The objective of this study was to investigate underlying mechanisms of long-term effective weight loss after laparoscopic sleeve gastrectomy (LSG) and effects on the medial orbitofrontal cortex (mOFC) and cognition.
Methods
A total of 18 individuals with obesity (BMI ≥ 30 kg/m2) underwent LSG. Clinical data, cognitive scores, and brain magnetic resonance imaging scans were evaluated before LSG and 12 months after LSG. We employed voxel-based morphometry analysis and seed-based resting-state functional connectivity (RSFC) analysis to assess LSG-induced structural and functional changes in mOFC. Partial correlation analysis and univariate and multivariate linear regression models were used to explore associations among biochemical indexes, neuroimaging, cognition, and weight loss.
Results
No significant improvement in general cognition was found after LSG. Decreases in gray matter volume of the bilateral mOFC and increases in RSFC of the right mOFC were observed 12 months after LSG. Weight loss was associated with RSFC, general cognitive scores, and triglyceride changes. Multivariate linear regression model revealed gray matter volume of the left mOFC and working memory scores at baseline explained 55.2% of the variation in weight loss.
Conclusions
These findings suggest that mOFC imaging and cognitive scores could serve as biomarkers for predicting persistent weight loss after LSG, which provides a solid foundation for a potential target for neuromodulation research.
{"title":"Medial orbitofrontal cortex structure, function, and cognition associates with weight loss for laparoscopic sleeve gastrectomy","authors":"Xin Li, Wen Zhang, Yan Bi, Yanjie Duan, Xitai Sun, Jiu Chen, Xin Zhang, Zhou Zhang, Zhengyang Zhu, Bing Zhang","doi":"10.1002/oby.24207","DOIUrl":"10.1002/oby.24207","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The objective of this study was to investigate underlying mechanisms of long-term effective weight loss after laparoscopic sleeve gastrectomy (LSG) and effects on the medial orbitofrontal cortex (mOFC) and cognition.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A total of 18 individuals with obesity (BMI ≥ 30 kg/m<sup>2</sup>) underwent LSG. Clinical data, cognitive scores, and brain magnetic resonance imaging scans were evaluated before LSG and 12 months after LSG. We employed voxel-based morphometry analysis and seed-based resting-state functional connectivity (RSFC) analysis to assess LSG-induced structural and functional changes in mOFC. Partial correlation analysis and univariate and multivariate linear regression models were used to explore associations among biochemical indexes, neuroimaging, cognition, and weight loss.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>No significant improvement in general cognition was found after LSG. Decreases in gray matter volume of the bilateral mOFC and increases in RSFC of the right mOFC were observed 12 months after LSG. Weight loss was associated with RSFC, general cognitive scores, and triglyceride changes. Multivariate linear regression model revealed gray matter volume of the left mOFC and working memory scores at baseline explained 55.2% of the variation in weight loss.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>These findings suggest that mOFC imaging and cognitive scores could serve as biomarkers for predicting persistent weight loss after LSG, which provides a solid foundation for a potential target for neuromodulation research.</p>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 2","pages":"308-320"},"PeriodicalIF":4.2,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774012/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhengting Liang, Huibo Qin, Binbin Su, Yanping Bao, Michael V. Vitiello, Gang Hu, Yunhe Wang
Objective
The objective was to evaluate the longitudinal patterns of central and general obesity, identify their genetic and behavioral risk determinants, and investigate the association of distinct obesity trajectories beyond middle age with subsequent cognitive decline and the risk of developing dementia in late life.
Methods
Using a nationally representative, longitudinal, community-based cohort, we examined trajectory patterns of obesity over a 14-year span beyond middle age employing latent mixture modeling. We then evaluated their relationship with subsequent cognitive decline through linear mixed models and with the risk of developing dementia using Cox models, adjusting for confounding variables.
