Explained and unexplained racial and regional inequality in obesity prevalence in the United States

ABSTRACT

Objective: There are substantial racial and regional disparities in obesity prevalence in the United States. This study partitioned the mean Body Mass Index (BMI) and obesity prevalence rate gaps between non-Hispanic blacks and non-Hispanic whites into the portion attributable to observable obesity risk factors and the remaining portion attributable to unobservable factors at the national and the state levels in the United States (U.S.) in 2010.

Design: This study used a simulated micro-population dataset combining common information from the Behavioral Risk Factor Surveillance System and the U.S. Census data to obtain a reliable, large sample representing the adult populations at the national and state levels. It then applied a reweighting decomposition method to decompose the black-white mean BMI and obesity prevalence disparities at the national and state levels into the portion attributable to the differences in distribution of observable obesity risk factors and the remaining portion unexplainable with risk factors.

Results: We found that the observable differences in distribution of known obesity risk factors explain 18.5% of the mean BMI difference and 20.6% of obesity prevalence disparities between non-Hispanic blacks and non-Hispanic whites. There were substantial variations in how much the differences in distribution of known obesity risk factors can explain black-white gaps in mean BMI (?67.7% to 833.6%) and obesity prevalence (?278.5% to 340.3%) at the state level.

Conclusion: The results from this study demonstrate that known obesity risk factors explain a small proportion of the racial, ethnic and between-state disparities in obesity prevalence in the United States. Future etiologic studies are required to further understand the causal factors underlying obesity and racial, ethnic and geographic disparities.     

Does obesity put your brain at risk?

Background and aimsThe negative impact of obesity on the brain is an issue of increasing clinical interest. Hence, this review summarized evidence linking obesity with brain morphology (gray and white matter volume), brain function (functional activation and connectivity), and cognitive function.MethodsA criticals review of the relevant published English articles between 2008 and 2022, using PubMed, Google Scholar and Science Direct. Studies were included if (1) an experimental/intervention study was conducted (2) the experiment/intervention included both high fat diet or body weight, whether it could counteract the negative effect brain morphological or functional change. Critical analysis for a supporting study was also carried out.ResultsBrain dysfunction can be recognized as result from neuroinflammation, oxidative stress, change in gut-brain hormonal functionality decrease regional blood flow or diminished hippocampal size and change in gut-brain hormonal functionality; which collectively translate into a cycle of deranged metabolic control and cognitive deficits, often obesity referred as changes in brain biochemistry and brain function. Recently, a few changes in brain structure and functions could be traced back even to obese children or adult. Evidence here suggested that obesity elicits early neuroinflammation effects, which likely disrupt the normal metabolism in hypothalamus, and hippocampus result from brain insulin resistance. The mechanisms of these robust effects are discussed herein.ConclusionBrain disease is inseparable from obesity itself and requires a better recognition to allow future therapeutic targeting for treatment of obesity. Additional research is needed to identify the best treatment targets and to identify if these changes reversible.     

English obesity policies: To govern and not to govern

Problem definitions constitute a crucial part of the policy process. In 2008 the Labour Government presented a plan to reduce the obesity prevalence in England. Only three years later the Conservative–Liberal Government introduced a plan on the same topic, which it presented as new and innovative. The aim of this study is to analyse the respective governments’ problematisations of obesity and to identify similarities and differences. Despite the different hues of the two governments, the programmes are surprisingly similar. They seek to simultaneously govern and not to govern. They adhere to liberal ideals of individual choice and they also suggest initiatives that will lead people to choose certain behaviours. Both governments encourage the food and drink industry to support their policies voluntarily, rather than obliging them to do so, although Labour is somewhat more inclined to use statutory measures. The Conservative–Liberal plan does not represent many new ideas. The plans are characterised by the paradox that they convey both ideas and ideals about freedom of choice as well as about state interventions to influence people's choices, which could be seen as incompatible, but as the study shows in practice they are not.     

“Obesity paradox” in coronary artery disease

Obesity used to be among the more neglected public health problems, but has unfolded as a growing medical and socioeconomic burden of epidemic proportions. Morbid obesity is linked to traditional cardiovascular risk factors like, hypertension, hyperlipidemia and diabetes, and suspected to incur increased morbidity and mortality in the Western and even third world populations. This patient cohort is also at greater risk to develop coronary artery disease. Recent population-based registries revealed that 43% and 24% of all cases of coronary revascularization were carried out in overweight and obese patients, respectively. However, despite evidence of a positive correlation between obesity and increased cardiovascular morbidity, some authors have described a better clinical outcome in overweight and obese patients, a phenomenon they coined “obesity paradoxon”. Thus, there is an ongoing debate in light of conflicting data and the possibility of confounding bias causing misconception and challenging the “obesity paradox”. In this review article we present the current evidence and throughly discuss the validity of the “obesity paradoxon” in a variety of clinical settings.     

Non alcoholic fatty liver disease and risk of incident diabetes in subjects who are not obese

Background and aims

It is not known whether non alcoholic fatty liver disease (NAFLD) is a risk factor for diabetes in non obese, non centrally-obese subjects. Our aim was to investigate relationships between fatty liver, insulin resistance and a biomarker score for liver fibrosis with incident diabetes at follow up, in subjects who were neither obese nor centrally-obese.

西格列汀联合二甲双胍治疗肥胖型2型糖尿病的疗效及对体脂含量情况分析

目的研究肥胖型2型糖尿病患者联合采用西格列汀、二甲双胍治疗的临床效果。方法选择2018年10月—2020年4月该院100例肥胖型2型糖尿病患者为研究对象,采用随机数表法分成常规组和治疗组,每组50例。常规组予二甲双胍治疗,治疗组予二甲双胍+西格列汀治疗。比较两组治疗效果、血糖指标、体脂含量、胰岛功能指标及不良反应。。结果两组治疗效果比较,差异有统计学意义(P<0.05)。治疗后常规组血糖指标高于治疗组,差异有统计学意义(t=8.183、4.828、18.158,P<0.05)。治疗后常规组体脂含量高于治疗组,差异有统计学意义(t=5.993、7.657、4.420,P<0.05)。治疗后两组胰岛功能比较,差异有统计学意义(t=5.898、5.283、16.033,P<0.05)。常规组不良反应总发生率低于治疗组,但差异无统计学意义(χ²=0.136,P=0.712)。结论西格列汀、二甲双胍联合治疗肥胖型2型糖尿病效果确切。