Thyroid Hormone Therapy

The thyroid is a small butterfly-shaped gland at the base of the neck that produces two primary hormones: T4 (thyroxine) and T3 (triiodothyronine). T4 is the storage form the gland releases in the largest quantity; T3 is the active form that actually drives cellular metabolism. Most of the T3 your body uses is not made by the thyroid directly but converted from T4 in peripheral tissues, particularly the liver and kidneys. That conversion step matters enormously, and it is one of the places where thyroid problems hide.

When thyroid hormone falls below what your body needs — the condition called hypothyroidism — metabolism slows across every system at once. Energy production drops, body temperature falls, digestion slows, cognition dulls, hair and skin change, and weight becomes difficult to control regardless of diet and exercise. Thyroid hormone therapy treats this deficiency directly by restoring hormone to the level your tissues actually require.

Thyroid disease is far more common than most patients realize. The American Thyroid Association estimates that about 20 million Americans have some form of thyroid disease and that up to 60 percent of those affected are unaware of their condition. Women are five to eight times more likely than men to develop a thyroid problem, and risk rises sharply during perimenopause, after pregnancy, and through other major hormonal transitions — precisely the periods when symptoms are most likely to be attributed to something else.

The single largest reason thyroid dysfunction goes undiagnosed is that most evaluations measure only TSH — thyroid-stimulating hormone, the pituitary signal that tells the thyroid to work harder. TSH is a useful screening test, but it is an indirect measure. It tells you what the pituitary thinks is happening, not how much active hormone is reaching your cells.

Reference ranges compound the problem. Laboratory ranges for TSH are built from broad population samples that include people with undiagnosed thyroid disease, which makes the "normal" range wider than the range in which most people actually feel well. A result of 4.0 mIU/L may be flagged as normal by a lab report while representing meaningful underperformance for the individual in front of you. Treating the flag rather than the patient is how symptomatic people get told their thyroid is fine.

Conversion problems are invisible on a TSH-only panel. A patient can produce adequate T4, and therefore show a reassuring TSH, while converting that T4 poorly into active T3. Chronic stress and elevated cortisol, chronic illness, nutrient deficiencies, and certain medications can all impair conversion. Without a free T3 measurement, this patient looks euthyroid on paper and feels hypothyroid in life.

Finally, autoimmune thyroid disease often begins long before standard numbers move. Hashimoto's thyroiditis — the most common cause of hypothyroidism in the United States — is driven by antibodies that attack thyroid tissue gradually. Thyroid peroxidase (TPO) and thyroglobulin antibodies can be elevated for years while TSH and T4 remain in range, and a panel that never tests antibodies never sees it coming.

Evaluation at The Riegel Center begins with a full thyroid panel rather than a single screening value. That panel includes TSH, free T4, free T3, reverse T3, and thyroid antibodies (TPO and thyroglobulin). Each measurement answers a different question, and the answers only make sense together.

TSH indicates how hard the pituitary is pushing the thyroid. Free T4 shows how much storage hormone is actually available to tissue rather than bound up and inactive. Free T3 shows how much active hormone is present at the cellular level, which is the number most closely tied to how a patient feels. Reverse T3 identifies whether T4 is being shunted into an inactive form — a pattern often seen with chronic stress, inflammation, or illness. Antibodies identify autoimmune thyroid disease, which changes both the prognosis and the monitoring plan.

Dr. Riegel interprets these results against optimal ranges and against your symptoms, not against the broad reference range alone. Two patients with identical TSH values can have very different clinical pictures, and the difference usually shows up in free T3, reverse T3, or antibody status. This is the same principle he applies across hormone medicine: laboratory data defines the physiology, but symptoms define whether treatment is working.

Thyroid function and reproductive hormones are tightly interconnected, which is why evaluating one without the other produces incomplete answers — and why a hormone specialist is well positioned to sort out symptoms that a thyroid-only workup cannot.

