Hormone Guide · Finding the Cause

Why I look for environmental factors in hormonal disorders

The gynaecological work-up is done, the values are known, and the question has still been left open. That is when I look at a signalling system with four weak points and at what can rattle them from the outside.

SJ
Shukri Jarmoukli · Physician · Area of focus: integrative medicine · ViveCura Berlin
Four-level grid Endocrine disruptors, mould, metals, inflammation When the search adds nothing 29 sources with DOI or PMID
ViveCura BlogHormone Guide › Environmental Cause-Finding
Why I am writing this

I send this text to patients after the consultation, because one question stays open that never quite fits into an appointment. Why do I look at the flat, the job and the inflammatory load when the problem is a menstrual cycle? The short answer is in this article. The long answer is that a hormone value checks only one of four points at which a signal can fall apart.

You are sitting there with a lab report on which everything is within range. Estradiol matching the cycle day. TSH unremarkable. Prolactin normal. The ultrasound was without findings, or with a finding that already has a name.

And still something is off. The cycle has become restless. Your skin reacts differently than it used to. The second half of the cycle feels like a different person. The exhaustion does not sit in your legs but behind your forehead.

Many women know this pattern. The work-up was correct and complete. It ruled out what had to be ruled out. It simply answers a different question from the one you came with. It answers: is there a disease here for which a treatment exists. Your question is: why is my system out of rhythm.

Those are two different questions. Both are legitimate. For the first there are guidelines, for the second there is a grid, a few good studies and many open spots. That is exactly what I am writing about here.

What you will find in this article

  • Why a normal blood value checks only one of four levels
  • The four-level grid: production, transport, receptor, breakdown
  • Search direction one: endocrine disruptors from the environment
  • Search direction two: mould toxins and zearalenone
  • Search direction three: cadmium and lead
  • Search direction four: silent inflammation
  • When this search is worthwhile and when it explicitly is not
  • What tests can do and what they cannot
Guideline professional society or agency Human observation or cohort Animal model rat, sheep, primate Cell culture in the lab, not in the body Method laboratory comparison or review, not a guideline

These labels sit next to every study from here on. In this field they are the single most important distinction. Leave them out and a rat study turns into a statement about your cycle. That happens constantly online, and it is the reason this topic has a poor reputation.

When the work-up is sound and the question remains

Picture two kinds of consultation. In one, the point is to confirm or rule out a diagnosis. That is precise work with clear rules. In the other, the point is to understand a course of events. That is blurrier, slower and needs more time than a standard appointment usually has.

The gynaecological work-up delivers the first, and it delivers it well. It clarifies whether PCOS lies behind your symptoms, or endometriosis, a thyroid disease, a prolactinoma, an early perimenopause. These distinctions are not incidental. They decide about treatments that can genuinely change something.

That is why the order in this article is not negotiable: the gynaecological work-up remains the foundation. The environmental perspective comes on top and never in its place.

Read this before you read on

There are symptoms for which no cause-finding runs in the background, but a prompt appointment is due. These red flags include:

  • bleeding after menopause, meaning after a year without a period
  • very heavy or suddenly and markedly changed bleeding
  • lower abdominal pain with fever
  • acute, one-sided, severe lower abdominal pain
  • unintended weight loss
  • visual disturbances or new severe headaches, especially together with milk discharge from the breast
  • rapidly progressing virilisation, meaning quickly increasing body hair, a deeper voice, pronounced hair loss on the head
  • your period stops for three months or longer without a pregnancy

These are not environmental questions. These are reasons to see a doctor, and soon. With acute severe lower abdominal pain, with very heavy bleeding and faintness, or with high fever this applies immediately: call the emergency services, 112 in Germany and across the EU, rather than booking an appointment in a few days.

I want to underline the last point. A period that stops for months can point to functional hypothalamic amenorrhoea and equally to a premature exhaustion of ovarian function, primary ovarian insufficiency. Both can matter not only for the cycle but also for bone density. The Endocrine Society explicitly names bone loss as a possible complication of functional hypothalamic amenorrhoea. That belongs in a medical work-up before anyone thinks about plasticisers.

Let us stay with the second kind of consultation. Often someone sits there with a diagnosis that explains only half of the symptoms. PCOS explains the irregular cycle, not the headaches. Endometriosis explains the pain, not the exhaustion since the move.

At this point a sentence regularly turns up that I do not like: they found nothing. It is not accurate. They searched very carefully for certain things and did not find them. That is something else.

A change of perspective

An unremarkable finding is not a blank page. It is an answered question.

The question was: is one of the known diseases with a tested treatment behind your symptoms. The answer was no. That is good news and valuable information. It just does not end the search, it moves it.

The second sentence that often falls: maybe it is psychological. That one is too quick for me as well. Not because the mind plays no part. Rather because it usually comes at the end of a list that has been worked through.

I want to be clear here about why routine care stops at this border. It is not disinterest. A guideline may only recommend what studies support with a tested consequence. Meaning: if we measure this and act on it, people are measurably better off. For environmental diagnostics in hormonal complaints exactly that kind of study is missing. The mechanisms are not missing. The intervention studies are.

That is not an omission. That is the method by which guidelines are built, and it has a good reason. It protects people from investigations whose benefit nobody has shown. Added to this are training priorities and time budgets: environmental toxicology is not at the centre of gynaecological training, and a detailed exposure history takes more time than a routine appointment usually allows.

What I do differently is therefore not better. It is a different frame. In my private practice I have more time for the history, I ask routinely about housing, occupation and exposures, and I work with probabilities rather than exclusions. Many colleagues would do the same if the frame allowed it. That comes at a price: I move more often in the territory of assumption. Which is why this text states at every point how certain something is.

And now you know why I keep asking when the work-up was clean.

Hormones are a signalling system, and signalling systems have four weak points

Think of a radio message. For a message to arrive, four things are needed. A transmitter that sends it. A transmission path along which it travels. A receiver that can pick it up at all. And someone who clears the old message from the buffer so the new one has room.

If one of these four fails, the message does not arrive properly. But the fault looks different each time. And, this is the point: if you only measure how loudly the transmitter is sending, you miss three faults out of four.

The organising grid of this article

Four points at which a hormone signal can fall apart

1
Production

Ovary, adrenal gland and thyroid make what hypothalamus and pituitary order. Here enzymes, building blocks and control signals mesh together.

2
Transport

Most sex hormones travel bound, above all to SHBG and albumin. How much stays free co-determines how much arrives at all.

3
Receptor

At the receiver it is decided what the signal sets off. A foreign substance may occupy the site, imitate the signal or block it.

4
Breakdown

The liver rebuilds hormones in two steps, the gut co-determines whether they leave the body or come back. Here the old message is cleared.

This grid is not mine. It follows directly from the Endocrine Society's definition of endocrine active substances: agents that may interfere with hormone biosynthesis, hormone metabolism or hormone action. DOI: 10.1210/er.2009-0002

Now the question becomes concrete. An estradiol value in the blood measures level one, meaning what is circulating right now. It says little about how much of it is freely available, whether the receptor is currently responding well and whether breakdown is keeping up.

