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BioTE HRT/BHRT MetaAnalysis
Introduction
Hormone replacement therapy (HRT) is used to treat menopausal symptoms in women. Most women who take HRT for menopausal reasons are given an estrogen/progesterone combination, except those who have had a hysterectomy, as they do not need progesterone. HRT has shown to improve muscle function, lower mortality in younger postmenopausal women and protect against brain aneurysms. Data suggests that estrogen, in particular, can decrease the risk of heart disease when taken early in postmenopausal years.1 HRT (testosterone) is also prescribed to a growing number of men to reverse the gradual age-related decline of testosterone.2 Use of hormone therapy changed when the 2002 Women’s Health Initiative3, a 15 year investigation that was stopped three years early when a preliminary review of the data showed that women taking the combination of estrogen and progesterin had a higher rate of breast cancer, heart disease and stroke.4 Based on these findings and the concern about health risks attributed to hormone therapy, doctors became less likely to prescribe it.5 However, a recent 2011 study found a slightly lower risk of breast cancer and no significant increase risk of heart disease, blood clots, stroke or early death among women taking estrogen only compared with women with hysterectomies who took placebo.6 Doctors, in the meantime, started to prescribe bioidentical hormone therapy (BHRT). Bioidentical hormone therapy (BHRT) is a compound that is identical to the natural molecules that the body produces. The term does not indicate the source of the hormone, but refers to the chemical structure. In addition, BHRT is not made from animal waste; rather they are formulated from soy products or yams by pharmacists to match the body’s hormones identically. As a result, patients are likely to benefit from the use of human hormones without the side-effects associated with non-human hormones. In addition to menopausal symptoms mentioned earlier, hormone loss is also associated with an increased likelihood of heart disease, bone loss, decreased cognitive function, loss of muscle mass, reduced sex drive, restless leg syndrome, mood swings, hair loss, osteoporosis, depression, weight gain, and thinning of the skin.7 BHRT has shown to have specific benefits such as improving cognitive function8,9 , improving mood10-13 and sleep14,15 , reducing neuronal secretion of Alzheimer’s β-amyloid peptides16 , and improving sexual function, muscle strength and body composition9. The newest technique is the implanting of a time-released pellet underneath the skin on the buttocks. By implanting the dosage beneath the skin, the implants consistently release small, physiologic doses of hormones providing optimal therapy. BioTE® Medical Hormone Pellet Therapy is the only method of hormone therapy that provides sustained hormone levels throughout the day for up to four to six months without any “roller coaster” effect as seen with oral and transdermal forms of hormonal therapy. Because the pellets are completely natural, Pellet Therapy is ideal for patients wanting the benefits of a natural hormone, without the drawbacks of a synthetic. Pellets contain a natural plant source of estrogen and testosterone. A compounding pharmacist, using strict federal guidelines, compounds the estrogen and testosterone utilized in the pellets. These pellets, which are smaller than a grain of rice, are placed in the fatty tissue underneath the skin and most closely mimic the actions of healthy ovaries and testicles with regards to hormone release into the bloodstream. The implantation procedure is easily performed in the doctor’s office. Abstract
There have been many articles published regarding the benefits of HRT and BHRT; particularly in breast cancer, prostate cancer, cardiovascular protection, and bone building/osteoarthritis. The purpose of this white paper is to summarize the results of these articles by each disease entity. Please note, however, that most of the articles did not specify HRT or BHRT, but the hormone therapy itself, such as estrogen, progestin and testosterone. Prostate Cancer
