Estrogen Dominance: what could really be behind PMS, hormone chaos and the feeling of being a stranger in your own body.
For the woman who has already been everywhere and still has no answer.
You function. But something is not right.
I bet you know this feeling.
Not sick enough to be really sick. But also not well enough to be really well. You get up in the morning and ask yourself why, after eight hours of sleep, you still feel as if you had not slept at all. Why your belly bloats every other week like yeast dough. Why your breasts ache so much that you cannot lie on your side at night. Why on some days you are your own best friend, and three days later you cannot bring up any understanding for the same people.
You went to the gynecologist. She measured. She nodded. She said: everything within the normal range. And you went home, somehow relieved. And somehow even more frustrated than before.
Because you know: there is more.
Let me tell you something you have probably never heard quite like this:
Your body does not lie. It is sending you very clear signals all the time. The problem is not your body. The problem is that most measurements are too coarse to see what your body is trying to tell you.
And the other thing I want to tell you, before we begin: You are not crazy. You are not dramatic. And what you are experiencing has a biochemical explanation. One that we are going to look at together. Without jargon. Without panic. But with real depth.
1. The ratio. Not the value.
Okay, let us start with what most people misunderstand, and indeed before they even know what estrogen dominance is.
Estrogen dominance sounds as if you have too much estrogen. Sometimes that is true. But mostly it is much more subtle. And much more interesting.
Imagine two musicians who are supposed to play a piece together.
Estrogen is the violin: loud, alive, brilliant, full of energy. Progesterone is the cello: warm, grounding, calm, the anchor. When the violin plays too loud, no beautiful piece arises. But the problem can also be that the cello is simply too quiet. It is not the violin playing wrong, it is the cello that is missing.
Estrogen dominance is almost always a problem of the cello. Not a problem of estrogen alone.
What estrogen really is, and why it is wonderful
Estrogen is not your enemy. Estrogen makes you alive. It builds up the endometrium, protects your bones, keeps your joints supple, makes your hair full and your skin radiant. It lifts your energy in the first half of the cycle. It is the reason you sometimes have weeks where you feel like you have everything in hand.
Estrogen rises in the first half of the cycle, the so-called follicular phase, up to ovulation. That is its job. That is beautiful. The problem begins when, after ovulation, the counterweight does not come.
Progesterone: the hormone without which you cannot really recover
Progesterone is the hormone of the second half of the cycle. It is produced in the corpus luteum, that is, in the tissue that arises after ovulation from the ruptured follicle. And here comes the decisive part, remember it:
No ovulation. No corpus luteum. No progesterone.
It is that simple. No supplement in the world can compensate for this as long as ovulation does not happen.
Progesterone does not only act in the uterus. In the brain a part of it is converted to allopregnanolone. This is what is called a neurosteroid, it activates the GABA system, the most important calming system of your nervous system. The body's own relaxation switch. When progesterone is missing or falls too early, you lose this switch. Sleep becomes shallower. Stimuli feel stronger. Mood swings explode. Inner restlessness comes out of nowhere.
What you call PMS? That is not weak nerves. That is neurobiology. That is measurable. That has a name.
MacLean JA & Hayashi K. investigated the actions of progesterone and progesterone resistance in gynecological disorders.
Core finding: the imbalance between estrogen and progesterone leads to estrogen dominance and progesterone resistance and is directly linked with gynecological disorders such as endometriosis, PCOS, fibroids and endometrial hyperplasia.
MacLean JA & Hayashi K. Progesterone Actions and Resistance in Gynecological Disorders. Cells. 2022;11(4):647. DOI: 10.3390/cells11040647It is not genetics, just because mom had it too. When your mother also had PMS, when your sister also struggles, when your cycles are all similarly difficult: this does not mean that you are genetically condemned to it. It could mean that you were exposed to the same environmental toxins in the same household. That you ate similarly. That stress in your family left similar biochemical patterns. Or that you all had the same lack of sleep, of magnesium, of safety. Genes load the gun. Lifestyle pulls the trigger. And the trigger is something you can influence.
2. Why your lab result still does not tell you what is going on
You went to the doctor. Everything is normal. But you are not normal.
I do not say that harshly. I say it with full respect for what you are going through. But I hear this sentence so often: everything is normal. And the woman sits across from me and looks at me as if I had just told her she was imagining all of this.
What matters to me here: hormones are not static numbers. They are a story that unfolds over the entire month. A single value tells you about as much as if you looked out the window once and claimed to know what the weather was like for the past month.
