Dear readers,
She is thirty-eight, she is exhausted in a way that sleep does not fix, her hair is coming out in the shower, she is cold when nobody else is cold, and she has gained eleven pounds without changing a thing. She has been to a doctor about it. Her TSH came back at 3.1, she was told it was normal, and the visit ended there. By the time she reaches me she has usually stopped expecting anyone to find anything, which is its own kind of injury, separate from the illness.
I want to be fair to the physician who saw her first. A TSH of 3.1 sits inside the laboratory’s reference range, and if you have twelve minutes and a full waiting room, that is where the workup stops. But a single number from the pituitary is not a picture of a system that touches every cell in the body, and it is certainly not an answer to the question that actually matters, which is why any of this is happening in the first place.
Dr. Izabella Wentz, the integrative pharmacist whose work has shaped how a generation of clinicians thinks about this disease, describes the conventional approach as pouring hormone into a leaking bucket. You can keep refilling it, and for some people that is enough. But if nobody asks why the bucket is leaking, you are managing a number rather than treating a person. That question, asked seriously and answered patiently, is the whole of my approach to thyroid disease.
Hashimoto’s is the diagnosis, even when nobody says the word
Hashimoto’s thyroiditis is the most common autoimmune disease in the world and the cause of the overwhelming majority of hypothyroidism in this country. Yet a remarkable number of women are handed a levothyroxine prescription and never told they have an autoimmune condition at all, because if the treatment is the same either way, the reasoning goes, the label does not change anything.
It changes everything. Autoimmunity is a disease of the immune system that happens to be attacking the thyroid, and the immune system is influenced by things you can actually reach: what you eat, what is living in your gut, what nutrients you are depleted in, how much stress you are carrying, and what you are exposed to. A thyroid that has already been destroyed cannot be talked back into working. An immune process that is still in motion is a different situation entirely.
It lands on women roughly seven to eight times as often as on men, and the biology behind that is real. The X chromosome carries a disproportionate share of immune genes, estrogen modulates immune activity directly, and pregnancy asks a woman’s immune system to tolerate another person for nine months and then reset, which is why the year after a birth is one of the most common moments for thyroid autoimmunity to surface. A great many women date their symptoms to that year and were told it was simply what having a baby feels like.
The timeline matters too. Antibodies appear years, sometimes decades, before the TSH moves. The gland compensates until it cannot, and during that entire window a patient can feel progressively worse while every standard test comes back unremarkable. That window is precisely where intervention has the most to offer, and it is precisely the window conventional practice tends to ignore.
The panel I run, and the numbers I actually aim for
TSH is the pituitary’s opinion of your thyroid rather than a measure of thyroid hormone in your tissues, and it lags behind change by about six weeks. I still use it. I simply do not let it testify alone. Most laboratories flag values above 4.5, a range built from a population that includes a great many people with undiagnosed thyroid disease. In practice, most of my patients feel best with a TSH somewhere between roughly 0.5 and 2, and I treat that as a target to discuss rather than a rule to impose, because the person matters more than the range.
Free T4 and free T3 measure the unbound hormone available to your cells. Total measurements are distorted by carrier proteins that shift with pregnancy, oral contraceptives, and oral estrogen therapy, which describes a large share of the women I see. T4 is essentially a prohormone; T3 is the active form that binds receptors and does the work, and the conversion between them happens in the liver, kidney, and tissues through enzymes that do not perform identically in everyone. Two women on the same dose with the same TSH can have meaningfully different free T3 levels, and only one of them feels well. That is not a mystery. It is a conversion problem, and you will never see it if you do not measure it.
Reverse T3 is the inactive form the body produces when it deliberately steers conversion away from active hormone, which it does under stress, illness, inflammation, caloric restriction, and low iron. I check it, and I want to be precise about how I use it. I do not treat a reverse T3 number, because there is no validated target and no evidence that pushing it down improves outcomes. I read it as a signal pointing upstream. When it is elevated, my question is what your body is responding to, and the answer is usually somewhere in the chapters that follow.
TPO antibodies and thyroglobulin antibodies are the tests most often missing from the chart in front of me. A positive TPO antibody with a normal TSH is not a negative workup. It is the diagnosis, arriving early, and it identifies a woman who is significantly more likely to progress and who deserves monitoring, attention around pregnancy, and a real conversation about what can be influenced. TSH receptor antibodies answer the opposite question, distinguishing Graves’ disease from a thyroid that is inflamed and leaking stored hormone, and they matter in pregnancy because they cross the placenta.
Alongside the thyroid panel I check the nutrients that determine whether any of it works: ferritin and a full iron panel, vitamin D and B12. In this framework we are aiming higher than the laboratory’s lower limit. Ferritin in the range of ninety to one hundred ten is where hair regrowth and energy tend to return, which is a long way above the fifteen that most labs will call normal, and B12 nearer seven hundred than three hundred. Two cautions I will not skip: I check iron studies before anyone supplements iron, because iron overload is a real condition and pushing ferritin in the wrong person causes harm, and vitamin D is a fat-soluble hormone that I dose and monitor rather than guess at.
