FauntLeRoy Naturopathic Medicine
CONDITION DEEP DIVE
Thyroid
The following is a detailed guide to the main types thyroid disorders (Hypothyroidism, Hashimoto's Grave's Disease). The goal is to educate so you can better understand this disease and how to manage it with both natural and conventional options. I want to empower you in your journey with thyroid disorder. We can have healthy, happy lives and I'm here to give you my expert medical expertise to assist you.
Thyroid Disorders
Comprehensive Thyroid Care: Understanding the Root Causes of Thyroid Imbalances
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Thyroid Overview:
The thyroid is a small, butterfly-shaped gland at the front of your neck, and it has an important job. It makes the hormones that set the pace for your whole body, which is why a problem there can show up in so many places at once: your energy, mood, heart, digestion, even how clearly you think. When the thyroid makes too little hormone, too much, or the immune system gets involved, you feel it everywhere. That is also why thyroid problems are so easy to miss or blame on something else.
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Not all thyroid disorders are the same. Hypothyroidism, Hashimoto’s thyroiditis, Graves’ disease, thyroid nodules, and thyroiditis each have different causes, patterns, and treatments. Two people can feel exactly alike and have very different problems, so the first step is figuring out which one you are dealing with.
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Common Thyroid Conditions We Help Patient With:
Hashimoto's Thyroiditis
Hypothyroidism
Graves' Disease & Hyperthyroidism
Thyroid Nodules
Thyroiditis
Postpartum Thyroid Changes
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Symptoms That May Be Related to Thyroid Dysfunction:
Fatigue
Weight changes
Brain fog
Hair loss
Mood changes
Temperature sensitivity
Menstrual changes
Basic Physiology:
Don’t worry, to start I’ll keep this simple. To make sense of how thyroid conditions are treated, it helps to know the three main hormones: TSH, T4, and T3. It starts in the brain with the pituitary gland, which makes TSH. TSH travels through the bloodstream to the thyroid, a gland at the front of your neck, and tells it to make T4 and T3. (TSH is the hormone we check most often on labs.)
T4 and T3 are sent out like messengers to nearly every cell in your body, where they help set the pace of your metabolism, or how quickly your cells use energy. Because of this, they influence your energy, body temperature, heart rate, digestion, weight, and mood. T4 is mostly a storage form. Your tissues convert it into T3, the active form that does most of the work, and they do it only as needed, which keeps your body from running too fast. The numbers come from iodine: T4 has four iodine atoms attached and T3 has three. That is why your body needs a little iodine from your diet to make thyroid hormone; it is a building block.
Without enough iodine, the thyroid can’t finish building T4 and T3. It keeps making the backbone of these hormones, but can’t complete it, so the gland fills up with unfinished product (thyroglobulin) and keeps expanding. That enlargement is called a goiter, which is a big tumor like growth on the thyroid which is easy to see as it sits right on the front of a person's neck. Thankfully with iodized salt we rarely see these goiters any more; but the point is that understanding the physiology of the thyroid and the thyroid hormones is vital towards understanding the diseases of the thyroid and how to treat them.
How I Evaluate Thyroid Health:
Every thyroid evaluation I do begins with a conversation. I want to hear your symptoms in your own words and understand your full health history, including whether thyroid disease runs in your family, because that context helps us know what to look for. My approach to labs is comprehensive and respectful. TSH is the most helpful single test, but it isn’t the whole story, and I’m glad to help you make sense of free T3, free T4, and other markers. I also check thyroid antibodies, which are often overlooked but can point to an autoimmune cause like Hashimoto’s disease. Depending on your situation, I may also look at nutrient levels. Selenium, iron, vitamin D, and B12 all play a role in how the thyroid works, and a shortfall in any of them can sometimes contribute to how you feel. Lifestyle and environment are part of the picture as well. Sleep, stress, and diet all influence thyroid health, and the thyroid is especially sensitive to radiation, a well-recognized risk factor for thyroid disease and thyroid cancer. That is why I ask about exposure history instead of assuming it doesn’t matter. My goal is for you to leave with a clear understanding of what is happening in your body and why, so that your treatment plan is built on real evidence.