The most important sentence in this article

A normal blood value checks one of four levels.

That is not a reproach to laboratory medicine. It is a description of what a level can measure and what it cannot. For the most common questions, that one level is entirely enough. For the question of why a system has slipped out of rhythm, it is sometimes not.

For the second level there is a lab value you have probably seen on a report before: SHBG. That is the transport protein for sex hormones. It is the bus they travel in, and it co-determines how many get off at the stop.

Review, mechanism, predominantly cell culture What steers transport

A research group in Barcelona has compiled what steers SHBG production in the liver. For a long time BMI counted as the most important factor and a high insulin level as the explanation for low SHBG in obesity, without a mechanism ever having been described.

The newer findings show a different picture: liver fat content is a strong determinant of circulating SHBG, and pro-inflammatory cytokines may downregulate SHBG production. The molecular pathways of this regulation are described, and the paper explicitly presents them as putative mechanisms.

For you this means: a low SHBG is rarely an isolated hormone problem. More often it is a pointer towards liver, blood sugar and inflammatory load. Level two therefore hangs on things an estradiol value does not depict at all.

Simo R, Saez-Lopez C, Barbosa-Desongles A et al. Novel insights in SHBG regulation and clinical implications. Trends Endocrinol Metab. 2015;26(7):376-83. DOI: 10.1016/j.tem.2015.05.001 · PMID: 26044465 [Mechanism Review]

On to the third level, the receptor. Something happens here that the image of key and lock explains well. A hormone made by the body is the matching key. A foreign substance can be a key that also fits the lock but turns it only halfway. Or one that gets stuck in the lock.

The Endocrine Society has compiled these pathways in two detailed statements, in 2009 and 2015. Named are estrogen-like and antiandrogenic effects, interference with thyroid pathways, with the fat metabolism switch PPAR-gamma, with retinoid pathways, with steroidogenic enzymes and with neurotransmitter systems. This is not a fringe position. It is the position of a large endocrinological professional society.

Guideline, scientific society statement What the professional society says and what it explicitly does not say

For the second statement, EDC-2, an Endocrine Society author group reviewed five years of literature across seven fields, among them female reproduction, the thyroid and glucose metabolism. Only work with adequate controls and case numbers was included, and for animal studies only exposure ranges relevant to humans.

The result: causal links between exposure and disease patterns are supported by animal models and are compatible with the available epidemiological data in humans. In the same breath the authors caution against inferring causality in humans, because the study designs are too heterogeneous to carry broad conclusions.

Exactly this double sentence is the stance of this article. It legitimises looking in this direction. And it explicitly does not permit asserting a cause in an individual case.

Gore AC, Chappell VA, Fenton SE et al. EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals. Endocr Rev. 2015;36(6):E1-E150. DOI: 10.1210/er.2015-1010 · PMID: 26544531 [Review, Guideline]

On to the fourth level, breakdown. Estrogens are rebuilt in the liver in two steps and then moved out via bile and gut. If that route is sluggish, more stays in circulation than the transmitter ordered. That is a chapter of its own, which I am not opening here. If you want it in more detail, it is under lowering estrogen naturally via the liver.

Why four such different things belong in one chapter

A plasticiser, a mould toxin, a heavy metal and a silent inflammation have nothing to do with each other at first glance. At second glance they do: they act at different points of the same system. The plasticiser at the receptor. The mould toxin at receptor and control centre. The heavy metal at the receptor and at the producing enzymes. The inflammation at the control centre and at the transport protein.

That also explains why symptoms in this field are rarely of a single type. When a control centre becomes quieter, that affects more than the cycle. It also helps steer thyroid, stress axis and appetite. Which is why in these cases someone so often sits there whose cycle, sleep, skin and digestion are all restless at once.

One final point on level one, so that no wrong impression arises. There are good reasons to take hormone measurement seriously, and there are rules about when which value is informative at all. Measuring progesterone on cycle day three makes about as much sense as reading the August rain gauge for January. Which test shows something when is under hormone testing: which test when.

And now you know why I keep asking after the lab report rather than stopping.

Search direction one: endocrine disruptors from the environment

The most common objection comes quickly and it is legitimate: the amounts are tiny. A little plasticiser from a packaging cannot rearrange a menstrual cycle.

The argument holds in classical toxicology. There the rule is: more poison, more effect. With hormones this works differently, for a simple reason. Hormones themselves operate in tiny amounts. Estradiol sits in the range of picograms per millilitre. A system designed for signals that small does not respond by the rules of a poisoning.

Review, cell culture plus animal model plus epidemiology Why the dose question runs differently here

A large author group systematically worked through two concepts: low-dose effects and non-monotonic dose response curves. Non-monotonic means that the curve changes direction within the range examined.

The result: such curves are common both for the body's own hormones and for endocrine active chemicals. From this follows the paper's central sentence: where they occur, the effect of low doses cannot be predicted from the effect of high doses.

For you this means: the sentence "the amount is too small" is no proof when it comes to endocrine disruptors. It is an assumption that does not automatically hold in this field. Conversely, it does not follow that every small amount is harmful. It only follows that you cannot calculate it, you have to measure it.

Vandenberg LN, Colborn T, Hayes TB et al. Hormones and endocrine-disrupting chemicals: low-dose effects and nonmonotonic dose responses. Endocr Rev. 2012;33(3):378-455. DOI: 10.1210/er.2011-1050 · PMID: 22419778 [Mechanism Review]

Now to the human data. And here it gets interesting, because the honest numbers are smaller than the topic sounds online.

Human study, prospective observation, 706 cycles Plasticisers, bisphenol A and cycle length

221 women who had stopped contraception and were trying to conceive collected first morning urine daily for up to six months and documented their bleeding days. 706 cycles were analysed, and eleven phthalate metabolites plus bisphenol A were measured.

What was observed: in the middle exposure tertile the luteal phase was 0.5 days shorter than in the lowest tertile for one phthalate metabolite, and 0.8 days shorter for bisphenol A. In the highest tertile the effect was smaller, 0.4 days in each case, and the confidence interval included zero. That is precisely the non-monotonic shape just described, and it also means: this study does not show a simple more-is-worse line. For follicular phase length, for time to pregnancy and for early pregnancy loss no association appeared. For one phthalate group there were even fewer early losses.

For you this means two things. The effect is measurable, so the system is responsive. And it is small, clearly under a day. The authors themselves write that the findings would need confirming in further human studies.

Jukic AM, Calafat AM, McConnaughey DR et al. Urinary Concentrations of Phthalate Metabolites and Bisphenol A and Associations with Follicular-Phase Length, Luteal-Phase Length, Fecundability, and Early Pregnancy Loss. Environ Health Perspect. 2016;124(3):321-8. DOI: 10.1289/ehp.1408164 · PMID: 26161573 [Cohort, n=221]

The next example is instructive because it shows how easily an arrow gets drawn in the wrong direction in this field.

Human study, cross-sectional, case-control Bisphenol A in women with PCOS

A group compared 71 women with PCOS and 100 controls, matched for age and body mass index. Bisphenol A was measured in blood.