The timing problem
Progesterone measured on day 14 tells you almost nothing meaningful. Because on day 14 you are at ovulation, where progesterone is physiologically still hardly present. Progesterone belongs in the luteal phase, ideally around day 19 to 22 of a 28-day cycle. If it is measured there and is low, that has weight. If it is measured at the wrong time, that tells you: nothing.
In routine care, progesterone is often measured for different questions than a targeted workup of the luteal phase. A single value then says little about the second half of the cycle. That is no reproach to anyone, it is a question of the question being asked. If you suspect that your complaints sit in the luteal phase, ask specifically for a measurement on day 19 to 22.
The ratio problem
Imagine that estrogen has had five glasses of wine tonight. Progesterone has had only one glass. Both values are "normal". But the effect in the body is that of someone coming home drunk, because the ratio is off.
Exactly that happens in the body. Estrogen can be within range, progesterone too, and yet the ratio of the two can be so out of balance that all the PMS symptoms are there. The lab does not see this when only individual values are looked at.
The xenoestrogen problem
And then there is something that no standard lab measures: foreign substances that behave like estrogen. Xenoestrogens from plastic, from mold toxins, from cosmetics, from certain foods. They can bind to your estrogen receptors, activate hormonal signaling chains and thereby raise the estrogen-like total effect in your body. But they do not appear as estradiol in the blood panel. They are invisible in the standard test.
That is why a woman can have perfect lab values and still have severe symptoms. Because what is burdening her is simply not measured.
The CGM idea: making visible what is invisible
In my practice I sometimes use a continuous glucose monitor (CGM), a small patch on the arm that shows at every moment how blood sugar reacts to every meal. Why am I telling you this here?
Because it is the same principle as with hormones: the snapshot in the resting state shows nothing. The curve over time shows everything. I wish we had the same tool for hormones. Until then, we need cycle-appropriate measurements, the right panel and the right timing.
3. Cortisol: your body cannot make alarm and progesterone at the same time
Stress is no excuse. Stress is biochemistry. And this biochemistry could have been sabotaging your hormone life for years.
I will show you why in a moment. But first an honest conversation about the word stress.
When I ask patients whether they are stressed, many say: "No, I am actually relaxed." And then they tell me about 55-hour work weeks, children who have to be made ready in the morning, sleep under seven hours, the feeling of never really winding down, and an inner monologue that keeps running at 11 in the evening. That is stress. Even if you do not experience it as such.
The pregnenolone fork: a model that is disputed
Cortisol and progesterone go back to the same precursor. It is called pregnenolone. In functional medicine a picture is often derived from this, according to which the body switches in favor of cortisol under chronic stress and the progesterone budget shrinks. That picture carries the name pregnenolone steal.
I mention it here because you will meet it everywhere. But let me say at once: endocrinologically this model is disputed. Steroid formation runs separately in the adrenal cortex and the corpus luteum, and there is no shared pool from which something could be stolen. What appears better supported is the route through the brain. Let us look at that now.
The HPO axis: when the brain no longer gives the order
Chronically high cortisol levels could moreover inhibit the higher-level control center of the hormone system: the hypothalamic-pituitary-ovarian axis. HPO axis for short.
This is how it works in the normal state: the hypothalamus (a region in the brain) gives the start signal with GnRH. The pituitary releases LH and FSH. The ovaries produce estrogen and progesterone. A precise, wonderful system.
Under chronic stress, cortisol could dampen these GnRH pulses. Less GnRH means less LH. Less LH means: weaker ovulation. Weaker ovulation means: a poorer corpus luteum. A poorer corpus luteum means: less progesterone. The cello falls silent.
Koch CE et al. investigated the interactions between circadian rhythms and stress.
Core finding: the stress axis and the inner clock are closely coupled. A disturbed day-night rhythm can shift cortisol regulation. The authors point out explicitly that a large part of these data comes from animal models and that transfer to humans has to be examined carefully. The chain from cortisol via LH to ovulation quality is a physiological consideration, not a result of this work.
Koch CE et al. Interaction between circadian rhythms and stress. Neurobiology of Stress. 2017;6:57–67. DOI: 10.1016/j.ynstr.2016.09.001The most insidious thing: your nervous system knows no difference
The saber-toothed tiger back then. The presentation tomorrow morning. The 57 unanswered emails. The child who does not sleep at night. For your nervous system, alarm equals alarm. It releases cortisol without asking questions.
