After the initial excitement in the first half of the 20th century about the flood of synthetic and animal hormones being used on humans, by WW2 it was becoming obvious that only purified appropriate human hormones should be used for human hormone replacement HRT – ie endocrine system replacement – insulin, growth hormone, estrogen, progesterone, testosterone, DHEA,cortisol, thyroid etc.

There was already carnage among pregnant women from synthetic estrogen – stilbestrol -apparent by 1949- before the lunatic shotgun Chicago Lying-In trial of stilbestrol (Dieckmann WJ 1953 -it was finally banned only in 1976) now affecting these women, their children and grandchildren  with every reproductive and cancer complication known ( Herbst AL  1971-2012).

And then there was the rubbish of Robert Wilson’s 1966 Feminine Forever book promoting premarin for Wyeth, and the further expose of oral horse estrogen by the Seamans’ book (1978 Women and the Crisis in Sex Hormones), and by 1980 Brian Henderson’s exposure of breast carcinoma increasing from about 12yrs of HT onwards using oral premarin even before provera became conventional as PremPak.

Yet we had human hormone replacement- implants, creams,  – of estradiol, progesterone, testosterone already marketed in RSA by Schering by 1944;

and William Masters and Grody already in 1953 had proven in the first, 13month HRT RCT that combined physiological (optimally dose-titrated) 20:1 testosterone-estradiol injection (later marketed as Mixogen, Primodian Depot) in elderly women within months rescued more than half from progressive dementia and frailcare.

But within 3 years Masters had been bought over by Wyeth to instead promote Premarin- “for womens’ convenience”. That gross fraudulent reasoning against all the evidence persisted through to the badly planned Womens Health Initiative started in the mid-nineties- the biggest, $billion trial ever, funded by and based on Wyeth’s already long-discredited USA-Canadian Premarin/Prempak – which in turn led to the ridiculous Million Women Study in UK.

Planned since the early 1990s, the publication of the protocol of the WHI in 1998 showed that it included few young health postmenopausal women for whom the Prem/Provera combination was either conventional or appropriate- but it shockingly included mostly elderly women in whom there was no evidence that good could be expected. (We stopped using such oral non-human xenohormones in the early 1990s because of the poor results they gave compared to human hormones as in all other branches of endocrinology). Then came the premature termination of the WHI trial based on bad science in 2002 and 2003. We in the International Menopause Society pleaded for good evidence-based sense in managing women permanently with appropriate human HRT- largely ignored by the Americans and UK – resulting in the KEEPS study planned in 2003 to try to undo the seriously misdirected zealous abandonment of appropriate HT (we were at the major KEEPS planning meeting in Vienna) .

Now the KEEPS results confirm that in the medium term (5year), lower dose premarin, or lowerdose estrodiol patch, with intermittent human progesterone, does no harm when started appropriately at menopause in well women – and parenteral estrogen if anything does better than oral premarin, without any of the risks of premarin and provera.

The KEEPS trial results were announced early October2012:

as we expected from the 5year study,  with no alerts

– with less premarin (than used in WHI), vs E2 patch  +- progesterone orally-

-both estrogens show   no harm, uniform trend to better . 

Hence the best regime  for both benefits and zero risks  remains lowdose  parenteral estrogen eg BiEst cream , balanced with progesterone cream, for all-system protection; plus if needed testosterone cream for low energy/mood/sexuality. .

SO there is no longer excuse, defence for not advising EVERY women to take some appropriate balanced human HRT from menopause onwards.

ACKNOWLEDGEMENTS: Our stubborn farsighted pioneers of parenteral human HRT – as creams, depot-injections and implants-  from the Ascended Masters Selye, William Masters, Greenblatt, de Kruif, Schleyer-Saunders, Gelfand and Gambrell,  to colleagues Dennis Davey, John Studd, Malcolm Whitehead, Henry Burger, Sue Davis and Lee Vliet-have been fully validated – thanks to current other IMS  and Andropause stalwarts and fellow enthusiasts like (in random memory order) Drs Harman, Naftolin, Sturdee, Gennazzanni, Simon, Shapiro, Gooren, Northrup, Lee, Dalton, Marshall, Schneider, Stephenson,  Farmer,Al-Azzawi, Saad, Lunenfeld, Bhasin, Bhana, Golding, Wu, Morley, Nieschlag, Behre, Handelsman, Hansen, Shippen, Notelowitz, Gutowitz, Thornley, Cheifitz,  Utian, Wang, Carruthers, Holman, Alperstein, Stumpf, Bornmann et alia, whom I acknowledge as my patient inspirations and sponsors over the past decades . 

