National Center for Chronic Disease Prevention and Health Promotion

PurposeTo assess the association of sustained obesity with medical expenditures and risk of hospitalization over time.DesignRetrospective cohort study.SettingThis study used linked data from ambulatory electronic medical records and medical claims.SampleAdults aged 17-64years with (1) continuous enrollment in an insurance plan and (2) weight measured each year over ≥5 calendar years during 2013-2020.MeasuresOutcome variables were annual medical expenditures and annual risk of hospitalization. Covariates included sustained obesity or sustained severe obesity (reference: sustained healthy weight), year, age, sex, race, and US Census region.AnalysisGeneralized estimating equations were used to assess how excess costs and risk of hospitalization increased with sustained obesity or severe obesity over 8years.ResultsObesity-associated excess expenditures grew from $1105 or 20% in year 1 to $5229 or 49% in year 8. The relative risk of hospitalization grew from 13% in year 1 to 159% in year 8 among persons with sustained obesity (versus those with sustained healthy weight). Differences were higher for those with severe obesity, and higher among females (compared to males) and those aged 40-64years (compared to those aged 17-39years).ConclusionsThis study's findings provide evidence of a compounding effect of sustained obesity on medical expenditures and hospitalization risk over time. These findings underscore the importance of efforts that promote and support healthy lifestyles, including community access to healthy foods and physical activity for all.

The constituents of tobacco smoke that specifically contribute to lung cancer risk have yet to be fully identified. We evaluated associations between biomarkers of potentially harmful constituents-polycyclic aromatic hydrocarbons (PAHs), tobacco-specific nitrosamines (TSNAs), nicotine, and volatile organic compounds (VOCs)-and lung cancer incidence among US women. In a case-cohort study nested within the Sister Study (women aged 35 to 74 years at baseline, enrolled 2003 to 2009), data were obtained for a random subcohort and all remaining incident lung cancers through September 2017 (median follow-up 9.6 years), stratified by race and ethnicity (Hispanic, non-Hispanic Black, non-Hispanic White, others) and smoking status (current, former, never). The analytic sample included 356 cases and 433 non-cases. We quantified 30 biomarkers in baseline urine samples and calculated hazard ratios (HRs) for associations between one-unit increase in biomarker concentrations (log-scale) and lung cancer incidence using weighted Cox regression models adjusted for urinary creatinine and demographic, health, and lifestyle factors. Among women who were currently smoking at enrolment, positive associations were observed for biomarkers of PAHs (naphthalene, phenanthrene, pyrene, fluorene; HRs 1.4 to 5.3), TSNAs (particularly 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK); HRs : 1.3-2.2), and VOCs (xylene, acrylamide, acrylonitrile, 1,2-dibromoethane/vinyl-chloride/ethylene-oxide/acrylonitrile, acrolein, styrene/ethylbenzene, benzene, dimethylformamide/methylisocyanate, 1,3-butadiene, crotonaldehyde, isoprene; HRs : 1.6-4.4). Associations with biomarkers of most PAHs, NNK, xylene, and dimethylformamide/methylisocyanate remained after additional adjustment for smoking frequency, duration, and nicotine metabolites. In women who did not smoke, positive associations were observed for styrene/ethylbenzene and dimethylformamide/methylisocyanate biomarkers. Exposure to PAHs, TSNAs and several VOCs through tobacco smoking were associated with increased lung cancer risk among women.

Public health programs may benefit from demonstrating the value of their allocated resources and funds in addition to program outcomes and impacts. Resources for funding are scarce and competitive. Program implementers and program decision makers can consider economic evaluations to demonstrate the value of resources used to deliver an intervention. Results of economic evaluation may be used by programs to assess effectiveness, sustainability, and make decisions about different approaches to a prevention program. While economic evaluations include several different analyses, they all require a program cost analysis. Conducting a program cost analysis accounts for the direct as well as the often overlooked indirect costs (e.g. donated materials or volunteer time) required for implementation. Programs may attempt to estimate program costs for budgeting purposes, however budgetary information does not completely account for the full cost of implementing a program. An evaluation-oriented cost analysis is more appropriate as it allows for estimations of expected annual funding, comparisons across intervention sites, and cost per person served, among other benefits. The aim of this presentation is to provide public health practitioners and implementers of public health programs an overview of how incorporating cost analyses into broader program evaluations may provide a fuller understanding of the intervention and its impact. This presentation will first provide a brief overview of economic evaluations, then describe key principles in cost analyses such as type of resources to account for, perspective of the analysis, and key calculations and terms in quantifying costs. Finally, we will highlight publicly available resources related to cost analyses.

