u/Phew-ThatWasClose

The other day, one of the many that is not this one, yesterday to be precise, I wrote a big long post about estrogen. Buried in the middle of that post was a brief paragraph about how Slynd can help with PMDD symptoms by shutting down the ovaries, but can also cause hypoestrogenism. Then today there is a post on the other sub describing exactly that. So I want to highlight it.

Slynd (Slinda in Europe) is a progestin only pill (POP) made of Drosperinone (DRSP). Slynd is one of only two POPs that can effectively shut down ovulation. The other is Cerezzette which is made of desogestrel and is awful for women with PMDD so we won’t talk about it. But be aware if someone you know is on Cerezzette most of this applies to them as well. The rest of the POPs are mini-pills, not designed to stop ovulation (though they might) and basically just an oral form of an IUD which have their own issues. For now we focus on Slynd.

Slynd is a progestin only pill (POP) made of Drosperinone (DRSP). Drosperinone is the progestin in Yaz. Even though it is a synthetic, not bioidentical, progestin drosperinone was designed to behave exactly like natural progesterone. So it is the kindest, gentlest, best progestin available.

What happens is this: Slynd stops ovulation. It shuts down the ovaries. The ovaries are where the estrogen is made. The estrogen is made by the follicules in the ovaries. With the ovaries shut down, the cycle is shut down, there are no follicules. So no estrogen. None at all.

That’s fine. For a few days. The existing Estradiol (E2) takes a bit to clear and then the hypoestrogenism (hypo = too little) starts to kick in and eventually leads to profound hypoestrogenism (way too little) after a week or two. The symptoms of hypoestrogenism can be far worse than the symptoms of PMDD. So she quits and we’re back to “I’ve tried everything and nothing works.”

But really she just needs some estrogen. Often the reason she’s on Slynd in the first place is because she was taken off a Combined pill to avoid the estrogen. But that is the synthetic Ethyl Estradiol (EE) in the COC. EE increases the risk of blood clots and can contribute to stroke if she has migraine with aura. It’s not “estrogen” that is the problem. It is that one specific form of estrogen.

The patch, used for HRT, contains a bioidentical Estradiol (E2) and delivers it directly to the blood stream. Bioidentical E2 is as close to natural as you can get and has none of the side effects EE has. It does not increase the risk of blood clots and does not increase the risk of stroke.

Interestingly hypoestrogenism is uncommon because Slynd is not as effective as it could be. Generally “shutting down the ovaries” means convincing the hypothalamus there is plenty of hormone circulating already so it doesn’t need to prod the system into producing Follicule Stimulating Hormone (FSH) or Lutenizing Hormone (LH). But Slynd just barely gets there. In about 93% of cases Slynd only manages to mostly convince the hypothalamus all is well and the hypothalamus will still produce a little pulse of GnRH to prod the pituitary gland into making a little FSH which results in a little follicular growth in the ovaries and a little estrogen is produced. Just enough actually. It’s as if the system is permanently stuck on day 7.

The other 7% just need supplemental estrogen so Slynd+patch “should” do the trick.

There are so many variables to this PMDD thing. Just looking at it from a different perspective can sometimes help. Which factor is most important in your situation? When I started writing this post I just wanted to explain the difference between the three main kinds of estrogen. It kinda got out of hand. There’s a TL;DR at the end. Even that is kinda long.

Some chick once said of a different post: “This reads like a gynecologist that doesn’t fully understand PMDD but read some books and likes big words and over explaining.” I substituted acronyms for some of the big words. If that helps. :)

There are three main kinds of estrogen. Ethinyl Estradiol (EE), Estradiol (E2) and Estetrol (E4). Some small amount of estrogen is used by the body for other purposes, like regulating the immune system, but mostly it’s all about the reproductive cycle. During the reproductive cycle natural estrogen (E2) is produced by the ovaries. Technically the corpus luteum which is a temporary structure in the ovaries that makes hormones during luteal. If you really want to know the corpus luteum is made of the ruptured follicule that released the egg. We can go as far into the weeds as you want, just ask.

Anyway, E2 is produced by the ovaries during luteal and released into the bloodstream quickly reaching the uterus which responds to increased E2 levels by growing and thickening it’s inner lining. The E2 is made by the corpus luteum which used to be the follicule which released the egg. The egg is on it’s way!!! The uterus responds by making a lining for the egg to implant in should it need to.

Ethinyl Estradiol (EE) is a synthetic estrogen that is in every COC since the beginning of COCs, save Nextstellis. That is why it was created – to be in COCs. When you take an oral contraceptive the first thing it does is run through the digestive system. That includes the liver. The liver is adept at getting rid of estrogen because in the normal course of things the body is done with the estrogen by the time it gets to the liver. So the liver will destroy any E2 it sees. Consequently you can’t put E2 in an oral contraceptive and expect it to ever reach the bloodstream. For contraceptive purposes that is where you need it, in the bloodstream, because you want the hypothalamus to see it and think there is plenty so no more is needed and …. tra-la-la.

So EE was specifically designed to be difficult for the liver to eliminate while also looking enough like E2 to fool the hypothalamus. Fun fact: The liver has a secondary means to eliminate molecules it cannot break down and that is to encase them in sugar. The sugar encased molecule is then inert and passed to the intestines to be eliminated as waste. There the bacteria in the intestines eat the sugar releasing the EE which then goes back into the bloodstream. This is why the EE can last up to 36 hours in the body and why daily pills can be taken daily. It is also why COCs can fail if you are sick and take an antibiotic. The antibiotic kills the bacteria so the bacteria don’t eat the sugar and release the EE back into the blood so the blood clears of EE in about 2 hours leading to possible ovulation and/or a resurgence of PMDD symptoms.

