T3 (Triiodothyronine)

T3 (triiodothyronine) is the metabolically active derivative of thyroxine, the hormone that directly promotes respiration and energy production in virtually all tissues. 3 Peat identified T3 as the basic anti-stress hormone, a co-factor for cellular energy production whose presence reinforces the organism's structure and function. 4 While the thyroid gland secretes a small portion of active T3, approximately 70% is produced in the liver through the enzymatic conversion of thyroxine (T4), a process that depends critically on the availability of glucose and allows metabolism to be sensitively adjusted to nutritional status. 3

The distinction between T3 and its pro-hormone T4 is central to Peat's critique of modern thyroid therapy. Peat argued that T4 alone, when administered to women or stressed individuals, often fails to restore metabolism because it can suppress the pituitary's thyroid-stimulating hormone and shut off the gland's own T3 output without being adequately converted to the active hormone in the liver. 7 He cited experiments showing that T4 added to brain, heart, and muscle tissue suppressed oxidative metabolism, while T3 universally increased respiration. 2 This conversion block is frequently driven by estrogen, which interferes with liver function and shifts metabolism toward fatty acid oxidation, wasting oxygen and preventing T4-to-T3 conversion. 10 Consequently, Peat observed that women are about five to ten times more likely to have thyroid problems than men, and that a physiological mixture of T3 and T4—imitating the gland's natural secretion ratio—is the most practical therapeutic approach. 2

The biological activity of T3 is not reliably indicated by standard lab measurements. Peat stressed that free T3 is a laboratory concept, and that T3 bound to its transport proteins, particularly transthyretin, can demonstrably enter cells, mitochondria, and nuclei. 5 Because T3's actions can be inhibited by polyunsaturated fatty acids, reverse T3, and excess thyroxine, the absolute serum level of T3 cannot be used alone for diagnosis. 5 Reverse T3 partly occupies the same response sites as active T3, competing against it, and can accumulate when local clearing enzymes are blocked by stress substances. 11 Peat instead recommended functional assessments: T3 promotes rapid cholesterol utilization, so serum cholesterol rises in hypothyroidism; it prevents unnecessary lactic acid production, making blood lactate a useful marker; and it regulates serum sodium, magnesium, calcium, and glucose. 5 He also noted that a person's temperature and pulse rate before and after T3 administration reveal whether it is affecting metabolic rate. 1

Therapeutic T3 use requires attention to dosage, ratio, and route. Peat noted that a typical effective oral dose is 5 mcg of T3 with each meal, and that the half-life of T3 is only about 12 hours to a day, compared to T4's two-week half-life, meaning TSH changes can occur within hours of T3 supplementation. 2 The optimal ratio of T3 to T4 varies by individual; those under estrogenic or stress-induced conversion blocks often do better on higher T3 ratios such as 1:2 or 1:1, and Georgi Dinkov has reported preferring a ratio closer to 3:1 by supplementing additional T3. 10 Topically applied T3 can be very beneficial for rashes and other skin problems, with local concentration remaining high if the solution penetrates about half a centimeter before dilution by blood, though Peat doubted enough would be absorbed to correct general hypothyroidism. 2 T3 is also the precursor for pregnenolone, produced from active thyroid hormone, cholesterol, and vitamin A in the mitochondria, positioning T3 as foundational to all downstream steroid hormone synthesis. 2