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Bio-identical hormones have a molecular structure that is identical to hormones that are naturally produced by the human body, and are intended to replace these hormones when their levels decline due to aging, disease, or surgery. In order for replacement hormones to fully replicate the function of hormones which were originally naturally produced and present in the human body, the chemical structures must match exactly. Synthetic non-bio-identical hormones have similar but not identical structures, so they are not the “perfect fit” for hormone replacement.
Researchers have long held that there are significant differences between hormones that are natural to humans (bio-identical) and synthetic (non-bio-identical) preparations. The structure of the hormone, not the sources, is the key. The term “bio-identical” does not indicate the source of the hormone. Bio-identical hormones are chemically processed from precursors found in yams or soy plants, yet they are identical to the hormones produced by the human body; hence the term “bio-identical plant-derived hormone.” These hormones are able to follow normal metabolic pathways so that essential active metabolites are formed in response to hormone replacement therapy. Synthetic – “patented,” “conventional,” “artificial,” or “horse” – hormones have been chemically altered, and are not identical in structure of activity to the naturally-occurring hormones they are intended to replace.
Most major studies have either failed to distinguish among types and dosages of HRT used in the study, or examined only the use of synthetic non-bio-hormones (as in the case of the Women’s Health Initiative). Side chains can be added to a natural substance to create a product that can be patented by a manufacturer and profitable to mass produce, and therefore a drug company has an incentive to fund research as to the use and effectiveness of synthetic non-bio-identical hormones. However, bio-identical substances cannot be patented, so scientific studies are less numerous on natural hormones. Structural differences inherent to non-bio-identical hormones may be responsible for side effects that are experienced when non-bio-identical hormones are used for replacement therapy.
Today’s women prefer natural hormones. In a survey of a nationally representative sample of 1,009 women aged 40 and older, 83% said they would prefer to use hormones that are similar to their own body’s hormones. Bio-identical hormones include estriol (E3), estradiol (E2), estrone (E1), progesterone, testosterone, dehydroepiandrosterone (DHEA), and pregnenolone.
The three types of hormones typically prescribed for bio-identical hormone replacement therapy (BHRT) are estrogens, progesterone, and androgens. The precise components of each woman’s therapy need to be determined after physical examination, medical history, and laboratory testing are considered. Close monitoring is essential to ensure that appropriate dosage adjustments are made.
The term “estrogen” actually refers to a group of related hormones, each with a unique profile of activity. The three principle estrogens in humans are estriol (E3), estradiol (E2), and estrone (E1). The use of one or more of these hormones is referred to as Estrogen Replacement Therapy (ERT). These hormones are often prescribed in combination to re-establish a normal physiologic balance.
Estriol has been shown to be clinically effective for the treatment of menopausal symptoms and problems, including vaginal atrophy, dryness, vaginal infections, painful intercourse, incontinence, and recurrent urinary tract infections.[1] Estradiol is the primary estrogen of ovarian origin and the major form of estrogen in premenopausal women. Estrone (made from the conversion of estradiol and androstenedione) is the primary estrogen in post-menopausal women.
C-reactive protein (CRP) is one of the main independent predictors of cardiovascular events. Oral post-menopausal ERT increases CRP levels by a first-pass hepatic effect. These elevated levels of CRP may be responsible for the early increased cardiovascular risk that has been reported shortly after women begin oral combined HRT using NON bio-identical synthetic hormones. However transdermal 17beta-estradiol has shown no significant effect on CRP in either short-term or long-term use.[2]
Despite studies reporting the risks associated with synthetic hormones, conjugated equine estrogens remain the most frequently prescribed form of ERT. Metabolites (breakdown products) of these synthetic estrogens have been linked to the development of breast cancer.[3] [4]
In addition to treating menopausal symptoms, ERT has been shown to be effective in decreasing the risk of colorectal cancer, and has potential for treating patients with Multiple Sclerosis and arthritis.
Natural bio-identical progesterone is commonly prescribed for perimenopausal women to counteract the condition known as “estrogen dominance.” Perimenopause is the time between the onset of changes in hormonal secretions and menopause, and is characterized by fluctuating hormones. Estrogen dominance occurs when a woman produces smaller amounts of progesterone than normal relative to estrogen levels.