What was observed: in the PCOS group the value was higher, 1.05 versus 0.72 nanograms per millilitre. The difference persisted when lean and overweight women were considered separately. Bisphenol A correlated weakly with testosterone, androstenedione and insulin resistance.

And now the part many guides leave out: the authors themselves point out that androgens influence the breakdown of bisphenol A. The higher value may therefore be a consequence of the hormone pattern rather than its cause. No direction can be read off this study.

Kandaraki E, Chatzigeorgiou A, Livadas S et al. Endocrine disruptors and polycystic ovary syndrome (PCOS): elevated serum levels of bisphenol A in women with PCOS. J Clin Endocrinol Metab. 2011;96(3):E480-4. DOI: 10.1210/jc.2010-1658 · PMID: 21193545 [Case-control, cross-sectional, n=171]

The methodologically cleanest work in this chapter comes from a large cohort of women and concerns an endpoint that leaves nobody cold: the timing of menopause.

Human study, prospective cohort, 5466 person-years PFAS and the timing of natural menopause

1120 women aged 45 to 56 who had not yet reached menopause were followed from 1999 to 2017. PFAS were determined in blood by mass spectrometry. The prospective design was chosen deliberately, because PFAS levels rise after menopause and cross-sectional studies can therefore produce a false direction.

What was observed: 578 women reached natural menopause during this time. Comparing the highest with the lowest tertile, hazard ratios ranged from 1.26 to 1.31. In the cluster with the highest overall burden versus the lowest it was 1.63, which corresponded to a menopause a median of two years earlier.

For you this means: here an environmental factor is linked to a clinically meaningful endpoint, in a design that accounts for the obvious pitfalls. It also shows how much effort is needed before such an association becomes credible at all.

Ding N, Harlow SD, Randolph JF et al. Associations of Perfluoroalkyl Substances with Incident Natural Menopause: The Study of Women's Health Across the Nation. J Clin Endocrinol Metab. 2020;105(9):e3169-82. DOI: 10.1210/clinem/dgaa303 · PMID: 32491182 [Cohort, n=1120]

And then there is the historical observation that set this field in motion in the first place. It comes from an animal experiment and from the year 1993.

Animal model, primates, very small groups Dioxin and endometriosis in rhesus monkeys

A colony of rhesus monkeys was chronically exposed to dioxin for four years. Ten years after the end of exposure, laparoscopy was used to look for endometriosis.

What was observed: in the lower dose group 3 of 7 animals had moderate to severe endometriosis, in the higher group 5 of 7. In the control group it was 33 percent, and among 304 unexposed animals at the same facility the frequency was 30 percent. Frequency and severity rose with the dose.

For you this means: this is an important historical observation and at the same time a very small study. Seven animals per group, a control group already at a third, and an animal model. It justifies a question. It does not justify a diagnosis.

One addendum belongs here, because it is rarely told. The same lead author showed in 2001 that the exposed animals also carried raised blood levels of dioxin-like PCBs, and that the severity of endometriosis correlated with the concentration of one of those PCBs. The effect therefore cannot be attributed to dioxin alone. Rier SE, Turner WE, Martin DC et al. Toxicol Sci. 2001;59(1):147-59. DOI: 10.1093/toxsci/59.1.147 · PMID: 11134554

Rier SE, Martin DC, Bowman RE et al. Endometriosis in rhesus monkeys (Macaca mulatta) following chronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. Fundam Appl Toxicol. 1993;21(4):433-41. DOI: 10.1006/faat.1993.1119 · PMID: 8253297 [In vivo, primate]

That leaves the question of how the agencies see it. And here lies the most honest news of this whole chapter: they see it differently.

Counterweight and context

When two agencies weigh the same data differently

The European Food Safety Authority reassessed bisphenol A in April 2023 and derived a tolerable daily intake of 0.2 nanograms per kilogram of body weight. That is a reduction by a factor of 20,000 compared with the temporary value from 2015. Immunological endpoints were decisive.

The German Federal Institute for Risk Assessment does not support this derivation. It cites methodological and scientific inconsistencies in the reassessment and arrives at its own guidance value of 0.2 micrograms per kilogram per day, meaning a value higher by a factor of 1000. A formal divergence procedure was conducted between the European institutions involved.

Quoting only one of these numbers creates a false picture of agreement. In this field, science does not speak with a single voice. Several institutions weigh the same data differently, and that is part of the picture.

What follows from this for everyday life? Very little drama and a few low-risk directions. Fewer hot foods in plastic, less receipt paper in the hand, ventilating after renovation, sparing use of fragrance. Physically these steps are low-risk, their benefit in an individual case cannot be proven, and they carry one side effect that is rarely discussed: they can lead into a spiral of avoidance. How I handle that is further down, in the paragraph against compulsive control. The concrete list is under xenoestrogens in everyday life, there with the sources and without panic.

And now you know why I ask about packaging, occupation and renovations.

Search direction two: mould toxins and the mycoestrogen zearalenone

I ask this question almost always, and it almost always comes as a surprise: was there ever water damage where you live? A damp corner? A move after which something changed?

The reason for the question is a word with a firm place in toxicology: mycoestrogen. There really are mould toxins whose main action is estrogen-like. This is not a fringe opinion. It is written in a regulatory risk assessment.

Regulatory document, risk assessment Why zearalenone is assessed as estrogenic

The responsible panel of the European food authority assessed zearalenone, a metabolite of Fusarium fungi that reaches food mainly via grain and grain products.

It was assessed explicitly on the basis of its estrogenic action as the critical endpoint. Meaning: the limit value was not derived from organ damage but from the hormonal effect itself.

For you this means: the sentence "there are mould toxins with estrogenic action" is toxicology assessed by an agency. What was assessed there was the substance and its intake via food. What was not assessed is household mould as the cause of a hormone problem. Those are two different things.

EFSA Panel on Contaminants in the Food Chain (CONTAM). Scientific Opinion on the risks for public health related to the presence of zearalenone in food. EFSA Journal. 2011;9(6):2197. DOI: 10.2903/j.efsa.2011.2197 [Guideline]

How such a substance intervenes in the control centre is shown particularly vividly by a rat study. It explains the mechanism. And it works with doses far above anything found in a flat.

Mechanism in the animal model

How zearalenone acts on the control centre in the rat experiment

  1. Immature female rats received zearalenone for five days at three dose levels. Estradiol served as positive control, corn oil as control.
  2. In the highest dose group and in the estradiol group the typical signs of precocious puberty appeared: earlier vaginal opening, heavier uterus, markedly higher blood levels of FSH, LH and estradiol.
  3. In the hypothalamus, GnRH and the signalling molecules Kiss1 and GPR54 were raised, at both mRNA and protein level. This describes the pathway: the mycoestrogen acts at the control centre, not only at the ovary.
  4. Most changes were still present at the middle dose, none at the lowest. From this the authors derived, for this experiment, a NOAEL of 0.2 and a LOAEL of 1 milligram per kilogram of body weight per day.