EE has an unfortunate side effect in that it encourages the liver to over-produce clotting factors which leads to an increase risk of blood clots. What happens is this: When she takes the pill it dissolves in the stomach and heads to the liver. The liver is inundated with estrogen, up to 100x what it normally sees. Ordinarily the liver would just destroy all that estrogen and be done. But because it can’t breakdown the synthetic EE, and because of the recycling system outlined above, the concentration remains high.

The only time a liver naturally experiences a prolonged high concentration of estrogen is when birth is imminent, so the liver prepares for birth. The liver over-produces clotting factors because it is preparing for a possible post-partum hemorrhage. And if she takes a COC continuously the liver will over-produce clotting factors 24/7/52.

Most COCs also contain a progestin, like levonorgestrel, with high androgenic properties. These progestins bind to the androgen receptors in the liver which tells the liver not to make more clotting factors. So the liver does not create clotting factor after all So a COC with levonorgestrel paired with ethinyl estradiol doesn’t increase the risk of blood clots. Phew! That was a long way to go for nothing.

Levonorgestrel (LNG) is a synthetic progesterone derived from testosterone. Yes, the same testosterone that gets blamed for aggressive behavior in men. 19-nortestosterone to be exact. That is where it gets it’s androgenic (mannish) properties from. They literally take a testosterone molecule, do some science, and end up with LNG.

And LNG is 50-100 times more potent than natural progesterone. That, in fact, was the point. LNG was designed to be far more potent that natural progesterone so you could fit enough in a pill to be effective. And the effect is ridiculous.

LNG also has a binding affinity that is roughly 323% higher than natural progesterone. About 323%. Maybe more, maybe less. And that binding affinity leads to a roughly 6,000 – 24,000% increase in residence time. Natural progesterone might attach to progesterone receptors in the hypothalamus for a few minutes at a time. LNG attaches and stays for 3-12 hours. That means the receptor is active, doing receptor stuff, all frickin day.

It’s almost exactly like the face huggers in Alien. The LNG gloms on to the progesterone receptor and will not let go. And it’s a frickin testosterone molecule so it’s really irritating. For a woman with PMDD this is exactly what you don’t want. She’s already irritable from the disorder and now the COC that is supposed to help regulate her cycle makes it worse.

LNG was/is the worst, or the best, depending on your perspective. Effective as contraceptives but all first, second, and third generation progestins have more or less the same issues. They are all derived from 19-nortestosterone and have more or less androgenic effects depending on the specific formulation. Which means side effects like irritability, weight gain, acne and facial hair. Moreover science found that the more they tweaked the base testosterone to get rid of unwanted side effects, the less androgenic the formulation became, and the more people started having blood clots.

So that’s not good. Science recognized the problem and worked to create a better progestin. The goal was to create a synthetic that behaved exactly like natural progesterone and drosperinone (DRSP) was the result. DRSP is derived from spironolactone, not testosterone, which means it not only doesn’t have androgenic properties, it actually has anti-androgenic properties. Instead of side effects like irritability, weight gain, acne and facial hair it has the side effects of not those things. Is a kinder gentler progestin that increases her calm. As a bonus spironolactone is a diuretic so DRSP also reduces bloating.

And that is why Yaz is the top recommended COC for PMDD. Yaz, Yasmin, and their generic equivalents contain DRSP as their progestin. Yaz is the only COC approved by the FDA for treating PMDD and is specifically called out by name in the RCOG treatment guidance.

But Yaz still pairs DRSP with EE and EE causes the liver to create clotting factor unless an androgenic progestin is there to prevent it. DRSP is anti-androgenic. So Yaz increases the risk of blood clots. And even though that is because of the EE it’s the DRSP that gets the blame. Other COCs don’t cause blood clots and the difference is the progestin – so it must be because of the progestin. So the reasoning goes.

Statistically turning 35 doubles your chances of having a blood clot so many doctors will discontinue Yaz at age 35. But for a healthy (18.5 ≤ BMI ≤ 24.9 ) woman who doesn’t smoke the risk doubles from 1/1000 to 2/1000. Still considered “uncommon” by WHO standards. And compare that to the 100% certainty of PMDD symptoms returning.

Still she may need to / be forced to go off Yaz, or any COC, for some reason. Often COCs are discontinued if she experiences migraines with aura because the EE can interact with the Cortical Spreading Depression (thing that causes the aura) to cause a stroke. So whatever the reason she may have to stop her COC.

To still prevent ovulation the only options are now Progestin Only Pills (POPs) and the only options there are levonorgestrel or norethindrone which are both based on testosterone and highly androgenic which is why POPs are not recommended for treating PMDD in the first place. That and they do not reliably stop ovulation anyway.

Except for Slynd. Slynd is DRSP. Remember PMDD is an abnormal reaction to normal hormonal changes. The point of all this is to prevent ovulation and introduce a steady state so the changes don’t happen. Slynd can do that with just 33% more DRSP than Yaz and no EE. But now (it’s always something) there is no estrogen at all in the system, synthetic or natural, and estrogen is important. Profound hypoestrogenism (systemically near zero estrogen) causes symptoms like hot flashes, severe night sweats, deep depressive slumps, and a rapid drop in bone mineral density. So we need some.

Enter the patch.

