Part 5: The Bioidentical Hormone Debate: Are Bioidentical Bioidentical Hormones (Estradiol, Estriol, and Progesterone) Safer or More Efficacious than Commonly Used Synthetic Versions in Hormone Replacement Therapy?

Written by BIH of Decatur on . Posted in Uncategorized

Discussion Physicians must translate both basic science results and clinical outcomes to decide on the safest, most efficacious treatment for patients. Evidence-based medicine involves the synthesis of all available data when comparing therapeutic options for patients. Evidence-based medicine does not mean that data should be ignored until a randomized control trial of a particular size and duration is completed. Rather, it demands an assessment of the patientcare_ref_serv_923_current available data to decide which therapies are likely to carry the greatest benefits and the lowest risks for patients.

Progesterone, compared with MPA, is associated with greater efficacy, patient satisfaction, and quality of life.  More importantly, molecular differences between synthetic progestins and progesterone result in differences in their pharmacological effects on breast tissue.   Some of the pro-carcinogenic effects of synthetic progestins contrast with the anticarcinogenic properties of progesterone, which result in disparate clinical effects on the risk of breast cancer.

Progesterone has an antiproliferative, antiestrogenic effect on both the endometrium and breast tissue, while synthetic progestins have antiproliferative, antiestrogenic effects on endometrial tissue, but often have a proliferative estrogenic effect on breast tissue.   Synthetic progestins show increased estrogen-induced breast tissue proliferation and a risk for breast cancer, whereas progesterone inhibits breast tissue proliferation and reduces the risk for breast cancer.

Until recently, estriol was available in the United States as a compounded prescription, but was banned in January;jsessionid=28AC80AEF73CC0019947E095714B5D5A8 by the FDA, which stated that it was a new, unapproved drug with unknown safety and effectiveness, although its symptomatic efficacy is generally not in question.192–196 The FDA has not received a single report of an adverse event in more than 30 years of estriol use. Estriol is also the subject of a US Pharmacopeia monograph. The FDA Modernization Act of 1997 clearly indicated that drugs with a US Pharmacopeia monograph could be compounded. It appears that the FDA took action, not because estriol is at least as safe and effective as current estrogens on the market, but in response to what was considered unsupported claims that estriol was safer than current forms of estrogen replacement and because there is no standardized dose. Estriol has unique physiologic properties associated with a reduction in the risk of breast cancer, and combining estriol with estradiol in hormone replacement preparations would be expected to decrease the risk for breast cancer.  In cardiovascular disease, synthetic progestins, as opposed to progesterone, negate the beneficial lipid and vascular effects of estrogen.

Transdermal bioidentical estrogen and progesterone are associated with beneficial cardiovascular and metabolic effects compared with the use of CEE and synthetic progestins.  BASED ON BOTH PHYSIOLOGICAL RESULTS AND CLINICAL OUTCOMES, CURRENT EVIDENCE DEMONSTRATES THAT BIOIDENTICAL HORMONES ARE ASSOCIATED WITH LOWER RISKS THAN THEIR NON-BIOIDENTICAL COUNTERPARTS. Until there is evidence to the contrary, current evidence dictates that bioidentical hormones are the preferred method of HRT.

Conclusion A thorough review of the medical literature supports the claim that bioidentical hormones have some distinctly different, often opposite, physiological effects to those of their synthetic counterparts. WITH RESPECT TO THE RISK FOR BREAST CANCER, HEART DISEASE, HEART ATTACK, AND STROKE, SUBSTANTIAL SCIENTIFIC AND MEDICAL EVIDENCE DEMONSTRATES THAT BIOIDENTICAL HORMONES ARE SAFER AND MORE EFFICACIOUS FORMS OF HRT THAN COMMONLY USED SYNTHETIC VERSIONS. More randomized control trials of substantial size and length will be needed to further delineate these differences.

Part 4: The Bioidentical Hormone Debate: Are Bioidentical Bioidentical Hormones (Estradiol, Estriol, and Progesterone) Safer or More Efficacious than Commonly Used Synthetic Versions in Hormone Replacement Therapy?

Written by BIH of Decatur on . Posted in Uncategorized


The WHI study demonstrated that the addition of MPA to Premarin® (a CEE) resulted in a substantial increase in the risk of heart attack and stroke. This outcome with MPA is not surprising because synthetic progestins produce negative cardiovascular effects and negate the cardioprotective effects of estrogen. Progesterone, in contrast, has the opposite effect because it maintains and augments the cardioprotective effects of estrogen, thus decreasing the risk for heart attack and stroke.

One mechanism contributing to these opposing effects for cardiovascular risk is the differing effects on lipids. Medroxyprogesterone acetate and other synthetic progestins generally negate the positive lipid effects of estrogen and show a consistent reduction in HDL,148,153–159,163 the most impo160566891-300x199rtant readily measured determinant of cardioprotection, while progesterone either maintains or augments estrogen’s positive lipid and HDL effects.

