9 Supported by research
T4 is an inactive thyroid hormone, whereas T3 is the active thyroid hormone.
"what she gave me is T4. That's the inactive thyroid hormone. There's there's this active thyroid hormone called T3." (said at 0:05:00)
In standard thyroid endocrinology, thyroxine (T4) is classified as a prohormone, whereas triiodothyronine (T3) is the primary biologically active hormone. T4 is secreted by the thyroid gland and converted in peripheral tissues to active T3 via outer-ring deiodination catalyzed by the iodothyronine deiodinase enzymes DIO1 and DIO2. T3 binds to nuclear thyroid hormone receptors with approximately 10- to 15-fold higher affinity than T4 to mediate canonical genomic actions. While emerging research demonstrates that T4 possesses weak intrinsic receptor activity and non-genomic membrane interactions, it primarily serves as a circulating precursor pool for local and systemic generation of active T3.
Lithium administration causes hypothyroidism.
"And so the lithium on top of it makes you hypothyroid." (said at 0:09:39)
Lithium therapy is well established to cause thyroid dysfunction, significantly increasing the risk of both subclinical and overt hypothyroidism. A comprehensive systematic review and meta-analysis published in The Lancet (McKnight et al., 2012) analyzing randomized controlled trials and observational cohorts found that patients receiving lithium had nearly six times the odds of developing clinical hypothyroidism compared with those receiving placebo (OR 5.78, 95% CI 2.00–16.67, p = 0.001) alongside an average increase in thyroid-stimulating hormone (TSH) of 4.00 iU/mL.
Conventional laboratory reference ranges define normal TSH levels as anywhere between 0.5 and 5.0 mIU/L.
"Like the TSH that they consider normal is anywhere between 0.5 and 5, basically." (said at 0:17:10)
Conventional laboratory reference intervals for thyrotropin (TSH) in non-pregnant adults typically span approximately 0.4 to 4.0–4.5 mIU/L (with some conventional assays and laboratories using cut-offs up to 5.0 mIU/L). The speaker's statement accurately captures the standard clinical reference range commonly used by clinical laboratories.
Natural desiccated thyroid formulations contain a blend of T4, T3, and T2.
"because that's for the people listening, it's a blend. It's a more natural blend of occurring blend, I should say, of T4, T3, and even T2." (said at 0:23:55)
Natural desiccated thyroid (NDT) preparations are manufactured from animal (typically porcine) thyroid glands. Because they are derived from whole glandular tissue rather than synthesized as isolated single molecules, NDT naturally contains a mixture of thyroid hormones and their metabolites, including thyroxine (T4), triiodothyronine (T3), and diiodothyronines (3,5-T2 and 3,3'-T2). Analytical testing using liquid chromatography–tandem mass spectrometry (LC-MS/MS) on thyroid glandular products confirms the presence of quantifiable levels of T4, T3, and T2 metabolites.
- supports: Determination of thyroid hormones in dietary supplements using liquid chromatography-tande… (Drug testing and analysis 2022) · cited 4x in the literature
"In this study, an LC-MS/MS method was developed and validated for the analysis of thyroxine (T4), 3,3',5-triiodo-l-thyronine (T3), 3,3',5'-triiodothyronine (rT3), 3,5-diiodothyronine (3,5-T2) and 3,3'-diiodothyronine (3,3'-T2) in dietary supplements." (abstract, methods, passage verified)
pubmedfull study (doi) - supports: 3,5-T2-an Endogenous Thyroid Hormone Metabolite as Promising Lead Substance in Anti-Steato… (Metabolites 2022) · cited 14x in the literature
"This narrative review focuses on 3,5-T2 effects on hepatic lipid and glucose metabolism and (non-)canonical mechanisms of action including its mitochondrial targets." (abstract, methods, passage verified)
pubmedfull study (doi)
Hypothyroidism causes myxedema, a proteinaceous edema visible in tissues under ultrasound.
"I could see it under ultrasound, Amie. I would actually put my ultrasound probe down and I would get this really foggy picture underneath and it was very difficult to really see the layers of the tissues that you should be able to see clearly. And I started asking all of my mentors in the space, like these old guys that have been doing ultrasound-guided injections forever. And I'm like, "Are you guys seeing hypothyroidism on on ultrasound?" And they were like, "What are you talking about?" I'm like, "It's myxedema. It's this proteinaceous edema and it's it's under the probe. I can see it."" (said at 0:14:03)
Hypothyroidism causes myxedema, a non-pitting edema characterized by the deposition of glycosaminoglycans and mucopolysaccharides (protein-carbohydrate complexes) in the skin and subcutaneous tissues. Published ultrasonographic studies of myxedematous skin lesions demonstrate distinct sonographic changes, including increased dermal and subcutaneous thickness, hypoechoic substance accumulation, and blurring/loss of definition of the anatomical boundaries between tissue layers, matching the host's description.