A transdermal patch can introduce a steady flow of estrogen to stabilize and regulate the system while not causing increased risk of blood clots or stroke. It can do this because it’s not EE, it’s E2 – bioidentical estradiol made from yams. Recall science could not put E2 in a COC because the liver would just destroy the E2 on the first pass before it ever reached the blood stream. But the patch delivers it directly to the blood stream. HaHAAA!! Why didn’t science just do that in the first place? Good question.

In 1965 transdermal technology didn’t exist. That and the focus wasn’t on women’s health, it was on preventing pregnancy and making preventing pregnancy as easy as possible. The point was profit and population control. After WWII “modern” medicine resulted in a sharp decrease in infant mortality. The baby boom wasn’t just soldiers returning home. It was also due to more babies surviving. Fear of overpopulation combined with the nacent women’s liberation movement to make easy contraception a popular idea. The Pill was the answer. Once a day, no worries.

There was a huge disaster in 2002-2005. Ortho-McNeil Pharmaceuticals did develop and market a transdermal patch called “Ortho Evra”. Unfortunately a lot of the information in this post was still unknown in 2002, specifically the side effects of EE. Even though they knew as early as 1961 that EE caused an increase in clotting risk they didn’t fully appreciate how bad it was because EE was always paired with a highly androgenic progestin. The Ortho Evra disaster is part of how they found that out.

Ortho Evra used a third generation progestin (norelgestromin) combined with EE to create a combined patch. You thought once daily was convenient! Ortho Evra was heavily marketed as a once a week thing with celebrity endorsements, fashion show sponsorships, magazine ads, and the whole nine yards. It was the sexy new modern birth control for the liberated woman of the next century. Then it started killing people.

EE is a big molecule. At the time transdermal technology was poorly understood. To force that big molecule through the skin the team packed in 5x as much EE as they needed, to create a pressure gradient. But apparently they didn’t do enough testing and the patch worked too well. The Ortho Evra patch delivers 60% more EE than oral contraceptives and does it all day. The liver gets way more EE and can never clear it so it’s creating clotting factor like mad.

Meanwhile norelgestromin is a third generation progestin developed to have fewer androgenic effects. That means it is less effective at countering the EE. More EE with less restrictions means more and more and more clotting factor which can cause deep vein thrombosis, heart attack, pulmonary embolism, and ischemic stroke. Not necessarily fatal but still awful and yes, people started to die. Young, healthy, hip, liberated women. Johnson and Johnson, Ortho-McNeil’s parent company, faced over 2400 lawsuits and it is estimated nearly 200 people lost their lives. Some few heart wrenching cases made national news. Ortho Evra was quietly pulled from the market in 2005.

The medical establishment has a long institutional memory and is understandably afraid of transdermal patches for treating women’s health issues. Today’s transdermals use E2 instead of EE but unless you can find a doctor who knows all these details, or who will believe you, it’ll be an uphill climb to get a patch added to your Slynd prescription. If only there were an all-in-one solution. How did we used to do it? Just one pill, no complications, that would be better.

Enter Nextstellis.

The only time a liver would naturally experience highly elevated estrogen levels is if a birth is imminent. By the eighth month E2 is at levels up to 100x normal and the liver responds by increasing clotting factor. But for Baby that can be a disaster. At that point baby is still getting oxygen and nutrients from mother across the placental barrier and that includes the high levels of E2. So baby’s liver protects itself by creating it’s own version of estrogen, estetrol (E4), and uses it to fill all the receptors in its liver so the E2 from mom can’t find purchase. Let that sink in. Baby’s liver creates it’s own estrogen (E4) to protect itself from mom’s estrogen (E2). And it does it by adding two additional hydroxyl groups to moms E2. Hence the names. Baby’s liver uses Mom’s E2 to create E4 to protect itself from too much E2.

Or at least that’s the current working theory. Officially science doesn’t know. But they do know that fetal estrogen cannot be broken down by adult livers. So making bioidentical E4 is a new way to get estrogen into the system via an oral contraceptive. Science can now make bioidentical E4 from soy proteins. Actually science has been able to do that since 1965 but only recently figured out a cost effective way to do it at scale. And they pair that with DRSP in a new COC called Nextstellis. Recall that DRSP is a synthetic progestin designed to behave exactly like natural progesterone. So the combination DRSP+E4 is as close to what the body does naturally as you can get, but in a pill.

TL;DR:

Ethinyl Estradiol (EE) is a synthetic estrogen designed to be difficult for the liver to destroy so that it could be put in a pill. This results in the liver being overwhelmed and it responds by increasing the production of clotting factors.

First, second, and third generation synthetic progestins are all based on testosterone. First and second generation have high androgenic properties. This results in unwanted side effects but also reduces the liver’s enthusiasm for producing clotting factors. Hence Combined Oral Contraceptives (COCs) don’t generally cause blood clots.

Some third generation progestins are tweaked to reduce the androgenic properties and some newer fourth generation progestins actually have anti-androgenic properties. When used in a combined pill, these progestins do not reign in the clotting factor production so there is higher risk.

Turning 35 doubles the risk of blood clots and many doctors will discontinue COCs at that point.

There are two Progesterone Only Pills (Slynd/drosperinone and Cerazette/desogestrel) that can effectively stop ovulation w/o estrogen. Desogestrel is another testosterone derivative so not ideal for women with PMDD. So Slynd can shut down ovulation. But then there is zero estrogen in the system.

Transdermal patches can put estrogen back in the system without increasing the risk of blood clots (or stroke) because they use bioidentical estradiol not synthetic ethinyl estradiol. Same thing for HRT. It’s just better estrogen.