For instance, the PEPI trial, a long-term randomized trial of HRT, compared a variety of cardiovascular effects including lipid effects of both MPA and progesterone in combination with CEE. While all regimens were associated with clinically significant improvements in lipoprotein levels, many of estrogen’s beneficial effects on HDL-C were negated with the addition of MPA. The addition of progesterone to CEE, however, was associated with significantly higher HDL-C levels than with MPA and CEE (a notable sparing of estrogen’s beneficial effects).

Fahraeus et al compared the lipid effects of synthetic progestins with progesterone in 26 postmenopausal women who had been receiving cutaneous estradiol for 3 to 6 months. Women received either 120 ⎧g of l-norgestrel or 300 mg of progesterone sequentially for another 6 months. Compared with the use of progesterone, l-norgestrel resulted in significant reductions in HDL and HDL-2.

Ottosson et al compared the lipid effects of estrogen when combined with either of 2 synthetic progestins, or bioidentical progesterone. Menopausal women were initially treated with 2 mg estradiol valerate (cyclical) for 3 cycles, and then were randomized to receive MPA, levonorgestrel, or progesterone. Serum lipids and lipoproteins were analyzed during the last days of the third, fourth, and sixth cycles. Those receiving estrogen combined with levonorgestrel had a significant reduction in HDL and HDL sub-fraction 2 (18% and 28%, respectively), as did those receiving MPA (8% and 17%, respectively). Conversely, there were no significant changes seen in the HDL and HDL sub-fraction levels with the use of progesterone.

Furthermore, a randomized trial by Saarikoski et al which compared the lipid effects in women using the synthetic progestin norethisterone and progesterone, those on synthetic progestin had a significant decrease in HDL, whereas those using progesterone had no decrease in HDL.

A number of studies have shown that coronary artery spasm, which increases the risk for heart attack and stroke, is reduced with the use of estrogen and/or progesterone.149–151-,174,179,180 However, the addition of MPA to estrogen has the opposite effect, resulting in vasoconstriction,149–151,174 thus increasing the risk for ischemic heart disease.SS_PR_090911heartdisease_intro

Minshall et al compared coronary hyperreactivity by infusing a thromboxane A2 mimetic in primates, which were administered estradiol along with MPA or progesterone. When estradiol was given with progesterone, the coronary arteries were protected against induced spasm. However, the protective effect was lost when MPA was used instead of progesterone.

Miyagawa et al also compared the reactivity of coronary arteries in primates pretreated with estradiol combined with either progesterone or MPA. None of the animals treated with bioidentical progesterone experienced vasospasm, while all of those treated with MPA showed significant vasospasm.

Mishra et al1 also found that progesterone protected against coronary hyperreactivity, while MPA had the opposite effect and induced coronary constriction.

In a blinded, randomized, crossover study, the effects of estrogen and progesterone were compared with estrogen and MPA on exercise-induced myocardial ischemia in postmenopausal women with coronary artery disease. Women were treated with estradiol for 4 weeks and then randomized to receive either progesterone or MPA along with estradiol. After 10 days on the combined treatment, the patients underwent a treadmill test. Patients were then crossed over to the opposite treatment, and the treadmill exercise was repeated.

Exercise time to myocardial ischemia was significantly increased in the progesterone group compared with the MPA group.

Adams et al1examined the cardioprotective effects of CEE and progesterone versus CEE and MPA in primates fed atherogenic diets for 30 months. The CEE and progesterone combination resulted in a 50% reduction in atherosclerotic plaques in the coronary arteries. This result was independent of changes in lipid concentrations. However, when MPA was combined with the CEE, almost all the cardioprotective effect (atherosclerotic plaque reduction) was reversed.

Other studies have shown that progesterone by itself or in combination with estrogen inhibits atherosclerotic plaque formation. Synthetic progestins, in contrast, have a completely opposite effect: they promote atherosclerotic plaque formation and prevent the plaque-inhibiting and lipid-lowering actions of estrogen.

Transdermal estradiol, when given with or without oral progesterone, has no detrimental effects on coagulation and no observed increased risk for venous thromboembolism (VTE). This result is in contrast to an increased risk for VTE with CEE, with or without synthetic progestin, which significantly increases the risk for VTE, whether both are given orally (eg, oral estrogen and oral synthetic progestin) as transdermal estrogen and oral synthetic progestin, or both estrogen and synthetic progestin given transdermally.

Medroxyprogesterone acetate also has undesirable intrinsic glucocorticoid activity, whereas progesterone does not have such negative effects and is a competitive inhibitor of aldosterone, which is generally a desirable effect.index

No changes in blood pressure are observed with progesterone in normotensive postmenopausal women, but a slight reduction in blood pressure is shown in hypertensive women.

Synthetic progestins can significantly increase insulin resistance, when compared with estrogen and progesterone.

