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Social Science & Medicine (1982) Nov 2023Obesity remains a significant public health concern globally with over one billion adults projected to be obese by 2025. To better understand the drivers of obesity and...
RATIONALE
Obesity remains a significant public health concern globally with over one billion adults projected to be obese by 2025. To better understand the drivers of obesity and to inform policy, it is important to explore the factors that influence obesity.
OBJECTIVES
The objective of this paper to examine if the crime rates in the neighbourhood or local area in which a person lives influences their likelihood of being obese. Thus, we seek to contribute to the literature on the determinants of obesity by asking the question: what is the effect of neighbourhood (i.e., postcode) crime on obesity? We also examine the pathways through which neighbourhood crime influences obesity with a focus on the role of social capital, physical activity and sleep quality.
METHODS
Using 14 waves of longitudinal data from the Household, Income and Labour Dynamics in Australia (HILDA) survey merged with official police statistics on crime rates at the postcode level, we apply identification strategies that address endogeneity arising from endogenous sorting and omitted variable bias.
RESULTS
We find that an increase in neighbourhood crime rates is associated with an increase in body mass index (BMI) and the likelihood of being obese. Exploring the pathways through which neighbourhood crime influences obesity, we find that social capital and physical activity are important channels, while sleep quality is not. The evidence also suggests that the effects of violent crime are more pronounced compared to property crime.
CONCLUSION
Our findings suggest that targeting crime, and in particular violent crime, which seems to be driving the findings, is a core mechanism for reducing BMI and maintaining healthy body weight. The mediating role of physical activity and social capital also suggest that public policy can specifically target these areas by providing interventions that promote social capital and physical activity even amidst high crime rates.
Topics: Adult; Humans; Crime; Australia; Exercise; Income; Obesity; Residence Characteristics
PubMed: 37832312
DOI: 10.1016/j.socscimed.2023.116289 -
Clinical and Molecular Hepatology Oct 2023
Topics: Humans; Non-alcoholic Fatty Liver Disease; Sarcopenia; Intra-Abdominal Fat; Obesity
PubMed: 37584065
DOI: 10.3350/cmh.2023.0250 -
Nature Communications Apr 2024Obesity is a well-established risk factor for human cancer, yet the underlying mechanisms remain elusive. Immune dysfunction is commonly associated with obesity but...
Obesity is a well-established risk factor for human cancer, yet the underlying mechanisms remain elusive. Immune dysfunction is commonly associated with obesity but whether compromised immune surveillance contributes to cancer susceptibility in individuals with obesity is unclear. Here we use a mouse model of diet-induced obesity to investigate tumor-infiltrating CD8 T cell responses in lean, obese, and previously obese hosts that lost weight through either dietary restriction or treatment with semaglutide. While both strategies reduce body mass, only dietary intervention restores T cell function and improves responses to immunotherapy. In mice exposed to a chemical carcinogen, obesity-related immune dysfunction leads to higher incidence of sarcoma development. However, impaired immunoediting in the obese environment enhances tumor immunogenicity, making the malignancies highly sensitive to immunotherapy. These findings offer insight into the complex interplay between obesity, immunity and cancer, and provide explanation for the obesity paradox observed in clinical immunotherapy settings.
Topics: Humans; Animals; Mice; Monitoring, Immunologic; Obesity; Diet; Neoplasms; Risk Factors
PubMed: 38565540
DOI: 10.1038/s41467-024-47359-5 -
BMC Women's Health Jul 2023Given the increase in the incidence of breast cancer during the past decades, several studies have investigated the effects of variables on breast cancer, especially... (Meta-Analysis)
Meta-Analysis
Given the increase in the incidence of breast cancer during the past decades, several studies have investigated the effects of variables on breast cancer, especially obesity. This systematic review and meta-analysis aims to evaluate any effects of obesity on breast cancer risk in women, before and after menopause, and in different continents.All forms of relevant literature examining any association between obesity and breast cancer, including cohort, case-control, and cross-sectional studies, were identified in the PubMed, Scopus, EMBASE, and Web of Science databases from January 1, 1990 until January 13, 2023. Body mass index (BMI) > 30 was used to indicate obesity. Every type of breast cancer was examined as outcome factors. The quality of the papers was evaluated using the Newcastle-Ottawa scale checklist. The Egger and Begg test was used to evaluate publication bias. To assess any extra impact of each research on the final measurement, a sensitivity analysis was carried out.One hundred and two studies were included in this meta-analysis. Respectively, 48 and 67 studies reported associations between obesity and breast cancer in pre and post menopausal women. Combining all studies, the pooled OR of the association between obesity and breast cancer in pre-menopausal women was OR = 0.93 CI: (0.85-1.1), (I = 65.4%), and for post-menopausal woman, OR = 1.26 CI: (1.19-1.34), (I = 90.5%).Obesity has a protective role in breast cancer among pre-menopausal women, but this relationship is statistically significant only in European women. The chance of developing breast cancer increases in post-menopausal women who are obese. This relationship is significant among Asian, North American, African and European women.