Results
Among the 4751 eligible participants (mean age, 58.7 [SD 8.1] years; 57% female), our analysis identified five distinct BMI trajectories and four WC trajectories spanning a 14-year period. In comparison with individuals in the low-stable BMI group, characterized by a consistent and healthy body weight (range, 22.8–22.9 kg/m2), those in the high-stable group, maintaining a stable obesity status (range, 34.3–35.4 kg/m2), exhibited an elevated risk of developing dementia (odds ratio [OR], 1.43; 95% CI: 1.02 to 2.00) and experienced a more accelerated cognitive decline over 6 years (difference in 6-year decline, −0.11 SD [95% CI: −0.18 to −0.03]). Similarly, when compared with participants in the low-stable WC group, indicating a stable and healthy WC (range, 76–79 cm), those in the high-increasing WC group, showing an increasing trend (range, 115–122 cm), demonstrated an increased risk of developing dementia (OR, 1.57, 95% CI: 1.01 to 2.49) and experienced a swifter cognitive decline (OR: −0.18 [95% CI: −0.28 to −0.07]).
Conclusions
General and central obesity trajectories beyond midlife with persistently high or increasing patterns were significantly associated with an increased risk of developing cognitive decline and dementia in late life. Longitudinal obesity patterns may assist in precise identification of older adults at risk of developing cognitive impairment for targeted intervention.
{"title":"Trajectories of general and central obesity beyond middle age in relation to late-life cognitive decline and dementia","authors":"Zhengting Liang, Huibo Qin, Binbin Su, Yanping Bao, Michael V. Vitiello, Gang Hu, Yunhe Wang","doi":"10.1002/oby.24208","DOIUrl":"10.1002/oby.24208","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The objective was to evaluate the longitudinal patterns of central and general obesity, identify their genetic and behavioral risk determinants, and investigate the association of distinct obesity trajectories beyond middle age with subsequent cognitive decline and the risk of developing dementia in late life.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Using a nationally representative, longitudinal, community-based cohort, we examined trajectory patterns of obesity over a 14-year span beyond middle age employing latent mixture modeling. We then evaluated their relationship with subsequent cognitive decline through linear mixed models and with the risk of developing dementia using Cox models, adjusting for confounding variables.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among the 4751 eligible participants (mean age, 58.7 [SD 8.1] years; 57% female), our analysis identified five distinct BMI trajectories and four WC trajectories spanning a 14-year period. In comparison with individuals in the low-stable BMI group, characterized by a consistent and healthy body weight (range, 22.8–22.9 kg/m<sup>2</sup>), those in the high-stable group, maintaining a stable obesity status (range, 34.3–35.4 kg/m<sup>2</sup>), exhibited an elevated risk of developing dementia (odds ratio [OR], 1.43; 95% CI: 1.02 to 2.00) and experienced a more accelerated cognitive decline over 6 years (difference in 6-year decline, −0.11 SD [95% CI: −0.18 to −0.03]). Similarly, when compared with participants in the low-stable WC group, indicating a stable and healthy WC (range, 76–79 cm), those in the high-increasing WC group, showing an increasing trend (range, 115–122 cm), demonstrated an increased risk of developing dementia (OR, 1.57, 95% CI: 1.01 to 2.49) and experienced a swifter cognitive decline (OR: −0.18 [95% CI: −0.28 to −0.07]).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>General and central obesity trajectories beyond midlife with persistently high or increasing patterns were significantly associated with an increased risk of developing cognitive decline and dementia in late life. Longitudinal obesity patterns may assist in precise identification of older adults at risk of developing cognitive impairment for targeted intervention.</p>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 2","pages":"405-415"},"PeriodicalIF":4.2,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774005/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Calorie labeling laws: who is affected and why?","authors":"Charles Courtemanche","doi":"10.1002/oby.24237","DOIUrl":"10.1002/oby.24237","url":null,"abstract":"","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 2","pages":"223-224"},"PeriodicalIF":4.2,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ammara Aqeel, Melissa C. Kay, Jun Zeng, Brianna L. Petrone, Chengxin Yang, Tracy Truong, Covington B. Brown, Sharon Jiang, Veronica M. Carrion, Stephanie Bryant, Michelle C. Kirtley, Cody D. Neshteruk, Sarah C. Armstrong, Lawrence A. David
Objective
We assessed the impact of a food-provisioning intervention on diet quality in children with obesity.