REFS:  THE NEW Published evidence from around the world, confirming the old:




2. Progesterone increases resistance of ophthalmic and central retinal arteries in climacteric women (nb Note that this article title from the latest Journal Climacteric (the North American Menopause Society) is nonsense – the drug this Brazilian trial used was not natural progesterone – but Provera- medroxyprogesterone- which should never electively be used for chronic oral use . But many ‘expert’ doctors refuse to think physiologically- so millions of women have suffered and died because of inexcusably wrong advice the past decade. Their doctors and the FDA should be sued- but you cant sue the USA Govt and the Big Pharma mafia that pays them $billions – without $millions to fund you) : CLIMACTERIC Posted online on October 9, 2012. (doi:10.3109/13697137.2012.720620) M. A. M. De SouzaB. M. De Souza* and S. GeberUnimontes Medical School, Montes Claros, Minas Gerais, Brazil

Objective To evaluate the effect of a synthetic progestin on the vascular resistance of the ophthalmic and central retinal arteries in climacteric women, compared to placebo, using transorbital ultrasound with Doppler velocimetry.

Methods  a prospective, randomized, double-blinded, placebo-controlled study with 216 climacteric women. Subjects were randomly allocated to one of two groups: either the group receiving placebo (one pill/day for 30 days) (n = 108) or the group receiving progestin (5 mg medroxyprogesterone acetate/day for 30 days) (n = 108). Transorbital Doppler velocimetric ultrasound was performed..

Results The mean ages of the participants in the study group and the control group were 54 ± 6.2 years (range 48–59 years) and 55 ± 6.8 years (range 46–60 years), respectively. When we compared the effect of the progestin on the central retinal artery before and after treatment, we observed a significant increase after the treatment in all Doppler indices. The same was observed when we compared the effect of the progestin on the ophthalmic artery. In the group of women receiving placebo, the Doppler indices were similar before and after treatment.

Conclusions Our results demonstrate the existence of a progestogenic vasoconstrictive effect in the ophthalmic and central retinal arteries. As this study provides new data, the observed effect needs further investigations to better elucidate its extent. Moreover, our findings may be particularly useful to others interested in understanding the vascular dynamics of the cerebral vessels and to researchers running clinical trials related to hormone replacement therapy.

3. By contrast using a cheap natural human biological supplement :

One-year effects of myo-inositol supplementation in postmenopausal women with metabolic syndrome CLIMACTERIC October 2012, 15, 490-495 (doi:10.3109/13697137.2011.631063)

A. SantamariaD. Giordano*, F. CorradoB. PintaudiM. L. InterdonatoG. Di ViesteA. Di Benedetto and R. D’Anna University of Messina , Italy

Objective To evaluate effect of myo-inositol treatment on some biochemical parameters of women affected by metabolic syndrome.

Methods Eighty outpatient postmenopausal women, affected by metabolic syndrome, were enrolled in a 12-month study. All women were treated with a low-energy diet, and then they were randomly assigned to myo-inositol 2 g b.i.d. (n = 40) or placebo (n = 40). All the women were evaluated for serum glucose, insulin, HOMA-IR (Homeostasis Model Assessment-Insulin Resistance), triglycerides, total and high density lipoprotein cholesterol, body mass index (BMI), waist circumference and blood pressure at baseline and after 12 months of treatment.

Results With the exception of BMI and waist circumference, after 12 months of treatment, all the parameters studied showed a significant improvement in the myo-inositol group compared to the control group. At the end of the study, in the myo-inositol group, the number of women without metabolic syndrome was eight (20%) whereas, in the control group, only one woman no longer had the metabolic syndrome after 12 months of diet.

Conclusions  Myo-inositol might be considered one of the insulin-sensitizing substances in the treatment of metabolic syndrome.

Understanding weight gain at menopause CLIMACTERIC October 2012, 15, 419-429 S. R. DavisC. Castelo-Branco*, P. ChedrauiM. A. LumsdenR. E. Nappi**, D. Shah†† and P. Villaseca the Writing Group of the International Menopause Society for World Menopause Day 2012 Universities of Monash Melbourne, Barcelona,  , Glasgow, , Pavia, Italy, Mumbai India, and Católica de Chile, 

Objective  to summarize the literature regarding the impact of the menopause transition on body weight and body composition.

Methods We conducted a search of the literature using Medline (Ovid, 1946–present) and PubMed (1966–2012) for English-language studies that included the following search terms: ‘menopause’, ‘midlife’, ‘hormone therapy’ or ‘estrogen’ combined with ‘obesity’, ‘body weight’ or ‘body composition’.