Hashimoto's thyroiditis causes the thyroid gland to appear jagged and smaller on ultrasound imaging.
"Like we can see it on ultrasound. It starts looking like Pac-Man attacked it, like jagged. It gets smaller." (said at 0:36:46)
Ultrasonographic imaging of Hashimoto's thyroiditis (chronic lymphocytic thyroiditis) characteristically demonstrates diffuse parenchymal heterogeneity, hypoechogenicity, and micronodularity/pseudonodularity separated by fibrous bands, which gives the thyroid gland an irregular, lobulated, or 'moth-eaten' appearance. Additionally, progressive autoimmune destruction of follicles and advancing fibrosis often lead to thyroid atrophy (volume reduction/shrinkage) in long-standing disease.
Patients can have autoimmune Hashimoto's thyroiditis with seronegative antibody test results.
"There are conditions—it's called seronegative antibodies—that we'll see a zero, but we know that that person has autoimmunity." (said at 0:40:00)
Published clinical and histopathological studies confirm that autoimmune thyroiditis (Hashimoto's thyroiditis) can occur in the absence of detectable circulating thyroid autoantibodies (anti-thyroperoxidase and anti-thyroglobulin antibodies), a condition recognized in the medical literature as seronegative autoimmune thyroiditis. In these patients, characteristic autoimmune lymphocytic infiltration of the thyroid gland and localized intrathyroidal autoantibody production can be present despite negative peripheral blood antibody assays.
- supports: Serum negative autoimmune thyroiditis displays a milder clinical picture compared with cla… (European journal of endocrinology 2014) · cited 53x in the literature
"Despite high sensitivity of current assays for autoantibodies to thyroperoxidase (TPO) and to thyroglobulin (Tg), some hypothyroid patients still present with negative tests for circulating anti-thyroid Abs. These patients usually referred to as having seronegative autoimmune thyroiditis (seronegative CAT) have not been characterized, and definite proof that their clinical phenotype is similar to that of patients with classic chronic autoimmune thyroiditis (CAT) is lacking." (abstract, background, passage verified)
pubmedfull study (doi) - supports: Seronegative Hashimoto thyroiditis with thyroid autoantibody production localized to the t… (Annals of internal medicine 1988) · cited 86x in the literature
"These studies show that lymphocytes capable of producing antithyroid antibodies can be present in the thyroid glands of patients with Hashimoto disease without evidence of a peripheral immune response, thus indicating that Hashimoto disease can exist as an organ-restricted autoimmune disorder." (abstract, conclusions, passage verified)
pubmedfull study (doi) - supports: Serum-negative chronic thyroiditis: an insidious nosographic entity cause of hypothyroidis… (Endocrine 2025) · cited 3x in the literature
"These results show that chronic serum-negative thyroiditis represents a nosographic entity, comparable to antibody-positive chronic thyroiditis and statistically correlated to an increase of post-operative hypoparathyroidism and pre-operative hypothyroidism." (abstract, conclusions, passage verified)
pubmedfull study (doi)
Nature-Throid is composed of 80% T4 and 20% T3.
"Dr. Tyna said when she was on Nature-Throid, that's 80% T4 and 20% T3." (said at 0:44:20)
Desiccated thyroid extract (DTE) formulations like Nature-Throid and Armour Thyroid adhere to USP specifications standardized to approximately 38 mcg of levothyroxine (T4) and 9 mcg of liothyronine (T3) per grain (65 mg). This corresponds to a T4:T3 weight ratio of approximately 4.22:1, which equates to roughly 81% T4 and 19% T3 (commonly referred to as an 80/20 ratio).
Active skeletal muscle is a major site for the conversion of T4 into active T3.
"And your muscle is a huge conversion site. Active skeletal muscle is a huge conversion site of T4 into the active form of T3." (said at 0:52:44)
Human kinetic and enzymatic modeling indicates that skeletal muscle, via type 2 iodothyronine deiodinase (D2), is the primary tissue responsible for extrathyroidal conversion of thyroxine (T4) into the active triiodothyronine (T3) pool in euthyroid individuals. Furthermore, experimental exercise studies demonstrate that physical activity directly increases D2 expression and enzymatic activity in skeletal muscle, accelerating local T4-to-T3 conversion.
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