When i found out my ovaries weren’t working i was compelled to find out all i can. It quickly became apparent that POI is just a big mystery and there’s not much anyone can do about it. I also noticed people mentioning DHEA though, in that it’s possibly helpful, although it is controversial.
DHEA (dehydroepiandrosterone) is an androgen, a male hormone. It’s the starting material that testosterone (that famous androgen) is made from, but it’s also a starting molecule for oestrogen. Both male and female humans make it in their bodies. Some people are not aware that females produce ‘male hormones’, but we do, mostly from the adrenal gland, but actually also in the ovaries. And these androgens are just now being recognised as important in ovulation. Walters 2015 is a great resource to learn more (although heavy with biochemistry concepts and jargon): http://www.reproduction-online.org/content/149/4/R193.full.pdf+html
Instead of delving into the mechanistic details of why DHEA might improve ovulation (we don’t know yet), we can assume that it does, and look for data to support this. My review of the data is by no means the most comprehensive, but a few days of work was enough for me to make a decision in regards to my personal situation. I started with a simple search on Google Scholar with the search terms ‘DHEA’ and ‘diminished ovarian reserve’. Then i limited to only those published this year. This gave me 31 documents to check. A lot of them were review articles, which was handy in that these would report on earlier studies. Others were not actually relevant, in that they only mentioned DHEA or ovarian reserve in passing. My aim was to find recent data that showed the effect of DHEA on ovaries like mine. This turned out to be only 3 studies.
Cui et al. used a mouse model, where the ovaries were damaged to make them resemble poorly functioning ovaries: http://europepmc.org/abstract/med/25790679
I don’t know enough to evaluate if this is an adequate model of POI/DOR, or how closely mouse ovulation mimics human ovulation. These issues should be addressed in the full-text of the article, but i only have access to the abstract. I’m not going to go to the trouble of trying to get a copy of the full text because the results in the abstract are not intriguing enough. The authors state that measures of ovarian function (including anti-mullerian hormone, AMH) increased in the mice given DHEA, as compared to mice who had not. This sounds promising, but perhaps isn’t at all. The authors state the results are statistically significant, with a p-value less than 0.05. This is the bare minimum that needs to be met in terms of statistically comparing two results ( of the mice treatment groups, in this case). But the authors don’t actually state the p-value, or the size of the result. This makes me think that the difference between the groups was very small. Additional evidence for this is that they state that AMH etc. increased in the DHEA group compared to the model group (with damaged ovaries). But they also had a ‘normal’ group, without damaged ovaries. Supposedly then the AMH etc. was a little higher than the model group, but not as high as the normal group.
If you are thinking, ‘well that’s ok, every small improvement is worthwhile, you perhaps can’t expect the treatment to completely reverse the damage and restore normal hormone levels’. But that is only one way of interpreting the data. We know all of these hormones fluctuate (even AMH!), so this small difference could very well just be ‘noise’, i.e. chance is involved because there is natural variance, there is no actual increase, it just appears that way.
Long story short, although i haven’t even seen the data, there is no strong evidence here (that’s what i’m after).
The next study was Tsui et al. http://www.tjog-online.com/article/S1028-4559(15)00025-X/pdf This one was very helpful. The entire article is available for free, and it includes a review of other studies done as well as new data. This data also purported to be promising due to small changes in ovarian function in patients who had low ovarian function. One obvious limitation of this study, is that there is no control group, another is that it is small (just ten patients). In fact this study closely resembles other studies on DHEA that have been criticised for the same reasons. At least this study was prospective. In terms of comparing to my own personal situation, these patients were not that ‘dire’. An FSH (follicle stimulating hormone) of ~15 IU/L is still within the normal range. And while an AMH of ~0.4 is a concern, it’s not the worst case. It was interesting to see that the inclusive criteria in the other studies (presented in Table 2) were similar. My conclusion therefore is that better studies might be warranted to improve the chances for ‘poor responders’ (not exactly the same as DOR/POI) but for those of us with menopausal hormone levels there is still no evidence that DHEA could help.
Thirdly, Vlahos et al. http://www.rbmojournal.com/article/S1472-6483(14)00551-3/abstract They state some hormonal improvements, although similar to the first study the size of the effect is conveniently left out of the abstract. I don’t have access to the full text but i will take on board their comment about ‘uncertain effectiveness’. This conclusion keeps on being mentioned, as in the review of Vardos et al. (http://www.rbmojournal.com/article/S1472-6483(14)00551-3/abstract) , who state: “Unfortunately despite the lapse of 5 years since the last publication, there is still a lack of robust evidence for most of the adjuvants searched and large well-designed randomised controlled trials are still needed” in reference to DHEA as well as other treatments/adjuvants for fertility.
Overall, there is just not enough evidence for me to bother trying to get my hands on DHEA. I’m glad i double-checked this as an option, and learnt a lot about ovaries in the process!
Since drafting this post i’ve read even more about DHEA. My decision is still the same, but there should be another DHEA-relevant post coming soon.