This is an animal model with high doses via gavage. It shows that the pathway exists. It does not show that it operates at the amounts a person meets in everyday life. Yang R, Wang YM, Zhang L et al. Mol Cell Endocrinol. 2016;437:62-74. DOI: 10.1016/j.mce.2016.08.012 · PMID: 27519634 [In vivo, rat]

In humans there is exactly one usable observation, and I am showing it to you with all its limitations, because online it is readily made larger than it is.

Human study, very small, case-control Zearalenone in the blood of girls with precocious puberty

At the University of Pisa, mycoestrogens were measured in the blood of 32 girls with central precocious puberty and 31 healthy controls.

What was observed: in 6 of the 32 girls, all from a limited area of Tuscany, zearalenone and alpha-zearalenol were detectable. At diagnosis, zearalenone correlated with height and weight, not with bone age. Under twelve months of treatment, the mycotoxin-positive girls grew faster. The authors phrase it cautiously, saying zearalenone is suspected as a triggering factor.

For you this means: six affected girls from a geographically limited region. That is a hint, not a proof. That is exactly how it should be cited.

Massart F, Meucci V, Saggese G, Soldani G. High growth rate of girls with precocious puberty exposed to estrogenic mycotoxins. J Pediatr. 2008;152(5):690-5. DOI: 10.1016/j.jpeds.2007.10.020 · PMID: 18410776 [Case-control, n=63]

And now comes the paragraph I consider the most honest of the whole article.

Where the evidence stops

104 studies, and not one of them in humans

A systematic review to PRISMA standard, registered in advance, searched the literature from 2000 to 2020 in three databases for work on Fusarium mycoestrogens and female reproduction.

104 studies from cell culture and animal models were included. They consistently support adverse effects: altered follicle profile in the ovary, disturbed cycle, thicker myometrium, in pregnancy placental haemorrhage and impaired fetal growth. And then the sentence that counts: not a single epidemiological study was found that met the inclusion criteria.

These endpoints come exclusively from cell and animal experiments. No statement about the course of a human pregnancy follows from them, and still less any offer to investigate such a thing.

Mechanistically well supported, human studies missing so far. That is the state of things. Anyone claiming more on the topic of mould and hormones is going beyond the data. Kinkade CW, Rivera-Nunez Z, Gorcyzca L et al. Toxins (Basel). 2021;13(6):373. DOI: 10.3390/toxins13060373 · PMID: 34073731 [Systematic Review]

Added to this is a distinction that almost always blurs online. Zearalenone is a food mycotoxin. It comes via grain, not via the wall of a room. Household mould is a different topic with different substances and a different evidence base.

Guideline, agency document What the WHO says about indoor dampness and mould

The WHO guideline on indoor air quality, 248 pages, compiled the evidence on dampness and mould growth.

Named as the most important effects: more respiratory symptoms, more allergies, more asthma and an influence on the immune system. The central recommendation is to prevent or minimise persistent dampness and microbial growth on interior surfaces and in building structures.

For you this means: the guideline names airways and immune system. It does not name the hormone system. Anyone connecting household mould with a hormonal disorder is arguing across intermediate steps and not from a guideline statement. I do that too, and I say that I am doing it.

World Health Organization Regional Office for Europe. WHO guidelines for indoor air quality: dampness and mould. Copenhagen: WHO; 2009. 248 pages. [Guideline]

How large is the demonstrated effect of housing dampness in the first place? A meta-analysis gives a usable order of magnitude for calibrating expectations.

Meta-analysis of observational studies Housing dampness and the airways

A working group pooled the published studies on dampness or mould in homes and respiratory infections or bronchitis, using fixed and random effects models.

What was observed: the pooled odds ratios lay between 1.38 and 1.50, with confidence intervals excluding one in each case. In the adjusted analyses bronchitis was at 1.45 and respiratory infections at 1.44. The estimated attributable risk proportions were 8 to 20 percent.

For you this means: household mould is demonstrably relevant in humans, but at a moderate magnitude, and for the airways. That is a good gauge of how strongly this card may be played.

Fisk WJ, Eliseeva EA, Mendell MJ. Association of residential dampness and mold with respiratory tract infections and bronchitis: a meta-analysis. Environ Health. 2010;9:72. DOI: 10.1186/1476-069X-9-72 · PMID: 21078183 [Meta-analysis, observational studies]
How I put this together

What I am saying here is an inference, not a guideline statement.

Established is: there are estrogenically active mould toxins, and damp homes can keep the immune system busy. Mechanistically plausible is: a persistently busy immune defence may affect the control centre of the cycle. Not established is the direct step from wall mould to hormonal disorder. That is why I ask about water damage, and why after a positive finding I do not say the cause has been found.

If you want to go deeper on mould: what mycotoxins are in the first place is under mycotoxins: the basics. Zearalenone in detail is under zearalenone as a mycoestrogen, and which symptoms fit a mould exposure at all is under mould symptoms at a glance. What to do about visible growth in the home is under mould in the home.

And now you know why I ask about the flat without turning it into a diagnosis.

Search direction three: heavy metals, above all cadmium and lead

Heavy metals are the topic most exaggerated online and least asked about in the consultation. I find both a shame, because in between there is a solid core.

The core is called metalloestrogen. Meant are metals that can dock at the estrogen receptor and set off a signal there. For cadmium this has been shown in the living animal, and the experimental design is elegant enough that I am happy to explain it to you.

Animal model, rat, plus exposure in the womb Cadmium imitates an estrogen effect in animals

Cadmium was given to rats whose ovaries had been removed. These animals no longer produce estrogen of their own. Whatever appears therefore cannot come from the body's own hormone.

What was observed: the weight of the uterus rose, the lining grew, progesterone receptor and complement factor C3 were upregulated. In the mammary gland, side branching and alveolar buds increased. Female offspring exposed in the womb entered puberty earlier and showed a larger glandular area.

For you this means: the term metalloestrogen is earned. It is supported in the animal model, cleanly shown and understandable in its mechanism. That does not transfer it to your cycle.

Johnson MD, Kenney N, Stoica A et al. Cadmium mimics the in vivo effects of estrogen in the uterus and mammary gland. Nat Med. 2003;9(8):1081-4. DOI: 10.1038/nm902 · PMID: 12858169 [In vivo, rat]

In humans it looks different, thinner and blurrier. The best bridge that exists comes from a large population-representative survey in the USA.

Human study, cross-sectional, population-representative Heavy metals in urine and sex hormones in blood

Data from 2728 adults in the US survey NHANES 2013 to 2016 were analysed. Fourteen heavy metals in urine were modelled against total testosterone, estradiol and SHBG in blood, individually and in a model for combined exposure.

What was observed: in women the exposure index of industrial pollutants was associated with a 20.6 percent lower estradiol. Cadmium, tin and lead dominated this association. In women after menopause it persisted, with cadmium and an arsenic compound standing out there. In men a different index showed a 5.35 percent lower SHBG.

For you this means: in the animal model the matter is clear, in humans there are so far only associations without direction. A cross-section measures everything at the same time. It cannot say what came first. The authors themselves write that further surveys are needed.