Results Whereas weight gain per se cannot be attributed to the menopause transition, the change in the hormonal milieu at menopause is associated with an increase in total body fat and an increase in abdominal fat. Weight excess at midlife is not only associated with a heightened risk of cardiovascular and metabolic disease, but also impacts adversely on health-related quality of life and sexual function. Animal and human studies indicate that this tendency towards central abdominal fat accumulation is ameliorated by estrogen therapy. Studies mostly indicate a reduction in overall fat mass with estrogen and estrogen–progestin therapy, improved insulin sensitivity and a lower rate of development of type 2 diabetes.

Conclusion The hormonal changes across the perimenopause substantially contribute to increased abdominal obesity which leads to additional physical and psychological morbidity. There is strong evidence that estrogen therapy may partly prevent this menopause-related change in body composition and the associated metabolic sequelae. However, further studies are required to identify the women most likely to gain metabolic benefit from menopausal hormone therapy in order to develop evidence-based clinical recommendations.

5 Hormone replacement therapy prescription – a disconnect between personal and patient prescribing Anna FentonNick Panay Climacteric Oct 2012,  15,  5: 409–410.

6. Body Identical Hormone Replacement.pdf
Climacteric 2012 supp 15: 1-2 Nick Panay full text.  
Climacteric. 2012 Apr;15 Suppl 1:3-10. What’s new in hormone replacement therapy: focus on transdermal estradiol and micronized progesterone Simon JA.The original conclusions of the Women’s Health Initiative study have been questioned as a result of the availability of age-stratified data. Initial concerns regarding the risk of coronary heart disease (CHD) in association with the use of hormone replacement therapy (HRT) have been replaced with concerns regarding thromboembolic disease, encompassing venous thromboembolism (VTE), particularly in younger postmenopausal women, and stroke, particularly in older women. The original publication of the study results led to a dramatic decrease in the use of oral HRT; however, the use of transdermal HRT has increased over recent years. Guidelines from the North American Menopause Society, the Endocrine Society, the International Menopause Society, and specific guidelines from the European Menopause and Andropause Society for the management of menopausal women with a personal or family history of VTE all contain positive statements regarding both transdermal estradiol and micronized progesterone. Unlike oral estrogens, transdermal estradiol has been shown not to increase the risk of VTE, or stroke (doses ≤ 50 μg), and to confer a significantly lower risk for gallbladder disease. Unlike some progestogens, progesterone is also not associated with an increased risk of VTE, or with an increased risk of breast cancer. Based on these data, which are now included in the guidelines, the use of transdermal estradiol and micronized progesterone could reduce or possibly even negate the excess risk of VTE, stroke, cholecystitis, and possibly even breast cancer associated with oral HRT use.

7. Its fitting that arch innovator,s promotors and defenders of premarin, and some who vehemently denied that oral HT causes increasing obesity, have at last changed the tune:

A decade post WHI, menopausal hormone therapy comes full circle – need for an independent commission CLIMACTERICAugust 2012, 15, 320-325 W. H. Utian Case Medical School, Cleveland, OhioThe sudden decision by the National Heart, Lung, and Blood Institute of the National Institutes of Health to terminate the estrogen–progestogen therapy arm of the Women’s Health Initiative (WHI) Study a decade ago now begs two questions: – has women’s health after menopause been helped or harmed as a result of the findings and the way in which they were presented, and, if harmed, what needs to be done to put things right?

Time and multiple reviews of specific publications from the WHI lead to the serious question whether a project designed to be of benefit to women’s health has boomeranged, and instead may have resulted in significant impairment to both the quality of life and physical health of postmenopausal women. It is therefore urgent to confirm whether this is so and whether corrective action needs be taken to prevent even more harm.

There are two obvious and immediate actions to be called for:

(1) The Food and Drug Administration (FDA) needs to revisit the black-box warnings on postmenopausal hormones. Specifically, there needs to be a separation of the advisories for estrogen alone from estrogen and progestogen combined usage.

(2) Justification is given to call for an independent commission to scrutinize every major WHI paper to determine whether the data justified the conclusions drawn.

Women progressing through and beyond menopause in the next decade need to be spared the unnecessary harm that may have been inflicted on their sisters of the previous decade.”

