Leisha Women, Autoimmunity, Iodine, the Gut and the Strange New Science of the Ovary!
I am not a doctor, nor do I want to approach health education from a place where someone else is expected to have all the answers. I am much more interested in what happens when we put our heads together, use science as an ally, and treat our own lived experience as a primary source of information about what is happening in the body. There is value in blood work, research and physiology, but there is also value in paying attention to patterns, timing, symptoms, emotions, food, environment and the things a woman already knows about herself. Perhaps the real understanding comes when we stop separating those things and start looking at the whole picture.
Women are disproportionately affected by autoimmune thyroid disease. I am one of those women entering my 60’s and looking, observing what is going on.
Research continues to point toward a complicated combination of sex hormones, immune regulation, genetics, epigenetics, environmental exposures and the microbiome. A 2025 review examining the differences between women and men with autoimmune thyroid disease concluded that the female predominance probably cannot be explained by one mechanism. Sex hormones appear important, but so do the X chromosome, fetal microchimerism, microbiota and environmental influences.
I also need to be careful when I say that I am seeing more Hashimoto’s because my clinical observation is different from looking at population statistics. I am just educating myself and others in the situation I find myself in.
A 2025 review looking across decades of Hashimoto’s research found prevalence estimates varying enormously around the world, somewhere around 5 to 10 percent globally, with some populations much higher and others considerably lower. Some studies suggest it has increased while others do not, and better testing, changing diagnostic practices, iodine exposure, environmental factors, lifestyle and actual biological changes may all be contributing. Still, something is happening in women that deserves a much wider conversation.
I Keep Coming Back to the Gut
The gut is always one of my first questions because the immune system and microbiome are inseparable from each other. We carry an extraordinary microbial ecosystem along the intestinal wall, and those organisms communicate continuously with immune cells, intestinal cells, the liver, the nervous system and the compounds circulating throughout the body. A 2026 review describes the gut-thyroid relationship as a genuine bidirectional system, with changes in the intestinal microbiome being associated with autoimmune thyroid conditions while thyroid function can also influence the intestinal environment. Researchers are looking at microbial metabolites, intestinal permeability, immune regulation and thyroid hormone metabolism as interconnected parts of that relationship.
That catches my attention because I do not think of the intestinal barrier as simply a wall that keeps things out. It is a living microbial interface. The organisms living there help determine what is transformed, what reaches the bloodstream, how immune cells are educated and how the body interprets what it encounters. We are only beginning to understand the number of conversations happening across that boundary.
It reminds me very much of the root zone of a plant. The root cannot really be understood without the rhizosphere surrounding it. Minerals can be present in the soil and still be biologically unavailable, while microbes transform compounds, exchange nutrients, influence signalling and interact with the defence systems of the plant. Human physiology is obviously different, but the ecological principle is familiar to me because biology works through relationships.
So when thyroid antibodies rise, I want to know what has happened in that intestinal ecosystem. How are the bowels functioning, what is being eaten, how diverse is the diet, and what happened before the thyroid pattern began? I want to know what has changed in digestion, bile flow and microbial ecology because looking at those questions does not diminish the importance of the thyroid. It gives the thyroid context.
Then I Ask About Stress, the Kidneys and the Adrenals
I have always thought of the thyroid, adrenals and kidneys as sisters. That is my language for them, but physiologically they are certainly not strangers. The adrenal glands sit above the kidneys and participate in our response to stress, blood pressure, fluid balance, mineral regulation and energy availability. The thyroid influences metabolism throughout the body, while the kidneys are constantly adjusting blood volume, minerals, filtration and metabolic waste and are themselves affected by thyroid hormones.
Research supports substantial communication between the hypothalamic-pituitary-adrenal axis, the HPA axis, and the hypothalamic-pituitary-thyroid axis, the HPT axis. Chronic stress and sustained cortisol signalling can alter thyroid hormone regulation and metabolism and may also influence immune processes involved in thyroid autoimmunity. The kidneys and thyroid affect each other as well. Thyroid hormones influence renal blood flow and filtration, while impaired kidney function changes thyroid hormone metabolism and laboratory patterns. The relationship goes in both directions.
So I keep asking questions that are rarely answered by a TSH result. How is the woman sleeping, and is she waking repeatedly through the night? Is her nervous system constantly alert? Has she been pushing through exhaustion for years? How is her blood pressure, hydration and mineral status, and how are her kidneys functioning? Has there been a major loss, an impossible relationship, financial stress, caregiving, fear or a situation she feels she cannot escape? These things are not separate from physiology simply because they do not fit neatly onto a thyroid blood panel.
Could There Also Be an Emotional Component?
I have become increasingly interested in what the body is experiencing emotionally when a chronic pattern begins. Stress biology already gives us a good reason to ask those questions because the nervous, endocrine and immune systems communicate continuously, but I am also interested in German New Medicine and some of the connections Dr. Ryke Geerd Hamer made between particular biological tissues and specific types of conflict.