Tao C, Li Z, Fan Y et al. Independent and combined associations of urinary heavy metals exposure and serum sex hormones among adults in NHANES 2013-2016. Environ Pollut. 2021;281:117097. DOI: 10.1016/j.envpol.2021.117097 · PMID: 33878511 [Cross-sectional, population-representative, n=2728]

And now the finding I consider indispensable, because it points the other way. Lead is generally regarded as the classic among fertility poisons. In one occupational medicine study, nothing of the sort was visible in the low exposure range.

Human study, retrospective observation, null finding Lead and time to pregnancy

At the Finnish Institute of Occupational Health in Helsinki, researchers examined how long it took women who were occupationally monitored for lead exposure to become pregnant. Grouping was by questionnaire and individual blood lead values.

What was observed: the adjusted ratios were 0.93, 0.84 and 0.80 across the three exposure levels, with all confidence intervals including one. The authors' conclusion: at the low exposures common at that time, lead was not associated with fertility. Only among the eight most heavily exposed women was the estimate 0.53, which the authors describe as a hint to be examined in a larger study.

For you this means: at the low exposures examined, no association appeared. Dose counts. "Lead disturbs fertility" is not supported in that blanket form.

Sallmen M, Anttila A, Lindbohm ML et al. Time to pregnancy among women occupationally exposed to lead. J Occup Environ Med. 1995;37(8):931-4. DOI: 10.1097/00043764-199508000-00007 · PMID: 8520955 [Cohort, retrospective]
A change of perspective

A null finding is not a boring finding. It is a yardstick.

Without the lead study this chapter would be one-sided. It shows where the line runs: relevant effects need relevant exposures. And it is the reason why, with heavy metals, I first ask about a plausible source and not first about a test.

Plausible sources are, for instance, smoking as the main source of cadmium, certain occupations, renovation of old buildings, drinking water pipes in very old houses. What blood and urine measurements each show and do not show is set out in detail under measuring heavy metals in blood or urine. Why I advise against hair mineral analysis for individual questions is under hair mineral analysis: useful or not.

And now you know why with metals I ask first about the source and then about the laboratory.

Search direction four: silent inflammation

This fourth direction is the least spectacular and in practice the most common. It has no name you can google, no flat you could renovate, and no substance you can avoid.

What is meant is a permanently slightly activated immune state. It arises not from an infection but from belly fat, from lack of sleep, from gut issues, from dental foci, from chronic stress, sometimes also from one of the other three search directions. And it has two points of attack on your hormone system, both well described.

The first point of attack is at the top, in the control centre. There is an animal model for this that takes the mechanism cleanly apart.

Animal model, sheep, acute endotoxin administration How an immune burden turns the cycle centre down

At the University of Michigan in Ann Arbor, a series of experiments in sheep examined the routes by which endotoxin disturbs the cycle. Endotoxin is a common model for an immune and inflammatory burden.

What was observed: in sheep without ovaries, endotoxin inhibited pulsatile LH release in two ways at once. First, less GnRH was released in pulses. Second, the pituitary responded less well to GnRH. Further experiments additionally showed that ovarian follicles responded less well to gonadotropins and that the estradiol-induced LH surge before ovulation was inhibited.

For you this means: the picture of inflammation turning the centre down is mechanistically grounded in the animal model. It is an acute experiment with endotoxin, not a model of chronic silent inflammation. That transfer is a transfer, and I name it as such.

Karsch FJ, Battaglia DF. Mechanisms for endotoxin-induced disruption of ovarian cyclicity: observations in sheep. Reprod Suppl. 2002;59:101-13. PMID: 12698976 [In vivo, sheep]

In humans there is a prospective cohort on this with a clear number and a built-in modesty.

Human study, prospective cohort, 1409 cycles Inflammatory marker and cycle length

In a cohort of women aged 30 to 44 who had been trying to conceive for less than three months, CRP was measured on cycle days two to four. The cycle was documented daily for up to four months. 1409 cycles from 414 women were analysed.

What was observed: there was no linear relationship between CRP and cycle length. But compared with a CRP below 1 milligram per litre, a CRP above 10 was associated with more than three times the odds of a long cycle of 35 days or more, adjusted odds ratio 3.7. The follicular phase was then on average 1.7 days longer.

For you this means two things. First the threshold: the effect appeared only above 10 milligrams per litre, so not in the range of slightly raised high-sensitivity CRP values. Second the direction: the authors write explicitly that it remains open whether inflammation changes the cycle or whether long cycles are a marker for more inflammation.

Harris BS, Steiner AZ, Faurot KR, Long A, Jukic AM. Systemic inflammation and menstrual cycle length in a prospective cohort study. Am J Obstet Gynecol. 2023;228(2):215.e1-215.e17. DOI: 10.1016/j.ajog.2022.10.008 · PMID: 36244407 [Cohort, n=414]
The counterweight without which the number misleads

CRP itself fluctuates with the cycle

In a prospective study, 259 women aged 18 to 44 were followed over up to two cycles, with up to eight measurements of CRP, estradiol, progesterone, LH and FSH per cycle, timed via a fertility monitor.

What was observed: CRP fluctuated markedly across the cycle. During the period, more women were classified as cardiovascularly raised, 12.3 versus 7.4 percent in other phases. A tenfold rise in estradiol went along with a 24.3 percent lower CRP, a tenfold rise in progesterone in the second half of the cycle with a 19.4 percent higher CRP.

So the arrow also points the other way: hormones influence the inflammatory marker. A single CRP value without the cycle phase noted is therefore hard to interpret. Gaskins AJ, Wilchesky M, Mumford SL et al. Am J Epidemiol. 2012;175(5):423-31. DOI: 10.1093/aje/kwr343 · PMID: 22306563 [Cohort, n=259]

The second point of attack of inflammation is the one I use most often in everyday practice, because it appears on every larger lab report: SHBG. You remember level two, transport. Pro-inflammatory messengers may downregulate SHBG production in the liver, and liver fat content appears to matter more than BMI alone.

Why I look at inflammation first

Of the four search directions, this one is the most common, the most measurable and the one where something is most likely to move. Sleep, belly fat, blood sugar and gut are not spectacular topics. They are the ones where work is most likely to pay off. Environmental factors come after that, not before.

How blood sugar and insulin fit into this picture is under insulin resistance and hormones in women. Why chronic stress is almost always part of it is under cortisol, stress and female hormones.

And now you know why I ask about sleep, gut and dental status before I talk about plasticisers.

When this search is worthwhile and when it explicitly is not

This is the section that decides whether this article is worth anything. Everything so far was mechanism and evidence. Now comes the question you actually have: does this concern me?

I will start with the sentence that stands above everything. From the fact that environmental factors can act hormonally it does not follow that every hormonal disorder has an environmental cause. The most common reasons for hormonal complaints are and remain sleep, stress, blood sugar, weight, thyroid and nutrients.

That is not a modesty formula. It is written, in other words, in an Endocrine Society guideline on functional hypothalamic amenorrhoea: chronic anovulation without a tangible organic cause, often linked to stress, weight loss, a very high exercise load or a combination of these. Explicitly a diagnosis of exclusion, and the work-up is meant to cover systemic and endocrinological causes.