For the first time in 80 years there is a new estrogen available. Estetrol (E4) is a bioidentical estrogen derived from soy that cannot be destroyed by the liver. Nextstellis pairs this with drosperinone (DRSP) in a new(ish) COC that has fewer side effects and is about as natural as you can get.

Hope that helps.

The book is a mashup of the wiki - which I wrote - plus highlights of posts and commentary from the sub - which ya'll wrote. So in my view I didn't write a book so much as compile one. We wrote a book. I just did the curating and formatting and the rest of the administrivia.

One big objection to the book is none of us have ever had PMDD, so what right do we (I) have to write a book about it. And my response is the book isn't about PMDD. It's a book by, for, and about partners.

But it also got me thinking about what else is out there. There are actually books, and chapters of books, about being a partner, written by women with PMDD, who have never been a partner. So fair is fair and I've been working on the book list in the wiki.

I am not trying to be exhaustive but I am trying to hit the highlights. I have a fair sampling of PMDD books in the list but it occurs to me we need some of the non-PMDD books as well, Classics like "The Body Keeps the Score" "Why Does He do That?" And "No More Mr. Nice Guy"

And so I turn to the community for recommendations. What have you read that made a difference?

We passed this milestone a few days ago and I'm not entirely sure it's really something to celebrate. But we're here. We're supporting each other. Hurrah for us!

Just five months since 7,000. Growth of the sub is accelerating. I assume that is due to greater awareness. Desperate partners typing "why does this keep happening?" and the AI sends them here. I hope people are finding what they need, if only validation that you're not alone. But if you're new check out the wiki and check out the book. Also check out the other resources linked up top and to the right.

When the book came out there was immediate, and severe, backlash. One common criticism was that I got the science wrong. There's very little science in the book so that was a puzzler. It's easy to criticize. Nevertheless I've started doing deep dives into the sciencey aspects of PMDD as they arise. The other sub maintains an excellent list of research articles if you are interested in exploring on your own.

The biggest take away I have from my research so far is this: Up to 80% of hysterectomies are unnecessary. If your loved one is leaning in that direction make sure you've both done the research and know exactly what and why.

I have an advanced math degree and have taught logic at the college level. When I say something "makes no sense" I'm not just whistling Dixie. I am not a medical professional - so I listen when medical folks say stuff and ask questions when things don't make sense. I'm smart, I can understand stuff, make it make sense.

I get extremely frustrated when people who should know better say "There is no point doing a hormone test because PMDD is not a hormone imbalance so results will come back normal". Absolute rubbish. I also get frustrated when people who should know better say "hormones fluctuate throughout the cycle so the results of a hormone test would be meaningless". Also absolute rubbish.

PMDD is not a hormone imbalance, but it sure looks like one, so that is the first thing to test for, to rule it out. Because if it is a hormone imbalance, like low progesterone, there is an easy fix. And the fix for that is completely different to how you treat PMDD. You don't know it's even potentially PMDD until after you've done a hormone test and results do come back normal.

"But hormones fluctuate so ..." If a medical professional says that to you find a different medical professional. That person is bad at their job. Progesterone, for example, fluctuates between 0.1ng/mL during the early follicular phase up to a maximum peak of 20 to 25 ng/mL durling luteal. If you do a blood test to measure progesterone and the results come back as 7ng/mL what does that mean? Depends on when you took the blood.

Fun fact: From 0.1 to 25 is a rise of 250x. That's three orders of magnitude. We often hear that PMDD is caused by the hormonal changes and that is why COCs help - because they level things out. But it isn't the changes so much as the rate of change, the velocity, that overwhelms the system.

Progesterone is at it's maximum on Day 21. That is when you do the blood test. If progesterone is below 10ng/mL on Day 21 that's a problem and that's not PMDD. If it's up closer to 20ng/mL then that's normal and you may have PMDD. On to the next step.

The next step is ruling out everything else. The other sub has an excellent chart in their wiki detailing what everything else is and how one might rule it out (about halfway down the page). Rather than duplicate their work I put similar information in our wiki in paragraph form. Read both.

The DSM-5 diagnostic criteria (G) states in part "The symptoms are not attributable to ... another medical condition". The ICD-11 similarly states "The symptoms are not a manifestation of another medical condition" is an "essential (required) feature". PMDD is clearly a diagnosis of exclusion according to the two most authoritative diagnostic manuals on the planet. Yet ...

RCOG and ACOG - the authorities on treating PMDD - also give guidance on diagnosing PMDD. Both RCOG and ACOG say to track symptoms for two months, and that's it. So when people tell you the only way to diagnose PMDD is to track symptoms for two months That is where they get that from. Both RCOG and ACOG repeat the tired old line that "there are no useful blood tests to confirm the diagnosis" which is flat out false.

PMDD is a diagnosis of exclusion. Every blood test will help confirm PMDD if it comes back normal. And every blood test is useful even if all it does is rule out one more possibility. And ruling out all other possibilities is required by the DSM-5 and the ICD-11

RCOG says that a clinician may order blood work if another cause is "clinically suspected" - leaving the definition of "suspected" up to the practitioner. Typically that means there are observable symptoms of that other disorder, but typically the observable symptoms are also symptoms of PMDD. ACOG goes further and cautions that while blood work is permissible in the diagnostic process too much testing may cause anxiety in the patient. Wouldn't want that.

It's as if RCOG and ACOG are trying to discourage doing routine blood tests. And a cynic might well conclude that is exactly what they are doing. Blood tests cost money. Having the patient fill out paper charts for two months is free.