The results presented are derived from literature published on prostate cancer between 2001 and 2011. Some cases of prostate cancer were newly diagnosed17 and most of the men were older in age (≥ 50 years).18-21 The size of the studies ranged from 7122 to 295023 patients and the majority of the articles indicated that the patients’ prostate cancer was treated with testosterone or testosterone with estrogen.17, 19, 20, 21, 23-25 In one article androgen suppression therapy was given26 and in another article there was no treatment given.27 Administration of testosterone and estrogen varied and was comprised of implants, injections and transdermals. Endpoint measurements included prostate zonal volume, 22 T serum and PSA levels, 17, 20,23,24,27 overall progression-free and cancer-specific survival.20, 24, 26 Results indicated that patients receiving testosterone had decreased prostate zonal volume irrespective of therapy up to middle age and increased thereafter.22 There was also improvement in quality of life23 and no evidence of increased risk of prostate cancer; 26 however there was no difference in survival between regular therapy vs. intermittent hormone therapy.23 Results also indicated that administration of testosterone promoted growth of benign prostatic nodules and enhanced pre-existing prostatic malignancy.18 One article was inconclusive regarding T level and prostate cancer risk after testosterone treatment.20 Patients receiving testosterone alone showed an increased risk of prostate cancer in men with low testosterone24 and patients receiving both testosterone and estrogen with high Gleason scores had lower testosterone and estradiol serum levels.17 Androgen suppression therapy, on the other hand, reduced disease progression and improved overall survival.26 Osteoporosis/Bone Density
A review of published articles on osteoporosis and /or bone density published between 1976 and 2010 are summarized. Study size ranged from 1228 to 16729 patients and follow-up ranged from 6 months30, 31 to over 14 years.28 All of the articles except for one indicated that the patients’ osteoporosis/bone density loss was treated with estrogen/estradiol,28,30,32-42 testosterone 29,31,43- 52or a combination of estradiol and testosterone.53-62 The remaining article indicated no treatment.63 Hormone replacement therapy was administered as subcutaneous or percutaneous implants,28,35,37,38,40,41,47,48,54-56,58,60-62 transdermal patches53,59 and oral tablets.36,39 Endpoint measurements included vertebral/femoral bone density,37,47,53,55,56,60-62 bone mineral density,28,29- 36,38,40,4-44,48-52,54,57-59 bone volume,34,35 muscle mass,44 strength,45 and hormone and serum levels.37,44,46,48-50,58 Results indicated that patients receiving HRT had an increase in bone density, bone mineral content, bone formation, wall thickness and serum E2 levels.28-38,42-49,51,54,56,58,60,62 HRT also showed an improvement in muscle mass, strength, body composition, mood, libido, cardiovascular function and quality of life.30,39,42-46,49,50,54,59 Markers of bone formation improved as well as cancellous bone volume and there was a reduction in body fat and total cholesterol.30,35,43,50,58 There was also a reduction in bone fractures, myocardial infarctions and cancer.39,41 It was noted that subcutaneous estrogen was more effective than oral estrogen47and that implants maintained or increased bone density whereas patches reduced bone density.53 Cardiovascular Protection
