0.53, -0.19], p < 0.001) and Chao 1 (SMD = -0.42, 95% CI = [-0.68, -0.17], p = 0.001), but no significant differences were found for Simpson, observed species, phylogenetic diversity, richness, abundance-based coverage estimator, and evenness (p ranged from 0.081 to 0.953). Over 75% of the included studies reported significant differences in β-diversity. Although there was substantial interstudy heterogeneity, especially for analyses at the phylum, class, and family levels, the majority of the included studies showed alterations in the depletion of anti-inflammatory microbes (i.e., Ruminococcaceae and Coprococcus) and the enrichment of proinflammatory microbes (i.e., Fusobacterium and Escherichia) in patients with NAFLD. Perturbations in gut microbiota were associated with NAFLD, commonly reflected by a reduction in beneficial species and an increase in the pathogenic species.
AU  - Su, X.*
AU  - Chen, S.*
AU  - Liu, J.*
AU  - Feng, Y.*
AU  - Han, E.*
AU  - Hao, X.*
AU  - Liao, M.
AU  - Cai, J.*
AU  - Zhang, S.*
AU  - Niu, J.*
AU  - He, S.*
AU  - Huang, S.*
AU  - Lo, K.*
AU  - Zeng, F.*
C1  - 68677
C2  - 54883
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
TI  - Composition of gut microbiota and non-alcoholic fatty liver disease: A systematic review and meta-analysis.
JO  - Obes. Rev.
VL  - 25
IS  - 1
PB  - Wiley
PY  - 2024
SN  - 1467-7881
ER  - 

TY  - JOUR
AB  - Non-alcoholic fatty liver disease (NAFLD) is a disorder characterized by excessive accumulation of fat in the liver that can progress to liver inflammation (non-alcoholic steatohepatitis [NASH]), liver fibrosis, and cirrhosis. Although most efforts for drug development are focusing on the treatment of the latest stages of NAFLD, where significant fibrosis and NASH are present, findings from studies suggest that the amount of liver fat may be an important independent risk factor and/or predictor of development and progression of NAFLD and metabolic diseases. In this review, we first describe the current tools available for quantification of liver fat in humans and then present the clinical and pathophysiological evidence that link liver fat with NAFLD progression as well as with cardiometabolic diseases. Finally, we discuss current pharmacological and non-pharmacological approaches to reduce liver fat and present open questions that have to be addressed in future studies.
AU  - Demir, M.*
AU  - Bornstein, S.R.
AU  - Mantzoros, C.S.*
AU  - Perakakis, N.
C1  - 68018
C2  - 54496
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
TI  - Liver fat as risk factor of hepatic and cardiometabolic diseases.
JO  - Obes. Rev.
VL  - 24
IS  - 10
PB  - Wiley
PY  - 2023
SN  - 1467-7881
ER  - 

TY  - JOUR
AB  - Obesity is a chronic, multifactorial, relapsing disease. Despite multicomponent lifestyle interventions, including pharmacotherapy, maintaining bodyweight loss is challenging for many people. The pathophysiology of obesity is complex, and currently approved pharmacotherapies only target a few of the many pathways involved; thus, single-targeting agents have limited efficacy. Proglucagon-derived peptides, glucagon, and the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), represent attractive targets for managing obesity and metabolic disorders because they may have direct roles in multiple mechanisms including satiety, energy homeostasis, and lipolytic activity. Unimolecular dual and triple agonists targeting glucagon and incretin hormone receptors have been shown to promote bodyweight loss, lower glucose levels, and reduce food intake in animal models of obesity. Multiple dual receptor agonists are in clinical development for the treatment of obesity, including GLP-1/GIP and GLP-1/glucagon receptor agonists. The extent to which glucagon contributes to treatment effects remains to be understood, but it may promote bodyweight loss by reducing food intake, while concomitant GLP-1 receptor agonism ensures normal glucose control. Further research is required to fully understand the molecular mechanisms of action and metabolic effects of both dual and triple receptor agonists.
AU  - Del Prato, S.*
AU  - Gallwitz, B.
AU  - Holst, J.J.*
AU  - Meier, J.J.*
C1  - 63389
C2  - 51417
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
TI  - The incretin/glucagon system as a target for pharmacotherapy of obesity.
JO  - Obes. Rev.
PB  - Wiley
PY  - 2021
SN  - 1467-7881
ER  - 

