Sex differences in the association of vital exhaustion with regional fat deposition and subclinical cardiovascular disease risk.

OBJECTIVE: Vital exhaustion (VE) is more strongly associated with cardiovascular disease (CVD) risk for women than men. This study examined whether sex differences in associations of VE with CVD risk markers are accounted for by unique associations of VE with regional adiposity. METHODS: The study enrolled 143 persons (18-55 years) without diagnosed conditions. VE was assessed by the Maastricht questionnaire. CVD indices were measured using the euglycemic-hyperinsulinemia clamp, resting blood pressure, and blood draws. Regional adiposity was measured using computed tomography and 2-D echocardiography. This cross-sectional study employed a path analysis approach, including relevant covariates. RESULTS: Of the cohort, aged 38.7 ± 8.4 years, 65% were men, and 41% were obese. The final model had excellent fit (χ2(36) = 36.5, p = .45; RMSEA = 0.009, CFI = 0.999). For women, but not men, the model indicated paths from VE to: 1) lower insulin sensitivity (B = -0.10, p = .04), and higher total cholesterol to HDL ratio (B = 0.12, p = .09), triglycerides (B = 0.10, p = .08), and C-reactive protein (B = 0.08, p = .09) through visceral adiposity; 2) higher mean arterial pressure (B = 0.14, p = .04), lower insulin sensitivity (B = -0.09, p = .08), and higher C-reactive protein (B = 0.12, p = .07) through subcutaneous adiposity; 3) lower insulin sensitivity (B = -0.07, p = .08) and higher total cholesterol to HDL ratio (B = 0.16, p = .03) through liver adiposity; and 4) higher C-reactive protein (B = 0.08, p = .09) through epicardial adiposity. CONCLUSION: Results extend prior evidence by showing that the association of VE with CVD risk in women is linked with specific regional adiposity elevation. Further study of adiposity-related mechanisms in women who experience early decline in vitality may inform clinical targets for CVD prevention.

Association of cardiometabolic health factors with age-related executive function and episodic memory.

Although decline of cognitive abilities in late life is regarded as a common facet of aging, there is inter-individual variability in this decline. Possible contributors are cardiometabolic risk factors associated with cerebrovascular dysfunction, but a dearth in unifying health-cognition models confound exactly how these risk factors mediate age-related changes in executive function (EF) and episodic memory. This study investigated the indirect effect of age on these cognitive abilities via cardiometabolic risk factors using a structural equation modeling approach. Participants included 738 adults (64% female) ranging from 21 to 85 years of age (M = 47.47, SD = 18.28). An exploratory factor analysis was applied to an EF battery yielding a two-factor solution, consisting of inhibition and cognitive flexibility, that showed acceptable fit (χ2(48) = 101.84, p < .001, CFI = .980, RMSEA = .039, SRMR = .035). The EF latent factors were then included in a confirmatory factor analysis exploring the indirect role of age on episodic memory and EF via blood pressure, cholesterol, triglycerides and body mass index. The theoretical model demonstrated acceptable fit, χ2(108) = 204.071, p < .001, CFI = .972, RMSEA = .035, SRMR = .035. Blood pressure was associated with lower cognitive flexibility (ß = -.20, p < .001) and there was a significant indirect effect of age on episodic memory through cognitive flexibility (ß = .07, p = .021). Results support the "Executive Decline Hypothesis" of age-related episodic memory decline and specifically implicate lower blood pressure control and cognitive flexibility in these changes.