A review of published articles on cardiovascular protection published between 1984 and 2012 are summarized. Study size ranged from 14 women64 to 2,416 men65 and follow-up ranged from 6 weeks 66, 67 to 5 years.65 Treatment included testosterone,65,66,68-70or a combination of estradiol alone followed by testosterone 64,67,73,74 or estrogen and progesterone,71 or estradiol and nomegestrol acetate.72 Hormonal treatment was administered as subdermal or subcutaneous implants,64,66,72-74 injections,68 transdermals71or oral tablets.68,71 Endpoint measurements focused on cholesterol levels, HDL, LDH,64,71-74 sex-hormone body globulin (SHBG),65body fat,73 insulin levels, 71T-levels,65-67, BMI,71 systolic blood pressure,71 oxygen consumption70 and 6-minute walk tests.67 Results in patients treated with a combination of estradiol and testosterone showed a reduction in total cholesterol and LDL with an increase in HDL thus offering cardiovascular protection.64, 67,73,74 Body fat was reduced in patients taking estradiol alone73 and patients taking estrogen with progesterone or nomegestrol acetate had reduction in cardiovascular risk factors.71 Results in patients taking only testosterone showed improvement in functional capacity associated with heart failure, reduction in total cholesterol and SHBG, and a reduced risk of cardiovascular disease.65,66,68-70 Hormone implants showed similar changes in lipid profiles compared with oral forms of hormones.64 Breast Cancer
A review of the published literature between the years 1941 and 2013 is summarized and focuses on women with breast cancer or history of breast cancer and pre and post-menopausal women and the effects of HRT. Three articles studied female monkeys, 75 mice76 and transsexuals, 77 respectively. Study size ranged from six patients78 to over one million79 and follow-up ranged from 3 months to 32 years.80 Treatment consisted of a variety of hormones that included progestins, 81,82 estradiol/estrogen,80,83-92 testosterone 78,93-96,105,106 and combinations of arimidex and testosterone,97 estrogen and testosterone, 75,77,98-101estrogen and progestagen, 79,102,103, testosterone and anastrozol,104 and BHRT.107 The hormones were administered as subcutaneous pellets/implants, patches, injections or orally. Endpoint measurements included progression and recurrence of breast cancer, 76,78,93,97,101 relative risk of invasive breast cancer, 76,79,81,83,87,88,91,94,95,98-100,105,106 plasma T levels,105 Rosner/Colditz breast cancer score,105 quality of life, 83,90,96 overall survival, 79,80,86,87,103 ease of menopausal symptoms, 84,96 and relative risk of hormone therapy. 89,101,102 Endpoint measurements in female monkeys focused on mammary epithelial proliferation, 75 in transsexuals tumor or cancer development, 77 and in mice tumor progression rate and survival.76 Patients taking estrogen showed improvement in menopausal symptoms, 83, 84 no increase in the risk of recurrence of breast cancer or of death, 80,81,85-88,90-94,96,99-102,105 a reduced risk of colorectal cancer and osteoporosis, 92 a reduction in fractures and myocardial infarctions and an increase in bone density.90 Prevention or reduction in estrogenic cancer risk was found in patients taking a combination of estrogen and testosterone,80,93,99-101 mortality rate did not increase due to breast cancer,80,86 and testosterone counteracted proliferation of breast cells and exerted a protective role. 93,94,96,99 A combination of estrogen and progestins had mixed results. Some studies found a low risk of breast cancer and no trend in increasing breast cancer with increasing duration of HRT; 81,102 whereas, other studies noted that use of HRT increased the risk of breast cancer compared to women never on HRT. 79, 82,103 Patients treated with testosterone/androgens showed an ease in menopausal symptoms, 94, 97 cardiovascular benefits, 96 and no risk or recurrence of breast cancer.94, 97 However, an excess of testosterone was found to be the principal growth stimulator of breast cancer.106 It was also found to be beneficial to implant testosterone at the operation site in women 78and a study with BHRT found it to be safer than synthetic HRT.107 A study using a combination of testosterone and anastrozole showed an improvement in menopausal symptoms without increasing estradiol levels.104 Results in a study on transsexuals found that a combination of testosterone and estrogen increased the probability of tumors with the duration of exposure to cross-sex hormones.77 Mammary epithelial proliferation was noted to increase in female monkeys after receiving a combination of testosterone and estradiol, 75 and 131 l-norcholesterol (radiotherapy) prevented local regional recurrence and metastatic spread after tumor resection in mice.76 Conclusion