The honest side-by-side

When an environmental search becomes sensible and when it does not

Speaks for it
  • The symptoms fit no simple picture, and the work-up has nonetheless been completed.
  • Several systems are affected at once: cycle, skin, sleep, digestion, mood, concentration.
  • There is a clear time link to a move, a water damage or a renovation.
  • The occupation brings exposure with it, for example workshop, laboratory, hairdressing, construction, cleaning, agriculture.
  • The course does not match the known explanations, for instance because it began too abruptly.
  • The symptoms improve noticeably on holiday or during a longer absence from home.
Speaks against it
  • Sleep, stress, blood sugar, weight, thyroid and nutrients are not yet sorted.
  • The symptoms fit well with an already established diagnosis, and its treatment has not been exhausted.
  • There is no plausible exposure, neither at home nor at work nor in the history.
  • The search would delay an indicated work-up, a necessary operation or fertility treatment.
  • The burden of searching itself would be greater than the possible gain.
  • The wish behind it is more to finally have a cause than to answer a question.

No single criterion decides. It is about the cluster. If there are four points on the left and none on the right, the question becomes sensible. And the other way round just the same.

On the fourth point on the right I will be blunt, because it is the most important. Time is a real factor in some situations. When trying to conceive. With endometriosis involving organs. With unexplained bleeding. Anyone who puts an environmental search first in such situations gains no insight but loses months. Cause-finding runs alongside medical care, never in its place and never before it.

What I explicitly am not saying

Nowhere in this article does it say that you should change an ongoing treatment. That applies to the pill, to hormone replacement therapy, to metformin, to antiandrogens, to GnRH analogues and to thyroid hormones. All of these are prescription-only medicines. Metformin and antiandrogens are frequently used off label in PCOS, meaning outside their approved indication, which requires medical counselling and also affects the question of who pays. All the more reason: whether a prescription still fits is a good question, and it belongs in a conversation with the doctor who issued it. Every adjustment belongs under medical supervision.

Equally: PCOS and endometriosis are medical diagnoses. They are made by a doctor and treated by a doctor. An environmental question alongside is an addition. It is no reason to postpone a recommended work-up or an indicated operation.

Why that matters so much is shown by a look at the guidelines themselves. The international PCOS guideline of 2023 comprises 254 recommendations and practice points, GRADE-based, carried by 39 organisations from 71 countries. Environmental factors, mould or heavy metals do not appear there in the recommended basic work-up. The ESHRE guideline on endometriosis of 2022 with 109 recommendations states explicitly that for most treatment options no firm recommendations could be formulated on the basis of the available evidence. In Germany the S2k guideline on endometriosis is added to this, AWMF registry number 015-045, current version from 2025.

How I read this restraint

The guidelines are silent on environmental diagnostics not out of ignorance. They are silent because the decisive study is missing.

What is missing is not the mechanism. That is set out in the Endocrine Society statements. What is missing is the intervention study: the work showing that women are measurably better off when this diagnostic work is done and acted upon. As long as it is missing, no guideline can recommend it. That is sound work, and I think it is right. It only does not mean the question is wrong. It means it has not been answered yet.

In my practice this means: I ask the question when the cluster speaks for it. I do not ask it first. And I treat it as a question and not as an explanation, as long as I have only an association and no cause. That is clinical observation and approach, not a study result.

And now you know when this search contributes something and when it gets in the way.

What tests can do and what they explicitly cannot

When people discover this topic, the first impulse is almost always the same: then just let me test for it. I understand the impulse well. And I have to dampen it, because in this field it rarely leads to an answer.

The principle first, and it holds without exception: no available test proves a cause. At best it shows an exposure. From exposure to an explanation of your symptoms is a long way, and no lab value covers that way on its own.

Method check, laboratory comparison, not a guideline document Hair mineral analysis put to the test

A hair sample from a healthy volunteer was split and sent to six commercial laboratories that together handled around 90 percent of mineral analyses in the USA. The same sample, six reports.

What was observed: for twelve minerals the difference between the highest and lowest reported value exceeded a factor of 10. For 14 of 31 minerals analysed by at least three laboratories there were statistically conspicuous extreme values. The reference ranges also differed so much that almost every mineral was classified as high, normal or low depending on the laboratory. The authors' recommendation: not to use such analyses to assess individual nutrient status or suspected environmental exposures.

For you this means: as a tool for your individual question this test is not usable. That is not a suspicion, that has been measured.

Seidel S, Kreutzer R, Smith D, McNeel S, Gilliss D. Assessment of commercial laboratories performing hair mineral analysis. JAMA. 2001;285(1):67-72. DOI: 10.1001/jama.285.1.67 · PMID: 11150111 [Method check, laboratory comparison]

With the mycotoxin urine test the problem lies elsewhere. It does measure something. It is just that a positive finding is so common that on its own it says little.

Human study, biomonitoring, cross-sectional How often mycotoxins are detectable in urine

447 first morning urine samples from 439 pregnant women in rural Bangladesh were examined by mass spectrometry for 35 mycotoxins.

What was observed: in only 17 of 447 samples, meaning 4 percent, none of the examined mycotoxins was detectable. Ochratoxin A was found in 95 percent, citrinin in 61 percent of samples. In 63 percent several mycotoxins occurred at once.

For you this means: if almost every sample in a studied population is positive, then a positive finding alone explains no symptoms. The numbers come from Bangladesh and are not one to one transferable to Germany. The logic behind them is.

Kyei NNA, Cramer B, Humpf HU et al. Assessment of multiple mycotoxin exposure and its association with food consumption: a human biomonitoring study in a pregnant cohort in rural Bangladesh. Arch Toxicol. 2022;96(7):2123-2138. DOI: 10.1007/s00204-022-03288-0 · PMID: 35441239 [Cross-sectional, biomonitoring, n=439]

What counts more in my consultation than a test result

  • The timeline. When did it start, and what was different in the three months before.
  • The exposure history. Homes, occupations, renovations, hobbies, water damage, including those from childhood.
  • The pattern across systems. Does it affect only the cycle or at the same time skin, sleep, gut and head.
  • The absence test. Does anything change when you are somewhere else for two weeks.
  • The risk question. Is a possible measure low-risk, affordable and sustainable in everyday life.

With inflammatory markers there is an additional peculiarity that is often overlooked in everyday practice: a CRP value without the cycle phase noted is hard to place, because it fluctuates with the cycle itself. Anyone measuring should note which cycle day it was.

And on hormone measurement itself: it is sensible when timing and question match. Which value shows what and when is set out in detail under hormone testing: which test when.

The paragraph against compulsive control

Now comes something that matters more to me than all the numbers before it. Environmental topics have a property that can make them risky: they are never finished.

There is always another packaging you could replace. Another piece of furniture that might off-gas. Another test you could do. Anyone who starts checking everything will always find something. And the more you find, the more the fear grows instead of the clarity.

I see this regularly, and I describe it as an observation, not as a study result. Someone who starts with a good question sometimes eats only five foods half a year later and sleeps worse than before. Then the search has cost more than it brought.

