I reversed osteoporosis without drugs

Thank you. You have confirmed what I have believed for some time but have just run into roadblocks with my doc's. The WHI has really screwed us over.

Can you please provide your age?
I am 62 and planning to start Evenity for 1 year. Then I am seriously considering HRT to lock in gains instead of reclast.
Just curious if you’ve had any issues with HRT if post menopause.

I was 62 when I went on HRT and am 68 now. I've been on a very low dose of .025 most of that time with no issues at all. I recently went to see Dr Felice Gersh who is an integrative gynecologis is well versed on the use of HRT and she wanted me to increase my dose to .05 for better effect. I tried it and had too much breast tenderness for my comfort so I went down to .0375 and have had no discomfort or issues on that dose.

Thank you since I am 62 that is very helpful. And do you do Estradiol and Testosterone or Estradiol and Progesterone??
My HRT doc was recommending starting with testosterone but I’m not sure…..
And was there a reason why you took it while on Evenity vs starting it afterwards?

One out of 8 women gets breast cancer and 80% of those are fed by hormones. I would love to see studies that update or counter the WHI. As a hormonal breast cancer patient (10 years ago) this option is not possible for me. I hope people are getting genetic testing at least, before going on HRT.

I have been reading about Estriol, used as a cream externally on the minor or major labia, as a way to repair any damage from menopause, like dry and painful sex, as well as assisting with maintaining bone integrity. It is advertised as a 'weak' estrogen with very little effect on breast tissue. This is an excerpt from the company I am considering: "Many women experience vaginal dryness and their practitioner decides to use Estradiol. There is significant research that finds low dose vaginal ESTRIOL is more effective at repairing the vaginal tissue – WITHOUT increasing the level of circulating estradiol in the rest of the body. So chances are, the small amount of estriol in the cream used consistently will repair the tissue. It is also considered wise to make sure that any estradiol is balanced by progesterone. Estrogen is a proliferative hormone – which means it makes cells grow. Progesterone has the opposite effect – it stops estrogen from growing too many cells. Estradiol is the strongest type of estrogen and should be balanced by bioidentical progesterone, not synthetic progestins." Does anyone have any knowledge or experience with Estriol?

@kanieben there are many different views on whether "progesterone has the opposite effect- it stops estrogen from growing too many cells." Some studies say it encourages breast cancer (progesterone receptors in cancer cells), some say it helps and some say it is neutral.

My breast cancer testing showed that my cancer was 95% responsive to estrogen and 80% responsive to progesterone.

I encourage everyone to read about the complexities of this here https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7156851/ particularly the section on HRT for menopause. It seems to say use for 5 years is safe. With so many contradictions in studies, clearly more research is needed. These studies do not appear to use bioidentical hormones.

Menopausal hormone therapy and breast cancer risk
The relationship between risk of breast cancer and use of menopausal hormone therapy has been investigated in many epidemiologic studies. A 1997 review by the Collaborative Group on Hormonal Factors in Breast Cancer brought together and reanalyzed data from 51 epidemiologic studies that represented about 90% of the worldwide evidence on this topic (140). The main analyses of the relation between risk of breast cancer and use of hormone therapy included 53,865 postmenopausal women (17,949 cases and 35,916 controls) with known age at menopause and use of menopausal hormone therapies. The results show that the increase in the relative risk of breast cancer associated with each year of use in current and recent users is small. Therefore, inevitably some studies show significant associations and others do not. However, combination of the results across many studies has the advantage of reducing such fluctuations. The increased risk of breast cancer was not significant until 5 years of menopausal hormone therapy use. For women who used menopausal hormones for 5 years or longer, the relative risk was 1.35 (95% CI: 1.21–1.49). The risk was reduced after discontinuing menopausal hormone therapy use and largely, if not completely, disappeared after about 5 years. Information about the hormonal constituents of the menopausal hormone therapy preparations used the most was available for only 4,640 (39%) of eligible women. The women in the main analysis had their breast cancers diagnosed on average in 1985, when the type of hormone used was predominantly estrogen alone; only 12% of the women used estrogen and progestogen combinations. There was no significant variation in the relative risk of breast cancer according to the formulation or dose of the estrogen used by most women, and no evidence of marked differences between menopausal hormone preparations containing estrogen alone and those containing both estrogen and progestogen.

In a later review (196), data from 8 randomized controlled trials and 19 epidemiologic studies were used to determine whether there is an association between menopausal hormone therapy use and breast cancer. The review also addressed a number of other questions, including whether data exist to show a differential effect from use of menopausal hormone therapy products, doses, regimens, and routes of administration. The results show that the average risk of breast cancer with use of estrogen alone was 0.79 (95% CI: 0.61–1.02) in 4 randomized trials involving 12,643 women, whereas the risk with estrogen-progestin use was 1.24 (95% CI: 1.03–1.50) in 4 randomized trials involving 19,756 women. In contrast, the average relative risks reported in the epidemiologic studies were higher in current users: 1.18 (95% CI: 1.01–1.38) for estrogen alone and 1.70 (95% CI: 1.36–2.17) for estrogen-progestin; however, the risks were not as strong in ever users: 1.08 (95% CI: 0.97–1.20) and 1.31 (95% CI: 1.12–1.53), respectively (196).