That was once brilliant, because the saber-toothed tiger was gone after a few minutes. The problem today: the alarm runs continuously. Not for minutes. For months. For years. And at some point the system starts to save. And it saves first on things that are not about survival. Reproduction, for example.
You will deliberately not find case histories from my practice here. What I can describe instead is the pattern. When sleep rhythm, morning light and training intensity are adjusted over several weeks, many women report milder complaints in the second half of the cycle. That is a clinical observation without study evidence, not a success rate, and it cannot be transferred to every woman. Whether anything follows from it in an individual case can only be clarified in a personal conversation.
4. Blood sugar: the silent saboteur almost no one has on the radar
May I ask you an uncomfortable question?
What did you eat for breakfast this morning? Oats with fruit? Toast? Coffee and then nothing for a while?
I am not asking to shame you. I ask because in my practice I keep experiencing the same surprise: a woman who considers herself to eat well wears a blood-sugar sensor for three days, and then we sit together and look at the curves. And the curve looks like a rollercoaster ticket.
A breakfast of oats with fruit and honey, followed by coffee with oat milk, counts as very clean for many people. In the sensor trace one often sees a steep rise afterwards and an equally steep fall, even when the values themselves stay within range. Some women report inner restlessness, concentration problems and cravings during exactly those phases in the late morning. What is usually missing in such breakfasts is protein and fat, which can buffer the rise. Whether that is connected in an individual case can only be judged individually, and a sensor trace alone proves no cortisol reaction.
What does this have to do with hormones?
Everything. Because when blood sugar rises, the pancreas releases insulin. Insulin is no evil hormone, it is essential for life. But chronically elevated insulin levels could affect several hormonally relevant processes, and indeed at the same time.
First: insulin could activate aromatase. This is an enzyme that sits in fat tissue and converts androgens to estrogen. More insulin, more aromatase activity, more estrogen from your fat tissue, and that completely independent of what your ovaries are doing.
Second: chronically high insulin levels could disturb ovulation. In PCOS exactly this mechanism is well documented.
Third: when blood sugar crashes after a spike, your body reacts with cortisol as counter-regulation. And cortisol, as we have already discussed, could inhibit progesterone synthesis.
A single breakfast can therefore become a whole chain: blood-sugar spike, insulin spike, cortisol counter-regulation, and through that possibly a dampened ovulation with less progesterone. Every morning. Over years. This chain is physiologically plausible. As a whole it is not proven in humans in this form.
Chang KJ et al. summarized the molecular and cellular mechanisms of polycystic ovary syndrome in a review article.
Core finding: insulin resistance and the resulting hyperinsulinemia are among the central mechanisms in PCOS and can go along with disturbed ovulation. This is a narrative review, not an original measurement series. The step from there to aromatase activity in fat tissue is a physiological consideration that this work does not itself test.
Chang KJ, Chen JH, Chen KH. The Pathophysiological Mechanism and Clinical Treatment of Polycystic Ovary Syndrome: A Molecular and Cellular Review of the Literature. Int J Mol Sci. 2024;25(16):9037. DOI: 10.3390/ijms25169037"Healthy" eating is not automatically hormone-friendly eating. You can eat vegan, gluten-free, organic and whole-food, and still send your blood sugar through the roof every morning. When every meal consists of carbohydrates without enough protein and fat, the hormonal damage is real. Independent of whether the food appears on the Instagram nutrition plan of your favorite account. The goal is not eat less. The goal is: protein first. Then the rest.
5. Your gut helps decide. Every night. Without your knowledge.
Here comes something most women have never heard, although it could have a huge influence.
The liver is a wonderful organ. It packages excess estrogen, attaches a kind of tag to it that says: please excrete. This packaged estrogen reaches the gut via bile. It is meant to leave with the stool.
But then your gut residents come along. Billions of bacteria. And some of them produce an enzyme called beta-glucuronidase. This is the little saboteur that tears the tag back off the packaged estrogen. The estrogen is set free. And because the gut absorbs everything floating freely in it, the estrogen ends up back in the bloodstream.
This is no error. It is a system known as the "estrobolome", the hormonal recycling of the gut. With a healthy gut flora it is in balance. With dysbiosis, that is, an imbalance of gut bacteria, this recycling could become excessively active. Too much estrogen returns. The ratio tips. Your body turns up.
Ashonibare VJ et al. investigated the axis between gut microbiota and gonadal function.
