95; [95% CI: 1.11 to 3.39], p?<?0.001), whereas the prevalence of somatic symptoms did not significantly differ between menopausal groups. Prevalence was positively correlated with CES-D depression risk categories. Participants in the high risk group were more likely to experience VMS (OR: 3.01; [95% CI: 1.68 to 5.36]) and somatic symptoms (OR: 14.58; [95% CI: 3.36 to 63.27]) relative to participants who scored 15 or less on the CES-D. Table 2 displays the means and standard deviations of VMS and somatic symptoms according to menopausal and depressive symptomology status. The parameters of the mediation analyses are shown in Table 3a. The multiple regression model with covariates explained 11% of the variance in VMS scores as a function of depression and menopausal status (R2?=?0.11 [95% CI: <a href="http://en.wikipedia.org/wiki/Thalidomide
">Thalidomide 0.03 to 0.18]). The effect sizes of path a (Cohen's d?=?0.30) and path b (��2?=?0.04) were small according to conventional guidelines. There were fewer symptoms of depressed affect at post- than peri-menopause (a?=??0.41 [95% CI: ?0.87 to ?0.08]) and participants with elevated depressive symptoms tended to report more frequent VMS (b?=?0.06 [95% CI: 0.01 to 0.10]) holding Ixazomib nmr
the covariates constant at both paths and controlling for the effect of menopausal status at path b ( Table 3b). There was a direct effect of menopausal status on VMS (c��?=??0.15 [95% CI: ?0.30 to ?0.05]). The BCa CI of the indirect effect excluded zero and the point estimate indicated a reduction in the frequency of VMS through depression (ab?=??0.023 [95% CI: ?0.063 to ?0.002]). The indirect effect explained 3% of the maximum possible indirect effect based on the model without covariates (K2?=?0.033; SE?=?0.01 [95% CI: 0.006 to 0.075]). The multiple regression model with covariates explained 27% of variance in somatic symptom scores as a function of the antecedent and mediator variables (R2?=?0.27 [95% CI: 0.16 to 0.37]). The effect size at path b was large (��2?=?0.24) and the unstandardized coefficient indicated that somatic symptoms increased with depressive symptoms (b?=?0.08 [95% CI: 0.06 to 0.10]) controlling Selleckchem LY2835219
for the covariates and menopausal status. The BCa CI of the indirect effect excluded zero and indicated fewer somatic symptoms at post- relative to peri-menopause through depression scores (ab?=??0.03; SE?=?0.01 [95% CI: 0.069 to 0.005]). The indirect effect explained 8% of the maximum possible effect based on the proposed model without covariates (k2: 0.08 [95% CI: 0.01 to 0.15]). Menopausal symptoms may vary from peri- to post-menopause transition as an indirect function of depressive symptomatology and the present findings provide support for this hypothesis. From peri- to post-menopause, depressed affect mediated a decline in the frequency of VMS and somatic symptoms, controlling for the effects of income, parity, and tobacco use.