Menopausal symptoms are associated with subclinical atherosclerosis in healthy recently postmenopausal women climacteric August 2012, 15, 4 , 350-357 , A. AugouleaE. ArmeniD. RizosA. AlexandrouM. CreatsaM. Kazani*, G. Georgiopoulos*, A. LivadaA. Exarchakou & K. Stamatelopoulos*University of Athens, Greece

Objectives To determine whether menopausal symptoms are associated with changes in arterial structure and function in healthy, recently postmenopausal women.

Methods One hundred and ten postmenopausal women aged 45–55 years were included in the present cross-sectional study. Menopausal symptoms were recorded by the Greene Climacteric Scale. Anthropometric measures, blood pressure, serum lipids, glucose, insulin, sex and thyroid hormones were determined in each individual. Arterial structure, function and stiffness were assessed by intima–media thickness (IMT), flow-mediated dilation and pulse-wave velocity, respectively.

Results Women with moderate to severe hot flushes had increased IMT compared to women with no or mild hot flushes (IMT in women with no hot flushes 0.61±0.08 mm, IMT in women with mild hot flushes 0.62±0.11 mm, IMT in women with moderate to severe hot flushes 0.67±0.11 mm; p = 0.034). This difference was independent of cardiovascular risk factors like age, menopausal age, smoking, blood pressure, adiposity, lipid levels, insulin resistance or hormone levels. No association was detected between psychological or psychosomatic symptoms and arterial indices. Furthermore, menopausal symptoms were not associated with serum sex steroids or thyroid hormone levels.

Conclusions Carotid IMT, a surrogate marker of subclinical atherosclerosis and cardiovascular risk, was found to be increased in women with vasomotor symptoms as compared to asymptomatic women. This association was independent of cardiovascular risk factors or endogenous hormone levels. It remains to be elucidated whether the presence of menopausal symptoms is an additional cardiovascular risk factor requiring preventive intervention

9. International Menopause Society comments on BMJ paper on HRT and menopause. 09 October 2012 Effect of hormone replacement therapy  on cardiovascular  events inrecently  postmenopausal women: randomised trial. BMJ. 2012 Oct 9;345:\ Schierbeck LLRejnmark LTofteng CLStilgren LEiken PMosekilde LKøber LJensen JE.


Department of Endocrinology, Hvidovre Hospital, Denmark. full text. OBJECTIVE: To investigate the long term effect of hormone replacement therapy on cardiovascularoutcomes in recently postmenopausal women. DESIGN: Open label, randomised controlled trial. Denmark, 1990-93. PARTICIPANTS: 1006 healthy women aged 45-58 who were recently postmenopausal or had perimenopausal symptoms in combination with recorded postmenopausal serum follicle stimulatinghormone values. 502 women were randomly allocated to receive hormone replacement therapy and 504 to receive no treatment (control). Women who had undergone hysterectomy were included if they were aged 45-52 and had recorded values for postmenopausal serum follicle stimulating hormone.

INTERVENTIONS: In the treatment group, women with an intact uterus were treated with triphasic estradiol and norethisterone acetate and women who had undergone hysterectomy received 2 mg estradiol a day. Intervention was stopped after about 11 years owing to adverse reports from other trials, but participants were followed for death, cardiovascular disease, and cancer for up to 16 years. Sensitivity analyses were carried out on women who took more than 80% of the prescribed treatment for five years.

MAIN OUTCOME MEASURE: The primary endpoint was a composite of death, admission to hospital for heart failure, and myocardial infarction.

RESULTS: At inclusion the women on average were aged 50 and had been postmenopausal for seven months. After 10 years of intervention, 16 women in the treatment group experienced the primary composite endpoint compared with 33 in the control group (hazard ratio 0.48, 95% confidence interval 0.26 to 0.87; P=0.015) and 15 died compared with 26 (0.57, 0.30 to 1.08; P=0.084). The reduction incardiovascular events was not associated with an increase in any cancer (36 in treated group v 39 in control group, 0.92, 0.58 to 1.45; P=0.71) or in breast cancer (10 in treated group v 17 in control group, 0.58, 0.27 to 1.27; P=0.17). The hazard ratio for deep vein thrombosis (2 in treated group v 1 in control group) was 2.01 (0.18 to 22.16) and for stroke (11 in treated group v 14 in control group) was 0.77 (0.35 to 1.70). After 16 years the reduction in the primary composite outcome was still present and not associated with an increase in any cancer.

CONCLUSIONS:    After 10 years of randomised treatment, women receiving hormone replacement therapy early after menopause had a significantly reduced risk of mortality, heart failure, or myocardial infarction, without any apparent increase in risk of cancer, venous thromboembolism, or stroke.


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