Dr. Ron’s Research Review – November 21, 2012

This week’s research review focuses on hypercholesterolemia and steroid deficiency.

In 2002, Dzugan proposed a new hypothesis of the etiology and pathogenesis of hypercholesterolemia. %. (Dzugan and Arnold Smith 2002)

They evaluated 20 patients with hypercholesterolemia who received hormonorestorative therapy (HT) with natural hormones. Hundred percent of patients responded.

Mean serum TC was 263.5 mg/dL before and 187.9 mg/dL after treatment.

Serum TC dropped below 200 mg/dL in 60.0%.

In 2011 they retrospectively analyzed 43 hypercholesterolemic patients treated with HT. HT therapy included a combination of several agents such as pregnenolone, dehydroepiandrosterone (DHEA), triestrogen, progesterone, testosterone, hydrocortisone, and vitamin D-3. (Dzugan, Rozakis et al. 2011)

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 31 women, 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.

Dr. Ron


Excerpts

HT is defined as a multi-hormonal therapy with the use of chemically identical formulas to human hormones (anthropo-identical) and is administered in physiologic ratios with dose schedules intended to simulate the natural human production cycle at optimal levels.

For restoration of estrogen, progesterone, and testosterone we utilize topical gels because they contain highly lipophilic molecules with low molecular weight, are very well absorbed through the skin, may use adipose tissue as a reservoir, and facilitate individualized dose of prescription.

The typical formulation for Triest gel (E3:E2:E1 – 90:7:3) was 1.25–2.5 mg/mL, progesterone 5–10% – 50–100 mg/mL, and testosterone 5–10% – 50–100mg/mL.

In cases of insufficient absorption with gel we utilized drops of Triest (E3:E2:E1 – 80:10:10) at 5mg/ml, progesterone at 50 mg/mL, and testosterone at 50 mg/mL.

Pregnenolone, DHEA, and hydrocortisone were used in oral form (capsules or tablets). The pregnenolone dose ranged from15 mg to 300 mg, DHEA from 15 mg to 200 mg, and hydrocortisone from 2.5 mg to 10 mg.

Vitamin D-3 was used in the doses that ranged from 1000 IU to 5000 IU.

Dosages were individually selected during HT to produce physiologic serum levels typical for healthy individuals between the age of 20 and 30 years for both genders

We administered hormones in doses sufficient to restore the optimal level that was defined as the level of hormones in the upper one third of normal range from the testing laboratory.


Articles

Correction of steroidopenia as a new method of hypercholesterolemia treatment

         (Dzugan, Rozakis et al. 2011) Download

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. MATERIAL AND 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.

Hypercholesterolemia treatment: a new hypothesis or just an accident?

            (Dzugan and Arnold Smith 2002) Download

A new hypothesis concerning the association of low levels of steroid hormones and hypercholesterolemia is proposed. This study presents data that concurrent restoration to youthful levels of multiple normally found steroid hormones is able to normalize or improve serum total cholesterol (TC). We evaluated 20 patients with hypercholesterolemia who received hormonorestorative therapy (HT) with natural hormones. Hundred percent of patients responded. Mean serum TC was 263.5 mg/dL before and 187.9 mg/dL after treatment. Serum TC dropped below 200 mg/dL in 60.0%. No morbidity or mortality related to HT was observed. In patients characterized by hypercholesterolemia and sub-youthful serum steroidal hormones, our findings support the hypothesis that hypercholesterolemia is a compensatory mechanism for life-cycle related down-regulation of steroid hormones, and that broadband steroid hormone restoration is associated with a substantial drop in serum TC in many patients.

References

Dzugan, S. A. and R. Arnold Smith (2002). "Hypercholesterolemia treatment: a new hypothesis or just an accident?" Med Hypotheses 59(6): 751-6.

Dzugan, S. A., G. W. Rozakis, et al. (2011). "Correction of steroidopenia as a new method of hypercholesterolemia treatment." Neuro Endocrinol Lett 32(1): 77-81.