Dysregulated autophagy contributes to liver steatosis, yet its regulation under distinct metabolic contexts remains poorly defined. Here, we identify bile acids (BAs) as critical modulators of hepatic autophagy. Circulating BA levels are elevated in human subjects with liver steatosis and independently associated with increased hepatic steatosis risk. High-fat diet (HFD) feeding increases circulating BA levels, while simultaneously reducing hepatic autophagic flux in mice, whereas pharmacological inhibition of farnesoid X receptor (FXR) enhances autophagy and alleviates steatosis in the livers of HFD-fed mice. Mechanistically, circulating BAs promote hepatic acetyl-CoA production through FXR-induced acyl-CoA oxidase 1 (ACOX1), which in turn suppresses autophagy by increasing the mechanistic target of rapamycin complex 1 (mTORC1) signaling. Similar to HFD feeding, prolonged fasting elevates BA levels and hepatic lipid accumulation, while concurrently upregulating hepatic miR-378, a positive regulator of BA synthesis. Although miR-378 exerts a cell-autonomous pro-autophagic effect during short-term fasting, it paradoxically drives lipid accumulation by suppressing hepatic autophagy via BA/FXR/ACOX1/acetyl-CoA axis in a non-cell-autonomous manner during either HFD feeding or prolonged fasting when BA action becomes considerable. Together, our study uncovers BAs as a previously unrecognized class of inhibitors of hepatic autophagy during prolonged fasting and in metabolic dysfunction-associated steatotic liver disease (MASLD), providing novel insights into context-dependent autophagic regulation of hepatic lipid metabolism and potential therapeutic strategies for MASLD.

Preventing Chronic Disease (PCD) is a peer-reviewed electronic journal established by the National Center for Chronic Disease Prevention and Health Promotion. PCD provides an open exchange of information and knowledge among researchers, practitioners, policy makers, and others who strive to improve the health of the public through chronic disease prevention.

Despite the ongoing youth mental health crisis and reports of spiking eating disorder rates, especially in rural and underserved areas, epidemiologic data on these patterns remain scarce. To help address this gap, the objectives of our study were to document the prevalence of key disordered eating behaviors in a representative sample of youth from Alaska (a state with a vast geographic area and significant rural and remote populations), examine differences across sociodemographic subgroups, and identify mental health correlates. Participants were those from the 2023 Alaska Youth Risk Behavior Survey, a cross-section of traditional (n = 1129) and alternative (n = 418) high school students in grades 9-12. We estimated weighted proportions of youth reporting past-month binge eating or unhealthy weight control behaviors (UWCBs), overall and by grade, sex/gender, race/ethnicity, and weight status; we then fit a series of logistic models to quantify associations between each outcome and indicators of mental distress and substance use. Approximately one-half of Alaska youth engaged in disordered eating in 2023, with female youth, racial/ethnic minority youth, and youth of higher weight status having inequitably higher prevalence. Youth who reported depression, anxiety, suicide ideation or attempts, alcohol use, e-cigarette use, or other substance misuse had significantly higher odds of both binge eating and UWCBs; conversely, cigarette use was not associated with either outcome. These findings collectively underscore the urgent need to include eating disorders within broader conversations regarding the ongoing youth mental health crisis, especially as it pertains to impacts on rural areas of the US. Ongoing surveillance at the state and federal levels, enhanced screening, and large-scale prevention efforts are warranted to address this growing public health threat.