TY  - JOUR
AB  - Several reviews have been conducted to assess the association between greenspace and overweight or obesity, but the conclusions were inconsistent. However, an updated comprehensive review and meta-analysis is warranted, because several high-quality papers have been published more recently. The objectives of this study are to systematically and quantitatively assess the evidence for a link between greenspace with overweight/obesity and to make specific recommendations for further research. We searched three English language databases, four Chinese language databases and the reference lists of previously published reviews for epidemiological studies on greenspace and overweight/obesity published before January 2020. We developed inclusion criteria, screened the literature and extracted key data from selected papers. We assessed methodological quality and risk of bias, and we graded the credibility of the pooled evidence. We also performed sensitivity analyses. Fifty-seven records met our inclusion criteria and were included in the study. Most studies were cross-sectional designs (81%) and were from developed nations (88%). More than half (55%) of the included studies found beneficial associations between greenspace and overweight/obesity in overall or subpopulations. Our meta-analytical results showed that greater normalized difference vegetation index was associated with lower odds of overweight/obesity in a statistically significant fashion (odds ratio [OR]: 0.88; 95% CI: 0.84, 0.91) but not residential proximity to greenspace (OR: 0.99; 95% CI: 0.99, 1.00), proportion of greenspace (OR: 0.96; 95% CI: 0.85, 1.08) or number of parks in an area (OR: 0.99; 95% CI: 0.97, 1.01). However, we detected high between-study heterogeneity in two of the four meta-analyses, which reduced the credibility of the pooled evidence. Current evidence indicates that there might be an association between greater access to greenspace and lower odds of overweight/obesity. However, additional high-quality studies are needed to more definitively assess the evidence for a causal association.
AU  - Luo, Y.N.*
AU  - Huang, W.Z.*
AU  - Liu, X.X.*
AU  - Markevych, I.*
AU  - Bloom, M.S.*
AU  - Zhao, T.
AU  - Heinrich, J.*
AU  - Yang, B.Y.*
AU  - Dong, G.H.*
C1  - 59697
C2  - 49016
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
TI  - Greenspace with overweight and obesity: A systematic review and meta-analysis of epidemiological studies up to 2020.
JO  - Obes. Rev.
VL  - 21
IS  - 11
PB  - Wiley
PY  - 2020
SN  - 1467-7881
ER  - 

TY  - JOUR
AB  - In early childhood, individuals with Prader-Willi syndrome (PWS) experience excess weight gain and severe hyperphagia with food compulsivity, which often leads to early onset morbid obesity. Effective treatments for appetite suppression and weight control are currently unavailable for PWS. Our aim to further understand the pathogenesis of PWS led us to carry out a comprehensive search of the current and emerging therapies for managing hyperphagia and extreme weight gain in PWS. A literature search was performed using PubMed and the following keywords: “PWS” AND “therapy” OR “[drug name]”; reference lists, pharmaceutical websites, and the ClinicalTrials.gov registry were also reviewed. Articles presenting data from current standard treatments in PWS and also clinical trials of pharmacological agents in the pipeline were selected. Current standard treatments include dietary restriction/modifications, exercise, and growth hormone replacement, which appear to have limited efficacy for appetite and weight control in patients with PWS. The long-term safety and effectiveness of bariatric surgery in PWS remains unknown. However, many promising pharmacotherapies are in development and, if approved, will bring much needed choices into the PWS pharmacological armamentarium. With the progress that is currently being made in our understanding of PWS, an effective treatment may not be far off.
AU  - Tan, Q.*
AU  - Orsso, C.E.*
AU  - Deehan, E.C.*
AU  - Triador, L.*
AU  - Field, C.J.*
AU  - Tun, H.M.*
AU  - Han, J.C.*
AU  - Müller, T.D.
AU  - Haqq, A.M.*
C1  - 57743
C2  - 47947
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
TI  - Current and emerging therapies for managing hyperphagia and obesity in Prader-Willi syndrome: A narrative review.
JO  - Obes. Rev.
VL  - 21
IS  - 5
PB  - Wiley
PY  - 2020
SN  - 1467-7881
ER  - 

TY  - JOUR
AB  - Obesity is associated with both structural and functional changes of the central nervous system. While gray matter alterations in obesity point to a consistent reduction with increasing body mass index (BMI), volumetric changes in white matter are more complex and less conclusive. Hence, more recently, diffusion tensor imaging (DTI) has been employed as a highly sensitive tool to investigate microstructural changes in white matter structure. Parameters of diffusivity and anisotropy are used to evaluate white matter and fibre integrity as well as axonal and myelin degeneration. Fractional anisotropy (FA) is the most commonly used parameter as it is the best estimate of fibre integrity. The focus of this review was on the relationship between obesity and brain alterations assessed by DTI. Altogether, these studies have shown a loss of white matter integrity with obesity-related factors, especially in tracts within the limbic system and those connecting the temporal and frontal lobe. More specifically, multiple studies found an inverse association between BMI and FA in the corpus callosum, fornix, cingulum and corona radiata in elderly and young adults as well as children. Furthermore, significant interactions were observed between BMI and age, pointing to accelerated ageing of white matter structure in obese.
AU  - Kullmann, S.
AU  - Schweizer, F.*
AU  - Veit, R.*
AU  - Fritsche, A.
AU  - Preissl, H.
C1  - 43290
C2  - 36567
CY  - Hoboken
SP  - 273-281
TI  - Compromised white matter integrity in obesity.
JO  - Obes. Rev.
VL  - 16
IS  - 4
PB  - Wiley-blackwell
PY  - 2015
SN  - 1467-7881
ER  - 