Topics: Female; Humans; Breast Neoplasms; Risk Factors; Cross-Sectional Studies; Menstruation; Obesity
PubMed: 37496015
DOI: 10.1186/s12905-023-02543-5 -
Frontiers in Endocrinology 2024Obesity is a heterogeneous condition which results from complex interactions among sex/gender, sociocultural, environmental, and biological factors. Obesity is more... (Review)
Review
Obesity is a heterogeneous condition which results from complex interactions among sex/gender, sociocultural, environmental, and biological factors. Obesity is more prevalent in women in most developed countries, and several clinical and psychological obesity complications show sex-specific patterns. Females differ regarding fat distribution, with males tending to store more visceral fat, which is highly correlated to increased cardiovascular risk. Although women are more likely to be diagnosed with obesity and appear more motivated to lose weight, as confirmed by their greater representation in clinical trials, males show better outcomes in terms of body weight and intra-abdominal fat loss and improvements in the metabolic risk profile. However, only a few relatively recent studies have investigated gender differences in obesity, and sex/gender is rarely considered in the assessment and management of the disease. This review summarizes the evidence of gender differences in obesity prevalence, contributing factors, clinical complications, and psychological challenges. In addition, we explored gender differences in response to obesity treatments in the specific context of new anti-obesity drugs.
Topics: Female; Humans; Male; Anti-Obesity Agents; Obesity; Sex Factors
PubMed: 38765954
DOI: 10.3389/fendo.2024.1349794 -
Cancer Research Mar 2024Overweight and obesity are identified by a high body mass index (BMI) and carry significant health risks due to associated comorbidities. Although epidemiologic data...
UNLABELLED
Overweight and obesity are identified by a high body mass index (BMI) and carry significant health risks due to associated comorbidities. Although epidemiologic data connect overweight/obesity with 13 cancer types, a better understanding of the molecular mechanisms underlying this correlation is needed to improve prevention and treatment strategies. In this study, we conducted a comprehensive analysis of molecular differences between overweight or obese patients and normal weight patients across 14 different cancer types from The Cancer Genome Atlas. Using the propensity score weighting algorithm to control for confounding factors, obesity-specific mutational features were identified, such as higher mutation burden in rectal cancer and biased mutational signatures in other cancers. Differentially expressed genes (DEG) in tumors from patients with overweight/obesity were predominantly upregulated and enriched in inflammatory and hormone-related pathways. These DEGs were significantly associated with survival rates in various cancer types, highlighting the impact of elevated body fat on gene expression profiles and clinical outcomes in patients with cancer. Interestingly, while high BMI seemed to have a negative impact on most cancer types, the normal weight-biased mutational and gene expression patterns indicated overweight/obesity may be beneficial in endometrial cancer, suggesting the presence of an "obesity paradox" in this context. Body fat also significantly impacted the tumor microenvironment by modulating immune cell infiltration, underscoring the importance of understanding the interplay between weight and immune response in cancer progression. Together, this study systematically elucidates the molecular differences corresponding to body weight in multiple cancer types, offering potentially critical insights for developing precision therapy for patients with cancer.
SIGNIFICANCE
Elucidation of the complex interplay between body weight and the molecular landscape of cancer could potentially guide tailored therapies and improve patient management amid the global obesity crisis.
Topics: Humans; Overweight; Obesity; Neoplasms; Body Mass Index; Comorbidity; Tumor Microenvironment
PubMed: 38190709
DOI: 10.1158/0008-5472.CAN-23-1463 -
Critical Care (London, England) Sep 2023Respiratory mechanics is a key element to monitor mechanically ventilated patients and guide ventilator settings. Besides the usual basic assessments, some more complex... (Clinical Trial)
Clinical Trial
BACKGROUND
Respiratory mechanics is a key element to monitor mechanically ventilated patients and guide ventilator settings. Besides the usual basic assessments, some more complex explorations may allow to better characterize patients' respiratory mechanics and individualize ventilation strategies. These advanced respiratory mechanics assessments including esophageal pressure measurements and complete airway closure detection may be particularly relevant in critically ill obese patients. This study aimed to comprehensively assess respiratory mechanics in obese and non-obese ICU patients with or without ARDS and evaluate the contribution of advanced respiratory mechanics assessments compared to basic assessments in these patients.
