So, just so you all know: Trans. Girls. Get. Periods.
First lets get this out of the way… Yes, trans women can have periods. No, we do not menstruate, but if your definition of “period” is so narrow so as to only include a flow of blood, then you are not living in the 21st century. I’m not going to spend time justifying this, it’s been done better by others. The purpose of this post is to explain the beginnings of how and why, as I have come to understand them.
Disclaimer: I am not a doctor, but being trans necessitates a degree of understanding of human biology and endocrinology, and I have made a hobby out of learning as much about endocrinology as I can without medical school. I am constantly reading clinical and academic papers on the inner workings of the human body, and this has given me a lot of insight into how these systems function.
For purposes of brevity I use the terms women, men, female and male to refer to individuals whose bodies are primarily estrogenic or androgenic, regardless of if that is by organic or artificial processes. This does not refer to the particular organs a person has, and I denote organ specific conditions were appropriate.
Additionally, the use of “Trans Women” in the title and parts of this piece is a shorthand for individuals who were assigned male at birth and are now on estrogen hormone therapy. Not all transgender women take estrogen, and not all transgender people who take estrogen are women, their identities are just as valid and I do not wish to exclude them with the wording of this essay, but in some contexts it was hard to avoid. I apologize in advance for the binary-centric nature of this post.
It all starts with the hypothalamus, the CEO of Endocrine Systems. The hypothalamus excretes Gonadotropin-releasing hormone (GnRH), a tropic peptide that regulates the entire process. GnRH is received by the pituitary gland, which then in turn releases two other hormones: Luteinizing Hormone (LH) and Follicle Stimulating Hormone (FSH).
In people with testes, FSH supports the maturation of sperm, and in people with ovaries, FSH stimulates the maturation of ovarian follicles into gametes. As the follicles reach maturation, they start to excrete large amounts of estradiol, and this is what causes the first estradiol surge in a 28 day cycle. One or more follicles fully mature into a gamete and the rest spin down until next month.
LH causes the production of testosterone in both the testes and the ovaries, but in the ovaries that testosterone is immediately metabolized into estrogens. LH also induces luteinization of mature ovarian follicles (hence the name), which produces progesterone and even more estrogens, and triggers ovulation.
In both cases of estradiol and testosterone, the presence of those hormones affects the GnRH pulses that hypothalamus produces, in a negative feedback regulation loop. Too much E or T in the system, the hypothalamus closes the valve; too little and it opens the valve.
The hypothalamus pulses approximately every 60 to 120 minutes. The frequency of the pulses effects which hormone is released (lower frequency skews towards FSH and high frequency triggers LH), and the intensity of the pulse controls how much.
In males this is a persistent pulse frequency and intensity, except during moments of sexual excitement when the pulses grow stronger and faster (thus increasing LH output) in order to boost testosterone and sperm production. In females, however, things act differently; estradiol also has a positive feedback effect on GnRH production that kicks off in estrogen dominated systems.
At a critical threshold of estradiol levels, the GNRH1-5 genes activate a genomic response that causes fluctuations in GnRH rhythms, essentially changing what the brain perceives as it’s proper baseline on a day to day basis over the course of a monthly cycle. These rhythms cause the rise and fall of LH and FSH in the patterns which stimulate the ovulation and menstrual cycle, including the dramatic spike that occurs half way into the cycle in order to induce ovulation.
In short, the hypothalamus has two modes, T dominant and E dominant. If you’re running on estrogen, your genes tells the hypothalamus to cycle your hormone levels, regardless of if you actually have ovaries. The hypothalamus doesn’t know there’s nothing there to listen to those signals, it just knows how much estrogen it expects to be in the blood stream, and it responds accordingly with regulation of GnRH output.
But here lies the rub: Trans women’s estradiol and progesterone levels do not rise and fall with these cycles, they remain constant. Injection and transdermal dosages have rise and falls on the scale of 1-2 weeks, and those on pills experience it on the scale of hours, nothing approaching the rise and fall that aligns with LH and FSH shifts. This means that the hypothalamus is constantly responding to levels that rarely match what it expects for that point in the cycle (broken clock, as it were), and producing in response to what it expects vs what it find.
Without ovaries, tho, there’s nothing to respond to these LH and FSH fluctuations, right? Well… not exactly.
The ovaries are far from the only point source for estradiol. Numerous organs throughout the body produce both estrogen and testosterone. The adrenal gland, adipose fat deposits, bone marrow, muscles and even the breasts themselves all produce estrogen and progesterone through various means. Most of the hormones are used up locally within the cells they’re produced in, but a portion of it can and does escape into the blood stream, and the majority of adrenal production is released directly into the blood stream.
How does this factor in to period symptoms? Well, mammary glands have been shown to be reactive to LH levels, as does the adrenal gland. As the LH levels fluctuate across a cycle, these sources respond in kind to produce, or not produce, estrogen and progesterone. The breast tissue source fits in with why these symptoms don’t typically become obvious until a year or more into transition, as it requires breast development to reach a degree of critical mass. This estrogen obviously does not approach the degree of fluctuation that comes with ovaries, but it doesn’t take much of a shift in estrogen levels to cause mental reactions. Every transfem on hormone therapy has experienced the emotional turbulence that comes with a change in dosage, or the depression that comes with either missing a dose or even being at the end of their injection cycle.