Methods
Participants (n = 33, aged 6–11 years) were randomly assigned to either usual care (intensive health behavior and lifestyle treatment) or intervention (usual care + food provisioning; high-fiber, low-dairy diet) for 4 weeks. The primary outcome was a change in child diet quality at Week 4. Secondary outcomes were changes in weight, food insecurity, gut microbiome composition (16S ribosomal RNA), and dietary intake, measured via an objective DNA-based biomarker (i.e., FoodSeq). Genomic dietary data were analyzed against a larger pediatric adolescent obesity cohort (n = 195, aged 10–18 years) from similar households.
Results
Intervention demonstrated changes across all assessed diet components and was more effective than usual care in increasing whole grain (β = 0.20, 95% CI: 0.05 to 0.34; p = 0.013) and fiber (β = 2.52, 95% CI: 1.28 to 3.76; p < 0.001) and decreasing dairy (β = −1.31, 95% CI: −2.02 to −0.60; p = 0.001). FoodSeq results, highly concordant with grocery orders (adjusted R2 = 0.65; p < 0.001), indicated a dietary shift toward low-energy-density plant taxa in the intervention relative to a prior survey of diet in a related cohort (β = 8.64, 95% CI: 5.18 to 12.14; p < 0.001). No significant changes were observed in microbiome, weight, or food insecurity.
Conclusions
Our study supports the potential of dietitian-guided food provisioning for improving diet quality in children with obesity and demonstrates an objective genomic approach for evaluating dietary shifts.
{"title":"Grocery intervention and DNA-based assessment to improve diet quality in pediatric obesity: a pilot randomized controlled study","authors":"Ammara Aqeel, Melissa C. Kay, Jun Zeng, Brianna L. Petrone, Chengxin Yang, Tracy Truong, Covington B. Brown, Sharon Jiang, Veronica M. Carrion, Stephanie Bryant, Michelle C. Kirtley, Cody D. Neshteruk, Sarah C. Armstrong, Lawrence A. David","doi":"10.1002/oby.24205","DOIUrl":"10.1002/oby.24205","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>We assessed the impact of a food-provisioning intervention on diet quality in children with obesity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Participants (<i>n</i> = 33, aged 6–11 years) were randomly assigned to either usual care (intensive health behavior and lifestyle treatment) or intervention (usual care + food provisioning; high-fiber, low-dairy diet) for 4 weeks. The primary outcome was a change in child diet quality at Week 4. Secondary outcomes were changes in weight, food insecurity, gut microbiome composition (16S ribosomal RNA), and dietary intake, measured via an objective DNA-based biomarker (i.e., FoodSeq). Genomic dietary data were analyzed against a larger pediatric adolescent obesity cohort (<i>n</i> = 195, aged 10–18 years) from similar households.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Intervention demonstrated changes across all assessed diet components and was more effective than usual care in increasing whole grain (β = 0.20, 95% CI: 0.05 to 0.34; <i>p</i> = 0.013) and fiber (β = 2.52, 95% CI: 1.28 to 3.76; <i>p</i> < 0.001) and decreasing dairy (β = −1.31, 95% CI: −2.02 to −0.60; <i>p</i> = 0.001). FoodSeq results, highly concordant with grocery orders (adjusted <i>R</i><sup>2</sup> = 0.65; <i>p</i> < 0.001), indicated a dietary shift toward low-energy-density plant taxa in the intervention relative to a prior survey of diet in a related cohort (β = 8.64, 95% CI: 5.18 to 12.14; <i>p</i> < 0.001). No significant changes were observed in microbiome, weight, or food insecurity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our study supports the potential of dietitian-guided food provisioning for improving diet quality in children with obesity and demonstrates an objective genomic approach for evaluating dietary shifts.</p>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 2","pages":"331-345"},"PeriodicalIF":4.2,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143026208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kenny Arbuckle, Reema Sharma, Frannie E. Drake, Abigail Usiyevich, Sarah Usman, Bridget A. Matikainen-Ankney
Objective
Obesogenic diets induce persistent changes in physical activity and motivation. It remains unclear whether these behavioral changes are driven by weight gain or exposure to obesogenic diets themselves. We investigated how exposure to a high-fat diet (HFD) in the absence of obesity affected physical activity, food motivation, and circadian patterns in mice.