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Proper Lab Testing:
The vitamin Biotin (also called vitamin B7) found in many hair, skin, and nail supplements, can interfere with thyroid labs. Please stop all biotin supplements 72 hours before you have a thyroid lab blood draw. Many thyroid tests use biotin in the lab process itself, so extra biotin in your blood can throw off the results, making TSH look falsely low and thyroid hormones falsely high. That can make a normal thyroid look overactive and lead to the wrong diagnosis.
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The five most important labs for assessing thyroid function, regardless of age, are:
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TSH: The hormone the pituitary releases to stimulate the thyroid. It is elevated in hypothyroidism and suppressed in hyperthyroidism, which makes it the best first screening test.
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Free T4: The unbound, usable portion of T4. It is read alongside TSH to tell overt thyroid disease from subclinical disease.
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Free T3: The unbound, active hormone. It is most useful for confirming hyperthyroidism, especially when TSH is suppressed and free T4 is normal.
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TPO antibodies: Antibodies against thyroid peroxidase, the enzyme that helps attach iodine to thyroglobulin. They are positive in most people with Hashimoto’s and can appear before TSH changes.
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Thyroglobulin antibodies (TgAb): Antibodies against thyroglobulin, the protein backbone of thyroid hormone. Some people with autoimmune thyroid disease are positive for this and negative for TPO, so testing both avoids missing it.
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Approach / Treatment Philosophy
My approach to thyroid care is to first identify the root cause of the thyroid disorder, then carefully match the treatment to the underlying cause. Lifestyle modification, nutrition, targeted supplementation, and prescription medication are all tools, and each is most effective in the clinical situation it fits. The task is determining which one your thyroid requires at each stage.
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In the early stages of thyroid disease, when labs remain within the normal range, lifestyle changes, correcting nutrient deficiencies, and evidence-based natural products can meaningfully support thyroid function, and I use them whenever they are appropriate. These are covered in detail below.
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In other cases, the thyroid can no longer produce enough hormone. This occurs in Hashimoto’s thyroiditis once enough thyroid tissue is affected, and in patients who have had the thyroid surgically removed for thyroid cancer or another condition. Nearly every cell in the body depends on thyroid hormone, and no supplement can replace a hormone the body is not producing. When the gland cannot supply it, the appropriate treatment is thyroid hormone replacement medication, dosed to restore normal physiologic levels.
In every case, my approach philosophy is consistent. Identify the cause, then guide you to the tool that corrects it.
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Iodine: A Key Nutrient for Thyroid Health
Iodine: Not Too Much, Not Too Little
The body cannot make iodine, so all of our iodine must come from our diet. As discussed above, the thyroid builds T4 and T3 hormones from iodine. T4 carries four iodine atoms, and T3 carries three. The thyroid works best when dietary intake stays within range.
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Too little iodine limits thyroid hormone production. This is how goiters develop, and it can also lead to hypothyroidism. Too much iodine also impairs thyroid function. Excess iodine, most often from well intentioned supplements, can suppress hormone production and cause hypothyroidism in some people. In others, particularly those with thyroid nodules, it can drive overproduction and cause hyperthyroidism. Unfortunately, this natural nutrient is not safe at every dose. That is why science has a recommended intake ranges.
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The Right Amount
For a non-pregnant adult, the recommended dietary allowance is 150 µg (micrograms) per day. Total intake should stay well below the tolerable upper limit of 1,100 µg per day. In the US, food usually meets this need. Good sources are iodized salt, dairy, bread, and seafood. Most non-pregnant adults need no iodine supplement. Needs rise during pregnancy and breastfeeding, to about 250 µg per day. The American Thyroid Association recommends a prenatal vitamin containing 150 µg of iodine during pregnancy.
Where Supplements Go Wrong
Thyroid support supplements often rely on iodine and kelp. The amount in the bottle is frequently not the amount on the label. In a laboratory analysis of commercial kelp products, supplements contained up to 5,600 µg of iodine per dose, and the labeling was often inaccurate.
Here is what those numbers mean. The highest dose is about 37 times the daily requirement. A single dose contained more than a month’s worth of the iodine your body needs. It is also about 5 times the safe upper limit. The FDA caps kelp supplements at 225 µg of iodine per daily serving. The highest dose measured is about 25 times that cap.