Jerilynn Prior, M.D., of the University of British Columbia in Vancouver, has presented evidence that progesterone can stimulate new bone formation in women with osteoporosis. This may indicate a role for progesterone use, alone or combined with estrogen which reduces bone loss, in improving Bone Mineral Density.[5] [6]
The Postmenopausal Estrogen/Progestin Interventions (PEPI) Trial confirmed that synthetic progestins partially negate the beneficial effects on cholesterol levels that result from taking estrogen. Natural progesterone, on the other hand, maintains benefits of estrogen on cholesterol while minimizing the side effects associated with synthetic progestins such as medroxyprogesterone acetate.[7]
The administration of 17 alpha-hydroxyprogesterone caproate or progesterone suppositories to women with high-risk pregnancies has significantly reduced the incidence of preterm birth.[8]
Approximately one in ten new mothers suffers from postpartum depression, or postnatal illness (PNI). “Unfortunately, women who have had PMS are prone to develop postnatal illness, but the good news is that PNI can be prevented by receiving progesterone” immediately after delivery. Women who have had postpartum depression once have about a 68% chance of recurrence after another pregnancy, but trials of prophylactic progesterone worldwide have shown that it is possible to reduce this recurrence rate to 7%.[9]
Mayo Clinic researchers surveyed 176 women taking natural micronized progesterone who had previously taken synthetic progestins to see if natural progesterone, when compared to synthetics, made a difference in the women’s overall quality of life, menopausal symptoms, and satisfaction with HRT. After one to six months, the women reported an overall 34% increase in satisfaction on micronized progesterone compared to their previous HRT, reporting these improvements: 50% in hot flashes, 42% in depression, and 47% in anxiety. Micronized progesterone was also more effective in controlling breakthrough bleeding.
Hermsmeyer, Miyagawa and Frank of Oregon Health Sciences University and USC School of Medicine compared medroxyprogesterone acetate (MPA) with natural progesterone as the progestin in HRT and studied the corresponding effect on coronary artery vasospasm. This research showed that progesterone plus estradiol protected against vasospasm, but MPA plus estradiol did not. In the past, the selection of MPA over progesterone has been based on familiarity and convenience. Based on these results, formulations of natural progesterone would appear to be the wiser choice.[10] [11]
Recently, attention has turned to the addition of the androgens testosterone and dehydroepiandrosterone (DHEA) to ERT in order to alleviate recalcitrant menopausal symptoms and further protect against osteoporosis, loss of immune function, obesity, and diabetes. ERT may represent incomplete preventive hormonal treatment in postmenopausal women because it does not directly address the declines in serum testosterone associated with hysterectomies and age-related gender-independent decline in DHEA and DHEA-sulfate. Additionally, ERT may cause relative ovarian and adrenal androgen deficiency, creating a rationale for concurrent physiologic androgen replacement.[12]
The addition of testosterone to conventional hormone therapy for postmenopausal women does not increase and may indeed reduce the hormone therapy-associated breast cancer risk, thereby returning the incidence to the normal rates observed in the general, untreated population.[13]
Every woman is unique. Therefore, it is a sensible approach for the patient to work together with her physician to individualize hormone replacement therapy. Bio-identical HRT can be customized by Dr. Maxwell in the needed strength and dosage form and administered via the most appropriate route to meet each woman’s unique needs.
By doing thorough, comprehensive testing, you also rule out other conditions which either mimic, or co-exist with, hormonal imbalance. The tests are easily ordered through our website, and the results are securely accessible to you on-line. They may also be forwarded to the physician of your choice if you wish.
[1] Menopause. 2004 Jan-Feb; 11(1):49-56
[2] Arterioscler Thromb Vasc Biol. 2004 Oct; 24(10);e164-7
[3] Proc Soc Exp Biol Med, 217(1);6-16
[4] Chem. Res Toxicol, 11(9);1105-11
[5]Endocrine Reviews, 11(2): 386-398
[6] Canadian Journal of Obstetrics/Gynecology & Women’s Health Care, 3(4): 178-84
[7] JAMA 1995; 273(3): 199-208
[8] Obstet Gynecol. 2007 Oct; 110(4): 865-72
[9] Once A Month, by Katharina Dalton, M.D., ©1999, p. 246
[10] Natural Medicine, 3(3): 324-7 and
[11] J Am Coll Cardiol 1997; 29(3): 671-80
[12] Obstetrics & Gynecology, 90(6): 995-8
[13] Menopause, 2004 Sep-Oct; 11(5): 531-5