Methods
C57Bl6/J mice were given ~80% of their daily calories in an HFD, known as isocaloric feeding, along with ad libitum access to laboratory chow. Weekly weights, physical activity levels, circadian patterns, operant behavior, and peripheral blood metabolic markers were measured to determine how an isocaloric HFD affected behavior and physiology. Following this period, the same cohort was exposed to an ad libitum HFD to monitor changes in weight gain and physical activity.
Results
An isocaloric HFD did not significantly increase weight or change physical activity levels. An isocaloric HFD decreased motivation for sucrose pellets but did not alter weight gain with ad libitum HFD exposure.
Conclusions
An isocaloric HFD was associated with decreased motivation for sucrose, as observed in reports of rodent models of obesity. These findings suggest that exposure to an obesogenic diet, even in the absence of significant weight gain, can induce behavioral changes associated with obesity.
{"title":"Isocaloric high-fat diet decreases motivation in the absence of obesity","authors":"Kenny Arbuckle, Reema Sharma, Frannie E. Drake, Abigail Usiyevich, Sarah Usman, Bridget A. Matikainen-Ankney","doi":"10.1002/oby.24227","DOIUrl":"10.1002/oby.24227","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Obesogenic diets induce persistent changes in physical activity and motivation. It remains unclear whether these behavioral changes are driven by weight gain or exposure to obesogenic diets themselves. We investigated how exposure to a high-fat diet (HFD) in the absence of obesity affected physical activity, food motivation, and circadian patterns in mice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>C57Bl6/J mice were given ~80% of their daily calories in an HFD, known as isocaloric feeding, along with ad libitum access to laboratory chow. Weekly weights, physical activity levels, circadian patterns, operant behavior, and peripheral blood metabolic markers were measured to determine how an isocaloric HFD affected behavior and physiology. Following this period, the same cohort was exposed to an ad libitum HFD to monitor changes in weight gain and physical activity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>An isocaloric HFD did not significantly increase weight or change physical activity levels. An isocaloric HFD decreased motivation for sucrose pellets but did not alter weight gain with ad libitum HFD exposure.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>An isocaloric HFD was associated with decreased motivation for sucrose, as observed in reports of rodent models of obesity. These findings suggest that exposure to an obesogenic diet, even in the absence of significant weight gain, can induce behavioral changes associated with obesity.</p>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 2","pages":"243-249"},"PeriodicalIF":4.2,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774000/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143019294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Thiamine deficiency is common after bariatric surgery, but patients with obesity may be deficient in thiamine even before surgery. The purpose of this research was to determine the prevalence of thiamine deficiency in patients with obesity at a medical weight-management clinic and assess the relationship between recent weight loss and thiamine deficiency.
Methods
For this observational study, medical records were reviewed for patients (n = 146) at the nonsurgical obesity medicine and preoperative bariatric surgery clinic at a Veterans Affairs Medical Center between January 1, 2012, and January 31, 2019. Thiamine deficiency was defined as a value less than the test reference range. χ2 tests were used to assess differences in thiamine deficiency by race, gender, and type 2 diabetes status. Logistic regression was used to evaluate the relationship between weight loss and thiamine deficiency.
Results
Thiamine deficiency was found in 32.2% of patients. There were no differences in the prevalence of deficiency by gender, race, or type 2 diabetes status. Weight loss was associated with increased risk for deficiency, although this was not statistically significant (odds ratio = 2.04, 95% CI: 0.79–5.27).
Conclusions
Approximately one-third of patients evaluated had a test result indicating thiamine deficiency. All people with obesity may benefit from additional nutritional screening.
