tissue euthyroidism is the net result of multiple steps including conversion of the prohormone T4 into its active metabolite T3, which is ultimately responsible for signaling at the end-organ target level
The circulating and intracellular pools of T3 of treated hypothyroid patients (i.e. devoid of endogenous TH production) depend entirely on the conversion of exogenous l-T4 into T3
The substitution of l-T3 for l-T4 caused a significant weight loss
The substitution of l-T3 for l-T4 caused a significant reduction in lipid parameters
Despite the increase in serum T3, the l-T3 treatment did not cause major changes in cardiovascular or musculoskeletal function, as indicated by the echocardiographic and maximal exercise tolerance tests and DXA studies.
The changes in serum lipid metabolism parameters are similar to the effects observed with drugs approved for the treatment of dyslipidemia
This differential response appears to be limited to the lipid metabolism and SHBG, whereas no differences in indices of insulin resistance were detected. This is remarkable because hyperthyroid states are associated with an increase in hepatic gluconeogenesis (37), and overt thyrotoxicosis is a known cause of secondary diabetes.
TH action is increased in the liver, and the SHBG increase supports this hypothesis
Similarly, no significant differences were observed in blood pressure, heart rate, or endothelial vascular function
In conclusion, the results of this pharmacology, proof-of-concept study indicate that replacement therapy of hypothyroidism with l-T3, compared with l-T4 causes weight loss and favorable changes in the lipid profile without appreciable side effects
Crossover study finds T3 versus T4 results in more weight loss, improved lipid management and increased SHBG without any adverse cardiovascular effects. The T3 was dosed 3 x daily due to its short half life compared to T4.
High serum rT3 may result from a decreased peripheral metabolism of thyroid hormones due to the aging process itself and/or disease and may reflect a catabolic state.
This study points to an association between a low-normal TSH and cognitive decline in the elderly. An association is not causative, but functional hypothyroidism does result in cognitive impairment, so the association would logically fit. The results of this study do as well.
T3 shown increase weight loss, lower LDL, decrease apolipoprotein B, decrease T cholesterol versus T4. This flies in the face of conventional medical dogma, that T 4 (synthroid, levothyroxine) is the only route of thyroid replacement. In fact, this suppports the use of armour thyroid, a T4/T3 combination.
The importance of the recognition of the effects of thyroid disease on the heart also derives from the observation that restoration of normal thyroid function most often reverses the abnormal cardiovascular hemodynamics
Here is an interesting finding: low free T3 is significantly associated with increased cardiovascular and all-cause mortality in 7 prospective study on hospitalized patients.
Low T3 post MI is associated with increased CHF, morbidity and mortality. Article discusses thyroid hormones and cardiac function/remodeling post infarct. The article also lays the ground work for a new study of T3 in patients post MI to be followed for 6 months.