Estrogen raises thyroid-binding globulin, the protein that carries thyroid hormone through the bloodstream. More binding protein means more hormone is bound and less is free and biologically available. This is why women starting estrogen therapy, or going through the estrogen fluctuations of perimenopause, sometimes need their thyroid status reassessed even though the thyroid gland itself has not changed.

Cortisol interferes from another direction. Chronically elevated cortisol from prolonged stress suppresses the conversion of T4 into active T3 and can push more T4 toward reverse T3 instead. A patient in that state has a functioning thyroid gland and a genuine shortage of active thyroid hormone at the tissue level.

The symptom overlap is the practical problem. Fatigue, weight gain, brain fog, hair thinning, low mood, and cold intolerance appear in both hypothyroidism and perimenopausal hormone decline. A woman treated for menopause whose thyroid is never fully evaluated may improve only partially and conclude that hormone therapy did not work for her — when the missing piece was thyroid all along. Evaluating both at once avoids months of that guesswork.

Thyroid hormone replacement is not one product. Several preparations exist, and the right choice depends on your labs, your symptoms, and how well your body converts T4 to T3.

Levothyroxine, a synthetic form of T4 identical to the hormone the thyroid produces, is the most widely prescribed treatment and the preparation the American Thyroid Association identifies as the standard of care for hypothyroidism. For most patients it is effective, predictable, and well tolerated, because the body converts it to T3 as needed.

A subset of patients, however, continues to have symptoms on T4 alone despite a normalized TSH — often those with impaired T4-to-T3 conversion. For these patients, combination therapy that supplies both T4 and T3 is sometimes used. Desiccated thyroid extract, which contains both hormones in a fixed ratio derived from animal thyroid, is another option some patients ask about. The American Thyroid Association does not recommend desiccated thyroid extract as routine first-line therapy, citing the absence of long-term outcome data and the non-physiologic T4-to-T3 ratio it delivers. Dr. Riegel reviews the evidence and the trade-offs with patients rather than defaulting to a single answer for everyone.

How thyroid hormone is taken affects how well it works. Absorption is meaningfully reduced by food, and by calcium supplements, iron, and certain acid-reducing medications, which is why thyroid hormone is typically taken on an empty stomach and separated from those products by several hours. Dose changes take time to register — thyroid hormone has a long half-life, and levels generally need six to eight weeks to stabilize before retesting gives a meaningful result. Patience during titration is part of doing this correctly.

At The Riegel Center, thyroid treatment is one component of a complete hormonal evaluation rather than a standalone prescription. Dr. Riegel measures thyroid function alongside estradiol, progesterone, total and free testosterone, DHEA-S, and cortisol, because the interactions among them determine how a patient actually feels. Correcting thyroid while leaving a significant sex-hormone deficiency untreated — or the reverse — produces partial results and a frustrated patient.

Treatment is dosed to the individual and adjusted deliberately. Starting doses are conservative, particularly in older patients and those with cardiac history, and are titrated upward based on repeat laboratory testing and symptom review rather than on a fixed schedule. Follow-up testing confirms that free T4 and free T3 are landing in the optimal range and that TSH has not been suppressed too far, since over-replacement carries real risks to bone density and heart rhythm.

This approach reflects a career built specifically on hormonal medicine. Dr. Riegel began with four years of hormone research at UT Southwestern Medical School and has spent more than thirty years in clinical hormone practice, developing roughly forty proprietary bioidentical formulations along the way. Thyroid has been part of that work throughout, because no serious evaluation of fatigue, weight change, or cognitive fog is complete without it.

Evaluation also clarifies when the thyroid is not the answer. Iron deficiency, sleep apnea, depression, poorly controlled metabolic disease, and sex-hormone decline can each produce a hypothyroid-looking symptom picture with a normal thyroid. Identifying which of these is actually driving your symptoms is the point of testing broadly at the outset, and it is what allows treatment to be aimed at the real cause.