Osteoporosis

Edward Lichten, M.D.,PC
555 South Old Woodward Suite #700
Birmingham, MI 48009 
248.593.9999

 

Muscle Wasting and
Generalized Strength
 Improves with Testosterone!

Excerpts of this material come from presentations from the 10th World Congress on Human Reproduction held on May 4-8, 1999 in Salvador, Bahia, Brazil. The opinions or views expressed do not necessarily reflect the recommendations of the UMDNJ Medical School who sponsored distribution of this materials.

Osteoporosis Video Testimonial


Osteoporosis in Women

 Few people know that half of the elderly females
who fracture their hip will die within 6 months!

That is why the prevention of osteoporosis is so important.

Few people know that anabolic steroids (testosterone, DHEA and human growth hormone) play the pivital role in overall well being in the postmenopausal woman. Although estrogen deficiency is recognized as a major risk factor for the development of osteoporosis, research is showing that anabolic steroids may be even more important in maintaining bone and muscle composition.

There are two processes involved in osteoporosis: bone formation and bone resorption. The problem with osteoporosis is that the bone is resorbed with calcium and structural integrity leached out of the bone while the process of reformation is slowed. In the young woman, these two opposite forces cancel each other out so the bone remains strong. In the pre-menopausal woman (over 40), there is gradual increase in resorption. If the woman is not active and not on estrogen replacement (including oral contraceptives), she may lose 15-20% of her bone density before the menopause. That is why pre-menopausal estrogen and anabolic steroid replacement is so important.

Lichten's Pearls

1. All women lose bone and muscle mass in their 40's.

2. May correlate loss of testosterone with loss of sex drive.

3. Testosterone replacement may be a bio-identical 1-4% cream applied sparingly daily.

4. Testosterone replacement may be 25-50mg of Testosterone Cyprionate intramuscular with 1cc B12 every 2 weeks.

5. Increased facial hair is natural at 40-60 due to shift in testosterone/ estradiol balance. Treat with spirolactone 50 - 100mg twice daily as it blocks conversion of testosterone to dihydro-testosterone.

 


Two recent studies[1,2] in aging men and women showed the levels of free testosterone and estradiol correlated directly with bone mineral density. Jassal [3] found that low bio-available testosterone was an independent predictor of height loss and subsequent vertebral fractures in postmenopausal women. And the Rancho Bernardo study [4] correlated not only estradiol (estrogen) but also testosterone and sex hormone binding globulin to subsequent loss in height. When low plasma values for testosterone were measured or suspected, there was significant correlation to documented height loss no matter whether the woman took estrogen or not.

What does this mean?
Those individuals with the lowest anabolic steroid level (testosterone, DHEA) have the most bone loss, fracture rate and muscle weakness.

C. Longcope [4] found that women who naturally produced more testosterone had less vertebral crush fractures than controls. The most important factor was blood levels.

How does testosterone affect bone? Testosterone not only spares bone it also stimulates the body to make more bone. And as testosterone has been shown to directly  build more muscle, the action of the muscle pulling on the bone is to make a stronger bone.

Research by Raisz [5] showed that the addition of small amounts of testosteroneincreased average bone formation by 50% over 3 months. All the measurements used for osteoporosis listed below were improved on testosterone:

Bone ResorptionBone Formation
deoxypyridinolineBSAP-bone specific alkaline phosphatase
pyridinolineC-terminal procollagen peptide
hydroxyprolineosteocalcin

The results of the study showed that the addition of a testosterone preparation to a menopausal woman's osteoporosis prevention program was 41% better than estrogen alone (relative to BSAP measurements). Not only does short term testosterone stimulate bone formation it does not lessen the benefit of estrogen on bone formation.

The Definitive Study
Davis[6] and colleagues investigated the effects of estrogen-androgen therapy on bone mineral density in a prospective, 2-year, single-blind trial in 34 menopausal women. Patients were randomized to receive either estradiol (50mg) pellets or estradiol (50mg) plus testosterone (50mg) pellets once every 3 months. Bone mineral density was assessed using dual-energy x-ray absorptometry. Both treatment groups had significant increases in total body, lumbar vertebrae (L1-L4) and hip bone mineral density compared with baseline values. There was a trend for a more rapid increase in bone mineral density in patients receiving estrogen-androgen therapy In addition, these patients also experienced a significantly greater increase in total body (P<0.008). vertebral L1-L4 (P<0.001), and trochanteric (P<0.005) mineral density compared with estradiol alone. Davis et al. concluded that estrogen-androgen, given as implanted pellets, was more effective in increasing bone mineral density in the hip and lumbar spine than estradiol alone.

Treatments with oral estrogen and testosterone are not as effective as implanted pellets
Two other randomized, double-blind studies concluded that androgen therapy was of value to the menopausal women. Watts[7] evaluated oral estrogen (1.25 mg conjugated esterified estrogen) with 2.5 mg methyl-testosterone with 1500 mg of calcium daily. With estrogen and androgen there was a significant increase in bone density of the lumbar spine after 12 and 24 months (P<0.001). Placebo and estrogen only were not significantly different. The authors concluded that bone density of the hip and lumbars increase significantly with estrogen-androgen supplementation.

Barrett-Connor [8] came to the identical conclusion in her study of 291 women with surgical menopause. At the end of the 2-year study, she reported that women receiving the higher dose of estrogen-androgen had a 4.3% and 3.5% increase from baseline in lumbar spine and total hip. The higher dose schedule of estrogen was not able to do half as well.

