Introduction
The present study aimed to examine the impact of age at menopause on the type 2 diabetes mellitus (T2DM) risk in postmenopausal women.
Material and methods
We included 4,968 postmenopausal women from the National Health and Nutrition Examination Survey 2011–2018. Age at menopause was measured by single year and categorically (< 40 years, 40–44 years, 45–54 years, 55 years and above). The outcome variable T2DM was measured with self-report and fasting blood glucose level. We performed logistic regression to estimate the odds ratio (OR) (95% confidence interval [CI]). Linear regression was used to examine the correlation between age at menopause and age at T2DM.
Results
Of the 4,968 postmenopausal women, 796 (16.0%) had T2DM after menopause. The mean age at menopause was 44.2 years. The mean age at T2DM was 57.2 years. Adjusting for potential confounders, the ORs for the association between age at menopause of < 40 years, 40–44 years and ≥ 55 years and T2DM were 1.97 (95% CI: 1.47–2.63), 1.27 (95% CI: 0.90–1.79) and 0.98 (95% CI: 0.66–1.45), respectively, compared to women having menopause at age 45 to 54 years. Each increase by 1 year in age at menopause was associated with a 3% reduction in the prevalence of T2DM (95% CI: 2–5). Age at menopause was significantly correlated with age at T2DM. Each 1-year increase in age at menopause might lead to a decrease of 0.39 years in age at T2DM.
Conclusions
Premature menopause was associated with increased T2DM risk in women. The earlier menopause occurs, the younger is the age at which T2DM may occur.
Introduction:
Previous studies have suggested an association between insulin resistance (IR) trajectories and adverse changes in cardiac structure and function in nondiabetic populations. We studied the associations between IR trajectories and incident heart failure (HF) and all-cause death in nondiabetic participants of the Atherosclerosis Risk in Communities (ARIC) study. We hypothesized that long-term moderate and high IR levels would increase the risk of incident HF and all-cause death.
Methods:
We included 7,835 participants (3,505 men and 4,330 women) aged 45-64 from the ARIC study without diabetes mellitus at any visit, and no history of prevalent HF, myocardial infarction, stroke, arterial or coronary surgery, or cancer at baseline. We estimated IR using Homeostatic Model Assessment-Insulin Resistance (HOMA-IR), triglyceride to high-density lipoprotein cholesterol ratio (TG/HDL-C), triglyceride glucose (TyG) index and metabolic score for IR (METS-IR). Serum insulin was not available at visits 2 and 3, so HOMA-IR was calculated for visits 1, 4, and 5. Latent class analysis identified two HOMA-IR trajectories, low-increasing and high-increasing, and three trajectories for TG/HDL-C, TyG index, and METS-IR: low-increasing, moderate-stable, and high-decreasing. We employed Cox proportional-hazards models to examine the associations of IR trajectories with incident HF and all-cause death adjusting for potential confounders.
Results:
Compared to participants in the low-increasing group, those in the high-increasing group of HOMA-IR were more likely to have incident HF and all-cause death (Table 1). For TG/HDL-C, TyG index and METS-IR, we found an increased risk of incident HF in the moderate-stable and high-decreasing groups relative to the low-increasing group. For all-cause death, consistent associations were found only in women (Table 1).
Conclusions:
Reduction of insulin resistance in nondiabetic individuals may be a suitable target for prevention strategies to reduce cardiovascular disease.
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