Low dose hydrophilic statins are the preferred agents for females at risk of osteoporosis

OBJECTIVES: The correlation between atherosclerosis and osteoporosis, independent of age, is clear. Multifactorial co-dependence between bone mineral density (BMD) and statin dose has been proposed. It is hypothesised that inhibition of the synthesis of cholesterol will also inhibit the synthesis of sex hormones and Vitamin D, negatively affecting BMD. This study aims to evaluate hydrophilic and non-hydrophilic statins effect on osteoporosis and analyse any possible superiority of one agent over the other within the group. METHODS: We identified 538 caucasian females who had a DEXA scan performed between 2002 and 2016 (age 60–89) in one DEXA center in Mid-West Ireland. A DEXA T-score results were analysed in the current study. Two hundred fifty females were not on statin therapy, and 323 females were on statin therapy. Females on therapy were separated into the atorvastatin group (N = 190), rosuvastatin group (N = 97), and pravastatin group (N = 36), comprising low dose and high dose groups. All anonymised data were analysed with SPSS statistical. To test the hypothesis that lower bone density is associated with high dose statins, an independent sample t-test was performed. The one-way between-groups ANOVA test was used to test the hypothesis that the BMD level depended on the statin's potency. RESULTS: Statin-naïve females have a statistically higher bone mineral density in the lumbar spine, t (538) = 3.42, p < 0.05 and in hip t (538) = 4.99, p < 0.05 than females on statin therapy. There was a significant difference in patient's age between the group, and no significant correlation was found between the patient's age and type of statin or bone density. In the atorvastatin group statistically, significant results were obtained both for spine and hip bone mineral density, t (188) = −5.61, p < 0.05 and t (188) = −3.62, p < 0.05, respectively. In the rosuvastatin group, statistically, a significant result was noted for bone mineral density of hip t (95) = −3.52, p < 0.05. This demonstrates a dose-dependency between bone mineral density and the dose of the statin. The independent between-group ANOVA yielded a statistically significant effect, F (2, 59) = 6.69, p < 0.05, η2 = 0.21 in the spine. Thus, patients on lipophilic statins had statistically lower BMD than females on hydrophilic statins. Multilinear regression analysis identified that age is not a statistically significant contributor in our analysis; however, the trend of decrease in bone mineral density with women's age is acknowledged by authors. CONCLUSIONS: The study results support the theory that bone mineral density decreases with an increase in a statin dose, and hydrophilic statins, like pravastatin, have a better metabolic profile in the lumbar spine than lipophilic agents.