{"title":"Thiamine deficiency in US veterans with obesity","authors":"Elizabeth Costello, Jennifer Kerns","doi":"10.1002/oby.24210","DOIUrl":"10.1002/oby.24210","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Thiamine deficiency is common after bariatric surgery, but patients with obesity may be deficient in thiamine even before surgery. The purpose of this research was to determine the prevalence of thiamine deficiency in patients with obesity at a medical weight-management clinic and assess the relationship between recent weight loss and thiamine deficiency.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>For this observational study, medical records were reviewed for patients (<i>n</i> = 146) at the nonsurgical obesity medicine and preoperative bariatric surgery clinic at a Veterans Affairs Medical Center between January 1, 2012, and January 31, 2019. Thiamine deficiency was defined as a value less than the test reference range. χ<sup>2</sup> tests were used to assess differences in thiamine deficiency by race, gender, and type 2 diabetes status. Logistic regression was used to evaluate the relationship between weight loss and thiamine deficiency.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Thiamine deficiency was found in 32.2% of patients. There were no differences in the prevalence of deficiency by gender, race, or type 2 diabetes status. Weight loss was associated with increased risk for deficiency, although this was not statistically significant (odds ratio = 2.04, 95% CI: 0.79–5.27).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Approximately one-third of patients evaluated had a test result indicating thiamine deficiency. All people with obesity may benefit from additional nutritional screening.</p>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 2","pages":"416-421"},"PeriodicalIF":4.2,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774014/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143019300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Marthe de Roo, Catharina A. Hartman, Alfred Wagtendonk, Hans W. Hoek, Jeroen Lakerveld, Tina Kretschmer
Objective
We examined BMI development across changes in the built environment during the transition from adolescence to young adulthood and explored the moderating role of genetic risk.
Methods
We used longitudinal data from individuals aged 16 to 25 years in the TRacking Adolescents' Individual Lives Survey (TRAILS) that we linked to built environment data for 2006, 2010, and 2016 from the Geoscience and Health Cohort Consortium (GECCO). We fitted a latent growth model of BMI and examined associations of changes in fast-food restaurant density and walkability with changes in BMI (n = 2735), as well as interactions of changes in fast-food restaurant density and walkability with genetic risk (n = 1676).
Results
Changes in fast-food restaurant density (e.g., Δ2010–2006: β = −0.04, 95% CI: −0.11 to 0.03) and walkability (e.g., Δ2010–2006: β = −0.05, 95% CI: −0.14 to 0.05) were not associated with BMI changes. Additionally, genetic risk did not moderate these associations.
Conclusions
We found limited evidence that moving to neighborhoods with higher fast-food restaurant density or less walkability was associated with BMI changes or that genetic risk moderated these associations. Our findings suggest that associations between the built environment and BMI changes during the transition into young adulthood are likely small.
{"title":"Interplay between genetic risk and built neighborhood conditions as predictor of BMI across the transition into adulthood","authors":"Marthe de Roo, Catharina A. Hartman, Alfred Wagtendonk, Hans W. Hoek, Jeroen Lakerveld, Tina Kretschmer","doi":"10.1002/oby.24213","DOIUrl":"10.1002/oby.24213","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>We examined BMI development across changes in the built environment during the transition from adolescence to young adulthood and explored the moderating role of genetic risk.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We used longitudinal data from individuals aged 16 to 25 years in the TRacking Adolescents' Individual Lives Survey (TRAILS) that we linked to built environment data for 2006, 2010, and 2016 from the Geoscience and Health Cohort Consortium (GECCO). We fitted a latent growth model of BMI and examined associations of changes in fast-food restaurant density and walkability with changes in BMI (<i>n</i> = 2735), as well as interactions of changes in fast-food restaurant density and walkability with genetic risk (<i>n</i> = 1676).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Changes in fast-food restaurant density (e.g., Δ2010–2006: <i>β</i> = −0.04, 95% CI: −0.11 to 0.03) and walkability (e.g., Δ2010–2006: <i>β</i> = −0.05, 95% CI: −0.14 to 0.05) were not associated with BMI changes. Additionally, genetic risk did not moderate these associations.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>We found limited evidence that moving to neighborhoods with higher fast-food restaurant density or less walkability was associated with BMI changes or that genetic risk moderated these associations. Our findings suggest that associations between the built environment and BMI changes during the transition into young adulthood are likely small.</p>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 2","pages":"385-394"},"PeriodicalIF":4.2,"publicationDate":"2025-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774011/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143019291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"GLP-1 receptor agonists and retained gastric content: Is it much ado about nothing?","authors":"Michael Camilleri","doi":"10.1002/oby.24215","DOIUrl":"10.1002/oby.24215","url":null,"abstract":"","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 2","pages":"221-222"},"PeriodicalIF":4.2,"publicationDate":"2025-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143019285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hanim E. Diktas, Michelle I. Cardel, Gary D. Foster, Monique M. LeBlanc, Stephanie L. Dickinson, Erin M. Ables, Xiwei Chen, Rebecca Nathan, Danielle Shapiro, Corby K. Martin
Objective
Food noise has received attention in the media, although no validated questionnaires exist to measure it. This study developed and tested the reliability and validity of the Food Noise Questionnaire (FNQ).