Testosterone, women and heart disease
Few data exist on the effects of testosterone on the development of coronary artery disease in women. The studies that examined the role of testosterone for these individuals have yielded conflicting results. Phillips [9] measured estradiol. testosterone, insulin, SHBG, DHEA-S, and risk factors for myocardial infarction in a group of 60 post-menopausal women undergoing coronary angiography. The authors found an association between elevated testosterone (P<0.008) and cholesterol (P<0.01) levels and the development of coronary artery disease. This association was also seen in a subset of 49 postmenopausal women who had no history of a myocardial infarction (P<0.05).

In a larger analysis using data from the Rancho Bernardo study, Barrett-Connor and Goodman-Gruen[10] prospectively examined the association between androstenedione, total and bio-available testosterone, estrone, and total and bio-available estradiol concentrations and the risk of death from cardiovascular and ischemic heart disease. Data were collected over a 19-year period from 651 postmenopausal women, none of whom were undergoing hormone replacement therapy. Follow-up during this time was 99.9%. Age-adjusted concentration of sex hormones did not differ significantly in women with and without a history of heart diseas at baseline and did not predict cardiovascular death or death from ischemic heart disease. In addition, estrogen concentrations were not associated with significantly more favorable risk factors for heart disease, and testosterone was not associated with less favorable risk factors. However, they were not priveleged to see Dr. Lichten's data which showed that the duration on Estrogen not the level was directly related to lowering insulin and decrease in heart disease. Based on the results of Barrett-Connor's study, the data do not support either a causal or preventive role for androgens and cardivoascular mortality in older women.

Androgens are Necessary for Muscle Building and to Prevent Wasting States
Work with patients with AIDs and wasting states established that no compound maintains muscle mass and weight as well as testosterone. Because of the toxicity of oral methyl-testosterone, other preparations have been used. The Androderm CIII patch delivers too little testosterone to be effective for the male and too much for the female. Testosterone injections weekly or bimonthly for months rarely results in scar formation and induration in the buttocks. We find that the testosterone pellets given every 2 months and the new form of testosterone pellets that lasts for months results in significantly less scar formation and induration.

Testosterone has been used for 40 years to build muscle. Small amounts such as the 50mg to 100mg testosterone pellet are very useful for the menopausal woman. It is a fact that the number one reason a man or woman enters a nursing home is because he or she is too weak to get out of a chair or off the toilet. With our ability to monitor patients, there is no contraindication for testosterone in the menopausal woman who is considering her future needs.

Men:
Men suffer from muscle wasting and osteoporosis, just less often than the female. The measurement of total testosterone and its division by sex hormone binding globulin should be .7 to 1.0 (both measurements in pmol/L). When the ratio falls below 0.5, the individual is at great risk for the development of hyper-insulinemia: obesity, heart disease, diabetes, high blood pressure and lipid abnormalities. The low testosterone results in loss of muscle and the loss of muscle results in thinner ligaments and bone osteoporosis. Men should consider testosterone laboratory testing at 40, 45 and every 2 years after 50. More than 60% of men at 50 will need testosterone replacement. See testosterone replacement.

References:

  1. Khosla S, Melton J, Atkinson EJ, et al. Relationship of serum sex steroid levels and bone turnover markers with bone mineral density in men and women. Journal of Clinical Endocrinology & Metabolism 1998;83:2266-2274.
  2. Ettinger B, Pressman A, Skarin P, et al. Associations between low leels of serum estradiol, bone density, and fractures among elderly women: the study of osteoporotic fractures. Journal of Clinical Endocrinology & Metabolism 1998;83:2239-2243.
  3. Jassal SK, Barrett-Connor E, Edelstein SL. Low bioavailable testosterone levels predict future height loss in postmenopausal women. Journal of Bone Mineral Research 1995;10:650-654.
  4. Longcope C, Baker RS, Hui SL, Johnston CC JR. Androgen and estrogen dynamics in women with vetebral crush. Maturitas 1984;6:309-318.
  5. Raisz L, Wiita B, Arthis A, et al. Comparison of the effects of estrogen alone and estrogen plus androgen on biochemical markers of bone formation and resorption in postmenopausal women. Journal of Clinical Endocrinology & Metabolism 1996;81:37-43.
  6. Davis SR, McCloud P, Strauss BH, Burger H. Testosterone enhances estradil's effects on postmenopausal bone density and sexuality. Maturitas 1995;21:227-236.
  7. Watts NB, Notelovitz M, Timmons MC, Addison WA, Wiita B, Downing LJ. Comparison of oral estrogens and estrogens plus adrogen on bone mnieral density, menopausal symptoms, and lipid-lipoprotein profiles in surgical menopause. Obstet Gynecology 1995;85:529-537.
  8. Barrett-Connor E, Timmons C, Young R, Wiita B, and the Estratest Working Group. Interim safety analysis of a two-year study comparing oral estrogen-androgen and conjuated estrogens in surgical menopausal women. Journal of Womens Health 1996;5:593-602.
  9. Phillips GB, Pinkernell BH, Jing TY. Relationship between serum sex hormones and coronary artery disease in postmenopausal women. Arteriosclerosis & Thrombosis 1997;17:695-701.
  10. Barrett-Connor E, Goodman-Gruen D. Prospective study of endogenous sex hormones and fatal cardiovascular disease in postmenopausal women. British Medical Journal 1995;311:1193-1196.


The information in this newsletter does not dictate an exclusive course of treatment or procedure to be followed and should not be construed as excluding other acceptable methods of practice.

 
 
Revised: November 10, 2008