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Excess iodine from supplements has been documented to cause thyroid dysfunction, including in people with no prior thyroid disease. If you take a supplement, keep the total added iodine well below the limit. Never use a product that does not state an exact microgram dose.
Why I Don’t Guess
My training includes the biochemistry of nutrition. I understand where iodine is used to build thyroid hormone and how it is absorbed in the gut. I know where it is found in food, and where it is missing from the diet. The right amount differs with the condition, body size, and many other factors. So I work from research, evidence, and established intake ranges.
I review every supplement a patient takes. I confirm exactly how much iodine it contains. Then I match the dose to the condition being treated.
Hypothyroidism
"Attention is the rarest and purest form of generosity"
- Simone Weil
Hypothyroidism
Overview: In hypothyroidism, the thyroid produces too little T4 (thyroxine) and T3 (triiodothyronine) to meet the body's needs. Because T3 is the active hormone that sets the metabolic rate of nearly every cell, a shortfall slows many systems at once: fatigue, weight gain, cold intolerance, constipation, dry skin, slowed cognition, low mood, bradycardia, and heavier or irregular menses.
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Labs - Why TSH rises while T4 and T3 fall. The pituitary continuously samples the circulating free T4 and free T3 and adjusts its output of TSH (thyroid-stimulating hormone) to keep them in range. When free T4 and free T3 drift down, the pituitary releases more TSH to drive the remaining thyroid tissue harder. The result is the pattern that surprises most people: TSH goes up as T4 and T3 go down. A high TSH is the feedback system calling for more hormone, not a sign of excess.
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The biochemical stages. Early in the disease, the gland can often hold free T4 within the reference range by responding to the elevated TSH. This combination (an elevated TSH with a normal free T4) is subclinical hypothyroidism. As functional thyroid tissue is lost, the compensation fails: free T4 falls below range and TSH climbs further. Free T3 is frequently preserved until relatively late, because the gland preferentially secretes T3 and because peripheral tissues upregulate deiodinase enzymes that convert T4 to T3. For this reason, a normal free T3 does not rule out meaningful hypothyroidism, and free T4 with TSH remains the more reliable pair for staging.
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The early destructive phase. When hypothyroidism results from autoimmune thyroiditis (Hashimoto's, below), the immune attack can rupture thyroid follicles and release preformed, stored T4 and T3 into the circulation. For a limited period this can raise free T4 and free T3 and suppress TSH, transiently resembling hyperthyroidism, before the gland settles into underactivity. This destructive phase is self-limited and is not the usual starting point; most people begin in the euthyroid or subclinical range.
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How it is diagnosed. TSH is the most sensitive first-line test, interpreted together with free T4, and free T3. TPO and thyroglobulin antibodies identify an autoimmune etiology.
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Treatment. Once the gland can no longer supply adequate hormone, physiologic levels are restored with thyroid hormone replacement. Levothyroxine is a medication that provides T4, structurally identical to the T4 the thyroid secretes; the body then converts it to T3 through its own deiodinase enzymes, at the rate each tissue requires. Dosing is titrated to TSH and free T4 and rechecked periodically.
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Where supportive care fits. Identifying and correcting documented deficiencies in iron, vitamin D, selenium, or B12 supports the pathways thyroid hormone depends on, and these markers are worth measuring (Duntas, Current Opinion in Endocrinology, Diabetes, and Obesity, 2023). These measures work alongside hormone replacement rather than in place of it once the gland's output is insufficient.
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What expert care adds. Taking levothyroxine the same way every day is as important as the dose itself. The most common reason a dose seems to stop working is timing. Levothyroxine should be taken at a consistent time on an empty stomach, and food and other pills should be held for a set interval afterward, because anything in the stomach at the same time can block the medication from being absorbed and lower how much actually reaches the bloodstream (Jonklaas et al., Thyroid, 2014). Many patients were never told this clearly, or were told once and understandably forgot. Getting the timing right is often enough to improve both the labs and how a person feels, without any change in dose.
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Pregnancy deserves special attention. Thyroid hormone needs rise early in pregnancy, often before many people realize they are pregnant, and the growing baby depends on the mother's thyroid hormone in the first trimester. Levothyroxine requirements commonly increase, and the dose frequently needs to be adjusted and the labs rechecked throughout pregnancy (Alexander et al., Thyroid, 2017). This is a time when close follow-up matters, and it is one of the areas where unanswered questions can have real consequences.