In summary, treatment with HRT and/or BHRT was found to improve quality of life and increased bone density, bone mineral density and muscle mass. Mood, libido and cardiovascular function improved and body fat was reduced, as well as cholesterol and LDH. Risk of prostate and breast cancer was reduced in the majority of the cases reviewed and there was an improvement in menopausal symptoms. Subcutaneous/percutaneous implants were the most common form of HRT/BHRT administration followed by transdermals and oral hormones. As with any medication, consultation with a physician is recommended to discuss personal risks and whether any version of HRT/BHRT is appropriate to be prescribed. Appendix A – References
1. www.medicalnewstoday.com. 2013 July 19. 2. Harvard Health Letter 2004 May. www.health.harvard.edu/health. 3. Stefanick M, Cochrane B, Hsia J. et. al. The WHI postmenopausal hormone trials. Ann Epidemiol 2003; 13:S78-S86. 4. Heiss G, Wallace R, Anderson GL, et al. Health risks and benefits 3 years after stopping randomized treatment with estrogen and progestin. JAMA 2008; 299:1036-1045. 5. Mayo Clinic Health Information Website. www.mayoclinic.com/health/hormone- 6. LaCroix AZ, Rowan T, Chlebowski RT, Manson JE. Health outcomes after stopping conjugated equine estrogens among postmenopausal women with prior hysterectomy. JAMA 2011; 305:1305-1314. 7. Hotze SF and Ellsworth DP. Point/Counterpoint: The case for bioidentical hormones. J Am Physicians and Surgeons 2008; 13:43-36. 8. Tan RS. Memory loss as a reported symptom of andropause. Arch Androl 2001; 9. Synder PJ, Peachey H, Berlin JA. Effects of testosterone replacement in hypogonadal men. J Clin Endocrinol Metab 2000; 85: 2670-2677. 10. Morita K, Her S. Progesterone pretreatment enhances serotonin-stimulated BDNF gene expression in rat c6 glioma cells through production of 5alpha-reduced neurosteroids. J Mol Neurosci 2008; 34:193-200. 11. Wang C, Swerdloff RS, Iranmanesh A, et al. Transdermal testosterone gel improves sexual function, mood, muscle strength, and body composition parameters in hypogonadal men. J Clin Endocrinol Metab 2000; 85:2839-2853. 12. Wang C, Alexander G, Berman N, et al. Testosterone replacement therapy improves mood in hypogonadal men – a clinical research center study. J Clin Endocrinol Metab 1996; 81:3578-3583. 13. Van Wingen GA. Progesterone selectively increases amygdale reactivity in women. 14. Paredes SD, Barriga C, Rodriguez AB. Melatonin and tryptophan as therapeutic agents against the impairment of the sleep-wake cycle and immunosenescence due to aging in Streptopelia risoria. Neuro Endocrinol Lett 2007; 28:757-760. 15. 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Five-year changes in bone density and their relationship to plasma estradiol and pretreatment bone density, in an older population of postmenopausal women using long-term estradiol implants. Gynecol Endocrinol 2003; 17:463-470. 39. Campagnoli C, Lesca L, Cantamessa C, et al. Long-term hormone replacement treatment in menopause: new choices, old apprehensions, recent findings. Maturitas 1993; 18:21-46. 40. Naessen T, Person I, Thor L, et al. Maintained bone density at advanced ages after long term treatment with low dose oestradiol implants. Br J Obstet Gynaecol 1993; 100:454-459. 41. Panax N, Versi E, Savvas M. A comparison of 25 mg and 50 mg oestradiol implants in the control of climacteric symptoms following hysterectomy and bilateral salpingo-oophorectomy. Br J Obstet Gynaecol 2000; 107:1012-1016. 42. Purdie DW, Ballard PA, Wahab M, et al. Bone mineral density (BMD) at lumbar spine and femoral neck in hysterectomised women treated with chronic oestradiol implantation. Maturitas (Abstract -F133) 1997. 