My guard rails

How I keep a question from becoming a trap

First: measures have to be low-risk, affordable and sustainably manageable. Everything else drops out, however good it sounds. Second: there is an upper limit for simultaneous changes. Three things, not thirty. Third: there is a point at which we look together at whether anything has moved, and if not, we stop.

And fourth, the most important point: when avoidance starts to dictate everyday life, food or relationships, that is not a sign of consistency. It is a signal that deserves to be taken seriously. If you notice that above all your eating is becoming narrow, you will find under understanding eating disorders: body and mind a text that is about exactly that.

Energy and a calm cycle are not a luxury. They are a large part of how free a life feels. Which is exactly why the search for them must not itself become a prison.

And now you know why I am sparing with testing and generous with listening.

Frequently asked questions

Why do my symptoms persist even though all my hormone levels are normal?

A blood value mainly measures how much of a hormone is currently in circulation. A signalling system, however, has four points: production, transport in the blood, reception at the receptor, and breakdown. A normal level does not rule out a problem at the other three points. That explains no symptoms, it only opens further questions: how do the hormones relate to one another, how high is the transport protein SHBG, what about sleep, blood sugar, thyroid and inflammatory load. Only once these questions are sorted is it worth looking outward.

What are endocrine disruptors in the first place?

The Endocrine Society defines them as substances from the environment, food and consumer products that may interfere with the production, metabolism or action of the body's own hormones. Named effects include estrogen-like and antiandrogenic actions, interference with thyroid pathways, with steroidogenic enzymes and with neurotransmitter systems. This is set out in two detailed scientific society statements, published in 2009 and 2015. DOI: 10.1210/er.2009-0002 and DOI: 10.1210/er.2015-1010. The authors' own caveat matters: the mechanisms are well described, while drawing a conclusion about an individual illness remains something to handle with care.

At which four points can a hormone signal be disturbed?

First at production, meaning in the ovary, adrenal gland and thyroid, directed by hypothalamus and pituitary. Second at transport, because most sex hormones travel bound to SHBG and albumin. Third at the receptor, where a foreign substance may occupy the site or amplify the signal. Fourth at breakdown, mostly in the liver and via the gut. This grid is the reason a plasticiser, a mould toxin, a heavy metal and a silent inflammation can appear in the same chapter. They act at different points of the same system.

Can mould in my flat affect my menstrual cycle?

For that step there are so far no robust human data. The WHO guideline on indoor dampness and mould names respiratory symptoms, allergies, asthma and effects on the immune system, not the hormone system. A meta-analysis on housing dampness found an odds ratio of 1.45 for bronchitis and 1.44 for respiratory infections. DOI: 10.1186/1476-069X-9-72. What can be argued is an indirect route: a lasting immune burden may affect the control centre of the menstrual cycle. That is an inference across intermediate steps and not a guideline statement.

What is zearalenone and why is it called a mycoestrogen?

Zearalenone is a metabolite of Fusarium fungi and reaches food mainly via grain. EFSA assessed it in 2011 explicitly on the basis of its estrogenic action as the critical endpoint. DOI: 10.2903/j.efsa.2011.2197. In the rat model it triggered precocious puberty via the kisspeptin pathway, with a NOAEL of 0.2 and a LOAEL of 1 milligram per kilogram per day. DOI: 10.1016/j.mce.2016.08.012. In humans the picture is different: a systematic review of 104 cell and animal studies found not a single epidemiological study that met the inclusion criteria. DOI: 10.3390/toxins13060373.

Are heavy metals really hormonally active, or is that overstated?

For cadmium the label metalloestrogen is supported, though in the animal model. In rats without ovaries, cadmium produced estrogen-typical changes in uterus and mammary gland, that is, where no endogenous estrogen was in play any more. DOI: 10.1038/nm902. In humans there are so far cross-sectional data: in the US survey NHANES an exposure index in women was associated with a 20.6 percent lower estradiol, with cadmium, tin and lead dominating this association. DOI: 10.1016/j.envpol.2021.117097. Cross-sectional means: measured at the same time, direction open.

What does a silent inflammation have to do with my menstrual cycle?

Two points of attack are described. In the sheep model, endotoxin dampened pulsatile LH release in two ways at once, through less GnRH and through a less responsive pituitary. PMID: 12698976. In humans, a prospective cohort found a CRP above 10 milligrams per litre associated with more than three times the odds of a cycle of 35 days or longer, adjusted odds ratio 3.7. DOI: 10.1016/j.ajog.2022.10.008. The authors themselves write that it remains open whether inflammation changes the cycle or whether long cycles are a marker for more inflammation.

What does a low SHBG on my lab report mean?

SHBG is the transport protein of the sex hormones. It co-determines how much free hormone reaches the receptor at all. A review describes liver fat content as a strong determinant of circulating SHBG, and that pro-inflammatory cytokines may downregulate SHBG production in the liver. DOI: 10.1016/j.tem.2015.05.001. A low SHBG is therefore not an isolated number but a prompt to look at the liver, blood sugar and inflammatory load. What follows from it belongs in a medical conversation and not in self-interpretation.

How do I recognise that an environmental search is worthwhile in my case?

No single criterion decides on its own, but there is a cluster that makes me pay attention: the symptoms fit no simple picture. Several systems are affected at once, meaning cycle, skin, sleep, digestion and mood. There is a time link to a move, a water damage or a renovation. The occupation brings exposure with it. The course does not match the known explanations. And the symptoms improve noticeably on holiday or during a longer absence from home. The more of these come together, the more sensible the question becomes.

When should I explicitly leave this search alone?

When sleep, stress, blood sugar, weight, thyroid and nutrients are not yet sorted. When the symptoms fit well with an already established diagnosis and the treatment intended for it has not been exhausted. When no plausible exposure is apparent. When the search would delay an indicated work-up, an operation or fertility treatment, because time is a real factor there. And when the burden of searching itself would be greater than the possible gain. From the fact that environmental factors can act hormonally it does not follow that every hormonal disorder has an environmental cause.

Which tests exist and what can they really show?

No available test proves a cause. In the case of hair mineral analysis, a split hair sample was sent to six laboratories: for twelve minerals the difference between the highest and lowest value exceeded a factor of 10, and almost every mineral was classified as high, normal or low depending on the laboratory. DOI: 10.1001/jama.285.1.67. Mycotoxins in urine are very frequently detectable in biomonitoring populations, in a cohort in Bangladesh only 4 percent of samples were completely negative. DOI: 10.1007/s00204-022-03288-0. A positive finding alone therefore explains no symptoms.

Why did my gynaecologist not look for this?

Because guidelines can only recommend what studies with tested consequences support. For environmental diagnostics in hormonal complaints exactly that is missing: there is no intervention study showing that such diagnostics change the course. The international PCOS guideline of 2023 with 254 recommendations therefore does not list environmental factors in the basic work-up. DOI: 10.1093/humrep/dead156. That is not an omission but the method by which guidelines are built. Added to this are training priorities and tight time budgets in routine care. The gynaecological work-up remains the foundation, the environmental perspective comes on top.

Do the regulatory agencies agree about bisphenol A?