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Finally, numbers and symptoms are read together. A TSH that falls inside the "normal" range is not always optimal for a given person, and persistent symptoms in someone who sits at the high end of normal deserve a real conversation rather than a quick dismissal. Other causes of the same symptoms, such as iron deficiency, are considered at the same time, so that nothing is missed and nothing is over-attributed to the thyroid alone.
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Hyperthyroidism
“Wherever the art of Medicine is loved, there is also a love of Humanity.”
- Hippocrates
Hyperthyroidism
What it is. Hyperthyroidism is an excess of circulating T4 and/or T3, which accelerates metabolism: tachycardia or atrial fibrillation, weight loss despite a preserved or increased appetite, fine tremor, anxiety, insomnia, heat intolerance, sweating, and frequent or loose stools. In older adults the presentation can be subtle; predominantly atrial fibrillation or unexplained weight loss.
Why TSH is suppressed. The same feedback loop runs in reverse. When free T4 and free T3 are elevated, the pituitary senses the excess and shuts down TSH secretion. The characteristic pattern is a suppressed (low or undetectable) TSH with a high free T4 and/or free T3. Free T3 is particularly informative in T3-predominant hyperthyroidism, where TSH is suppressed and free T4 can still read within range while free T3 is clearly elevated.
Common causes. The most frequent cause is Graves' disease (below). Others include autonomously functioning ("hot") nodules and toxic multinodular goiter, the transient hormone release of thyroiditis, and exogenous sources such as excess iodine or excess thyroid hormone intake. A radioactive iodine uptake scan helps separate causes that overproduce hormone (high uptake) from those that leak stored hormone (low uptake).
Why conventional treatment is central. Sustained elevation of T4 and T3 places measurable strain on the cardiovascular system and skeleton — atrial fibrillation, left ventricular changes, and accelerated bone loss — and at its most severe can progress to thyroid storm, a life-threatening emergency. Treatment is directed at the underlying cause and may include antithyroid medication (which blocks hormone synthesis), radioactive iodine, or surgery, coordinated with an endocrinologist.
Urgent signs. Fever, confusion, a very rapid or irregular heartbeat, or severe agitation warrant emergency evaluation.
Where supportive care fits. Once a treatment plan is in place, supportive care can address sleep, stress, and nutrition. Supplemental iodine and kelp are generally avoided, because an iodine load can aggravate certain forms of hyperthyroidism, particularly nodular disease (Farebrother et al., Annals of the New York Academy of Sciences, 2019).
Hashimoto's
Thyroiditis
“Out of your vulnerabilities will come your strength.”
- Unknown
Hashimoto's Thyroiditis
What it is. Hashimoto's thyroiditis is the most common cause of hypothyroidism in the United States and is autoimmune. The immune system progressively targets the thyroid, so over time the gland secretes less T4 and T3. The decline is gradual, which is why fatigue, weight change, hair thinning, cognitive slowing, and cold intolerance often build over years before antibodies are measured.
The antibodies. Most people with Hashimoto's have TPO (thyroid peroxidase) antibodies, and many also carry thyroglobulin antibodies; both can appear years before TSH changes. These antibodies are markers of the autoimmune process. The tissue destruction itself is driven largely by T-lymphocyte infiltration of the gland, which is why antibody titers correlate poorly with symptom burden or disease stage. Some people carry high titers with normal function for extended periods, while a smaller group is antibody-negative yet shows the characteristic hypoechoic ultrasound pattern.
Why TSH can fluctuate early. The autoimmune attack is patchy rather than uniform. Episodes of inflammation can release stored T4 and T3, producing a brief rise in free hormone and a dip in TSH before any underactivity is apparent. As functional tissue is lost, the pituitary compensates with higher TSH to keep free T4 in range, so TSH can rise while free T4 holds steady — the subclinical stage. When compensation ultimately fails, free T4 falls. Layered on top of the disease, TSH itself varies with time of day and recent meals, so a single reading can mislead in either direction, and trends are more informative than any one value.
