IV vitamin C and vitamin E was found to lower the mortality rate in those with critical illness at the 28 day mark. This study showed the safety and efficacy of IV vitamin C and vitamin E in those critically ill.
critical illness is associated with low TSH, reduced T3, and increased rT3 production. Inflammation is critically involved in this process. This study from JCEM shows how unreliable TSH and T4 are.
These observed changes, in correlation with a low T(3)/rT(3) ratio, may represent tissue-specific ways to reduce thyroid hormone bioactivity during cellular hypoxia and contribute to the low T(3) syndrome of severe illness.
Significant suppression of serum concentrations of 3,5,3'-triiodothyronine (T3) and elevation of serum concentrations of 3,3',5'-triiodothyronine (rT3) were seen
Critically ill patients found to be depleted in glutathione, vitamin C, Zinc, and too a lesser extent: vitamin E. The obvious treatment would be to replace those identified deficiencies
A good biomarker of intracardiac TH signaling would be helpful but has not been identified. In the absence of such a marker,
a rational, cautious therapeutic approach might be to restore and maintain over time biochemical euthyroidism as documented
by normal circulating levels of TSH, FT4, and FT3.
a low-T3 state resulting from altered peripheral TH metabolism secondary to caloric restriction is associated
with impaired cardiac contractility
Low-T3 syndrome is the central finding and defines the illness in a variety of acute and chronic severe nonthyroidal illnesses
with cardiac origin, including MI, HF, and surgically treated cardiac disease.1 Low circulating levels of T3 in the absence of primary thyroid hypofunction have been found in 20% to 30% of patients with
dilated cardiomyopathy.
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.
Is there something here missed on the authors. If one had ill intentions, could one not recommend a pregnant mother as the ideal candidate to program, or reprogram the offspring. Changes induced to F2 are called inter generational inheritance.