43. Isidori Am, Giannetta B, Greco EA, et al. Effects of testosterone on body composition, bone metabolism and serum lipid profile in middle-aged men: a meta-analysis. Clin Endrocrinol 2005; 63:280-293. 44. Lunenfeld B, Nieschlag E. Testosterone therapy in the aging male. Aging Male 45. Notelovitz M. Androgen effects on bone and muscle. Fertil Steril 2002; 77:S34-S41. 46. Nieschlag E, Behre HM, Bouchard P, et al. Testosterone replacement therapy: current trends and future directions. Hum Reprod 2004; 10:409-419. 47. Savvas M, Studd JWW, Fogelman I, et al. Skeletal effects of oral oestrogen compared with subcutaneous oestrogen and testosterone in postmenopausal women. Br Med J 297:331-333. 48. Zacharin MR, Pua J, Kanumakala S. Bone mineral density outcomes following long- term treatment with subcutaneous testosterone pellet implants in male hypogonadism. Clin Endocrinol 2003; 58:691-695. 49. Zitzmann M, Nieschlag E. Hormone substitution in male hypogonadism. Mol Cell 50. Bain J. Testosterone and the aging male: to treat or not to treat? Maturitas 2010; 51. Rhoden EL, Morgentaler A. Risk of testosterone replacement therapy and recommendations for monitoring. N Engl J Med 2004; 350:482-492. 52. Oettel M. The endocrine pharmacology of testosterone therapy in men. Naturwisssenschaften 2004; 91:66-76. 53. Anderson CHM, Raju KS, Forling MI, et al. The effects of surgical menopause and parenteral hormone replacement therapy on bone density, menopausal symptoms and hormone profiles. Maturitas 1997; 27(Suppl 1):S70. 54. Davis SR, McCloud PI, Strauss BJG, et al. Testosterone enhances estradiol’s effects on post-menopausal bone density and sexuality. Maturitas 1995; 21:227-236. 55. Garnett T, Studd J, Watson N, et al. A cross-sectional study of the effects of long- term percutaneous hormone replacement therapy on bone density. Obstet Gynecol 1991; 78:1002-1007. 56. Garnett T, Studd J, Watson N, et al. The effects of plasma estradiol levels on increases in vertebral and femoral bone density following therapy with estradiol and estradiol with testosterone implants. Obstet Gynecol 1992; 79:968-972. 57. Lobo RA. Androgens in postmenopausal women: production, possible role, and replacement options. Obstet Gynecol 2001; 56:361-376. 58. Panay N, Zamblera D, Sands R, et al. Low dose 25 mg oestradiol implants and 1 mg norethisterone as continuous combined hormone therapy: a prospective study. Br J Obstet Gynaecol 2002; 109:958-960. 59. Panay N. New products and regimens (since 2003). Climacteric 2007; 10 (Suppl 60. Savvas M, Studd JWW, Norman S, et al. Increase in bone mass after one year of percutaneous oestradiol and testosterone implants in post-menopausal women who have previously received long-term oral oestrogens. Br J Obstet Gynaecol 1992; 99:757-760. 61. Barlow DH, Abdalla HI, Roberts ADG, et al. Long-term hormone implant therapy – hormonal and clinical effects. Obstet Gynecol 1986; 67:321-325. 62. Studd J, Savvas M, Watson N, et al. The relationship between plasma estradiol and the increase in bone density in postmenopausal women after treatment with subcutaneous hormone implants. Am J Obstet Gynecol 1990; 163:1474-1479. 63. Brincat M, Kabalan S, Studd WW, et al. A study of the decrease of skin collagen content, skin thickness, and bone mass in the postmenopausal woman. Obstet Gynecol 1987; 70:840-845. 64. Farish E, Fletcher CD, Hart DM, et al. The effects of hormone implants on serum lipoproteins and steroid hormones in bilaterally oophorectomised women. Acta Endocrinol 1984; 106:116-120. 65. Ohlsson C, Barrett-Connor E, Shalender, et al. High serum testosterone is associated with reduced risk of cardiovascular events in elderly men. The MrOs (Osteoporotic Fractures in Men) Study in Sweden. J Am Coll Cardiol 2011; 58:1674-1681. 66. Worboys S, Kotsopoulos D, Teede H, et al. Subcutaneous testosterone implant therapy improves endothelium-dependent and independent vasodilation in postmenopausal women already receiving oestrogen. Heart Lung Circ 200; 9:A109. 