What’s the point of herbal HRT?

Like the gay movement during the peak of the HIV crisis, the trans community was forced to take our healthcare into our own hands due to the absolute disinterest, and often outright hostility, of the medical establishment. My typical girlfriend knows more about practical transition endocrinology than any endocrinologist I’ve talked to. Everybody being their own doctor brings with it a certain hostile attitude to even the idea of herbal transition. There’s various factors involved in this visceral reaction. The rest of this text is from a transfem perspective, but the same rationales would apply for transmasc or non-binary transition:

• Synthetic hormones for transition are poorly tested and poorly understood. Plant compounds are even less tested and not at all understood. Why discard what precious little reliability we have?

• Commercial plant products are not regulated. A lot of them are outright scams, selling flour or random vegetable debris for trendy expensive herbs.

• Even if there’s some real active principle, you can’t rely on the dosing, and nobody knows how much to dose.

• Phytoestrogens are ‘weakly’ estrogenic; i.e. they activate the estrogen receptors much less than endogenous estrogens. Even among the endogenous estrogens, only 1 out of 4 (E2, estradiol) is believed to induce strong feminising changes. And even with estradiol, feminisation is often subpar. Why stack the deck even worse against you?

• Even in anecdotes of herbs doing something, this usually involves doses that are much more expensive than the cost of hormones in any reasonable country that has a healthcare system.

• Moreover, weak estrogens may hog the receptors and outcompete E2 or other, better estrogens. If a trans person romanticises the idea of magical girl witch herbs and keeps taking high amounts of phytoestrogens after starting synthetic hormones, this may actually hinder their transition.

• Cis men have dysphoria over the idea of feminisation, and, not knowing what’s dysphoria or how to deal with it, panic. So a lot of reports on soy milk growing boobs have acquired the character of tabloid-panic urban folklore. (If only it was that easy!)

• Freshly hatched trans girls often are reluctant to commit to transition, having to fight back a lifetime of social gaslighting and take the step of outing oneself as a targeted minority. Dealing with the medical cistem is insult added to injury. It is a lot less stressful to buy some sketchy plant pills from Amazon. But the sketchy plant pills from Amazon will do nothing, especially without blocking T. The sooner the new chick finds her bravery and beats the cistem down into giving her the good stuff, the better off she’ll be.

• Also, hesitant trans girls may fall into the natural fallacy and think it’s safer to first try out things if they’re in herb form. (Taking liquorice long-term will damage your liver; E2 spray won’t.)

• Herbalism is based on traditional knowledge and tinged with varying degrees of mysticism/alternative medicine quackery.

All of these arguments are valid, and are the reasons why I wouldn’t replace industrial hormones for plants. I do have an argument against a pure WPATH-based, establishment-medicine, obey-your-doctor approach. Please observe Figure 1. below.

=> Figure 1. Argument against obeying your doctor.

These were fought for every step along the way:

• When I was gatekept for 6 months because ‘some people are delusional’ and ‘we need to make sure you are ~really~ trans’, I was also afraid of immigration trouble if I imported DIY hormones, and I didn’t yet know anyone who could give me some safely. So I dug into pubmed for anything that reduced testosterone or had estrogenic effects, and took the highest doses I could find of liquorice, spearmint and pueraria mirifica. By the time I was finally allowed to start synthetic HRT, I already had breast buds, had lost muscle bulk, and my T was down to around 100ng/dL.

• When a doctor refused to try upgrading gel to spray I insisted anyway. It bumped up my E2 from ~80 to 120pg/mL.

• When the doctor then told me 120pg/mL was too high, I started timing my blood tests so that I could explore higher doses, and did it anyway.

• I had to change doctors to safely expore the testicle technique from r/MtFHRT . It increased E2 to ~300 to ~350pg/ML.

• When my doctor refused to prescribe progesterone, I changed doctors and did it anyway.

• When the cistem was unable to provide injections, I got them from my community and did them anyway.