TY  - JOUR
AB  - Summary: Previously, a single nucleotide polymorphism (SNP), rs9939609, in the FTO gene showed a much stronger association with all-cause mortality than expected from its association with body mass index (BMI), body fat mass index (FMI) and waist circumference (WC). This finding implies that the SNP has strong pleiotropic effects on adiposity and adiposity-independent pathological pathways that leads to increased mortality. To investigate this further, we conducted a meta-analysis of similar data from 34 longitudinal studies including 169,551 adult Caucasians among whom 27,100 died during follow-up. Linear regression showed that the minor allele of the FTO SNP was associated with greater BMI (n=169,551; 0.32kgm-2; 95% CI 0.28-0.32, P<1×10-32), WC (n=152,631; 0.76cm; 0.68-0.84, P<1×10-32) and FMI (n=48,192; 0.17kgm-2; 0.13-0.22, P=1.0×10-13). Cox proportional hazard regression analyses for mortality showed that the hazards ratio (HR) for the minor allele of the FTO SNPs was 1.02 (1.00-1.04, P=0.097), but the apparent excess risk was eliminated after adjustment for BMI and WC (HR: 1.00; 0.98-1.03, P=0.662) and for FMI (HR: 1.00; 0.96-1.04, P=0.932). In conclusion, this study does not support that the FTO SNP is associated with all-cause mortality independently of the adiposity phenotypes.
AU  - Zimmermann, E.*
AU  - Ängquist, L.H.*
AU  - Mirza, S.S.*
AU  - Zhao, J.H.*
AU  - Chasman, D.I.*
AU  - Fischer, K.*
AU  - Qi, Q.*
AU  - Smith, A.V.*
AU  - Thinggaard, M.*
AU  - Jarczok, M.N.*
AU  - Nalls, M.A.*
AU  - Trompet, S.*
AU  - Timpson, N.J.*
AU  - Schmidt, B.*
AU  - Jackson, A.U.*
AU  - Lyytikäinen, L.-P.*
AU  - Verweij, N.*
AU  - Müller-Nurasyid, M.
AU  - Vikström, M.*
AU  - Marques-Vidal, P.*
AU  - Wong, A.*
AU  - Meidtner, K.*
AU  - Middelberg, R.P.*
AU  - Strawbridge, R.J.*
AU  - Christiansen, L.*
AU  - Kyvik, K.O.H.M.*
AU  - Hamsten, A.*
AU  - Jääskeläinen, T.*
AU  - Tjönneland, A.M.*
AU  - Eriksson, J.G.*
AU  - Whitfield, J.B.*
AU  - Boeing, H.*
AU  - Hardy, R.*
AU  - Vollenweider, P.*
AU  - Leander, K.*
AU  - Peters, A.
AU  - van der Harst, P.*
AU  - Kumari, M.*
AU  - Lehtimäki, T.*
AU  - Meirhaeghe, A.*
AU  - Tuomilehto, J.O.I.*
AU  - Jöckel, K.-H.*
AU  - Ben-Shlomo, Y.*
AU  - Sattar, N.A.*
AU  - Baumeister, S.E.*
AU  - Davey Smith, G.*
AU  - Casas, J.P.*
AU  - Houston, D.K.*
AU  - Marz, W.*
AU  - Christensen, K.*
AU  - Gudnason, V.G.*
AU  - Hu, F.B.*
AU  - Metspalu, A.*
AU  - Ridker, P.M.*
AU  - Wareham, N.J.*
AU  - Loos, R.J.F.*
AU  - Tiemeier, H.M.*
AU  - Sonestedt, E.*
AU  - Sørensen, T.I.A.*
C1  - 43797
C2  - 36761
CY  - Hoboken
SP  - 327-340
TI  - Is the adiposity-associated FTO gene variant related to all-cause mortality independent of adiposity? Meta-analysis of data from 169,551 Caucasian adults.
JO  - Obes. Rev.
VL  - 16
IS  - 4
PB  - Wiley-blackwell
PY  - 2015
SN  - 1467-7881
ER  -