CONCLUSION Estrogen with an osteoblast P4R-acting progestin ( EPT ) in these five published RCT provides Level 1 evidence that MPA caused significantly greater annual percent spinal BMD gains than the same dose of ET .
OBJECTIVE To assess whether progesterone ( P4 ) or osteoblast P4 receptor-acting progestin ( P ) contributed to estrogen ( E ) therapy-related  increased areal bone mineral density ( BMD ) in r and omized controlled trials ( RCT ) with direct r and omization to estrogen ( ET ) or estrogen-progestin ( EPT ) therapy .
Progesterone Therapy, Endothelial Function and Cardiovascular Risk Factors: A 3-Month Randomized, Placebo-Controlled Trial in Healthy Early Postmenopausal Women
Background Progesterone is effective treatment for hot flushes/night sweats . The cardiovascular effects of progesterone therapy are unknown but evidence suggests that premenopausal normal estradiol with also normal progesterone levels may provide later cardiovascular protection . We compared the effects of progesterone to placebo on endothelial function , weight , blood pressure , metabolism , lipids , inflammation and coagulation . Methods and Results We conducted a r and omized , double-blind , 3-month placebo-controlled trial of progesterone ( 300 mg daily ) among 133 healthy postmenopausal women in Vancouver , Canada from 2003–2009 . Endothelial function by venous occlusion plethysmography was a planned primary outcome . Enrolled women were 1–11 y since last menstruation , not using hormones ( for > 6 months ) , non-smoking , without diabetes , hypertension , heart disease or their medications . R and omized ( 1∶1 ) women ( 55±4 years , body mass index 25±3 ) initially had normal blood pressure , fasting lipid , glucose and electrocardiogram results . Endothelial function ( % forearm blood flow above saline ) was not changed with progesterone ( 487±189 % , n = 18 ) compared with placebo ( 408±278 % , n = 16 ) ( 95 % CI diff [ −74 to 232 ] , P = 0.30 ) .  Progesterone ( n = 65 ) and placebo ( n = 47 ) groups had similar changes in systolic and diastolic blood pressure , resting heart rate , weight , body mass index , waist circumference , total cholesterol , low-density lipoprotein cholesterol and triglyceride levels . High-density lipoprotein was lower ( −0.14 mmol/L , P = 0.001 ) on progesterone compared with placebo . Fasting glucose , hs-C-reactive protein , albumin and D-dimer changes were all comparable to  placebo . Framingham General Cardiovascular Risk Profile scores were initially low and remained low with progesterone therapy and not statistically different from placebo . Conclusions Results indicate that progesterone has short-term cardiovascular safety . Endothelial function , weight , blood pressure , waist circumference , inflammation and coagulation were unchanged as were lipids except for HDL-C. The statistically significant decrease in HDL-C levels was not clinical ly important ( based on lack of Cardiovascular Risk Profile change ) . Trial Registration Clinical Trials.gov
CONCLUSION Estrogen with an osteoblast P4R-acting progestin ( EPT ) in these five published RCT provides Level 1 evidence that MPA caused significantly greater annual percent spinal BMD gains than the same dose of ET .
OBJECTIVE To assess whether progesterone ( P4 ) or osteoblast P4 receptor-acting progestin ( P ) contributed to estrogen ( E ) therapy-related  increased areal bone mineral density ( BMD ) in r and omized controlled trials ( RCT ) with direct r and omization to estrogen ( ET ) or estrogen-progestin ( EPT ) therapy .