Clinical perspectives on hormone health, peptide therapy, metabolic wellness, gut health, and healthy aging — written for patients who want to understand the science behind their care, not just the summary.

Thyroid dysfunction is one of the most common and most commonly missed hormonal conditions in the US — affecting an estimated 20 million Americans, with up to 60% undiagnosed. The primary reason it gets missed is a testing problem: most standard care relies on a single marker, TSH, to evaluate a system that requires a much more complete picture.
Why isn't TSH alone enough to evaluate thyroid function?
TSH (thyroid-stimulating hormone) is a pituitary hormone — it measures how hard the pituitary gland is pushing the thyroid to produce hormones, not how much active thyroid hormone is actually reaching your cells. A normal TSH tells you that the pituitary-thyroid feedback loop is intact at that moment. It does not tell you how much T4 is being converted to the active T3 your cells actually use, whether that conversion is efficient, whether reverse T3 is blocking active hormone at receptor sites, or whether thyroid antibodies are attacking the gland. Patients with real, symptomatic thyroid dysfunction regularly have TSH in the normal range — and are told their thyroid is fine.
What thyroid tests should I ask for?
A complete thyroid evaluation at DNA Wellness includes:
TSH: Still useful as part of the picture — but only as one data point among several.
Free T4 (FT4): The primary hormone produced by the thyroid gland. "Free" means unbound and available to tissues — not attached to transport proteins. Total T4 can appear normal while free T4 is low.
Free T3 (FT3): The active form of thyroid hormone that enters cells and drives metabolic function. T4 must be converted to T3 — primarily in the liver, gut, and peripheral tissues — to be useful. Many patients convert T4 to T3 inefficiently, producing symptoms of hypothyroidism despite normal T4 levels.
Reverse T3 (rT3): An inactive mirror image of T3 that the body produces under stress, inflammation, caloric restriction, or illness. High reverse T3 blocks T3 receptors — meaning active hormone can't reach cells even when T3 levels appear adequate. This pattern is a common and frequently missed driver of hypothyroid symptoms.
TPO Antibodies (Anti-TPO): Thyroid peroxidase antibodies indicate Hashimoto's thyroiditis — an autoimmune attack on the thyroid gland. Hashimoto's is the most common cause of hypothyroidism in the US and can be present for years before TSH becomes abnormal. Identifying it changes the treatment approach.
Thyroglobulin Antibodies (Anti-Tg): A second antibody marker for autoimmune thyroid disease, included when Hashimoto's is suspected.
Subclinical hypothyroidism is defined conventionally as elevated TSH with normal T4 — meaning the pituitary is working harder than normal to drive thyroid output, suggesting the gland is underperforming, but T4 hasn't dropped below the reference range yet. By conventional standards, this is often watched rather than treated.
By functional medicine standards, it produces real symptoms that deserve attention:
Fatigue that doesn't improve with sleep
Cold intolerance — feeling cold when others are comfortable
Weight gain or difficulty losing weight despite normal diet and exercise
Constipation
Hair thinning or shedding — particularly from the outer third of the eyebrows
Dry skin and brittle nails
Depression and cognitive slowing — brain fog, slowed thinking, poor memory
High cholesterol — the thyroid regulates cholesterol metabolism; subclinical hypothyroidism elevates LDL
Muscle aches and joint stiffness
Heavy or irregular periods in women
The symptom burden of subclinical hypothyroidism is well-documented even when TSH is only modestly elevated. Waiting until TSH crosses an arbitrary threshold before treating means patients spend months or years symptomatic unnecessarily.
Hashimoto's thyroiditis is the most common cause of hypothyroidism — an autoimmune condition in which the immune system produces antibodies that attack and gradually destroy thyroid tissue. Over time, this destruction reduces the thyroid's ability to produce hormones, eventually producing clinical hypothyroidism.
The important distinction is that Hashimoto's is an immune system problem that happens to damage the thyroid — treating only the thyroid without addressing the autoimmune driver leaves a root cause unaddressed. Identifying Hashimoto's through antibody testing changes the clinical approach: it opens the door to dietary interventions (gluten and dairy removal have significant evidence for reducing antibody levels), immune modulation strategies, and monitoring designed around the autoimmune nature of the disease rather than hormone levels alone.
How is hypothyroidism treated beyond standard levothyroxine?
Standard hypothyroidism treatment in conventional medicine is levothyroxine (synthetic T4) — which addresses T4 deficiency but does not correct poor T4-to-T3 conversion, high reverse T3, or the autoimmune driver in Hashimoto's.
At DNA Wellness, Dr. Katherine Ortiz evaluates the full thyroid picture and may use:
Desiccated thyroid extract (DTE): A natural thyroid medication (Armour Thyroid, NP Thyroid, or compounded) containing both T4 and T3. Many patients whose symptoms don't fully resolve on levothyroxine alone respond significantly better to a T4/T3 combination.
Liothyronine (T3): Synthetic T3 added to levothyroxine for patients who convert T4 to T3 poorly — identified by low free T3 alongside adequate free T4.
Addressing reverse T3: High rT3 requires identifying and treating the underlying cause — typically chronic stress, inflammation, nutrient deficiencies (selenium, zinc, iron), or caloric restriction.
Autoimmune and gut-focused strategies for Hashimoto's: Dietary modification, vitamin D optimization, selenium supplementation, and gut health support all have evidence for reducing thyroid antibody levels and slowing autoimmune progression.
Can you have hypothyroid symptoms with a normal TSH? Yes. Patients with poor T4-to-T3 conversion, high reverse T3, or early Hashimoto's can have significant hypothyroid symptoms with a TSH in the normal range. A comprehensive thyroid panel — not TSH alone — is required to evaluate thyroid function completely.
What is the optimal TSH range for thyroid function? Conventional medicine defines normal TSH as approximately 0.4–4.5 mIU/L. Functional medicine providers typically aim for a more narrow optimal range of 1.0–2.0 mIU/L, particularly in symptomatic patients. The free T3 level, and how a patient feels at a given TSH, matters as much as the number itself.
Does thyroid medication cause weight loss? Thyroid optimization in hypothyroid patients often allows weight that was gained during untreated hypothyroidism to normalize — particularly when metabolic rate returns to normal. It is not a weight loss drug, but correcting thyroid function removes a significant metabolic obstacle.
Can diet affect thyroid function? Yes. Gluten has documented associations with Hashimoto's — the molecular similarity between gliadin (a gluten protein) and thyroid tissue (molecular mimicry) may drive autoimmune activity. Many Hashimoto's patients see meaningful antibody reduction on a strict gluten-free diet. Selenium, zinc, and iodine deficiency all impair thyroid hormone synthesis and conversion.
Is thyroid testing different for men and women? The same comprehensive panel applies to both. Thyroid dysfunction is significantly more common in women — particularly Hashimoto's — but men are affected too and are often less likely to be evaluated. The symptoms are the same regardless of sex.
If you have persistent fatigue, weight that won't move, cognitive slowing, hair loss, or cold intolerance — and you've been told your thyroid is normal based on TSH alone — Dr. Katherine Ortiz at DNA Wellness and Longevity Institute in Bonita Springs runs a comprehensive thyroid panel that gives you the full picture, not a single number.
Book your thyroid evaluation → (239) 250-7930 | defynaturalaging.com