Benzodiazepines may influence neurosteroid metabolism by virtue of their actions on translocator protein (TSPO; "peripheral benzodiazepine receptor").  The pharmacological actions of benzodiazepines at the GABA A receptor are similar to those of neurosteroids . Factors which affect the ability of individual benzodiazepines to alter neurosteroid levels may depend upon whether the individual benzodiazepine drug interacts with TSPO. Some benzodiazepines may also inhibit neurosteroidogenic enzymes reducing neurosteroid synthesis. 
While there has been no definite information published as to who should not take pregnenolone, on theoretical grounds, a few cautions can be suggested. Since pregnenolone (especially at high doses) may (in some people) increase estrogen or testosterone levels, I believe that men with prostate cancer (which may be worsened by testosterone) and women with breast or ovarian cancer (which may be worsened by estrogen) should probably take pregnenolone only with their doctors consent and supervision. Men with high PSA (prostate specific antigen) blood levels (possible indicator for undiagnosed or future prostate cancer) should also proceed with caution with pregnenolone use. Lastly, because of pregnenolones anti-GABA, pro-NMDA action, persons known to suffer from epileptic seizures or who are taking an anti-seizure medication such as Dilantin, Depakote or Tegretol should probably only use pregnenolone with their doctors supervision. Finally, as we age, the body produces ever-less of the enzyme which converts pregnenolone to DHEA. Thus, while supplementary pregnenolone taken during middle age and beyond will produce at least some normalization back toward more youthful (and healthful) levels of other steroid hormones, pregnenolone will not completely substitute for other steroid hormone supplements in those with medically demonstrated needs for various specific steroids ., DHEA, cortisol, estrogen, etc.
First, the normality of data was assessed using a Shapiro-Wilk test. Then, levels of hormones were compared between cases and controls using a matched paired -test or Wilcoxon test as appropriate. We also ran exploratory correlation analyses (Pearson’s or Spearman’s rho, as appropriate) to examine the associations between hormonal levels and other factors, including the severity of symptoms. If significant associations were detected, we subsequently adjusted for the severity of other symptom dimensions in multiple linear regression models to account for their potential confounding effect [ 7 ]. SPSS was used for all analyses.