Core finding: gut microbiota can influence circulating sex hormones, immune response and inflammation markers. The authors point out explicitly, however, that the majority of this evidence comes from animal studies and that robust human studies are still largely lacking.
Ashonibare VJ et al. Gut microbiota-gonadal axis: the impact of gut microbiota on reproductive functions. Frontiers in Immunology. 2024;15:1346035. DOI: 10.3389/fimmu.2024.1346035Sluggish bowel movements are very often taken for normal, especially when they have been there for years and are familiar in the family. From a functional-medicine point of view they are not trivial for the hormone household. The longer the packaged estrogen stays in the gut, the more opportunity beta-glucuronidase could have to cut it free again. That is why I always ask about digestion before we talk about hormones. Persistent constipation, blood in the stool or a sudden change in bowel habits, however, belong in a medical workup first, not in a self-experiment.
The liver: much more than a detoxification station
The liver is no trash bin into which you throw everything and hope that it somehow disappears. It is a highly precise metabolic organ that actively paces estrogen breakdown over two biochemical phases.
In phase 1, estrogen is converted into various metabolites. These can be harmless or problematic, depending on which path is preferred. In phase 2 the metabolites are made water-soluble for excretion. When the liver is under pressure from alcohol, chronic sleep deprivation, too many processed foods, heavy metals or mold toxins, phase 1 could stall. Estrogen metabolites accumulate. Some of them could themselves be hormonally active.
Brassicas like broccoli, cauliflower and Brussels sprouts therefore belong, in my view, in a hormone-friendly kitchen, together with enough fiber overall. Why I see it that way has to do with the interplay of liver and gut. An efficacy promise for a single food is expressly not intended here. Furthermore, the liver does its most important regenerative work at night. Bad sleep is bad liver management. And bad liver management could be hormonally expensive.
6. Xenoestrogens: when your environment burdens your hormone system
Now comes the part that first makes some people incredulous. And then frightens them.
Imagine that someone sneaks into your apartment, sits down in the seat of your partner and behaves as if he were your partner. The seat is taken. The signals run through. But it is not the right person. The system reacts anyway.
That is exactly what xenoestrogens do in your body. They bind to estrogen receptors and activate hormonal signaling chains, without appearing as estrogen in the blood panel. The standard lab does not measure them. They are invisible. But they can act.
BPA and phthalates: plastic that disguises itself as a hormone
BPA is a component of polycarbonate plastics. It is found in plastic bottles, canned foods, some dental materials. Its chemical structure resembles estradiol, the most active body-own estrogen, so strongly that it can bind to estrogen receptors.
Phthalates are plasticizers in PVC products: cosmetics, perfumes, shampoos, plastic packaging. Their breakdown product MEHP could trigger oxidative stress in follicle cells and impair follicle maturation. More plasticizer can migrate out of a plastic bottle that has stood for a longer time in the sun or in a hot car. One more word on thermal till receipts, because they are often mentioned in this context: BPA in thermal paper has been banned in the EU since 2020. Something has improved here. Substitutes such as bisphenol S are, however, also under discussion. Anyone who handles receipts daily at work can simply avoid holding them with damp or freshly creamed hands.
Blaauwendraad SM et al. conducted a prospective cohort study with 1,405 women and measured their urinary burden of bisphenols and phthalates three times during pregnancy.
Core finding: in this cohort, higher phthalate burdens were associated with lower average AMH levels over time. For bisphenol A no significant association was found in this study, and the individual findings after 6 and 9 years did not hold after correction for multiple testing. AMH is regarded as a marker of ovarian reserve. This is an association, not proof of causation.
Blaauwendraad SM, Dykgraaf RHM, Gaillard R, Liu M, Laven JS, Jaddoe VWV, Trasande L. Associations of bisphenol and phthalate exposure and anti-Müllerian hormone levels in women of reproductive age. eClinicalMedicine. 2024;74:102734. DOI: 10.1016/j.eclinm.2024.102734Tzouma Z et al. evaluated a decade of human epidemiological evidence on endocrine-active chemicals and fertility.
Core finding: systematic review of 14 observational studies published between 2014 and 2024. BPA, phthalates and PFAS were associated there with reduced ovarian reserve, with PCOS and with altered hormone levels. The authors call the evidence methodologically heterogeneous and speak of biological plausibility, not of proof.