For the analyses of the association of breast cancer risk by hormone formulation, dose, regimen and route of administration, the number of studies used in each group varies. For progestogen types, only 2 studies included risks with current exposure (139, 197). The analyses compared a C-21 related progestogen, namely MPA, with 2 C-19 related progestogens, norethindrone and levonorgestrel. Breast cancer risks with C-21 and C-19 related progestogens were virtually the same (2.14, 95% CI: 1.18–3.87 and 2.14, 95% CI: 1.68–2.72, respectively) (196). Only one study reported information on progestogen dose; the Women’s Health Study evaluated MPA dosages over the ranges of < 5 to 10 mg/day; the trend from lowest to highest dose was not significant (198).

Although the 2 major reviews of data reanalysis just described include a substantial number of studies (51 epidemiologic studies in one review, and 8 randomized controlled studies and 19 epidemiologic studies in the other review), none of these studies include progesterone data. However, this changed with the publication of results from the E3N study to investigate risk factors for cancer in women, including exogenous hormones (142, 199). Although oral progestins were used most widely in the E3N study, there was also substantial use of exogenous progesterone. The progestins included dydrogesterone, medrogestone, chlormadinone acetate, cyproterone acetate, promegestone, nomegestrol acetate, norethindrone acetate, and MPA.

In an updated report on the E3N cohort evaluating 80,377 postmenopausal women 40–65 years of age at enrollment and followed for up to 12 years, use of estrogen alone was associated with a 29% increased breast cancer risk (95% CI: 1.02–1.65) (199). This increased breast cancer risk with use of estrogen alone (almost exclusively estradiol compounds and mostly administered transdermally) differs from that of the WHI estrogen-alone trial which found a decreased risk with oral conjugated equine estrogens (200).

The association of estrogen-progestogen combinations with breast cancer risk varied significantly according to the type of progestogen (199). The RR was 1.00 (95% CI: 0.83–1.22) for estrogen-progesterone, 1.16 (95% CI: 0.94–1.43) for estrogen-dydrogesterone, and 1.69 (95% CI: 1.50–1.91) for estrogen combined with other progestogens, which included medrogestone, chlormadinone acetate, promegestone, nomegestrol acetate norethindrone acetate, and MPA; the increased breast cancer risk was consistent across these latter estrogen-progestogen formulations. Estrogen alone, estrogen-progesterone and estrogen-dydrogesterone did not differ significantly from one another in breast cancer risk, but the risks were all significantly lower than that of estrogen combined with the other progestogens. It should be noted that the chemical structure of dydrogesterone differs from that of progesterone only in that the methyl group at the carbon 10 is in the alpha-orientation and there is a double bond between carbons 6 and 7. The E3N study was the first epidemiologic study to show that estrogen-progesterone and estrogen-dydrogesterone combinations may be the least harmful menopausal hormone therapies with respect to postmenopausal breast cancer risk. However, more evidence is required to make firm clinical recommendations for use of these formulations, compared to other formulations, in managing menopausal symptoms.

HRT itself does not cause breast cancer. It can feed an already existing estrogen-driven cancer though. It's important to remember that in the WHI study, the 26% increase in breast cancer rates on HRT was actually a very, very small increase. It was sensationalized and the relative risk was reported not the absolute risk. In our daily lives, the risk of developing breast cancer between the ages of 50 and 60 is 2.33%. On HRT, according to that study, the risk increased from 2.33% to 2.94%. That's a tiny increase of 8 additional women per 10,000. And that was for women on Premarin – an oral estrogen from horse urine that contains a multitude of estrogens, along with synthetic progestin which some speculate might be the greater villain. Both are considered much less safe than transdermal estrogen and bioidentical progesterone so actual increased risk may even be smaller than was "concluded" by the study. For some people, any increase in risk is too much risk which I understand, particularly if there is previous breast cancer or a genetic risk. It's a really personal decision and one that should be explored with a menopausal specialist that has a thorough grasp of all the nuances.

I believe that estradiol is typically used for vaginal health though estriol may sometimes be used. In either case, it saturates and restores vaginal tissues, is not systemic and will not have an impact on your bones. They prescribe vaginal estrogen to women of all ages, even in their 90s as it is safe and will help to minimize the risk of UTIs which become more prevalent as we age. Estriol is the estrogen present during pregnancy. Estradiol is present throughout our lives and that is the form that is most often prescribed for menopausal symptoms, bone maintainance, vaginal health. Recently, there are new facial creams available using Estriol. Studies have shown skin enhancement and no systemic outcome.

@teb did you read what I posted? The conclusion was that 5 years was safe and that more research is needed on progesterone.

I would not quibble about anyone choosing HRT. Of course. I realize that hormones only feed already existing cancer cells and are not a cause. But it takes a long time for cancer to develop so we don't all know whether there are cells that will be fed by hormones- until the cancer is apparent.

I believe the WHI was skewed older which increased the risk in the results. Unfortunately there seem to be flaws in every study and many are contradictory, for just about every medical issue.

HRT is not technically "natural" but apparently nature didn't intend for us to live so long.