Period symptoms vary wildly in all women, cis and trans, but I have read accounts from transfeminine people describing every single common period symptom, save of course for actual menstruation. This includes:
- Cramping in the lower abdomen
- Water retention and Bloating.
- Gas, Diarrhea and other intestinal issues (“period shits”)
- Emotional instability and irrational thoughts (heightened depression, increased dysphoria)
- Muscle aches and pains, join pain, stiffness
- Beast engorgement and nipple tenderness
So what could cause these? Well lets tackle the first one and see if we find some answers.
In women with ovaries, the endometrium layer of the uterus that forms during the first half of the luteal phase of the cycle is rich with a lipid named Prostaglandin F2alpha (PGF2a). When the uterine lining breaks down, all that PGF2a is released into the surrounding tissue, as well as into the corpus luteum (the egg), catalyzing the destruction of the cell. Along with triggering a release of oxytocin, the PGF2a causes contractions in the muscle layer that surrounds the uterus. PGF2a also affects the intestinal and stomach lining, which is what causes period shits.
Ok, so what does that have to do with people who don’t have uteruses? F2a is not the only prostaglandin that causes muscle contractions. Prostaglandin E2 (PGE2) also causes muscle spasms in sufficient quantities, and is used to induce labor because of this effect. PGE2 is produced basically anywhere in the body that is under attack or has been damaged, but it is also formed in muscles, the intestines, adipose fat, and the mammary glands. Additionally, both PGE2 and PGF2a are produced by the thyroid and the adrenal glands. As shown above, mammary tissue and the adrenal gland have both been shown to respond to fluctuations in LH concentrations.
Adrenal released prostaglandins could absolutely cause contractions in the intestines and surrounding muscles, inflammation in the abdomen from the protaglandins would induce bloating, and prostaglandin surges in mammary tissue would explain breast engorgement and sensitivity. Some may scoff at the idea that these secretions could be sufficient to produce these symptoms, but the fact is we don’t know. Nobody has studied prostaglandin secretion in women who do not have ovaries. We simply do not know.
There’s a lot about all of this that we don’t know. Modern trans medical care is little more than a decade old (while trans hormone therapy has been around for well over a century, WPATH in its current incarnation has only existed since 2007, and the current Standards of Care, which were a significant improvement over previous versions, came out in 2011). Prior to that, transgender care was largely ignored, or considered a fringe practice. Additionally, the trans population is exploding in size right now because stigmas are reducing and awareness is climbing, people are coming out and starting hormone therapy in record numbers. Estimates of total transgender individuals have more than doubled in the last 5 years. Suddenly we’re learning all sorts of new things about the medical behavior of transgender individuals, but also medical science is just starting to pay attention. The medical community hadn’t even officially recognized that trans women could breastfeed until this year, which the trans community had known for decades.
No one is studying trans women’s periods (at least, that I could find). Many existing notions for how womens bodies work are based on the assumption that estrogen and progesterone fluctuations cause these reactions. I can’t find any research into responses to FSH outside of the ovaries, it’s just not been studied. I couldn’t even find data on LH and FSH levels in trans women, just a general expectation that it will be significantly lower than cis women because of the elevated estrogen levels.
Thus, the following is merely my conjecture on what is happening in the body, based on observations in myself and anecdotal accounts from other trans women.
At the start of the cycle the hypothalamus expects E to be its lowest, but because trans women control their estrogen levels artificially, the hypothalamus sees levels far higher than it anticipates and shuts down all production of GnRH, flat-lining LH and FSH output. During the last half of the follicular phase it expects to see levels closer to what actually is there, so pulses gradually pick up pace as it approaches a baseline. Then it hits the ovulatory phase and sends for an LH and FSH spike to attempt to induce ovulation (but of course there’s nothing to ovulate). Then we enter the luteal phase and once again the hypothalamus attempts to trigger a rise in anticipation of a pregnancy that can’t happen, and when it doesn’t the hypothalamus then again reduces output around day 22 in order to induce menstruation (which, again, can’t happen).
With every single repetition of my cycle I have been able to predict my mental state according to my position within the cycle, completely independent of my 5 day estradiol injection cycle.
- On days 1-6 I experience severe cases of gender and body dysphoria, and hightened depression. I become melancholy and my Rejection Sensitive Dysphoria becomes much easier to trigger. This is the time that I track as being my period, the difference in mental state is so stark that I can easilly recognize it day to day. My feminine voice will also be almost impossible to maintain on these days. I become very needy, and crave attention from my wife. My bowel movements become very sloppy (period poops), and I’ll start retaining water (the bloating is fierce). I’ll wait up each morning feeling very stiff, and my joints will hurt.
- Days 7-12 I usually feel very blah. I’ll have times of heightened dysmorphia where it becomes harder to see myself as feminine. My voice, again, fluctuates with that mental state.