Tzouma Z, Dourou P, Diamanti A, et al. Associations Between Endocrine-Disrupting Chemical Exposure and Fertility Outcomes: A Decade of Human Epidemiological Evidence. Life (Basel). 2025;15(7):993. DOI: 10.3390/life15070993Zearalenone: the mold substance that looks like estrogen
This is one of the most fascinating and frightening findings of modern hormone research.
Zearalenone (ZEA) is a mold-fungus toxin. It is formed by Fusarium mold that grows on grains: corn, wheat, oats, barley. It is heat-stable and survives cooking and baking. Grain products can therefore contain traces. In the EU there are binding maximum levels for this that are officially monitored. Everyday amounts are thus far below what was used in animal experiments. The topic can become relevant above all when an additional mold burden in the home comes on top.
And its chemical structure resembles 17-beta-estradiol so strongly that it can bind competitively to estrogen receptors. In livestock farming the effect has been described for decades: ZEA can trigger hyperestrogenism in animals, disturb the cycle, inhibit ovulation and cause infertility. In veterinary medicine ZEA has a fixed name: mycoestrogen.
Lv Q et al. investigated the reproductive toxicity of zearalenone and its molecular mechanisms.
Core finding: zearalenone and its metabolites can bind competitively to estrogen receptors and cause reproductive dysfunction. Mechanisms include oxidative stress, germ-cell apoptosis, DNA damage and cell-cycle arrest. In animal breeding, ZEA-contaminated feed leads to abortions and reproductive disorders.
Lv Q et al. Reproductive Toxicity of Zearalenone and Its Molecular Mechanisms. Molecules. 2025;30(3):505. DOI: 10.3390/molecules30030505You will deliberately not find case histories from my practice here. What I can describe instead is the pattern: in therapy-resistant courses it is worth asking about the living situation and about a possible mold burden. Visible mold in the bedroom or bathroom that keeps coming back is a piece of information that often does not come up in the history at all, because nobody suspects a connection. Whether anything follows from it in an individual case can only be clarified in a personal conversation. A connection between mold burden and fertility is so far not proven in humans.
7. Mercury and amalgam: when a dentist visit could change hormones
What I am about to tell you sounds far-fetched to some at first. Please read it through to the end anyway.
Mercury is a fascinating and frightening substance. It is the only metal that is liquid at room temperature. And once it enters the body, it behaves like a system hacker: it preferentially deposits itself in endocrine organs. In the thyroid. In the pituitary. In the ovaries.
Where does mercury in the body come from?
The most common sources in everyday life are amalgam fillings, also called "silver fillings". They consist of about 50 percent mercury. With chewing, with temperature differences, and in an acidic milieu, amalgam continuously releases tiny amounts of mercury vapor. Not dramatic, but steady. Over years. Over decades.
Added to this are deep-sea fish and seafood (especially tuna and swordfish), industrial exposures and certain occupational fields.
What mercury could do in the hormone system
Mercury binds with high affinity to sulfur groups of enzymes, that is its entry point. Among them are also selenoproteins, for example deiodinase. Deiodinase is the enzyme that converts inactive T4 to active T3, that is, to the thyroid hormone that actually acts in the cells. When mercury displaces selenium and blocks deiodinase, T4-to-T3 conversion could be disturbed. The result: lab values that look "normal", while at the cellular level too little active thyroid hormone arrives.
At the same time, high mercury burdens could trigger autoimmune processes via T-cell reactions that target thyroid tissue. An honest classification belongs here: the greater part of this evidence comes from animal studies. The human studies performed so far have not been able to confirm the findings from animal models conclusively. What I describe is a mechanistically plausible picture and a clinically observed pattern, not a proven connection.
Ursinyova M et al. investigated the connection between human mercury exposure and thyroid hormone status using 75 mother-child pairs.
Core finding: in this small study, mothers with amalgam fillings had lower average T4 and fT4 levels. Further associations appeared only in individual subgroups. The exposures were in the low range overall, the authors formulate conditionally throughout, and the informative value of a study of this size is limited.
Ursinyova M et al. The relation between human exposure to mercury and thyroid hormone status. Biological Trace Element Research. 2012;148(3):281–291. DOI: 10.1007/s12011-012-9382-08. The thyroid: the silent conductor of the hormone system
When women come to me with exhaustion, cycle disturbances and poor mood, I always also look at the thyroid. Always. Because it is so often overlooked and can trigger so much.
The thyroid produces T4 (thyroxine) and some T3. But most of the T3 your body needs is converted from T4 elsewhere: in the liver, the gut and other tissues. T3 is the active hormone. It is the gas pedal for cellular energy, for metabolism, mood, heart rate, body warmth.