Doctors who rely on symptom tracking alone can easily misdiagnose patients with PMDD when what they really have is PME (Premenstrual Exacerbation) of an easily treatable disorder. Symptoms that are manageable during follicular can easily arise during luteal just because the whole system is in flux and stressed.

So the 40-80% misdiagnosis rate starts to make sense. The diagnostic criteria are clear. But the diagnostic guidance, from the authorities who should know these things, are paltry. So it's up to you. Read everything, become the expert.

If you or your loved one is struggling with PMDD symptoms and haven't had the blood work done ... do it now.

ETA: Two (2) people have downvoted. Yet no comments or reports so ... why?

I got a little carried away in a recent post and stated that IUDs cannot stop the ovulatory cycle and so cannot stop PMDD symptoms. It was pointed out to me that that is incorrect and therefore I am a fount of misinformation and nobody should listen to anything I say. That last bit was implied, not actually stated. :)

My bad. IUDs can stop ovulation. In fact they often do. That is not a good thing.

What I said was this:

>IUDs do not have enough actual chemical in them to stop the ovaries from doing their thing and the cycle continues. For a woman with PMDD an IUD will not help. It can’t.

What I should have said is this:

All hormonal IUDs release levonorgestrel at a continuous low rate for 5-8 years. Mirena is the highest dose IUD and it starts out releasing ~21mcg/day which falls rapidly to ~14mcg/day in the first year and falls further to ~7mcg/day by the end of the 8 year lifespan.

IUDs are not designed to stop the ovulatory cycle. A COC like Levotar, which also contains levonorgestrel and is designed to stop ovulation, delivers a much higher dose (150mcg/day). IUDs can work using a lower dose because they are local to the uterus. What they are designed to do is plug the cervix (or cause the cervix to create a plug) so the sperm can't get in, and thin the uterine lining so an egg would have nowhere to implant even if a sperm did manage to get in. It is the thinning of the uterine lining that stops the period.

But not all of the chemical stays in the uterus. Some gets out into the bloodstream and some reaches the pituitary gland. Levonorgestrel is 50x-100x more potent than natural progesterone so sometimes even that small amount is enough to convince the pituitary gland not to manufacture and release Follicle-Stimulating Hormone (FSH) and Lutenizing Hormone (LH). And without direction from the pituitary gland the ovaries do not produce an egg and do not produce the hormones that cause PMDD. The hormonal cycle is stopped.

In fact this happens more often than one would think given the low doses. This from the Mirena insert:

This from the mirena insert:

>

In the first year the IUD prevents ovulation 65% of the time. That drops to 25% after 4 years. Note they are not claiming it prevents 65% of women from ovulating, just 65% of cycles across all the women in the study. IUDs do not reliably stop the ovulatory cycle for anyone. They are not intended to. But they may, as a side effect, and if a doctor is prescribing "birth control" there is a tacit assumption that is stopping the cycle since that is what "the pill" does. The doctor may even say it does.

As birth control IUDs work fine. But they are deceptive for women with PMDD because if they are operating under the assumption this is going to stop their hormonal cycle, and it does, they think they are cured. Hurrah! Then if their cycle comes back in a year, or two, or randomly, but their period doesn't ...

You can see where that would be problematic. If the symptoms return with no physical indication the cycle has returned then we're back in the denial phase. It can't be PMDD because her cycle has "stopped". So it must be you.

And there are all the other reasons IUDs are a bad idea for women with PMDD. This is just one more.

AI is pretty annoying – but this one made me smile.

>If a woman's premenstrual rage or despair is driven by the severe late-luteal prostaglandin surge seen in primary dysmenorrhea, endometriosis, or fibroids, it is a physical phenocopy of PMDD

That was after I told it to quit patronizing me. :)

I recently wrote a thing about IUDs and how they “should” not help with PMDD and could easily make matters worse. Nevertheless I consistently see posts and comments on the other sub about how IUDs do, in fact, help with PMDD symptoms. Why is that?

Those women do not have PMDD. But it surely looks like they do.

According to the diagnostic criteria PMDD is any 5 of a possible 11 symptoms that “are associated with clinically significant distress or interference with work, school, usual social activities, or relationships with others.” PMDD has an extremely high misdiagnosis rate (40-80%) and there are many conditions that look an awful lot like PMDD. Dysmenorrhea is one.

Too often women don’t get a proper diagnosis and experience years of frustration trying to treat a disorder they don’t have. Many in the medical community are unaware PMDD even exists, or have old fashioned biases like “Oh, that’s just the new name for PMS.” Often women have to do their own research and become convinced they have PMDD because all the symptoms line up and when they finally find a doctor who agrees with them it’s like the sun breaking through the clouds. Doctors themselves, the ones that are PMDD aware, often just listen to a list of symptoms and say “Yep, sounds like PMDD.”

But just because it happens during luteal doesn’t mean it’s PMDD. That is why it is so important to get the blood work done – to rule out a host of other things it could be. Beyond the blood work look to the symptoms. Treatment recommendations are what they are because they help most women with PMDD. The recommendation is a mono-phasic Combined Oral Contraceptive (like Yaz) and a low dose intermittent SSRI. But some doctors know only one solution for anything to do with the reproductive system and that solution is Birth Control – whatever birth control is handy.

The reason COCs work for PMDD is they shut down the ovaries. Then the hormonal cycle that is driven by the ovaries stops and the PMDD that is driven by the changes in the hormonal cycle stops. IUDs do not have enough actual chemical in them to stop the ovaries from doing their thing and the cycle continues. For a woman with PMDD an IUD will not help. It can’t.