• Based on Powers' theory of free E2 and SHBG feedback, I started a cycle that would go from a high of ~1000pg down to adrenals and repeat, figuring that it would hit the sweet spot at least part of the time and expose me to a variety of hormonal profiles.

• At this point I had nice Tanner 4 breasts, but less upper body subcutaneous fat than I’d like, puffed aureolæ with no nipples protusion, and development seemed stuck.

• I experimented with cycling, with the stop-and-go technique from r/estrogel, and finally started doing phytoestrogens again. A month after the last 2 experiments, my breasts plumped up noticeably, became sensitive again, and nipples seem to be changing into the Tanner 5 stage.

Now we need to add the disclaimers:

• I do a lot of self-experiments all the time with N=1. There’s no way to know what helped, if anything. Theoretically, it could even be that staying on track and doing just E2 gel and nothing else would have had even better results.

• I’m Brazilian. Women in my family are curvy and large-breasted. Could be my good results are from genetics alone and nothing I did made any difference.

• This is my 4th year of transition. Could be the timing was a coincidence and it just needed this long to round up.

But while my level of trust on this is low, I would still bet that some of the things I tried did something, and the body I have today is the cumulative result of all that—both the mainstream HRT and the sketchy. My first endo once told me confidently ‘trans women just don’t grow breasts very much on HRT’, and advised me to give up and save money for breast augmentation if I cared so much, and that if I didn’t want body hair I ‘should have been born Nordic’. He’s just convinced that feminisation is crappy and partial and that’s how it is. He also told me there’s a reason for the official recommendations for cyproterone + 80pg E2, and he would never prescribe anything but that. When I look at the mirror I wonder how he never connected the two things.

Let’s see some arguments in favour of experimentation in general, and of herbal approaches in particular.

Nobody knows how this thing works

Transition science is severely understudied. Heck, even cis women medicine is a second citizen. There’s no reliable model of how various hormones interact and the roles of gonadal vs. adrenal vs. tissue production vs. fluctuations in receptor density and how much sex-coded bodily changes are influenced by growth hormones etc. etc.

This does not mean that science is fake and you should replace it by Venus crystal meditation. It does mean that there’s a lot of room left for exploration. Very little research was ever even attempted on the quality of feminisation; most cis researchers don’t empathise with our needs enough to even ask that question, they look at us and think the problem is a risk of suicide, not that the problem is a hairy chest. A lot of biomedical research relies on terrible metholology, like correlational studies based on null-hypothesis significance testing, which is little more than flipping a coin at a question (this is why there’s so many headlines on ‘X cures cancer’ then ‘X causes cancer’ back-to-back). Most of these p-value-as-oracle studies never replicate; and capitalism ensures there’s no incentive to try to replicate in the first place.

Again, herbal medicine research is even worse. My point is the weaknesses of the current models, plus the poor results that have been normalised, plus the occasional outlier to the poor results, mean it makes sense to try out stuff out of the beaten track. Evidence for progesterone or dietary gynecomastia ranges from low quality to anecdotes; but that’s not far off from the evidence WPATH uses to still force poor American girls to take spiro.

Maybe weak estrogens play a role after all

Estrone (E1) used to be the villain in DIY transition communities. In typical approaches to treatment many year ago, trans girls used to be prescribed pills as first-line medication, rather than gel or patches. E2 pills will bump up your E1 beyond cis-girl ratios. Since E1 is a much ‘weaker’ estrogen, the community theory was that it would hog up the receptors and prevent the good stuff from working well. This seemed to be validated by the very frequent cases of women who changed from pills to injections and unstalled immediatelly, after years without subcutaneous fat deposit or body hair reduction or breast volume increase etc. Again, anecdotes, but Powers' early clinic reports seemed to validate this theory, because a large amount of his patients benefitted from injections in this very visible way.

That was until it came to fore (both in Powers' clinic and from further independent reports) that some women who were stalled on injections progressed immediately upon adding pills, or even switching from injections/transdermal to pills.