Why thyroid and estrogen dominance could be linked
Thyroid hormones influence SHBG, the sex-hormone-binding globulin. SHBG is the transport protein that binds estrogen and testosterone in the blood and thereby inactivates them. With a thyroid underfunction (hypothyroidism), SHBG drops. What that means: more free estrogen circulates in the blood. At the same time, estrogen breakdown in the liver slows. Hypothyroidism could thus indirectly favor estrogen dominance.
And the other way around: high estrogen levels raise thyroid-binding globulin (TBG), another transport protein. More TBG means: less free T3 and T4 for the cells. The thyroid has to produce more to achieve the same effect. A self-reinforcing loop is possible. Estrogen dominance and thyroid problems invite each other in.
TSH alone is not enough
In standard diagnostics, often only TSH is measured. TSH is the higher-level commander from the pituitary. But a normal TSH does not exclude that too little active T3 arrives in the cells. For that one would need to know fT3, fT4 and anti-TPO antibodies.
I see women with TSH within range but fT3 at the lower edge, elevated antibodies and classical hypothyroidism symptoms. A broader picture can help in such cases.
Iron, selenium and the thyroid: the invisible triangle
The conversion of T4 to T3 by deiodinase needs selenium as a cofactor. Selenium supply in Germany is rather tight, because the soils are low in selenium. A true deficiency is therefore not automatically present, but it can be measured. Selenium should not be dosed high on suspicion, the span between sensible and too much is narrow. Mercury can displace selenium, as we just saw. And iron deficiency impairs thyroid peroxidase (TPO), the enzyme that synthesizes T4 and T3 in the thyroid in the first place.
Iron deficiency can therefore directly slow thyroid synthesis. Poor thyroid impairs hormone metabolism. Hormone metabolism affects everything else. And all of this sometimes begins with a ferritin value of 14 µg/L that the lab calls "normal".
9. Iron deficiency: the overlooked foundation, without which nothing functions
Ferritin at 12. "Normal according to the lab". Exhausted nonetheless.
I experience this regularly. A woman comes because of hormonal complaints. Her ferritin is 12 or 14 µg/L. The lab says: within range. I say: that explains a lot of what you describe.
Iron deficiency is the most common micronutrient deficiency worldwide. And women in the reproductive phase are especially affected, because menstruation costs iron. The problem: the ferritin threshold from which an official deficiency is declared lies in many German labs at 12 to 15 µg/L. From a physiological point of view, that is far too low.
Badenhorst CE et al. investigated a contemporary understanding of iron metabolism in active premenopausal women.
Core finding: estrogen and progesterone actively influence iron regulation via hepcidin. Iron deficiency is widespread in premenopausal women, the female-specific causes are insufficiently researched and treated to date.
Badenhorst CE et al. A contemporary understanding of iron metabolism in active premenopausal females. Frontiers in Sports and Active Living. 2022;4:903937. DOI: 10.3389/fspor.2022.903937How iron deficiency could hit your hormone system
Iron is a cofactor of thyroid peroxidase (TPO), the enzyme that incorporates iodine into active thyroid hormones in the thyroid. With iron deficiency, TPO could not be sufficiently active: less T4, less T3, worse conversion. With this the loop closes: iron deficiency impairs the thyroid, the thyroid affects SHBG and estrogen breakdown, and all of this together could favor estrogen dominance.
Furthermore, your mitochondria, the power plants of every cell, need iron for the respiratory chain. Exhausted mitochondria mean exhausted cells, exhausted hormone production, exhausted you.
What I consider functionally favorable
In women with clear symptoms I look more closely at values below 30 µg/L, even without anemia. Ferritin above 50 µg/L is my personal orientation value in this, not an official threshold. What matters most to me is the order.
10. The pill: what it does, and what comes after
I do not judge. I inform. Because many women tell me they would have wished for more time for the questions they have about the pill.
The pill works essentially like this: synthetic estrogens and progestins (synthetic progesterone) are taken. The pituitary registers: hormones present. No LH surge. No ovulation. No natural cycle.
The monthly bleeding under the pill is no real period. It is a withdrawal bleed, because in the pill-free week the synthetic hormones stay away and the lining sheds. No ovulation. No progesterone. No allopregnanolone. No GABA boost.