Looking for the trigger
Dr. Wentz frames autoimmunity as requiring three things in combination: a genetic predisposition, a trigger, and intestinal permeability. You cannot change the first. The other two are where the work happens, and this is the part of the visit that takes an hour rather than twelve minutes, because it is essentially an investigation.
The gut comes first, both because it is nearly always involved and because it is the area where my practice is already built to look properly. The mechanical piece is simple and badly underappreciated: thyroid hormone is absorbed in the small intestine, and that absorption is impaired by celiac disease, H. pylori, atrophic gastritis, low stomach acid including the kind produced by years of acid-suppressing medication, and bacterial overgrowth. When a patient’s dose keeps climbing without explanation, she often does not have worsening thyroid disease. She has a gut that is not absorbing what she swallows.
The immune piece runs deeper. The majority of your immune system sits along your intestinal lining, and specific organisms have been repeatedly associated with thyroid autoimmunity, H. pylori and the intestinal parasite Blastocystis hominis among them, with treatment sometimes followed by falling antibody titers. I want to be careful with how strong a claim I make here, because association is not proof and the published evidence is thinner than the internet suggests. What I will say plainly is that when proper testing finds overgrowth, infection, insufficient digestion, or significant inflammation, treating it is worth doing on its own merits, and in a meaningful number of my patients the thyroid picture improves alongside the gut.
Food is the trigger patients ask about most. The relationship between Hashimoto’s and celiac disease is genuine, running through shared genetics, and celiac prevalence in Hashimoto’s patients is several times that of the general population, which is why I screen everyone before they change their diet rather than after, when the test stops working. If celiac disease is present, strict gluten avoidance is the treatment, full stop. If it is absent, I will be more honest with you than most of this field: the randomized trials of gluten-free eating in non-celiac Hashimoto’s are small and inconsistent, and one recent meta-analysis found thyroglobulin antibodies fell while TPO antibodies did not. What I also know, from watching a great many patients closely, is that a substantial number of them feel unmistakably better without gluten, and often without dairy, and that this shows up in symptoms long before it shows up in a titer. So I offer a structured elimination with a genuine reintroduction, we track how you feel and what your antibodies do, and then we decide based on your results rather than on anyone’s ideology, mine included.
Stress, sleep, and blood sugar belong on this list rather than in a footnote, and I will come back to them.
Toxic exposures are the category where I hold the most reservations. There is real evidence that halogen exposure, certain heavy metals, and some environmental chemicals influence thyroid function and autoimmunity, and there is also an enormous commercial industry selling detoxification protocols that have never been tested. I will look for a plausible, specific exposure in your history. I am not going to sell you a cleanse.
Selenium, myo-inositol, and the iodine warning
This is the rare supplement question with actual randomized data behind it. Selenium is the required cofactor for the enzymes that both build thyroid hormone and protect the gland from oxidative damage, and pooled trial data show that supplementation lowers TPO antibodies and modestly lowers TSH in Hashimoto’s, with effects appearing over three to six months. Myo-inositol works differently, improving how thyroid cells respond to TSH signaling, and the combination trials, most using six hundred milligrams of myo-inositol with a low dose of selenium, reported falling TSH and antibody levels along with better quality of life in early disease.
The honest footnote is that a 2026 meta-analysis comparing the combination against selenium alone confirmed the added benefit for TSH and thyroglobulin antibodies but did not find a significant additional effect on TPO antibodies specifically, and noted that the number of trials remains small. Nearly all of this research enrolled people whose thyroid was still producing hormone on its own, which is exactly the patient I most want to reach, and none of it replaces thyroid hormone once the gland has genuinely failed.
So I use this combination deliberately, most often in early or subclinical disease, and I measure antibodies and TSH before we start and again at six months so that we are deciding with evidence rather than momentum. Selenium has a genuinely narrow therapeutic window, so more is not better and I would rather you not add Brazil nuts to a supplement you are already taking.
Iodine deserves its own warning, because it is where well-meaning people get hurt. Iodine is necessary for thyroid hormone production, and in a gland under autoimmune attack, high-dose supplementation can accelerate the attack and worsen hypothyroidism. The doses circulating in wellness spaces are frequently many times what anyone with Hashimoto’s should take. If iodine belongs in your plan, it belongs there because we established a deficiency, not because a bottle promised thyroid support.
When an ultrasound helps, and when it does not
Ultrasound images the gland’s structure and tells you nothing about its function, so it is not part of every thyroid workup. I will often obtain one at the time of an initial Hashimoto’s diagnosis, because the characteristic changes confirm what the antibodies are telling us and a baseline is genuinely useful. Beyond that, I image when I feel a nodule, when the gland is enlarged or asymmetric, when there is pressure, difficulty swallowing, or a voice change, when a lymph node concerns me, when something turns up incidentally on other imaging, or when there is a history of neck radiation or thyroid cancer in the family.