Within the GNM interpretation, thyroid-gland patterns are often associated with speed and urgency. The person may experience something as happening too slowly, feel desperate to obtain something quickly, or feel unable to get rid of something quickly enough. Thyroid-duct patterns are interpreted somewhat differently and are associated more with helplessness, powerlessness or feeling unable to change an important situation.
I do not look at this and decide that every woman with Hashimoto’s must have experienced the same emotional conflict. Humans are far too complex for that. What interests me is going back to the beginning and asking what was happening when the thyroid pattern appeared. Was there an intense experience involving powerlessness, urgency, helplessness or feeling trapped? Did something happen that the person could not change, escape, speed up or slow down? Sometimes those questions open an entirely different part of the history.
GNM also uses the idea of “tracks,” meaning reminders associated with an original experience. A person, place, date, smell, conversation or similar situation may bring someone back into the same emotional and physiological response. Hamer described repeated movement between conflict activation and recovery as “hanging healing,” where the person never completely leaves the cycle because something keeps reactivating it.
Whether every detail of that model ultimately proves correct interests me less than continuing to ask the question. The body remembers patterns. Chronic physiological stress is real, and the brain does not need an event to be happening today in exactly the same form in order to respond to something it has learned from yesterday. The emotional history belongs in the conversation.
Then There Is Iodine, and This Gets Complicated
Iodine may be the most confusing part of the modern thyroid conversation because the opinions become extreme very quickly. Iodine is absolutely necessary for thyroid physiology because thyroid hormones themselves contain iodine. Without adequate iodine, the body cannot produce sufficient thyroid hormone, and significant deficiency can result in hypothyroidism and goiter. Iodine requirements are also particularly important during pregnancy and breastfeeding.
Then we reach the disagreement. I find this intriguing how the sciences actually argue amongst themselves. It is our job as individuals to consider it all and figure it out what makes sense to us.
Conventional thyroid organizations emphasize adequate iodine while warning that excess iodine can disturb thyroid function, particularly in people who already have thyroid autoimmunity. The American Thyroid Association advises against routine iodine supplements containing more than 500 micrograms per day and notes an adult tolerable upper intake level of 1,100 micrograms per day except in particular circumstances under supervision. There is research behind their concern, including population studies suggesting that very high iodine exposure may contribute to autoimmune thyroid patterns in susceptible individuals.
On the opposite end of the conversation are physicians such as Dr. David Brownstein and the late Dr. Guy Abraham, who have argued that iodine deficiency is much more widespread than generally recognized and that the body’s requirement for iodine extends far beyond the thyroid. Brownstein reports finding iodine deficiency in a very high proportion of his own patients and has been a prominent advocate of what Abraham called orthoiodosupplementation. Their protocols can involve iodine amounts far beyond standard nutritional recommendations.
I actually think the disagreement is worth exploring because completely opposing camps usually tell me there is more biology we have not fully understood. I do not think the useful question is simply whether iodine is good or bad. I want to know why both too little and too much can disturb the same organ, why one person appears to respond beautifully while another does not, and what else determines that response.
Nutrients do not function independently. The effects of iodine depend on the condition of the thyroid, nutritional status, selenium-dependent enzymes, kidney handling, hormone demand and probably other aspects of individual physiology that we have yet to fully understand. I would never look at a woman with thyroid autoimmunity and automatically conclude that she needs enormous amounts of iodine, but neither would I conclude that iodine has somehow become the enemy because antibodies are elevated. It is an essential element, and the more useful question is one of context, amount, timing and terrain.
And Then I Read This Research About the Ovary
Now we get to the part that made me say, holy cow. New science that can change our current views!
Northwestern University researchers have been studying what happens to ovaries after reproduction ends. We have traditionally talked about the ovary mainly in terms of eggs, fertility, estrogen and progesterone, and once reproduction ends there has been a tendency to think of the ovaries as organs that have essentially finished their important work.
Apparently, that may be completely wrong. A June 2026 study examined ovaries from young, reproductively old and post-reproductive mice. Researchers found the expected loss of follicles with age, but they also found increasing fibrosis, collagen deposition and major changes in gene expression. The post-reproductive ovaries began losing much of their reproductive molecular identity while developing what the researchers describe as an “immune-like” identity.
T cells increased, macrophages increased and multinucleated giant cells increased, while genes involved in both innate and adaptive immune responses became more active. Perhaps even more interesting, some of the genes increasingly expressed in the older ovaries coded for factors predicted to be secreted from the ovary, including immunoglobulin and complement-related signals. Researchers are now asking whether the aging ovary may be communicating inflammatory signals beyond itself and influencing other tissues in the body.
The Northwestern researchers describe the post-reproductive ovary as potentially changing from primarily a reproductive organ into something resembling an immune organ. They still do not know exactly what that means, and much of this particular work is being uncovered through animal models, but the implications are fascinating.
For decades we have talked about menopause primarily through the loss and fluctuation of reproductive hormones. Now we have researchers asking whether ovarian aging also changes immune signalling.
That is a very different conversation.
Could This Have Anything to Do With Female Autoimmunity?