What the pill can change in your body
First, it could deplete nutrients. Vitamin B6, B12, folate, magnesium, zinc, selenium. These nutrients are essential for neurotransmitter synthesis and hormone metabolism. What happens when, after ten years on the pill, you stop and selenium, zinc and B6 are depleted? The restart becomes harder.
Second, the pill strongly raises SHBG. This protein binds not only estrogen but also testosterone. Which means: less free testosterone. Less libido. Less energy. Less drive. And the curious thing: SHBG can remain elevated after stopping, sometimes for months.
Third, the pill could change the gut microbiome and thereby affect the estrobolome.
Post-pill: the restart no one explains
When you stop the pill, the body's own system has to start up again after months or years of suppression. That takes time. In some women it goes quickly. In many it takes three to six months until the cycle is stable.
What often happens during this time: an androgen rebound. The ovaries begin to produce again, sometimes overshooting. This can lead to acne, oilier skin, mood swings.
At the same time, the first cycles are often anovulatory. No ovulation, no progesterone. That means: a phase of potential estrogen dominance until the rhythm has settled again. This phase is transient. But it is real. And it deserves real support, not "just wait".
The pill suppresses your own cycle instead of replacing it. That is neither good nor bad. It is simply important to know. If you experience symptoms after stopping, this is no sign that your body is "broken". It can be a sign that it is taking up its own rhythm again.
11. What I measure in practice and why I do not start with the lab
When a woman comes to me, the conversation does not begin with a lab sheet. It begins with a long history. With real listening.
I ask: when do the symptoms appear? In which cycle phase? How do you sleep, really? What does your morning look like, from the first thought to the first bite? What do you eat and in what order? Have you ever lived in an apartment with visible mold? Did you have amalgam fillings, and when and how were they removed? Are you on the pill or have you stopped, and when? Are there thyroid disorders in the family?
Only when I understand this do I see which lab brings new information. Not everything at once. But what really moves us forward.
The basic hormone panel
- Sex hormones cycle-bound: estradiol on day 3 to 5, progesterone on day 19 to 22, LH, FSH, AMH (ovarian reserve)
- Thyroid complete: TSH, fT3, fT4, anti-TPO, anti-thyroglobulin (not only TSH)
- Iron status: ferritin, serum iron, transferrin saturation
- Nutrients: vitamin D, zinc in erythrocytes, selenium, magnesium, B12, folate
- Inflammation marker: hsCRP
- SHBG and free testosterone
- Fasting insulin and glucose on suspicion of insulin resistance
Extended diagnostics on suspicion of toxin exposure
- Heavy-metal analysis in blood or urine with corresponding history
- Mycotoxin analysis in urine with mold exposure history or therapy-resistant courses
- CGM sensor for blood-sugar profile
- HRV measurement as a functional marker of the nervous system
12. Seven levers. Today. Not next Monday.
And now the decisive step: from understanding to action.
I know how it is. You read something, nod inwardly, think "I will try that out", and a month later nothing has happened. Because everything sounds somehow doable, but nothing is really anchored.
Therefore I ask you: choose right now while reading two levers. Only two. And start tomorrow morning.
01 Protein first. Every morning.
Your breakfast can co-determine the blood-sugar curve for the whole morning. A meal with enough protein and fat can keep the blood-sugar rise flatter, and flatter curves mean less counter-regulation via cortisol. Concretely: eggs, skyr, cottage cheese, nuts, legumes. First protein. Then the rest.
02 Brassicas and ground flaxseeds daily.
Broccoli, cauliflower, Brussels sprouts and rocket belong, in my view, in a hormone-friendly kitchen, as do one to two tablespoons of freshly ground flaxseed and enough fiber overall. Why I see it that way has to do with the interplay of liver and gut. An efficacy promise for a single food is expressly not intended here. Two practical notes on flaxseed: drink enough with it, and leave it out if a narrowing of the bowel or a risk of ileus is known. The German Federal Institute for Risk Assessment recommends not exceeding about 15 grams of ground flaxseed per portion.
03 Two minutes of breath work. Three times daily.
This sounds almost laughably simple. An extended exhalation can address the parasympathetic system, that is, the counterpart to the stress system. Four seconds in. Six to seven seconds out. Two minutes, three times a day. That is your brake. Free of charge. Available everywhere.
04 Reduce xenoestrogens, without losing your mind.
You do not have to change everything at once. But three things you can change immediately: do not drink from a plastic bottle that has stood for a longer time in the sun or in a hot car. Do not hold thermal till receipts with damp or freshly creamed hands. Go through your cosmetics by INCI list for parabens and synthetic fragrances. This can reduce the daily intake from these sources.