- Days 13-16, the ovulatory phase, have me riding high and happy. My gender euphoria goes through the roof, my body confidence is high, and all I ever see in the mirror is a woman. My movements and other behaviors become subtly more feminine (I’ll notice my hips swing more when I walk, for example), and my voice feminisation is perfect on these days. My libido also spikes and I find myself much more affectionate towards my wife. This has been echoed by other transfems I know as well, with others around them even commenting on how they seem really well put together and alive during this time.
- Days 16-20 are simply normal; no significant behavior or mental shifts.
- Day 21-22 will be another day of great body feels. My breasts will swell on this day, sometimes as much as 2 cup sizes, and my hips swing a little broader than usual.
- Day 23 until the end of the cycle become increasingly tempestuous. I start to have mood swings and my emotional responses get stronger. I’ll get cranky easier and find myself more susceptible to road rage, but I also feel very happy when I swing high. This lasts until day 28-31, when I’ll suddenly crash into day 1 again.
This pattern has now repeated four times since I identified my cycle using a period tracker application, and I strongly believe it was happening for months prior to my noticing it. (Some have asked what app I use; I’m currently using Ovia, but it’s far from ideal. I’ve yet to find one that is actually good for trans women).
My suspicion is that medical science is totally wrong about the reception of LH and FSH in humans, especially FSH. Many of the studies into the responses of these hormones by individual parts of the body are based on observations in mice and cows, which have completely different estrous cycles from humans and massively different brain structures. Given the way that FSH fluctuates over the course of a female reproductive cycle, and how those fluctuations line up with the symptoms we experience, the correlation is just too strong to be coincidence.
Unfortunately, until somebody conducts a study of LH and FSH blood levels of male-assigned individuals on estrogen therapy who experience period cycles, we can never really be sure.
Today I may have found an answer for why the cycle has such an impact on mental state, in spite of even estrogen levels, and the cause of the happy phase that I experience around day 15. Several studies have found fluctuations in plasma oxytocin levels that correlated with the rise and fall of LH levels.
These results clearly demonstrate that, in spontaneously ovulating women, there is an approximate doubling of the circulating level of oxytocin associated with the time of ovulation. It is tempting to suggest that the elevated oxytocin concentrations play a part in the mechanism of ovulation. […] Subsequently, LH may contribute to the further stimulation of oxytocin release since Swaab and Jongkind (1971) showed that gonadotropic hormones are capable of activating neurosecretory activity in rats.
The above chart and text come from a paper published in 1981.
This 1991 paper found that post-menopausal women treated with hormone therapy experienced oxytocin spikes higher than untreated pre-menopausal women.
oxytocin levels also increased and were significantly elevated when the oestradiol level exceeded 2 pmol/ml [544pg/mL] […] The oxytocin levels appeared to be only partly related to the oestradiol level. It is possible that the stimulatory effect of oestradiol is antagonized by a concomitantly high progesterone level.
In other words, if your E and P are high enough, this amplifies the oxytocin production. This fits with another paper published in 2005 that found that women who were taking oral contraceptives experienced the opposite effect, with less oxytocin fluctuation across their cycles. Most oral contraceptives use synthetic progestins instead of bio-identical progesterone, which would not react the same way within the hypothalamus and pituitary glands, which is where oxytocin is produced. While the first paper I linked hypothesizes that this is caused by elevated LH, I believe that is a false correlation. It’s far more likely that the two are independently elevated in response to GNRh signals from the hypothalamus, and that the oxytocin release is not affected by the gonadotropic feedback loop.
Why is all this significant? Here’s some of the things Oxytocin is responsible, taken from wikipedia:
- Bonding and stimulation of maternal behavior
- Increases of empathy towards members of a shared group and encourages generosity
- Boosts social emotions, promoting trust and attachment while also increasing fallout from betrayal and envy.
- Modulation of fear response and anxiety
- Acts as an anti-depressant, and deficits have been shown to cause depression.
That last piece is key. Elevated oxytocin levels during the ovulatory phase would significantly reduce dysphoric depression, where reduced levels in the first and last weeks of a cycle would increase dysphoric depression. The other aspects aren’t dismissed either, however. Some trans women I’ve spoken to (as well as myself) have commented on feeling more socially confident around day 15.
Here’s another factoid from the wikipedia article that isn’t exactly relevant, but I thought it interesting:
It has also been shown that testosterone directly suppresses oxytocin in mice. This has been hypothesized to have evolutionary significance. With oxytocin suppressed, activities such as hunting and attacking invaders would be less mentally difficult as oxytocin is strongly associated with empathy.
What if the female brain needs oxytocin, and this is why having testosterone in our systems causes so much anguish, and starting HRT has such a significant impact on trans women? What if the male brain can’t handle those levels of oxytocin, thus producing the same effect for trans men? This would seem to align with why many trans men experience extreme dysphoria during breast feeding, which triggers oxytocin surges.
It has been shown that oxytocin differentially affects males and females. Females who are administered oxytocin are overall faster in responding to socially relevant stimuli than males who received oxytocin. Additionally, after the administration of oxytocin, females show increased amygdala activity in response to threatening scenes; however, males do not
Definitely food for thought.