METHODS
All intubated patients admitted in two ICUs for any cause were prospectively included. Gas exchange and respiratory mechanics including esophageal pressure and end-expiratory lung volume (EELV) measurements and low-flow insufflation to detect complete airway closure were assessed in standardized conditions (tidal volume of 6 mL kg predicted body weight (PBW), positive end-expiratory pressure (PEEP) of 5 cmHO) within 24 h after intubation.
RESULTS
Among the 149 analyzed patients, 52 (34.9%) were obese and 90 (60.4%) had ARDS (65.4% and 57.8% of obese and non-obese patients, respectively, p = 0.385). A complete airway closure was found in 23.5% of the patients. It was more frequent in obese than in non-obese patients (40.4% vs 14.4%, p < 0.001) and in ARDS than in non-ARDS patients (30% vs. 13.6%, p = 0.029). Respiratory system and lung compliances and EELV/PBW were similarly decreased in obese patients without ARDS and obese or non-obese patients with ARDS. Chest wall compliance was not impacted by obesity or ARDS, but end-expiratory esophageal pressure was higher in obese than in non-obese patients. Chest wall contribution to respiratory system compliance differed widely between patients but was not predictable by their general characteristics.
CONCLUSIONS
Most respiratory mechanics features are similar in obese non-ARDS and non-obese ARDS patients, but end-expiratory esophageal pressure is higher in obese patients. A complete airway closure can be found in around 25% of critically ill patients ventilated with a PEEP of 5 cmHO. Advanced explorations may allow to better characterize individual respiratory mechanics and adjust ventilation strategies in some patients. Trial registration NCT03420417 ClinicalTrials.gov (February 5, 2018).
Topics: Humans; Body Weight; Critical Illness; Obesity; Respiration, Artificial; Respiratory Distress Syndrome; Respiratory Mechanics
PubMed: 37667379
DOI: 10.1186/s13054-023-04623-2 -
Journal of Cachexia, Sarcopenia and... Feb 2024More than 650 million people are obese (BMI > 30) worldwide, which increases their risk for several metabolic diseases and cancer. While cachexia and obesity are at...
BACKGROUND
More than 650 million people are obese (BMI > 30) worldwide, which increases their risk for several metabolic diseases and cancer. While cachexia and obesity are at opposite ends of the weight spectrum, leading many to suggest a protective effect of obesity against cachexia, mechanistic support for obesity's benefit is lacking. Given that obesity and cachexia are both accompanied by metabolic dysregulation, we sought to investigate the impact of obesity on skeletal muscle mass loss and mitochondrial dysfunction in murine cancer cachexia.
METHODS
Male C57BL/6 mice were given a purified high fat or standard diet for 16 weeks before being implanted with 10 Lewis lung carcinoma (LLC) cells. Mice were monitored for 25 days, and hindlimb muscles were collected for cachexia indices and mitochondrial assessment via western blotting, high-resolution respirometry and transmission electron microscopy (TEM).
RESULTS
Obese LLC mice experienced significant tumour-free body weight loss similar to lean (-12.8% vs. -11.8%, P = 0.0001) but had reduced survival (33.3% vs. 6.67%, χ = 10.04, P = 0.0182). Obese LLC mice had reduced muscle weights (-24%, P < 0.0354) and mCSA (-16%, P = 0.0004) with similar activation of muscle p65 (P = 0.0337), and p38 (P = 0.0008). ADP-dependent coupled respiration was reduced in both Obese and Obese LLC muscle (-30%, P = 0.0072) consistent with reductions in volitional cage activity (-39%, P < 0.0001) and grip strength (-41%, P < 0.0001). TEM revealed stepwise reductions in intermyofibrillar and subsarcolemmal mitochondrial size with Obese (IMF: -37%, P = 0.0009; SS: -21%, P = 0.0101) and LLC (IMF: -40%, P = 0.0019; SS: -27%, P = 0.0383) mice. Obese LLC mice had increased pAMPK (T172; P = 0.0103) and reduced FIS1 (P = 0.0029) and DRP1 (P < 0.0001) mitochondrial fission proteins, which were each unchanged in Lean LLC. Further, mitochondrial TEM analysis revealed that Obese LLC mice had an accumulation of damaged and dysfunctional mitochondria (IMF: 357%, P = 0.0395; SS: 138%, P = 0.0174) in concert with an accumulation of p62 (P = 0.0328) suggesting impaired autophagy and clearance of damaged mitochondria. Moreover, we observed increases in electron lucent vacuoles only in Obese LLC muscle (IMF: 421%, P = 0.0260; SS: 392%, P = 0.0192), further supporting an accumulation of damaged materials that cannot be properly cleared in the obese cachectic muscle.