We do not know yet, but I certainly think the question is worth asking. The ovarian research does not prove that the aging ovary causes Hashimoto’s, and that is not what I am suggesting. What interests me is the possibility of another piece in the much larger female immune-endocrine picture that we have not known to look for.
Women already have a substantially greater tendency toward autoimmune thyroid disease than men, and researchers have been trying to understand the influence of estrogen, estrogen receptors, chromosomes, pregnancy, immune differences, fetal microchimerism and the microbiome on that disparity. Now we have researchers telling us that the ovary itself appears to change its immune character as it ages.
We also know that ovarian function and thyroid function communicate. Thyroid hormones influence reproductive physiology, ovarian hormones interact with thyroid and immune signalling, and neither system operates independently of the hypothalamus, pituitary, adrenals, gut, liver or kidneys. The endocrine system was never a collection of isolated glands working alone.
The question becomes particularly interesting when I think about the women I see entering their forties, fifties and sixties. Their ovarian hormone patterns, immune signalling, intestinal microbiome, sleep, metabolism and stress physiology may all be moving through profound transitions at the same time. Their kidneys and mineral regulation have experienced decades of metabolic demand, their nutritional history matters, including their iodine history, and their immune system itself is changing with age.
Then we measure thyroid antibodies and call the problem Hashimoto’s. Maybe that is an accurate diagnosis while still being an incomplete story.
We Have Been Studying Women in Pieces
This new ovarian research interests me because it exposes a problem that reaches far beyond the ovary. Medicine has divided women into specialties, with the endocrinologist looking at the thyroid, the gastroenterologist looking at the intestine, the gynecologist looking at the ovaries, the nephrologist looking at the kidneys, another specialist looking at the immune system and somebody else looking at stress, anxiety or sleep. Yet the woman carrying all of these organs is one biological ecosystem.
Researchers themselves are beginning to challenge that fragmentation. The Northwestern team specifically talks about understanding ovarian function across the entire female lifespan and not simply in relation to fertility and reproduction. They are investigating whether ovarian aging may influence cardiovascular health, bone health, metabolism, brain health and systemic aging. The ovary is beginning to look much less like an organ that simply stops working at menopause and much more like an organ that changes its job.
That is fascinating to me because it changes the questions we can ask. If the post-reproductive ovary is still biologically active and potentially producing immune and inflammatory signals, what does that communication mean for the rest of the female body? What happens when we put that beside the dramatic female predominance in thyroid autoimmunity, the hormonal changes of perimenopause and menopause, changes in the microbiome and decades of accumulated stress physiology?
We do not have all of those answers yet, and I am glad we do not because this is exactly where science gets interesting.
I Am Not Looking for One Cause
I do not think Hashimoto’s is going to turn out to be a simple iodine problem, a simple gut problem, a simple emotional conflict, a simple menopause problem or a simple genetic problem. Living systems rarely work that way, and the longer I work with both the human microbiome and the soil food web, the less interested I become in looking for one isolated cause.
I want to know what the microbial ecosystem is doing and what has happened to digestion, food, mineral availability and the intestinal environment. I want to look at the kidneys and adrenals because fluid balance, mineral regulation, stress physiology and thyroid metabolism are interconnected. I want to understand iodine without joining either extreme camp, and I want to know what happened emotionally before the thyroid changed and whether the woman is still cycling through the same stress pattern years later.
Now I also want to know what her ovaries are doing, In the 2026 ovarian research does not answer the thyroid question, but it opens another door. It suggests that an organ we thought had largely retired after reproduction may remain extraordinarily biologically active and may become increasingly involved in immune signalling as it ages.
For me, that is what makes this kind of science exciting. We keep dividing the body into glands, organs, hormones, immune pathways and diseases so that we can study them, and then biology keeps showing us that everything is talking to everything else.
Perhaps the thyroid was never meant to be understood alone. And, that is the foundation of Terrain Theory. Also, no women can be seen and treated as a “group”. Everyone is unique. And, I am not a doctor or a specialist but I definitely want to help people become educated.
So for the research….
Women and autoimmune thyroid disease:
https://pubmed.ncbi.nlm.nih.gov/40544184/ Gut-thyroid connection and microbiome:
https://pubmed.ncbi.nlm.nih.gov/42419219/ Stress, cortisol and thyroid function:
https://pubmed.ncbi.nlm.nih.gov/42376980/ Kidney-thyroid relationship:
https://pubmed.ncbi.nlm.nih.gov/39004740/ Iodine and Hashimoto’s, 2025 systematic review:
https://pubmed.ncbi.nlm.nih.gov/40558577/ American Thyroid Association position on iodine:
https://www.thyroid.org/ata-statement-on-the-potential-risks-of-excess-iodine-ingestion-and-exposure/ GNM thyroid material:
https://np.learninggnm.com/SBS/documents/thyroid_parathyroids.html New 2026 ovarian study, “The post-reproductive ovary shifts from a reproductive to an immune-like organ”:
https://pubmed.ncbi.nlm.nih.gov/42271623/ Northwestern’s easier-to-read article about the ovarian research:
https://news.northwestern.edu/stories/2026/08-2/reshaping-how-we-think-about-the-ovary-and-aging