The expression of vascular cell adhesion molecule-1 (VCAM-1) is one of the earliest events in the atherogenic process. Otsuki et al compared the effects of progesterone and MPA on VCAM-1 expression and found that progesterone inhibited VCAM-1. No such effect was observed with MPA.

Educate Yourself To Stay Healthy With Bio-Identical Hormone Replacement

Written by BIH of Decatur on . Posted in Men, Menopausal Research, Uncategorized, Women

In medicine there are many avenues to health.  Many will encourage exercise daily.  And this is good.  Others talk about a proper diet is most important… are what you eat.  And this is also true.  Weight control is seen as very important to live a long healthy life.
educate yourself
All these concepts are essential to live life to the maximum.

But our hormones have the most influence on your health.  As Suzanne Somers says in her book,  AGELESS: THE NAKED TRUTH ABOUT BIOIDENTICAL HORMONES   “Hormones are our life force; the decline of hormones is the hallmark of aging.  Without hormone replacement, we will end up mere shells of our former selves.”

Too often we let others tell us what they think is best.  “Take this pill.” “Put on this cream.” “Join a gym.” “Meditate, and take vitamin supplements.” And we will try all these things to preserve, or regain the youth and health we once had.

A suggestion might be to educate yourself, and make your own decision.

When we  learn how extremely important hormones are, even essential to our health, the next question may be, “What do I do next?”

You can call our office for a free consultation to learn more.  In the meantime, there are many excellent books on this subject that will encourage one to take advantage of this “life force”, Bio-Identical Hormone Replacement Therapy.

Books on Bio-Identical Hormone Replacement Therapy:
(suggested reading)

“The Hormone Solution, Stay Younger Longer” by Thierry Hertoghe
“Stay Young and Sexy with Bio-Identical Hormone Replacement”   by Jonathan Wright
“Testosterone for Life”   by Abraham Morgentaler
“The Savvy Woman’s Guide to Testosterone”  by Elizabeth Vliet
“Women’s Hormones” by Pamela Smith
The Testosterone Syndrome”  by  Eugene Shippen
“Bioidentical Hormones 101”  by  Jeffrey Dach
“You Don’t Have to Live With It”  by  Gino Tutera
“Natural Hormone Replacement”  by Jonathan Wright
“Natural Hormone Balance”  by  Uzzi Reiss

Low Testosterone – A Risk Factor for Heart Disease

Written by BIH of Decatur on . Posted in Men, Uncategorized

man with heart










The following article shows MEN who are low in testosterone are MORE  likely to die especially of heart disease.

Testosterone is a vasodilator and aids in blood flow to the heart. There are more receptor sites to testosterone in the heart muscle than any other muscle in the body. All this could explain the reason men live longer if their testosterone is normal.

What you see in the study is that in 930 men who already had coronary disease low testosterone was common. And of those men who had low testosterone, they were twice as likely to die. This, of course, suggest strongly that men with higher testosterone levels are more likely to live. Using bio-identical hormones to raise one’s testosterone to that of a younger person just makes sense.

ScienceDaily (Oct. 21, 2010) — Low testosterone levels seem to be linked to a heightened risk of premature death from heart disease and all causes, suggests research published online in Heart.

The finding refutes received wisdom that the hormone is a risk factor for cardiovascular disease. The researchers base their findings on 930 men, all of whom had coronary artery heart disease, and had been referred to a specialist heart centre between 2000 and 2002. Their heart health was then tracked for around 7 years.
On referral, low testosterone was relatively common. One in four of the men was classified as having low testosterone, using measurements of either bioavailable testosterone (bio-T) — available for tissues to use — of under 2.6 mmol/l or total testosterone (TT) of under 8.1 mmol/l.

These measures indicate clinically defined testosterone deficiency, referred to as hypogonadism, as opposed to a tailing off in levels of the hormone as a result of ageing.

During the monitoring period almost twice as many men with low testosterone died as did those with normal levels. One in five (41) of those with low testosterone died, compared with one in eight (12%) of those with normal levels.

The only factors that influenced this risk were heart failure (left ventricular dysfunction), treatment with aspirin or a high blood pressure drug (beta blocker) and low bio-T levels.

A low bio-T level was an independent risk factor for premature death from all causes and from heart disease, after taking account of other influential factors, such as age, other underlying health problems, smoking and weight.

Borderline levels of low total testosterone (15.1mmol/l) also increased the risk of an early death.

While high doses of testosterone found in anabolic steroids are harmful to health, the evidence suggests that low, rather than high, levels of the hormone, are associated with obesity, risky blood fats, and insulin resistance, all of which are risk factors for diabetes and heart disease, say the authors.

Men at high risk of these diseases may stand most to gain from testosterone replacement, they suggest.
An accompanying editorial points out that there is increasing interest in looking at the impact of testosterone replacement.