05 Sleep rhythm as hormone therapy.
Sleep acts on progesterone indirectly, but clearly. Progesterone arises after ovulation in the corpus luteum. When sleep is chronically short or irregular, that can impair ovulation quality via the stress axis, and a weaker corpus luteum can form less progesterone. Constant rise time, also at the weekend. Dim screen light in the evening. Sleep room cool and dark. This is no wellness recommendation. This is endocrine basic care.
06 Lab, cycle-bound and complete.
When you go to the doctor, ask explicitly for: progesterone on day 19 to 22, estradiol on day 3 to 5, ferritin, the complete thyroid (TSH plus fT3, fT4 and anti-TPO), vitamin D, zinc. Not only TSH. Not only hemoglobin. But the complete picture.
07 With persistent symptoms, ask about the temporal connection.
Did it begin after a dentist visit? After a move into a house with mold? After stopping the pill? After a long course of antibiotics? These questions are no esoterics. They are functional medicine. They show where to look.
13. Your self-check: who are you in this story?
Before you go to the doctor, before you order anything, before you change anything: ask yourself these questions.
Not for me. Not for the record. But so that you start to understand your own body instead of following it like a stranger.
Block 1: the temporal connection
- Did your symptoms begin in temporal connection with a dentist visit? With the removal or placement of amalgam fillings?
- Have you ever lived in an apartment or house with visible mold? Did your well-being worsen during this time?
- Has your hormone system changed after stopping the pill? When exactly, and for how long had you taken the pill before?
- Have you had frequent antibiotic treatments in recent years?
- Has your bowel pattern changed? Constipation, bloating, irregularity?
Block 2: your everyday life
- What do you eat first thing in the morning: carbohydrates or protein?
- Do you often feel sleepy after lunch, or have cravings in the late afternoon? (Possible sign of blood-sugar swings)
- Do you regularly sleep less than 7 hours?
- Are you often still on your phone or laptop in the evening?
- Do you drink daily from plastic bottles, or heat foods in plastic containers?
- Do you use many conventional personal-care and cleaning products?
Please seek prompt medical workup with:
- Suspicion of PCOS, endometriosis or fibroids (heavy or painful bleeding, wish for children)
- Persistent exhaustion that strongly limits daily life
- Thyroid symptoms: feeling cold, hair loss, unexplained weight changes
- Severe depression, panic attacks or pronounced PMDD
- Suspicion of serious toxin exposure
- Persistent constipation, blood in the stool or a sudden change in bowel habits
If you do not want to sort this out on your own: below this article you will find the option to arrange an appointment. No lab sheet first. Listening first, then measuring.
Sources
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- Chang KJ, Chen JH, Chen KH. The Pathophysiological Mechanism and Clinical Treatment of Polycystic Ovary Syndrome: A Molecular and Cellular Review of the Literature. Int J Mol Sci. 2024;25(16):9037. DOI: 10.3390/ijms25169037
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- Caporossi L, Viganò P, Paci E, et al. Female Reproductive Health and Exposure to Phthalates and Bisphenol A: A Cross Sectional Study. Toxics. 2021;9(11):299. DOI: 10.3390/toxics9110299
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- Balló A, Busznyákné Székvári K, Czétány P, et al. Estrogenic and Non-Estrogenic Disruptor Effect of Zearalenone on Male Reproduction: A Review. Int J Mol Sci. 2023;24(2):1578. DOI: 10.3390/ijms24021578
- Zhu X et al. The endocrine disruptive effects of mercury. Environ Health Prev Med. 2000;4(4):174–183. DOI: 10.1007/BF02931255
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- Pamphlett R et al. Mercury in the human thyroid gland. PLoS One. 2021;16(2):e0246748. DOI: 10.1371/journal.pone.0246748
- Badenhorst CE et al. Iron metabolism in active premenopausal females. Front Sports Act Living. 2022;4:903937. DOI: 10.3389/fspor.2022.903937
- Yang Q, Jian J, Katz S, Abramson SB, Huang X. 17beta-Estradiol inhibits iron hormone hepcidin through an estrogen responsive element half-site. Endocrinology. 2012;153(7):3170-3178. DOI: 10.1210/en.2011-2045
Shukri Jarmoukli | Doctor and mentor | Berlin
All information serves informational purposes and does not replace a medical diagnosis or treatment.