Ivf Success Rates After Miscarriage – Murmungee, Victoria

Testosterone and IVF success rates Research discussion

Our recent publication in JARG is probablyone of the more important publications of our androgen related, DHEA related, work inrecent years because it details to a very large degree how DHEA works. We now for 78years know that DHEA improves ovarian function in women with diminished ovarian reserve.We however really learned that empirically because we saw it work, we did not understandhow it worked. Now we understand that it works at least to a large degree via the conversionof DHEA to testosterone, testosterone is the main male hormone both in females and males.Testosterone in turn has been shown to be very, very important for the very early stagesof follicle maturation, long before follicles

really ovulate and release the egg; two tothree months removed, two to three months before that follicle reaches maturation andreleases an egg. So it is at these very, very early stages that testosterone is very importantfor growth and development of these maturing follicles. This was first learned a few yearsago in mouse experiments. We suspected that the same principle applied also to the human,but we had no evidence. This paper details now evidence how DHEA is converted to otherandrogens, and what the paper showed, what the study showed, is that there is a directrelationship between how well DHEA converts to testosterone with subsequent pregnancychances. To summarize it in one sentence:

The lower the testosterone of an infertilewoman with diminished ovarian reserve is at treatment start, and the higher the testosteronegoes after she gets DHEA supplementation, the higher the patient's pregnancy chancein IVF subsequently. And as we now understand, the reason for that is the DHEA that the patientingests is very quickly converted to DHEA sulfate and then on to testosterone and alsothe female hormone estradiol, but in the majority to testosterone. And it is that testosteronethat benefits the little follicles, but we see those effects only weeks to months laterand that is why we once again empirically now know for a number of years that it takesat least 6 weeks of taking DHEA, maybe a little

longer, to get the maximum effect. The reasonis because what we are actually treating is the very early stages of follicle maturation,while all fertility treatment over the last 50 years was geared only at the last two weeksof follicle maturation. The implications for treatment from thesefindings are actually very significant and we indeed have started to integrate them alreadyinto our treatment of fertility patients here at CHR. Probably the most important consequenceof these findings is that we no longer start IVF cycles until a patient has reached adequatetestosterone levels. We now know the range where we want the patient to be at a minimum.So in a way we are bringing, since most of

our patients are older, we are bringing theirtestosterone levels back to where they used to be when they were young. So that is themost important consequence of these findings and has pretty radically changed how we dothings at CHR. But the secondary finding is, in this study, that not all women convertthe DHEA to testosterone equally well. Indeed there are roughly 15% percent of women whoconvert very, very poorly, in other words you can give them DHEA and DHEA, for longertime as usual and still they will not raise their testosterone. And in these women wenow have started a al trial where we give them testosterone directly by applicationto the skin. It is a perspectively randomized

trial where we are trying to overcome theinability to properly convert DHEA to testosterone. This is also very important because DHEA isthe most abundant steroid hormone in our bodies and it is kind of the reservoir for otherhormones; and as I previously mentioned, DHEA is converted to both sex hormones, testosteroneand estradiol, so it is the reservoir for all sex hormones in the human body. But likeanything else different individuals have different abilities. The third finding of our recentstudy is that some of these differences in the ability to convert DHEA to testosterone,like anything is genetically controlled. And there appears to be a pretty strong statisticalassociation with a gene called FMO1 gene which

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