No, and that is the most honest news on this topic. In April 2023 EFSA derived a new tolerable daily intake of 0.2 nanograms per kilogram of body weight, a reduction by a factor of 20,000 compared with the temporary value from 2015, driven by immunological endpoints. DOI: 10.2903/j.efsa.2023.6857. The German Federal Institute for Risk Assessment does not support this derivation, cites methodological and scientific inconsistencies and arrives at a guidance value higher by a factor of 1000. A formal divergence procedure was conducted between the institutions involved.

What do I do if this topic pulls me into compulsive control?

Then that is a signal that deserves to be taken seriously. Environmental topics have a property that can make them risky: they are never finished. There is always another packaging, another piece of furniture, another test. When avoidance starts to dictate everyday life, food or relationships, the price is higher than the possible benefit. What makes sense then is to limit measures to a few low-risk and sustainably manageable points and to bring attention back to sleep, movement and nutrition. Anyone noticing that eating itself is becoming narrow will find under understanding eating disorders: body and mind a text on this.

Where this article connects to the rest of the cluster

This text is the map. The individual countries on it have their own articles, because they have their own evidence and their own practical questions. Depending on where you currently stand, one of these routes leads onward.

You want the overview first
Hormonal imbalance in women

The larger context, from which this article goes deeper into a single chapter.

You wonder what to change day to day
Xenoestrogens in everyday life

The practical side of endocrine disruptors, with concrete sources and without drama.

You are interested in the best documented mycoestrogen
Zearalenone and hormones

Zearalenone in detail, with the evidence and the limits of transferring it.

You do not know what mycotoxins are
Mycotoxins: the basics

The foundation, without which the rest of this topic is hard to place.

There was water damage where you live
Mould symptoms at a glance

Which symptoms fit a mould exposure at all and which do not.

You can see mould on the wall
Mould in the home

What to do in order when growth is visible, before you think about laboratories.

You are considering testing for metals
Heavy metals in blood or urine

What blood and urine each show, what they do not show and when it is worthwhile.

You have been offered a hair mineral analysis
Hair mineral analysis: useful?

Why this test is not suitable for individual questions as things currently stand.

You want to know which test fits when
Hormone testing: which test when

Timing and meaning of the standard values, sorted understandably.

Chronic stress is front and centre for you
Cortisol, stress and female hormones

The most common non-environmental reason for a cycle that has slipped.

You want to understand breakdown
Estrogen breakdown via the liver

The fourth level of the grid, in detail and with the limits of the evidence.

Your blood sugar is a topic
Insulin resistance and hormones

Why SHBG, blood sugar and cycle sit closer together than it looks.

If you want the detail on the substance
Bisphenol A and your hormones

The substance from tins and till receipts, the 2023 EFSA reassessment and what BPA free does and does not mean.

If plasticisers are the question
Phthalates: the plasticisers

Why phthalates affect testosterone rather than oestrogen, and where they come from in everyday life.

If you want to place drinking water and cookware
PFAS: the forever chemicals

Why the forever chemicals stay in the body for years and where individual avoidance reaches its limit.

If you are looking at the bathroom shelf
Endocrine disruptors in cosmetics

Parabens, UV filters and fragrances, sorted by what is documented and what is merely loud.

If the endometriosis trail interests you
Dioxins, PCBs and endometriosis

The 1993 monkey study, the Seveso cohort and what does and does not follow from them today.

If metals are part of the question
Heavy metals and female hormones

Cadmium as a metalloestrogen, lead and the bone store, and what blood, urine and hair analysis each show.

SJ

Shukri Jarmoukli

Physician · Area of focus: integrative medicine · ViveCura Berlin

I work in my private practice at the interface of conventional medicine, functional medicine and Clinical Psychoneuroimmunology. With hormonal complaints I am less interested in which value sits inside the reference range than in which question was left open after the work-up.

On environmental topics I am deliberately more reserved than you might expect from an integrative practice. The mechanisms are strong, the human data often are not, and no test proves a cause in an individual case. This article replaces neither medical advice nor a gynaecological work-up. It is meant to help you ask better questions at your next appointment.

ViveCura, Privatpraxis Shukri Jarmoukli, Skalitzer Straße 137, 10999 Berlin

Scientific sources

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Transparency on the evidence: what is established, what is plausible and what stays open
  1. Established by scientific society statements and agency assessments. That endocrine active substances can intervene via receptors, steroidogenic enzymes and further pathways has been compiled twice in detail by the Endocrine Society. That zearalenone is estrogenically active has been assessed by EFSA as the critical endpoint. This is the most robust part of this article.
  2. Established in humans, but with small effects. The associations between bisphenol A, or a phthalate metabolite, and the luteal phase were under one day. Anyone turning that into an explanation for severe symptoms is overstretching the data.
  3. Methodologically best secured is the PFAS cohort. It is prospective and takes into account that PFAS levels rise after menopause. It too shows an association and no proven cause in an individual case.
  4. On the topic of mould the human evidence ends early. The systematic review on Fusarium mycoestrogens found 104 cell and animal studies and not a single epidemiological study that met the inclusion criteria. Mechanistically well supported, human studies missing so far.
  5. Household mould and hormonal disorder is an inference. The WHO guideline names airways and immune system, not the hormone system. The step from immune burden to the cycle control centre is mechanistically plausible and has not been shown directly in humans for this route.
  6. For cadmium the picture is uneven. Clear in the animal model, in humans so far only associations without direction, because the available human data are cross-sectional.
  7. For lead no association appeared in the low exposure range with time to pregnancy. This null finding stands here deliberately, because the chapter would otherwise be one-sided.
  8. On the inflammation topic the direction is open. The association between a CRP above 10 milligrams per litre and long cycles has been shown in humans. At the same time CRP itself fluctuates with the cycle and falls as estradiol rises. An association whose direction is open.
  9. The sheep model is a transfer. It works with acute endotoxin administration, not with chronic silent inflammation. Transferring it to human everyday life is an assumption, not a measurement.
  10. The dioxin observation in rhesus monkeys is historically important and very small. Seven animals per group, a control group already at 33 percent, an animal model. On top of that, the same group showed in 2001 that the exposed animals also had raised PCB levels, so the effect cannot be attributed to dioxin alone. It justifies a question.
  11. The tests are the weakest part of the field. Hair mineral analysis is not usable as a tool for individual questions. A positive mycotoxin urine finding alone explains no symptoms, because it occurs very frequently in biomonitoring populations. The numbers from Bangladesh are not one to one transferable to Germany.
  12. The guidelines do not list environmental diagnostics as routine. That is because the decisive intervention study is missing, and not because the mechanisms are disputed. This restraint is explained here and not disputed.
  13. What I describe from my consultation is marked as observation and is not a study result. That applies to the order of my approach and to my experience with avoidance spirals.
  14. What deliberately does not appear here. No dosing recommendation, no elimination protocol, no product or laboratory recommendation, no prices and no advice to change, reduce or stop an existing medication. This applies explicitly to the pill, hormone replacement therapy, metformin, antiandrogens, GnRH analogues and thyroid hormones. Every adjustment belongs under medical supervision. From no section does it follow that a recommended work-up, an indicated operation or fertility treatment should be omitted or postponed.

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