IUDs prevent conception by increasing the amount of mucus in the cervix so the egg cannot get through to the uterus and by thinning the uterine lining so there is nothing for the egg to implant in if it does get there. That second part is the key. IUDs make the uterine lining so thin there is nothing to shed during menses. There is no reason to have a period and consequently, even though an IUD does not stop her cycle, it does stop her period.

How can PMDD persist when she doesn’t have her period? This is how. She still has her cycle.

Dysmenorrhea is characterized by extreme cramping before and during menses. Often comorbid with heavy flow (menorrhagia) and subsequent anemia (low iron). The extreme cramping is caused by an overabundance of prostaglandins. Extreme as in traumatic. Extreme to the point of causing psychological distress. And the prostaglandins that cause the contractions (and the cramping) in the uterus … that helps to sluff off the uterine lining during menses … are manufactured by the uterine lining. No lining = no prostaglandins = no contractions = no period.

Dysmenorrhea is a phenocopy of PMDD meaning it looks a lot like PMDD but isn’t. It has a different cause even though the symptoms are similar. The contractions and cramping start a couple days before her period starts to begin to loosen the lining. It looks like a premenstrual disorder because it starts premenstrually. And the contractions are severe enough to cause psychological trauma. She’s raging because she’s in tremendous physical pain.

Fortunately treating for PMDD will also stop dysmenorrhea because if you stop the reproductive cycle with a COC you also stop menses. Not by thinning the lining but by stopping the lining from forming in the first place. No period doesn’t mean no cycle. But no cycle does mean no period.

Similarly for endometriosis and submucosal fibroids. Both are forms of secondary dysmenorrhea which just means it’s dysmenorrhea symptoms caused by something else. Or it’s a Premenstrual Exacerbation (PME) of a known condition that results in symptoms like PMDD.

Endometriosis is a condition in which uterine lining grows outside the uterus. “Outside the uteris” is the pelvic cavity where basically everything is and endometriosis lesions can grow anywhere. Depending on where they are the lesions can cause a host of symptoms including bowel and urinary pain, pain during sex, nausea, constipation, infertility, chronic fatigue, nerve pain, and radiating leg pain.

All that can be exacerbated premenstrually for the same reason dysmenorrhea is. The signal that causes the uterine lining to start producing prostaglandins activates the external lesions as well. The prostaglandins outside the uterus cause inflammation, chemical burns, pelvic bleeding and continuous, high-amplitude trauma signals sent directly to the brain. It’s the trauma that produces the Rage.

As the name implies submucosal fibroids are fibroids that grow under the uterine lining on the uterine wall. They are permanent (benign) tumors that can only be removed by surgery and they disrupt the normal activities of the uterus just by being there. The uterus detects them as a foreign invaders and tries to expel them during menses by jacking up the production of prostaglandins precisely so the contraction will be extra violent. It doesn’t work so the system will try again next cycle. And the next and the next.

For both endometriosis and submucosal fibroids inhibiting/stopping the growth of the uterine lining mitigates/prevents symptoms. So if a woman with one of these conditions is misdiagnosed with PMDD, and incorrectly given an IUD or POP as the Birth Control method to stop the “PMDD”, it’ll work. Multiple errors compounded to make a happy accident. The patient is cured!

That seems really unlikely. You’d have to have an idiot doctor making multiple mistakes stumbling across an actual fix for the wrong disorder Clouseau style. But it’s more common than you’d expect. Estimates are 50% to 90% of women experience dysmenorrhea. Of those 15% to 20% experience severe dysmenorrhea. Taking the low end of both ranges (50% of 15%) means at least 7.5% of menstruating women experience extreme physical agony before their period every single month.

Endometriosis impacts roughly 10% of women and takes an average of 7-10 years to be properly diagnosed. Typically those women are initially mis-diagnosed with a premenstrual mood disorder because symptoms appear like clockwork every time the uterine lining starts producing prostaglandins.

Fibroids impact 70% - 80% of women with about 30% being large enough and positioned so the body reacts. 30% of 70% is 21% of women worldwide have fibroids significant enough to cause secondary dysmenorrhea.

Combined about 30% of women who menstruate have intense, undiagnosed or untreated physical pelvic disorders that look an awful lot like PMDD. Suddenly I’m wondering why we don’t see more “PMDD” being “cured” with IUDs and POPs. Indeed PMDD only affects 2-8% of women and is a diagnosis of exclusion. It’s only PMDD if it isn’t anything else. So why aren’t these pelvic cavity disorders being actively tested for during the PMDD diagnostic process?

Mostly because it’s hard. Lesions and fibroids are both really difficult to detect short of exploratory surgery and dysmenorrhea itself has no physical presence, nothing to look for. But primary dysmenorrhea has a multitude of symptoms and secondary dysmenorrhea caused by endometriosis or fibroids has those same symptoms. The symptomology is where we can see the difference.

Unlike PMDD secondary dysmenorrhea can cause constant low-grade fatigue, backaches, and bloating even during follicular, as well as diarrhea and pelvic pain during luteal. Psychological symptoms are directly related to the traumatic physical pain of the disorder not the hormonal shifts in the cycle.

Lets wrap this up as I’m starting to confuse myself. Basically this:

If your SO has PMDD and an IUD cured it that’s great. Likely she does not have PMDD. Who cares? Whatever it was is cured. But keep all this in mind because eventually that IUD has to come out. She can just put another one in and go another 5 years but life goes on and things change so be aware. Talk to your doctor about tracking down the real cause of symptoms so you're ready when the time comes.

