title: Correction of steroidopenia as a new method of hypercholesterolemia treatment.
abstract: OBJECTIVE
  In 2002 we proposed a new hypothesis of the etiology and pathogenesis of hypercholesterolemia. There is paucity of information in the literature regarding the association of steroidopenia and hypercholesterolemia. Our goal is to determine if the treatment of steroidopenia with hormonorestorative therapy (HT) to youthful levels will normalize total cholesterol (TC) levels.
  
  
  METHODS
  We retrospectively analyzed 43 hypercholesterolemic patients treated with HT. Laboratory workup included lipid profile, serum pregnenolone, dehydroepiandrosterone sulfate (DHEA-S), progesterone, total estrogen, cortisol, total testosterone, and vitamin D-3 levels at presentation with follow up ranging from 3 to 9 months. HT therapy included a combination of several agents such as pregnenolone, dehydroepiandrosterone (DHEA), triestrogen, progesterone, testosterone, hydrocortisone, and vitamin D-3.
  
  
  RESULTS
  HT lowered mean TC from 228.8 mg/dL to 183.7 mg/dL (19.7%) (p<0.05) in all patients. In 12 men of mean age 58, HT statistically significantly lowered TC from 227.9 mg/dL to 177.1 mg/dL (22.3%) (p<0.05). Apparently it did so mostly by lowering LDL and triglycerides (TRG) while HDL did not appreciably change. In 31women, mean age 57, TC declined from 229.2 mg/dL to 186.3 mg/dL (19%) (p<0.05). HDL, LDL, and TRG are also decreased to a statistically significant degree. These results were associated with statistically significant elevations in pregnenolone, DHEA Sulfate, testosterone, progesterone but not total estrogen, cortisol or vitamin D-3 changes in both men and women.
  
  
  CONCLUSIONS
  We conclude that correction of steroidopenia with the use of hormonorestorative therapy is an effective strategy for normalizing and maintaining cholesterol homeostasis.
authors.affiliation: Dzugan Institute of Restorative Medicine, Deerfield Beach, FL 33442, USA. dzugan@yahoo.com
authors.forename: Sergey A
authors.initials: SA
authors.lastname: Dzugan
authors.forename: George W
authors.initials: GW
authors.lastname: Rozakis
authors.forename: Konstantine S
authors.initials: KS
authors.lastname: Dzugan
authors.forename: Less
authors.initials: L
authors.lastname: Emhof
authors.forename: Sergey S
authors.initials: SS
authors.lastname: Dzugan
authors.forename: Constantinos
authors.initials: C
authors.lastname: Xydas
authors.forename: Christos
authors.initials: C
authors.lastname: Michaelides
authors.forename: Janet
authors.initials: J
authors.lastname: Chene
authors.forename: Michael
authors.initials: M
authors.lastname: Medvedovsky
mesh_terms: D002762:Cholecalciferol / Q000097:blood / Q000172:deficiency; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood / Q000378:metabolism; D004967:Estrogens / Q000097:blood / Q000172:deficiency; D005260:Female; D020249:Hormone Replacement Therapy / Q000379:methods*; D006728:Hormones / Q000097:blood* / Q000172:deficiency*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood / Q000172:deficiency; D006937:Hypercholesterolemia / Q000097:blood / Q000188:drug therapy*; D007006:Hypogonadism / Q000097:blood / Q000188:drug therapy*; D008049:Lipase / Q000097:blood; D008297:Male; D008875:Middle Aged; D011284:Pregnenolone / Q000097:blood / Q000172:deficiency; D011374:Progesterone / Q000097:blood / Q000172:deficiency; D012189:Retrospective Studies; D013739:Testosterone / Q000097:blood / Q000172:deficiency
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D004967:Estrogens; D006728:Hormones; D002762:Cholecalciferol; D013739:Testosterone; D011374:Progesterone; D019314:Dehydroepiandrosterone Sulfate; D011284:Pregnenolone; D008049:Lipase; D006854:Hydrocortisone