Methods
Participants (N = 400) successfully completed, the FNQ and a demographic questionnaire and self-reported weight and height. A subsample (n = 150) completed the FNQ 7 days later for test–retest reliability, and this subsample's first FNQ data were subjected to exploratory factor analysis. The remaining subsample (n = 250) completed two preoccupation with food questionnaires to test convergent validity, along with mood, anxiety, and stress questionnaires to test for discriminant validity. Confirmatory factor analysis was conducted using this subsample's FNQ data.
Results
Data from 396 participants were analyzed (4 participants did not complete all FNQ items). The FNQ had excellent internal consistency reliability (Cronbach α = 0.93) and high test–retest reliability (r = 0.79; p < 0.001; mean [SD] = 7.4 [1.0] days between administration). Factor analyses found that the five FNQ items loaded onto a single factor, with good fit indices (χ2[5] = 52.87, p < 0.001; root mean square error of approximation [RMSEA] = 0.20; comparative fit index [CFI] = 0.95; standardized root mean squared residual [SRMR] = 0.03). The FNQ showed good convergent (all r > 0.78; p < 0.001) and discriminant (all r < 0.39; p < 0.001) validity.
Conclusions
The FNQ provides a psychometrically reliable and valid measure of food noise, although further research is needed to evaluate its clinical utility.
{"title":"Development and validation of the Food Noise Questionnaire","authors":"Hanim E. Diktas, Michelle I. Cardel, Gary D. Foster, Monique M. LeBlanc, Stephanie L. Dickinson, Erin M. Ables, Xiwei Chen, Rebecca Nathan, Danielle Shapiro, Corby K. Martin","doi":"10.1002/oby.24216","DOIUrl":"10.1002/oby.24216","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Food noise has received attention in the media, although no validated questionnaires exist to measure it. This study developed and tested the reliability and validity of the Food Noise Questionnaire (FNQ).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Participants (<i>N</i> = 400) successfully completed, the FNQ and a demographic questionnaire and self-reported weight and height. A subsample (<i>n</i> = 150) completed the FNQ 7 days later for test–retest reliability, and this subsample's first FNQ data were subjected to exploratory factor analysis. The remaining subsample (<i>n</i> = 250) completed two preoccupation with food questionnaires to test convergent validity, along with mood, anxiety, and stress questionnaires to test for discriminant validity. Confirmatory factor analysis was conducted using this subsample's FNQ data.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Data from 396 participants were analyzed (4 participants did not complete all FNQ items). The FNQ had excellent internal consistency reliability (Cronbach <i>α</i> = 0.93) and high test–retest reliability (<i>r</i> = 0.79; <i>p</i> < 0.001; mean [SD] = 7.4 [1.0] days between administration). Factor analyses found that the five FNQ items loaded onto a single factor, with good fit indices (<i>χ</i><sup>2</sup>[5] = 52.87, <i>p</i> < 0.001; root mean square error of approximation [RMSEA] = 0.20; comparative fit index [CFI] = 0.95; standardized root mean squared residual [SRMR] = 0.03). The FNQ showed good convergent (all <i>r</i> > 0.78; <i>p</i> < 0.001) and discriminant (all <i>r</i> < 0.39; <i>p</i> < 0.001) validity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The FNQ provides a psychometrically reliable and valid measure of food noise, although further research is needed to evaluate its clinical utility.</p>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 2","pages":"289-297"},"PeriodicalIF":4.2,"publicationDate":"2025-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774004/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143019243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yan Emily Yuan, Andrea V. Haas, Bernard Rosner, Gordon H. Williams, Marie E. McDonnell, Gail K. Adler
Objective
Individuals who have metabolically healthy overweight/obesity (MHOO) do not have cardiometabolic complications despite an elevated BMI. Renin-angiotensin-aldosterone system (RAAS) activation and salt sensitivity of blood pressure (SSBP) are cardiovascular disease (CVD) risks, which are increased in individuals with higher BMI values. Little is known about the differences in RAAS activation and SSBP between MHOO and metabolically unhealthy overweight/obesity (MUOO) phenotypes.