Bodies are more diverse than universal models assume

I know a girl who took the minimum-dose E2 pill, 2mg, and got no serum E2 at all. 2mg is too little for most people but in her case it seemed to do nothing; her estradiol levels were, and still are, lower than cis men’s, and this with no interference from gonadal testosterone (she does GnRH blockers). She tried increasing it to 4mg, still a modest dose for most purposes. It made her sick. The effect was consistent and baffled doctors. That can’t happen; E2 has no overdose effects. But the reaction was clear; take 4mg, get sick. Even more interestingly, she actually feminised super well on 2mg oral E2. Eventually she got access to a lab that tests everything and found out that she gets absurdly high levels of E1. Like, scarily above normal levels of E1, from 1 minimum dose E2 pill. And she transitions fine on that.

Maybe doing the same thing all the time isn’t the best approach

Consider the anecdotes from r/estrogel. It seems that many trans women who were forced to stay off estrogens for a while, then went back, were surprised by the effects getting stronger than ever. Trying to imitate an uterine cycle has, in my read of self-reports at least, unclear results. But these cases involved longer breaks, 4 to 6 weeks, and seemed much more promising. The admin proposed, could FSH/LH be involved? Normally we try to nuke LH because of its role in increasing gonadal hormone production, but at least one study identified the otherwise uncommon high-LH high-E2 combo as a correlate to high breast growth in pubescent cis girls. If you periodically ‘reset’ then ‘accelerate’ your doses, the homeosthases will be catching up all the time, so you’ll be exposed to different hormonal ratios. Maybe some of them are necessary for full pubertal development. Maybe this speculation is all bunk and you’re wasting time if you do it, you could be soaking your receptors in E2 all along.

At this point what I recommend to new girls is, if whatever you doing is working for you, keep doing it as long as you can; if it’s not working try to shake up things a bit. Increase dosages, or decrease if it’s very high, change from pills to transdermal or transdermal to injections or add pills to spray or add P4 or remove P4. Change your T blocker, try monotherapy, do an orchi. Trust bodily changes you can see and feel over serum hormone levels. Trust mental subjective feelings.

And if you’re into this kind of thing, and want to play with it, maybe add a daily spoonful of pueraria to your cereal, sprout some fenugreek seeds and eat them regularly, DIY some lavender+tea tree essential oils on rosehip seed oil carrier and rub on breasts every night (patch test first!). Probably it will do little, or nothing. Maybe it will actually impair your HRT. Maybe it will surprise you. All I know for sure is I tried everything I could, and now boobs squishy.

Resilience

To this day, my country’s only brand of E2 spray doesn’t even mention the existence of transgender folk. It’s sold as medicine for menopause. And direct E2 supplementation for menopause seems to be getting out of favour in cis medicine. The moment cis women stopped doing estrogen injections, injections disappeared from the market. Most research we have on how to block T is for treating cis men with cancer. Blocking T and DHT turns out to stave off prostate cancer only temporarily, so now other avenues are being sought.

I’m writing this at a low point in a mishandled pandemic that’s being now treated as if it was over, for no other reason than capitalists wanting to see the profit graphs going up; while fascism is rising globally, government repression started targeting activists near me, and threats of war are a kind of opening salvo to the chill I get when I hear the springbirds singing in early February. What do we do when we can’t buy hormones anymore?

I would recommend everyone to look up how mix your own medicine, and stock some raws from factories (gang up with your crew; people can collaborate in different ways). But a diversity of strategy could be useful here. Not everybody everywhere will be able to access raw chemicals or keep around ethanol and a precision scale. Growing a garden is a lot more doable than a processing lab, and in some not-so-implausible scenarios, might be a good backup to unstable supply chains. Maybe herbal HRT is only a second-rate substitute, but it’s not nothing, it’s not just placebo. American kudzu doesn’t have all the estrogenic compounds of its relative Pueraria mirifica, but has a lot of them, and shows promise in cis HRT studies. American girls will ~never~ ever run out of kudzu.

I’m aware that this is just prepper silliness and the chances of any of this knowledge being actually useful are remote. But still, when I look at the news, I find it oddly comforting to know that stinging nettles tincture is a 5α-reductase inhibitor.