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Category: Basic Sciences/Biologics; Ankle; Diabetes; Midfoot/Forefoot Introduction/Purpose: Charcot neuropathic arthropathy (CNA) is a debilitating, rapidly destructive degenerative joint disease that occurs in diabetic, neuropathic midfoot. Clinicoradiologic assessment for CNA previously relied on Eichenholtz Stage. There is limited data on CNA histopathology. The goal of this study was to independently develop a histopathologic scoring system for Charcot neuropathic arthropathy. Methods: Retrieval of surgical pathology specimens from neuroarthropathic CNA patients (2012-2019) were analyzed to evaluate joint soft tissue and bone. Considering progression from large to small periarticular bone fragments to resolution, we devised and applied a CNA FEMASK-score (named after coauthors): 0= intraneural arteriolosclerosis; 1= large bone fragments without host histiocytic response; 2= mixed bone fragments with host histiocytic response; 3= small minute bone spicules resorption to fibrosis. Clinical modified Eichenholtz staging and outcome were then compared the CNA FEMASK-score to assess for associations between these three elements. Results: Forty-eight cases of CNA included 34 males and 14 females, mean age 60.3 and age range 28-83 years, with clinical diabetes mellitus (predominantly Type II) and longstanding neuropathy. Elevated HbA1C, Eichenholtz stage, American Society of Anesthesia score, and Charlson comorbidity index were predictive of amputation. Pathologic specimens varied from fixation tissue to amputation. In addition to neurotraumatic, neurovascular and inflammatory findings, a distinctive intraneural hyalinized arteriolosclerosis was observed. FEMASK-scores:1 = 10%, 2= 58%, and 3=32%. FEMASK-score comparisons were 98% accurate compared with the modified Eichenholtz criteria scores of each patient and 98% reproducible among pathologists. FEMASK 2 and 3 correlates strongly with amputation. Conclusion: Our novel CNA FEMASK-score classification, derived from the largest cohort of diabetic neuropathic specimens, is reproducible, explains pathophysiology, correlates with Eichenholtz, and predicts amputation. The unique intraneural vasculopathy observed contributes to CNA etiology.

Introduction: Worksites are promising venues for promoting health, given considerable time spent at work and opportunities for environmental change. Yet, the impact of worksite wellness programs (WWPs) on diet and adiposity, as well as the most relevant WWP components, are not established. Methods: Following MOOSE and PRISMA guidelines, we conducted a systematic review and meta-analysis of the impact of multi-component WWP trials (RCT or quasi-experimental) on diet and adiposity. Data were extracted in duplicate and pooled using inverse variance random effects meta-analysis. Pre-specified sources of heterogeneity (study design, world region, worksite type, duration, WWP components) were analyzed by meta-regression and subgroup analysis. Funnel plots, Begg’s, and Egger’s tests evaluated potential publication bias. Results: From 6612 abstracts, we identified 48 studies assessing WWPs and diet or adiposity. Most were in the US (54%) or Europe (23%), with diet (64%) and exercise/weight loss (20%) as main targets. Intervention components were variable (Figure). Most common outcomes were intakes of fruits and vegetables (F&V) (19 studies), total fat or fat subtypes (18), and dietary fiber (4); and BMI (35) and waist circumference (WC) (10). Median duration was 12 months (range: 1-48 mo). In pooled analyses, WWP increased intake of F&V, especially fruits (Figure). Significant effects were not identified for dietary fiber, total fat, or fat subtypes. WWP also reduced BMI (Figure) and WC (-2.03 cm, 95% CI:-3.88,-0.20). Trial duration significantly modified effects on BMI (2 ; 12+ mo: -0.16 kg/m 2 ; P-interaction=0.046); but not WC or F&V intake. Additional findings for heterogeneity, including WWP components, and publication bias will be presented. Conclusions: These novel findings support effectiveness of WWP for increasing F&V and reducing BMI and WC.

Background: Because long-term weight gain typically occurs insidiously (~1 lb/y) it is very difficult to study in RCTs and prospective cohorts provide crucial evidence on its key contributors. Most prior studies have evaluated how baseline diet, rather than change in diet that may be more physiologically relevant, relates to future weight gain. Aim: To evaluate and compare different methodological approaches for investigating how diet relates to long-term weight gain. Methods: Participants from 3 separate cohorts, the Nurses Health Study (NHS, n=50,422), Nurses Health Study II (NHS II, n=47,898), and the Health Professionals Follow-up Study (HPFS, n=22,557), free of obesity and chronic diseases at baseline, were included and followed for up to 20 y. Lifestyle, health status, and weight were assessed by questionnaires every 2 y, and diet by validated FFQ every 4 y. We assessed 3 different analytic approaches, including relations of 1) baseline diet at the start of each 4 y with weight change in the next 4 y; 2) 4-y change in diet with weight change in the same 4 y; and 3) 4-y change in diet with lagged weight change in the next 4 y. We compared these approaches evaluating consistency across cohorts, magnitudes of associations, and biological plausibility of findings. Results: Across the three methods, consistent, robust, and biologically plausible associations were only seen between changes in diet and changes in weight in the same 4 y (Figure). Findings evaluating baseline diet and lagged dietary change were less consistent across cohorts, far smaller in magnitude, and often not biologically plausible, suggesting presence of both bias and misclassification of the true relevant dietary metric. Conclusions: The methods used to analyze dietary habits and long-term weight gain are crucial. The most robust, biologically relevant, and consistent findings are seen when evaluating dietary change and weight change in discrete periods.

Poor diet is the leading cause of cardiovascular disease in the USA and globally. Evidence-based policies are crucial to improve diet and population health. We reviewed the effectiveness for a range of policy levers to alter diet and diet-related risk factors. We identified evidence to support benefits of focused mass media campaigns (especially for fruits, vegetables, salt), food pricing strategies (both subsidies and taxation, with stronger effects at lower income levels), school procurement policies (for increasing healthful or reducing unhealthful choices), and worksite wellness programs (especially when comprehensive and multicomponent). Evidence was inconclusive for food and menu labeling (for consumer or industry behavior) and changes in local built environment (e.g., availability or accessibility of supermarkets, fast food outlets). We found little empiric evidence evaluating marketing restrictions, although broad principles and large resources spent on marketing suggest utility. Widespread implementation and evaluation of evidence-based policy strategies, with further research on other strategies with mixed/limited evidence, are essential "population medicine" to reduce health and economic burdens and inequities of diet-related illness worldwide.