New Australian study below [1].
I remember reading old writings years ago that stated that, while women needed estradio [E2] for bone health, men only needed testosterone [T]. Made no sense, of course - why would there be two mechanisms? Men who had osteoporosis & very low T, also had low estradiol. Most male E2 comes from the aromatization of T. T supplementation in otherwise healthy men fixes the bone problem, but primarily because it restores E2.
The new paper politely opens with:
"There is increasing recognition that, in men, some biological actions attributed to testosterone (T) are mediated by estradiol (E2)."
The subject of addback E2 via low-dose patches has come up here a few times. There is a vlog post by Dr. Myers that is useful, but I have often wondered why the approach is not standard practice for men on ADT. If E2 dips below 12 pg/mL, prescribe the patch.
In the Australian study:
"E2 treatment reduced hot flushes and bone resorption."
When serum calcium levels dip, osteoclasts break down bone to obtain calcium (resorption). This is a short-term response which is followed by calcium uptake from the gut &, ultimately, osteoblastic activity to rebuild bone. For this we need some calcium in the diet, vitamin D, a few other things, & ... E2.
...
But perhaps doctors prefer to treat with a bisphosphonate because T is also very important?
Here is a 2013 paper from "Current opinion in endocrinology, diabetes, and obesity" (no doubt widely read by oncologists) [2]:
"Evidence from recent studies shows that the contributing role of testosterone to osteoporosis is modest and likely trumped by other factors such as estradiol levels. A few studies have documented an association between low testosterone levels and lower bone mineral density (BMD), increased prevalence of osteoporosis of the hip and low bone mass-related fractures. Other studies, however, have found that testosterone levels are not independent predictors of bone resorption or formation markers, BMD at the hip or incident fractures."
"Although male hypogonadism is associated with osteoporosis, estradiol is likely to be the more important hormone for bone health."
-Patrick
[1] ncbi.nlm.nih.gov/pubmed/295...
Eur J Endocrinol. 2018 Mar 16. pii: EJE-17-1072. doi: 10.1530/EJE-17-1072. [Epub ahead of print]
Short-term effects of transdermal estradiol in men undergoing androgen deprivation therapy for prostate cancer: a randomized placebo-controlled trial.
Russell N1, Hoermann R2, Cheung AS3, Ching M4, Zajac J5, Handelsman DJ6, Grossmann M7.
Author information
1
N Russell, Department of Medicine (Austin Health), The University of Melbourne, Melbourne, 3084, Australia nicholas.russell@austin.org.au.
2
R Hoermann, Innere Klinik I, Klinikum Lüdenscheid, Lüdenscheid, 58509, Germany.
3
A Cheung, Department of Medicine (Austin Health), The University of Melbourne, Heidelberg, Australia.
4
M Ching, Pharmacy Department, Austin Health, Heidelberg, Australia.
5
J Zajac, Medicine, University of Melbourne, Heidelberg, 3084, Australia.
6
D Handelsman, ANZAC Research Institute and Dept of Andrology, Dept of Andrology, Sydney, 2139, Australia.
7
M Grossmann, Medicine, Austin Health/ Northern Health, University of Melbourne, Heidelberg, 3084, Australia.
Abstract
OBJECTIVE:
There is increasing recognition that, in men, some biological actions attributed to testosterone (T) are mediated by estradiol (E2). This study used two low doses of daily transdermal E2 gel to assess effects on circulating E2 concentrations in men with prostate cancer with suppressed endogenous E2 production arising from androgen deprivation therapy (ADT). Secondarily, we aimed to assess short term biological effects of E2 addback without increasing circulating T.
DESIGN:
28-day randomised, placebo-controlled trial Methods: 37 participants were randomised to either 0.9 mg or 1.8 mg of 0.1% E2 gel per day, or matched placebo gel. Fasting morning serum hormones, quality of life questionnaires, and treatment side effects were evaluated at baseline, day 14 and day 28. Hot flush diaries and other biochemical measurements were completed at baseline and study end.
RESULTS:
Transdermal E2 significantly raised serum E2 from baseline to day 28 compared to placebo in the 0.9mg dose group (median 208 pmol/L; interquartile range 157-332), and in the 1.8mg dose group (median 220 pmol/L; interquartile range 144-660). E2 treatment reduced hot flush frequency and severity as well as beta carboxyl-terminal type 1 collagen telopeptide.
CONCLUSION:
In men with castrate levels of E2 and T, daily transdermal E2 0.9-1.8mg increases median serum E2 concentrations into the reference range reported for healthy men, but with substantial variability. E2 treatment reduced hot flushes and bone resorption. Larger studies will be required to test whether low dose E2 treatment can mitigate ADT-associated adverse effects without E2-related toxicity.
PMID: 29549104 DOI: 10.1530/EJE-17-1072
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How many of you are using tE2 as your only form of ADT?
