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low T3 associated with poor prognosis in cardiac patients.   Poor prognosis = death.  T3 is important in cardiac remodeling, which is inherently important with cardiac disease.

Fantastic review by Dr. Holtorf on reverse T3, leptin, and weight loss

what a silly study!  They look at free T4, the weakest thyroid hormone and found high levels to be associated with dementia.  However, they failed to assess free T3, the most biologically active, and reverse T3, inactive.  This study was like they intentionally blinded themselves of the body's physiology to study dementia.  This is the problem with a lot of research today: they have forgotten their foundation. Many older adults struggle with poor free T4 to free T3 conversion and high reverse T3 conversion.  So, without knowing what these clients were doing in these pathways makes their conclusion obsolete.

reverse T3 does not block T4 to T3 converson; but occupies T3 receptors and inhibits T3 stimulating receptors

Great review of the current understanding of thyroid hormone metabolism in cardiac tissue.  Low T3 and increased rT3 (via increased D3 activity) is CLEARLY associated with poor cardiac performance and post MI and CHF is associated with poor outcomes.  T3 is critical in cardiac remodeling and recovery post MI.  T3 is actually a vasodilatory in the coronary arteries.   Why a endocrinologist would call rT3 useless only points to their ignorance of the literature.

IV T3 was given to patients with chronic heart failure.  What the study found may surprise you: improved heart function (ventricular), improved BNP, decrease heart rate, no side effects.  T3 has been shown to be more predictive of cardiac death in those with cardiac disease, than elevated lipids or decreased ejection fraction.

T3 in the post MI individual decreases the MI infarct size and the progression to heart failure. What is really  interesting about this study is that the T3 induced mitochondrial biogenesis and activity which is a great thing in recovery of MI and also in disease i.e. cancer.  However, it appears to increase HIF-1alpha and angiogenesis which is stimulated by retrograde signaling.  There is a muddied picture here.  Because T3 stimulates oxidative phosphorylation and mitochondria biogenesis which is favorable for health.  However, in this study of rats, it induced HIF-1alpha and angiogenesis in post MI, which is favorable to recovery, yet this is unfavorable for cancer.    Yet oxidative phosphorylation is favorable to cancer prevention/elimination and MI recovery.

low T3 in sick euthyroid clients; severity correlated with decreasing T3

low free T3: elevated reverse T3 in critically ill patients

low free T3:elevated reverse T3 correlates with major depression and TSH and free T4 do not.

reverse T3 and the free T3:rT3 can be used to assess prognosis of those with CHF.

New study shows that T3 and thyroid hormone agonists reduce LDL.  This is independent that LDL receptors.  Previously, it was thought that T3 increased LDL receptor expression.  But, this study shows that T3 lowers LDL independent of the LDL receptors.  

T3 replacement in people with low T3 and cardiac dysfunction found to improve cardiac performance.

replacement therapy for hypothyroidism must include both T4 and T3

effects of systemic illness on thyroid function: elevated Reverse T3 and low free T3

weight loss in obese children with low TSH and free T3 indicates high risk or regain of weight.  The important value here is the free T3.

T3 increases mitochondrial oxidative phosphorylation. This has huge impacts on which hypothyroidism is currently managed (only evaluate TSH and T4) and disease implication. We know that decoupling of oxidative phosporylation and a shift to glycolysis and glutaminolysis (substrate-level phosphorylation) results in genomic mutability and cancer, then a low T3 has implications in cancer prevention

T3 induces beneficial oxidative changes in muscles through its interaction with mitochondrial receptors.  PGC-1alpha and PPAR-gamma were involved in this process.  The important point here is that T3 is increasing oxidative function of muscle through interaction with mitochondria.

This study finds that T3 increases enzymes in the oxidative phosphorylation pathways and not in the glycolytic pathways in mitochondria.  This has enormous health implications, especially in cancer.  This also casts doubt on the current traditional medical dogma of hypothyroid evaluation and management which gives no regard to T3 in testing or therapy.

oxidative stress decreased type 1 deiodinase activity and thus T4 to T3 conversion, resulting in increased rT3 production.  Of interesting note, Alpha lipoic acid increased type I deiodinase activity and T4 to T3 conversion.