What I do not do is rescan a stable gland every year out of diligence. South Korea offered neck ultrasounds broadly to people without symptoms and thyroid cancer diagnoses rose roughly fifteenfold, while deaths from thyroid cancer did not change, meaning an enormous number of people were biopsied, operated on, and given a cancer diagnosis for something that was never going to hurt them. About a third of Hashimoto’s patients have nodules, nearly all of them harmless. Restraint here is not neglect.
Thyroid hormone: getting the medication right
Roughly five to fifteen percent of people on levothyroxine alone continue to feel unwell with a perfectly normal TSH. That is millions of people, and telling them the number is fine is not a clinical answer.
Levothyroxine is still where most people should start. It is a single stable molecule with a long half-life and the best long-term safety data we have, and most patients do beautifully on it. The details determine whether it works: an empty stomach, thirty to sixty minutes before food or coffee, and four hours away from calcium, iron, and magnesium. Taken with breakfast and a multivitamin, it is a substantially different medication than the one I prescribed. I recheck at six weeks and I ask how you feel with the same seriousness that I read the lab.
Liothyronine, sold as Cytomel, is synthetic T3, and it is what I reach for when the free T3 is low, conversion appears to be the problem, or a patient remains symptomatic on adequate levothyroxine after the nutrient and gut work is done. The randomized trials of combination therapy have not shown consistent benefit across populations, and I take that seriously rather than dismissing it, though I also think those studies used fixed ratios and endpoints poorly suited to answering whether an individual feels like herself again. T3 has a short half-life and usually needs divided dosing, it requires real caution in older patients and anyone with cardiac disease or atrial fibrillation, and I will not suppress your TSH to chase a symptom, because the consequences for bone and heart are not theoretical.
Desiccated thyroid extract, including Armour Thyroid and NP Thyroid, contains both hormones in a fixed ratio richer in T3 than the human thyroid produces, and a significant number of patients tell me they feel better on it than on anything else. I believe them, and I prescribe it. You should also know that its regulatory footing is unsettled at the moment. These products have never been through FDA approval, which is more an accident of history than a verdict, but it does mean the batch-consistency guarantees applied to levothyroxine do not apply here and there have been potency recalls. In August 2025 the FDA notified manufacturers that it intended to act against unapproved animal-derived thyroid products with a twelve-month transition; in March 2026 the agency replaced that with a risk-based enforcement approach and a promise of formal guidance by this month; and one major pharmacy benefit manager dropped these products from its formulary in April. If you take desiccated thyroid, this does not mean stopping. It means we should have a plan instead of a surprise.
The stress axis
Patients ask me about adrenal fatigue constantly, and both the dismissive answer and the enthusiastic one are wrong.
The dismissive answer is that the adrenal glands do not get tired, which is technically true and clinically useless. The enthusiastic answer treats a mail-order saliva panel as a diagnosis, and those tests do not perform well enough to build a plan on. What is genuinely happening in most of these women is dysregulation of the hypothalamic-pituitary-adrenal axis, the system that governs the stress response, and its effects on the thyroid are measurable rather than metaphorical. Sustained cortisol elevation suppresses TSH release and pushes conversion away from active T3 and toward reverse T3. That is why a woman sleeping five hours, undereating, and training hard can produce a thyroid panel that looks mildly hypothyroid without having primary thyroid disease at all, and why medicating that panel treats the readout instead of the problem.
So this part of the plan is not glamorous and it is not optional. Regular meals with adequate protein so that your blood sugar stops swinging, a genuine sleep window, exercise that restores you rather than depletes you, and enough salt and fluid if your blood pressure runs low. I use adaptogens and targeted nutrients in some patients and find them helpful, while being straightforward that the evidence there is suggestive rather than definitive.
One thing in this territory is not optional at all. True adrenal insufficiency is uncommon but clusters with autoimmune thyroid disease, and starting thyroid hormone in someone who has it untreated can precipitate a genuine crisis. If there is unexplained low blood pressure, salt craving, darkening skin, low sodium, or a patient who felt distinctly worse after starting levothyroxine, that gets tested properly with a morning cortisol and a stimulation test, and it gets sorted first.
What this adds up to
A root cause approach is not a rejection of medication. I prescribe thyroid hormone, often generously, and I have no interest in withholding it while someone waits to see whether a diet works. What it means is that the prescription is the beginning of the conversation rather than the end of it, and that we spend the same energy asking why your immune system turned on your thyroid as we spend adjusting the dose.
The woman with the TSH of 3.1 was not exaggerating and she was not looking for a label. She was describing her own body accurately to people who were looking at too little information. She has antibodies, she has low ferritin, she has a gut that has been quietly miserable for a decade, and she has been running on four hours of sleep since her second child was born. None of that is visible on a single line of a lab report, and all of it is treatable.
If any of this sounds like your own chart, I would like to see the whole of it with you.
Reach out to our office at 703-866-4144 or schedule a free introductory call with us and let’s get you sorted the right way.
Best wishes,
Dr. Gajer
The Gajer Practice – The Science of Health, The Art of Transformation
