Previous studies demonstrated associations of endogenous sex hormones with diabetes. Less is known about their dynamic relationship with diabetes progression through different stages of the disease, independence of associations, and role of the hypothalamic-pituitary gonadal axis. The purpose of this analysis was to examine relationships of endogenous sex hormones with incident diabetes, prediabetes and diabetes traits in 693 postmenopausal women and 1,015 men aged 45-74 without diabetes at baseline participating in the Hispanic Community Health Study/Study of Latinos and followed six years. Baseline hormones included estradiol, luteinizing hormone (LH), follicle stimulating hormone (FSH), sex hormone-binding globulin (SHBG), dehydroepiandrosterone sulfate (DHEAS), and in men, testosterone and bioavailable testosterone. Associations were analyzed using multivariable Poison and linear regressions. In men, testosterone was inversely associated with conversion from prediabetes to diabetes (incidence rate ratio (IRR) for 1 SD increase in testosterone: 0.821; 95% CI 0.676, 0.997; p = 0.046), but not conversion from normoglycemia to prediabetes. Estradiol was positively associated with increase in fasting insulin and homeostatic model assessment of insulin resistance (HOMA-IR). In women, SHBG was inversely associated with change in glycosylated hemoglobin (HbA1c), post load glucose and conversion from prediabetes to diabetes (IRR = 0.62; 95% CI 0.44, 0.86, p = 0.005) but not from normoglycemia to prediabetes. Relationships with other hormones varied across glycemic measures. Stronger associations of testosterone and SHBG with transition from prediabetes to diabetes than from normoglycemic to prediabetes suggest they are operative at later stages of diabetes development. Biologic pathways by which sex hormones affect glucose homeostasis await future studies.

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Background: Surveillance systems rely on death records to monitor the most severe outcome of the opioid epidemic. However, few studies have linked data from hospital systems with death records to determine potential undercount of opioid-involved deaths occurring in hospitals. This study describes characteristics of decedents less likely to have an autopsy following an opioid-involved death in hospitals and estimates the resulting undercount. Methods: A probabilistic data linkage of hospital and medical examiner data involving 4,936 opioid-involved deaths among residents of Cook County, Illinois, US from 2016 to 2019. We included only hospital deaths that met a national case definition and presented with clinical signs of opioid overdose. Results: Decedents had higher odds of not having an autopsy if they were 50+ years, admitted to the hospital (aOR = 3.7: 2.1, 6.5), hospitalized for 4+ days (aOR = 2.2: 1.5, 3.1), and had a comorbid diagnosis of malignant cancer (aOR = 4.3: 1.8, 10.1). However, decedents exposed to heroin and synthetic opioids (aOR = 0.39: 0.28, 0.55), and concurrent exposure to stimulants (aOR = 0.44: 0.31, 0.64) were more likely to have an autopsy). Compared to estimates from the US Centers for Disease Control and Prevention (CDC), we observed undercounts of opioid overdose deaths ranging from 6% to 15%. Conclusions: Surveillance systems may undercount decedents that do not meet the typical profile of those more likely to have an autopsy, particularly older patients with chronic health conditions. Our undercount estimate likely exists in addition to the estimated 20%-40% undercount reported elsewhere. See video abstract at, http://links.lww.com/EDE/B990.