If your SO has PMDD and her doctor gave her an IUD and now she’s cranky all the time but has no period … likely she does have PMDD and her doctor is a doofus. Go read the other post about IUDs and why they don’t work for PMDD.

If your SO has been diagnosed with PMDD and is considering “birth control” talk about all this stuff. Specifically ask about symptoms like period pain, heavy bleeding, and diarrhea. Statistically it’s more likely to be some form of dysmenorrhea than PMDD.

If you do suspect dysmenorrhea try to rule that out. Typically, secondary dysmenorrhea has low-level symptoms all month (due to the underlying condition) then an extended, intense luteal flare. Primary dysmenorrhea has no underlying condition, so the only symptom is a short, but intense, luteal window - just one or two days before, and the first few days of, her period. Talk to your doctor about backing up two more days (starting day 24) and trying an NSAID, like prescription strength ibuprofen, to ward off possible inflammation caused by any excess prostaglandins. If that helps talk some more about possible endometriosis or fibroids.

Correctly treating the “PMDD” with a COC that shuts down the ovaries will also stop the dysmenorrhea if that’s what she has. But if what she has is secondary dysmenorrhea due to endometriosis or fibroids that is masking a time bomb. Symptoms disappear but the lesions or fibroids continue to spread and grow. Other causes of secondary dysmenorrehea, like adenomyosis, pelvic inflammatory disease (PID), and cervical stenosis are similarly masked by properly treating “PMDD”. It is important to get the diagnosis right so you treat what you have – even if the treatment ends up being the same damn thing.

But the single most important take away is this: IUDs do not help PMDD. If you read online about people who love their IUD because their “PMDD” symptoms went away don’t believe it. That’s fantastic for them but they should spend some time looking for the actually cause of their symptoms. If your loved one truly has PMDD and goes to the trouble and pain of getting an IUD fitted it will not help and will likely make things worse. At the very least try a mini-pill first to test for an adverse reaction before committing to an invasive semi-permanent procedure.

I intended to wrap it up six paragraphs ago. Sheesh. Does anybody have any questions?

Obligatory disclaimer – since apparently this is necessary now. Most women with PMDD are not Ragers. Most women with PMDD are not Abusers. PMDD doesn’t cause abuse. But PMDD can open the door, and here we are.

There is a second negative review of the book, this one written by a human. If I can follow the logic the basic premise seems to be you’re not allowed to say anything negative about your abuser if she also has PMDD because someone else with PMDD will think you are accusing them of being an abuser and then commit suicide.

It’s pretty twisted and I’m fairly confident it’s the same woman who once accused us, as a group, of forcing (her word) women with PMDD to not talk about anything substantive during luteal. At least I hope it’s the same woman – otherwise there’s two of them. But to be clear nobody is forcing anybody to do anything. Including – nobody is forcing partners to engage in conversations they don’t want to engage in. She can talk all she wants, but you don’t have to be there.

To be honest there are more than two. At this point I count at least seven, but I would estimate more like twenty. A small but vocal minority of women with PMDD hate the whole idea of a book centered on partners because it doesn’t talk about how awful PMDD is for her. They’ve hurled all kinds of accusations like the book overgeneralizes, stigmatizes, speaks in absolutes, portrays all women with PMDD in the same negative light, etc. Furthermore it’s not balanced, doesn’t take the science into account, gets the science wrong, is too blamey, pushes for accountability while also infantalizing the women by having the man manage the condition … just a lot of bad faith and emotional reasoning.

I won’t go into why all those accusations are off base because you can just read the book for yourself. It’s free. But I do want to touch on one thing … It’s worse for her.

So what? Is that really going to be the cornerstone of your position? That’s where you want to plant your flag? It sucks for everybody! But you want to claim the high ground because it’s slightly worse for you? Two things can both be true. My pain doesn’t decrease when you belittle it. If anything that’s part of the problem. We’re both in pain but only one of us is trying to do something about it.

Which is my second point – she can do something about it. We are here, on this sub, seeking advice and support from strangers, because we have tried everything we can think of and it hasn’t helped. In many cases what it hasn’t done is ... it hasn’t gotten her to do anything at all to help herself. If she felt better maybe she wouldn’t lash out so much. But in many cases she won’t even acknowledge there is a medical issue to consider.

So we’re left to fend for ourselves by taking a time out, or distancing, or shutting down. Then we get accused of disrespecting, or triggering her RSD, or stonewalling, or being avoidant. No shit Sherlock. Who wouldn’t want to avoid that garbage. I’m supposed to be “securely attached” while you tell me how awful I am for two weeks straight?

Which brings me to the third point – Is it though? Women with PMDD frequently report gaslighting themselves during follicular into thinking it wasn’t that bad. Symptoms like fatigue, overwhelm, and brain fog can contribute to misremembering. Certainly a lot of partners here report their PMDDer flat out denies having ever said or done the things she said or did during luteal. Again – not everybody – but here, in this context, luteal amnesia seems to be common.

Moreover, as HS pointed out two years ago (linked above), the hormonal cycle that caused all the chaos during luteal now makes her feel great during follicular. We have no such hormonal boost to help us “get over it”. It’s a disorder, a medical condition, so “don’t take it personally”. But that is a big ask when the PMDD makes it very personal indeed.

All of which is to say … we’re in this together, equals, a team. The couples that make it are the ones that can work together against the common enemy. If half the team is AWOL, or worse, discounting and belittling the other teammate, we’re doomed. Who has it worse is largely irrelevant. What can we do to make it better?

