Thyroid disorders are among the most common conditions in adults over 45, most prevalent in women, and most consistently undertreated in conventional primary care. The reason is not a failure of clinical awareness. It is a failure of the screening test most commonly used to evaluate thyroid function.

TSH — thyroid stimulating hormone — is the pituitary signal that tells the thyroid to produce more or less hormone. When TSH is elevated, the pituitary is calling for more thyroid output than it is receiving, which suggests hypothyroidism. When TSH is suppressed, the thyroid is producing more than needed, suggesting hyperthyroidism. For the majority of patients, TSH provides a reliable indirect measure of thyroid function and is adequate for screening purposes.

For a meaningful subset of patients, it is not enough. TSH reflects what the pituitary is signaling, not what the thyroid is producing, and not what the cells are actually receiving and using. A patient can have a TSH within the reference range and still have insufficient free T3 — the active form of thyroid hormone — reaching target tissues. A patient on levothyroxine with a normal TSH may still be converting T4 to reverse T3 rather than active T3, a pattern that produces hypothyroid symptoms despite a reassuring lab value. These scenarios are not rare. They are common enough to explain a substantial portion of patients who report continued fatigue, cognitive difficulty, cold intolerance, and weight resistance despite thyroid labs that their physician calls normal.

A complete thyroid evaluation includes free T3, free T4, reverse T3, and thyroid antibodies alongside TSH. The antibody panel — TPO antibodies and thyroglobulin antibodies — identifies Hashimoto’s thyroiditis, the most common cause of hypothyroidism in adults, which can be active and destructive for years before TSH moves outside the reference range. Identifying Hashimoto’s matters because it changes the monitoring strategy, the clinical conversation about symptoms, and the long-term treatment approach. A TSH that has not yet become abnormal does not mean autoimmune thyroid disease is not present and active.

The treatment question for subclinical hypothyroidism — TSH elevated but still within some definitions of acceptable range, free T4 at the lower end of normal — is one of the more contested areas in thyroid medicine. The conventional guidance has been to monitor without treating until TSH crosses a defined threshold. The clinical argument for treating symptomatic patients whose TSH is in the upper portion of the normal range, particularly when free T3 is low and symptoms are consistent with hypothyroid physiology, is stronger than the guideline threshold alone suggests. Dr. Stein approaches this conversation directly, explaining what the evidence supports for the individual patient rather than defaulting to population-based thresholds that may not fit the clinical picture in front of him.

Levothyroxine optimization is the other area where management most commonly falls short. Many patients on levothyroxine have been on the same dose for years without reassessment beyond TSH. Body weight changes, other medications, absorption factors, and the natural progression of thyroid disease all affect how much levothyroxine is needed and how it is utilized. A TSH maintained at the high end of the reference range on a stable dose is not necessarily optimal. A patient who feels well on a TSH of 1.2 and feels poorly on a TSH of 3.8 — both technically within range — deserves treatment calibrated to their symptom experience, not a population threshold.

The addition of T3 to thyroid treatment, through combination T4/T3 therapy or natural desiccated thyroid preparations, remains controversial in conventional endocrinology. The clinical evidence for benefit in patients who continue to have symptoms on levothyroxine alone is mixed but not absent. There is a subset of patients who respond better to T3 supplementation. Identifying that subset requires careful evaluation of free T3, reverse T3, symptoms, and response to therapeutic trial. It requires a physician willing to have the conversation and willing to manage the outcome with appropriate monitoring. Hormone evaluation at BRCM includes thyroid as part of the full hormonal picture, not as a separate and more limited clinical conversation.

For women in perimenopause and menopause, the thyroid picture is complicated by the symptom overlap between hormonal transition and thyroid dysfunction. Fatigue, cognitive changes, sleep disruption, weight changes, and mood instability are common to both conditions. A physician seeing these symptoms in a perimenopausal patient who does not evaluate both hormonal and thyroid status comprehensively will miss one or both contributions. The advanced diagnostics available to BRCM members are built to capture the full picture.

The American Thyroid Association patient resources provide accessible background on thyroid physiology and the current state of diagnostic and treatment guidelines. The clinical conversation with Dr. Stein goes beyond those resources to the specific patient in front of him and what the evidence supports for their situation.

To discuss thyroid evaluation or your current thyroid management, call (561) 483-5500 or schedule through the contact page.