CONCLUSIONS
Taken together, these results demonstrate that obesity is not protective against cachexia and suggest exacerbated impairments to mitochondrial function and quality control with a particular disruption in the removal of damaged mitochondria. Our findings highlight the need for consideration of the severity of obesity and pre-existing metabolic conditions when determining the impact of weight status on cancer-induced cachexia and functional mitochondrial deficits.
Topics: Humans; Male; Animals; Mice; Cachexia; Mice, Inbred C57BL; Mitochondria; Muscular Atrophy; Carcinoma, Lewis Lung; Obesity; Muscle, Skeletal
PubMed: 38062911
DOI: 10.1002/jcsm.13391 -
JMIR Public Health and Surveillance Feb 2024Previous studies have confirmed the separate effect of arterial stiffness and obesity on type 2 diabetes; however, the joint effect of arterial stiffness and obesity on...
BACKGROUND
Previous studies have confirmed the separate effect of arterial stiffness and obesity on type 2 diabetes; however, the joint effect of arterial stiffness and obesity on diabetes onset remains unclear.
OBJECTIVE
This study aimed to propose the concept of arterial stiffness obesity phenotype and explore the risk stratification capacity for diabetes.
METHODS
This longitudinal cohort study used baseline data of 12,298 participants from Beijing Xiaotangshan Examination Center between 2008 and 2013 and then annually followed them until incident diabetes or 2019. BMI (waist circumference) and brachial-ankle pulse wave velocity were measured to define arterial stiffness abdominal obesity phenotype. The Cox proportional hazard model was used to estimate the hazard ratio (HR) and 95% CI.
RESULTS
Of the 12,298 participants, the mean baseline age was 51.2 (SD 13.6) years, and 8448 (68.7%) were male. After a median follow-up of 5.0 (IQR 2.0-8.0) years, 1240 (10.1%) participants developed diabetes. Compared with the ideal vascular function and nonobese group, the highest risk of diabetes was observed in the elevated arterial stiffness and obese group (HR 1.94, 95% CI 1.60-2.35). Those with exclusive arterial stiffness or obesity exhibited a similar risk of diabetes, and the adjusted HRs were 1.63 (95% CI 1.37-1.94) and 1.64 (95% CI 1.32-2.04), respectively. Consistent results were observed in multiple sensitivity analyses, among subgroups of age and fasting glucose level, and alternatively using arterial stiffness abdominal obesity phenotype.
CONCLUSIONS
This study proposed the concept of arterial stiffness abdominal obesity phenotype, which could improve the risk stratification and management of diabetes. The clinical significance of arterial stiffness abdominal obesity phenotype needs further validation for other cardiometabolic disorders.
Topics: Male; Humans; Middle Aged; Female; Longitudinal Studies; Diabetes Mellitus, Type 2; Obesity, Abdominal; Vascular Stiffness; Ankle Brachial Index; Pulse Wave Analysis; Cohort Studies; Obesity
PubMed: 38329798
DOI: 10.2196/46088 -
JCI Insight Sep 2023Obesity promotes triple-negative breast cancer (TNBC), and effective interventions are urgently needed to break the obesity-TNBC link. Epidemiologic studies indicate...
Obesity promotes triple-negative breast cancer (TNBC), and effective interventions are urgently needed to break the obesity-TNBC link. Epidemiologic studies indicate that bariatric surgery reduces TNBC risk, while evidence is limited or conflicted for weight loss via low-fat diet (LFD) or calorie restriction (CR). Using a murine model of obesity-driven TNBC, we compared the antitumor effects of vertical sleeve gastrectomy (VSG) with LFD, chronic CR, and intermittent CR. Each intervention generated weight and fat loss and suppressed tumor growth relative to obese mice (greatest suppression with CR). VSG and CR regimens exerted both similar and unique effects, as assessed using multiomics approaches, in reversing obesity-associated transcript, epigenetics, secretome, and microbiota changes and restoring antitumor immunity. Thus, in a murine model of TNBC, bariatric surgery and CR each reverse obesity-driven tumor growth via shared and distinct antitumor mechanisms, and CR is superior to VSG in reversing obesity's procancer effects.
Topics: Humans; Mice; Animals; Triple Negative Breast Neoplasms; Caloric Restriction; Disease Models, Animal; Obesity; Bariatric Surgery
PubMed: 37698918
DOI: 10.1172/jci.insight.172868