Treatment. When the gland can no longer maintain adequate free T4 and free T3, physiologic levels are restored with thyroid hormone replacement, titrated to normalize TSH and free T4.
Where supportive care fits. Several supportive measures have evidence-based roles alongside hormone replacement:
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Selenium. In Hashimoto's, selenium supplementation consistently lowers TPO antibody levels, and in people not yet on thyroid medication it can modestly lower TSH; some report improved well-being (Huwiler et al., Thyroid, 2024; Zhang et al., Medicine, 2025). It modifies the autoimmune markers rather than curing the disease, and excess selenium is itself harmful, so the dose matters.
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Vitamin D. Low vitamin D is common in Hashimoto's, and correcting a documented deficiency may modestly reduce antibody levels in euthyroid, antibody-positive people with low baseline values; the effect diminishes once overt hypothyroidism is established (Sun et al., Frontiers in Endocrinology, 2025; Pleić et al., PLoS One, 2024).
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Diet. A balanced, anti-inflammatory pattern such as the Mediterranean diet — with adequate selenium, zinc, iron, and vitamin D — is a reasonable and broadly healthy foundation (Duntas, Current Opinion in Endocrinology, Diabetes, and Obesity, 2023). A gluten-free diet benefits those who also have celiac disease or genuine gluten sensitivity; it is not established as a treatment for Hashimoto's on its own (Larsen et al., Journal of Clinical Endocrinology and Metabolism, 2022; Virili et al., Reviews in Endocrine and Metabolic Disorders, 2024).
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Iodine. Additional iodine does not benefit Hashimoto's and can aggravate autoimmune thyroiditis; high-dose iodine and kelp are best avoided (Hu & Rayman, Thyroid, 2017).
Putting it together. Supportive measures can improve how a person feels and can favorably shift antibody levels, and they are worth doing well. They complement, rather than substitute for, thyroid hormone replacement once the gland's own output of T4 and T3 is insufficient.
Grave's Disease
“Great acts are made up of small deeds.”
- Lao Tzu
Graves' Disease
What it is. Graves' disease is the most common cause of hyperthyroidism and is autoimmune in origin. The immune system produces a stimulating antibody directed at the TSH receptor (TRAb, also measured as TSI) that mimics TSH and switches the thyroid on continuously, independent of pituitary feedback. The gland therefore overproduces T4 and T3 despite a fully suppressed TSH. Graves' can also involve the eyes (Graves' orbitopathy); proptosis, irritation, or diplopia, and may produce a diffuse goiter.
How it is diagnosed. Labs show a suppressed TSH with elevated free T4 and/or free T3. A positive TSH receptor antibody (TRAb/TSI) confirms the diagnosis. When the antibody is equivocal, a radioactive iodine uptake scan showing diffuse, increased uptake distinguishes Graves' from thyroiditis and from nodular disease.
Treatment. The three established options are antithyroid medication (such as methimazole, which inhibits thyroid peroxidase and thus hormone synthesis), radioactive iodine, and thyroidectomy. The choice depends on disease severity, eye involvement, pregnancy status and plans, goiter size, and patient preference, and is made together with an endocrinologist.
Where supportive care fits. Selenium is the supportive option with the most consistent supporting data in Graves'. Added to standard therapy, selenium has improved quality of life and eye outcomes in mild Graves' orbitopathy in some trials, though results vary and it functions as an adjunct to conventional treatment (Linn et al., Journal of Trace Elements in Medicine and Biology, 2025; Rayman, Lancet, 2012). Low vitamin D is common in Graves', so measuring and correcting a deficiency is reasonable (Luo et al., Medicine, 2026; Czarnywojtek et al., Journal of Clinical Medicine, 2023). Iodine and kelp are avoided. Smoking cessation is important, as smoking worsens Graves' orbitopathy.
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Disclaimer: The information on this website is for general educational purposes only. It is not a substitute for medical advice, diagnosis, or treatment from a qualified clinician who knows your history. Reading this site or contacting us through it does not create a doctor-patient relationship. Do not start, stop, or change any medication or treatment without talking to your prescribing provider. If you think you are having a medical emergency, call 911. Dr. Jason FauntLeRoy ND, is licensed in WA, MT. Content last reviewed 10/20/26.
"Attention is the rarest and purest form of generosity"
- Simone Weil