I was recently told that I “got the science wrong.” No help, no pointers, no advice, just a reprimand. Then I got accused of a bunch of stuff I didn’t do and called a “motherfucker”. Ahhhh, good times. Nevertheless I’ll try to get this in the ballpark and if I make a mistake I hope someone will correct me. Only without the drama.

The RCOG treatment tiers are what they are because they help most women with PMDD. PMDD has a fairly high misdiagnosis rate (estimates from 40-80%) which can also lead to treatment not helping, or the “wrong” treatment working great. Treating for PMDD when you don’t have it won’t help and accidentally treating the thing you do have will help. Add to that the reproductive system is shamefully understudied and really really complex and there is a great deal of variability in how women react to treatment.

Nevertheless there are these recommendations that are based in science and “should” be the first thing to try. But you have to get it right and the recommendations themselves are fairly cryptic. I’ve written about this before, probably will again, today let’s focus on hormonal IUDs and COCs. Copper IUDs just prevent pregnancy by being an effective spermacide. They do nothing for PMDD so we’ll ignore those.

TL;DR: Hormonal IUDs are crap for PMDD, as are many COCs

The idea behind introducing birth control is to eliminate the rise and fall of the hormones during the reproductive cycle. By taking a mono-phasic Combined Oral Contraceptive continuously the changes that cause PMDD symptoms are muted (if the ovaries remain active) or even eliminated (if the ovaries are shut down completely).

But a daily pill is a task. I can relate. I have a life threatening medical condition and I barely manage to take my pill a third of the time. IUDs are attractive because one office visit and a week or two adjusting and you’re set for years.

There are several reasons hormonal IUDs are not recommended for PMDD. The first is they are all progesterone only – not combined. That means if the ovaries do shut down there is no estrogen and estrogen is vital for all sorts of things, not the least of which is the immune system. But that’s a different post.

But truth is IUDs don’t shut down the ovaries. They lack enough actual hormone to do so. They work by thickening the cervical mucus so the egg can’t reach the uterus, and by thinning the uterine lining so the egg can’t implant if it does get there. So the ovaries are still working and the cycle continues.

Doctors will tell you (her) that IUDs are great. They are a really low dose of progestin, about a fourth of what is in a COC, and that works because it is local to the uterus. It’s right there. And very little makes it into the blood stream. And even if that were true … PMDD is a neurological disorder! So treating it with something that by design doesn’t affect the brain is … a little stupid.

And the progestin all of them use is levonorgestrel. All of them. In the US, Europe, Australia, Japan, China, India … all of them. And levonorgestrel is about the worst thing for PMDD. Wildly popular and effective for birth control, crap for hormone based mood disorders.

For starters Levonorgestrel is a synthetic progestin derived from testosterone. Yes that testosterone. The very hormone blamed for excess aggression in men. Consequently levonorgestrel has high androgenic (Man-like) properties. It increases the chances of side effects like acne and unwanted hair growth. That’s the canary in the coal mine. Visible symptoms that are easy to quantify. Science won’t say, but I have a hard time believing levonorgestrel doesn’t also cause mood changes. Anecdotal data from both subs supports that conclusion.

Levonorgestrel also has high “progestogenic” properties. That means that among progestins levonorgestrel is especially potent. About 50x-100x more potent than natural progesterone. This is part of why it’s ideal for IUDs. A low dose goes a long way so an IUD can last 5 years or more. But it also means that it’s a sledgehammer for folks with a sensitive system. It’ll bind to the progesterone receptors and not let go, leaving the natural (better) progesterone out in the cold. Rather than augment it will take over. So the thing derived from testosterone is in charge and science is bold enough to tell you high progestogenic properties can increase the chances of side effects like mood changes, fatigue, depression and weight gain.

All these factors combine to shatter the myth that IUDs are local to the uterus and therefore won't affect the brain. Levonorgestrel is 50x-100x more potent than natural progesterone so a little goes a long way, and at least a little does get into the bloodstream. And levonorgestrel, like all steroid hormones, is fat soluble. That means the blood/brain barrier does not exist so the levonorgestrel has free reign.

Many COCs also use levonorgestrel as their progestin. The dose there is about 5-10x the dose in an IUD and they will effectively shut down the ovaries. But the sledgehammer analogy still applies. Now there is an extremely potent progestin, derived from testosterone, just dominating the system. Anecdotal reports are often "Now she's just angry all the time." Gee - I wonder why?

Meanwhile Yaz is specifically recommended by RCOG, and the only COC approved by the FDA for treating PMDD, because it contains drosperinone as it’s progestin. Drosperinone is a fourth-generation (“newer” per RCOG) progestin that is derived from spironolactone. Spironolactone, in turn, is a diuretic. Drosperinone inherits Antimineralocorticoid properties from this lineage. That means it helps prevent bloating.

But also drosperinone has low progestenic properties, so it will augment instead of taking over, and anti-androgenic properties. The latter means it actively binds to the testosterone receptors, blocking the natural testosterone from binding, to help reduce agitation, irritability, and aggression.

That said drosperinone is still a synthetic progestin. Some women just don't tolerate a synthetic so even Yaz or Yasmine (same thing but 50% more estrogen) can cause an increase in symptoms. For some.

The birth control page at the other sub’s wiki has a chart with all the progestins listed. Highly recommend looking up the progestin in your loved ones BC and checking the chart.

Is very exciting. Somebody really hates the book.

I mean they really, really ... really ... hate the book.

They hate it so much they spent a good ten minutes prompting some A.I. to write a scathing four paragraphs. And let me tell you that A.I. didn't hold back. It got virtually everything wrong but ... with confidence!

You should read it. The review - I mean - but also the book. :)