Methods
We studied 1430 adults on controlled dietary sodium. Individuals in the MHOO group had BMI ≥ 25 kg/m2 without comorbidities (e.g., diabetes, dyslipidemia, hypertension, CVD), whereas individuals in the MUOO group had BMI ≥ 25 kg/m2 and at least one comorbidity. The control group included healthy individuals (BMI 18.5–24.9 kg/m2).
Results
BMI was similar between the MHOO (28.9 kg/m2) and MUOO groups (29.3 kg/m2; p = 0.317). On liberal sodium, the MUOO group had activated RAAS compared with the MHOO group, including higher plasma aldosterone concentration (mean [SD], 1.11 [0.48] ng/dL; p = 0.020), plasma angiotensin II levels (4.11 [2.0] pg/mL; p = 0.040), and percentage of individuals with plasma renin activity ≥ 1.0 ng/mL/h (+3.6%; p = 0.017). The MUOO group had higher SSBP than the MHOO group (6.0 [1.9] mm Hg; p = 0.002). Applying a zero-to-six-point metabolic health score found that a worse score was associated with higher measurements of RAAS activity and SSBP (p < 0.001).
Conclusions
Compared to the MHOO group, the MUOO group was characterized by an increase in the following two CVD risk factors: higher RAAS activity and SSBP on controlled sodium diets. Therapeutic interventions targeting the effects of angiotensin II and/or aldosterone may offer cardiometabolic protection for individuals with the MUOO phenotype.
{"title":"The renin-angiotensin-aldosterone system and salt sensitivity of blood pressure offer new insights in obesity phenotypes","authors":"Yan Emily Yuan, Andrea V. Haas, Bernard Rosner, Gordon H. Williams, Marie E. McDonnell, Gail K. Adler","doi":"10.1002/oby.24218","DOIUrl":"10.1002/oby.24218","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Individuals who have metabolically healthy overweight/obesity (MHOO) do not have cardiometabolic complications despite an elevated BMI. Renin-angiotensin-aldosterone system (RAAS) activation and salt sensitivity of blood pressure (SSBP) are cardiovascular disease (CVD) risks, which are increased in individuals with higher BMI values. Little is known about the differences in RAAS activation and SSBP between MHOO and metabolically unhealthy overweight/obesity (MUOO) phenotypes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We studied 1430 adults on controlled dietary sodium. Individuals in the MHOO group had BMI ≥ 25 kg/m<sup>2</sup> without comorbidities (e.g., diabetes, dyslipidemia, hypertension, CVD), whereas individuals in the MUOO group had BMI ≥ 25 kg/m<sup>2</sup> and at least one comorbidity. The control group included healthy individuals (BMI 18.5–24.9 kg/m<sup>2</sup>).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>BMI was similar between the MHOO (28.9 kg/m<sup>2</sup>) and MUOO groups (29.3 kg/m<sup>2</sup>; <i>p</i> = 0.317). On liberal sodium, the MUOO group had activated RAAS compared with the MHOO group, including higher plasma aldosterone concentration (mean [SD], 1.11 [0.48] ng/dL; <i>p</i> = 0.020), plasma angiotensin II levels (4.11 [2.0] pg/mL; <i>p</i> = 0.040), and percentage of individuals with plasma renin activity ≥ 1.0 ng/mL/h (+3.6%; <i>p</i> = 0.017). The MUOO group had higher SSBP than the MHOO group (6.0 [1.9] mm Hg; <i>p</i> = 0.002). Applying a zero-to-six-point metabolic health score found that a worse score was associated with higher measurements of RAAS activity and SSBP (<i>p</i> < 0.001).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Compared to the MHOO group, the MUOO group was characterized by an increase in the following two CVD risk factors: higher RAAS activity and SSBP on controlled sodium diets. Therapeutic interventions targeting the effects of angiotensin II and/or aldosterone may offer cardiometabolic protection for individuals with the MUOO phenotype.</p>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 2","pages":"321-330"},"PeriodicalIF":4.2,"publicationDate":"2025-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143019297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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