67. Worboys S, Kotsopoulos D, Teede H, et al. Evidence that parenteral testosterone therapy may improve endothelium-dependent and independent vasodilation in postmenopausal women already receiving estrogen. J Clin Endrocrinol Metab 2001; 86:158-161. 68. Conway AJ, Boylan LM, Howe C, et al. Randomized clinical trial of testosterone replacement in hypogonal men. Inter J Androl 1988; 11:247-264. 69. Giagulli VA, Triggiani V, Corona G, et al. Evidence-based medicine update on testosterone replacement therapy (TRT) in male hypogonadism: focus on new formulations. Cur Pharm Design 2011; 17:1500-1511. 70. Toma M, McAlister FA, Coglianese EE, et al. Testosterone supplementation in heart failure: a meta-analysis. Circ Heart Fail 2012; 111:315-321. 71. Cavender RK, Fairall M. Subcutaneous testosterone pellet implant (Testopel) therapy for men with testosterone deficiency syndrome: a single-site retrospective safety analysis. J Sex Med 2009; 6:3177-3192. 72. Barbosa IC, Coutinho EM, Oladapo L, et al. An open-label study of subdermal implants of estradiol-only versus subdermal implants of estradiol plus nomegestrol acetate: effects on symptom control, lipid profile and tolerability. Gynecol Endocrinol 2009; 25:269-275. 73. Davis SR, Walker KZ, Strauss BJG. Effects of estradiol with and without testosterone on body composition and relationship with lipids in postmenopausal women. Menopause 2000; 7:395-401. 74. Fletcher CD, Farish E, Hart DM, et al. Long term hormone implant therapy – effects on lipoproteins and steroid levels in post-menopausal women. Acta Endocrinol 1986; 111:419-423. 75. Dimitrakakis C, Zhou J, Wang J, et al. A physiologic role for testosterone in limiting estrogenic stimulation of the breast. Menopause 2008; 10:292-298. 76. Azab AK, Kleinstem J, Doviner V, et al. Prevention of tumor recurrence and distant metastasis formation in a breast cancer mouse model by biodegradable implant of 131 l-norcholesterol. J Controlled Release 2007; 123:116-122. 77. Mueller A, Gooren L. Hormone-related tumors in transsexuals receiving treatment with cross-sex hormones. Eur J Endocrinol 2008; 159:197-202. 78. Loeser AA. Mammary carcinoma response to implantation of male hormone and progesterone. Lancet 1941; 238:698-700. 79. Million Women Study Collaborators. Breast cancer and hormone replacement therapy in the million women study. Lancet 2003; 362:419-427. 80. Natrajan PK, Soumakis K, Gambrell RD. Estrogen replacement therapy in women with previous breast cancer. Am J Obstet Gynecol 1999; 181:288-295. 81. Juergen CD, Heinemann LAJ, Mohner S, et al. Breast cancer risk associated with different HRT formulations: a register-based case-control study. BMC Women’s Health 2006; 6:13. 82. 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Maturitas 2009; 62:76-80. 96. Glaser R, Wurtzbacher D, Dimitrakakis C. Efficacy of testosterone therapy delivered by pellet implant. Maturitas 2009; 68(Suppl 1):S73. 97. www.breastcancer.org/tips/menopausal/new_research. Arimidex-testosterone combo may ease menopausal symptoms. May 19, 2012, pg 2. 98. Tamimi R, Hankinson SE, Chen WY, et al. Combined estrogen and testosterone use and risk of breast cancer in postmenopausal women. Arch Intern Med 2006; 166:1483-1489. 99. Hofling M, Hirschberg AL, Skoog L, et al. Testosterone inhibits estrogen/progestogen-induced breast cell proliferation in postmenopausal women. Menopause 2007; 14:183-190. 100. Tutera G, Gambrell D. Marked reduction of breast endometrial and ovarian cancer in users of bio-identical estradiol and testosterone subcutaneous pellets. Maturatis 2009; 63(Suppl 1):S64. 101. Dimitrakakis C, Zava D, Marinopoulos S, et al. Low salivary testosterone levels in patients with breast cancer. BMC Cancer 2010; 10:547 102. 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The bioidentical hormone debate: are bioidentical hormones (estradiol, estriol, and progesterone) safer or more efficacious than commonly used synthetic versions of hormone replacement therapy? Postgrad Med 2009; 121:1-13.

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