The dangers of Low T3

At the heart of much supposed “controversy” in endocrinology is the role of T3 thyroid hormone testing and T3-based treatments for hypothyroidism.

Perpetuating this “controversy” is the continual restatement in research articles that T3 and T4-T3 combination therapy (of which Natural Dessicated Thyroid is a sub-type) is a “controversy.” Repeatedly saying it is controversial only serves to reinforce the controversy and dismisses it, if the persons stating it are not doing anything to resolve it.

Meanwhile, clinical practice shows little sign of an actively debated controversy. Most doctors conform to the T4-only recommendations for best practice because they are easy and cheap.  Adjusting Synthroid dosage to TSH levels to “normalize the TSH” has turned into a simple game of numbers that leaves many hypothyroid patients symptomatic and at risk.

As I show in my review of a journal article by Abdalla & Bianco (2014), biology teaches that a healthy plasma T3 level must be defended, and the TSH cannot be trusted to indicate adequate T3 levels.

The dangers of low-T3 in any patient can be logically hypothesized from many studies of “Low T3 Syndrome” and “Sick Euthyroid Syndrome” and “subclinical hypothyroidism”

A recent journal article (Rhee, et al, 2015) included a table outlining the associations between Low T3 and morbidity/mortality:

From Rhee’s Table 3: Studies of thyroid functional disease…

I’ve selected just the T3 findings:

Cardiovascular surrogates

  • Jaroszynski (2005):  Low FT3 (Delayed ventricular depolarization measured by signal-averaged EKG
  • Zoccali (2006): Low FT3 (in lowest tertile) = Decreased left ventricular systolic function and increased left ventricular mass; estimates attenuated to null with adjustment for IL-6 and serum albumin
  • Tatar (2011): Low FT3 (in lowest tertile) = Carotid artery atherosclerosis and increased arterial stiffness
  • Yilmaz (2011): Low FT3 (< median) = Impaired flow-mediated vasodilation
  • Meuwese (2013): Low FT3 (< median) = Increased vascular calcification

Mortality

  • Zoccali (2006): Low FT3 (tertiles) = Increased all-cause mortality
  • Enia (2007): Low FT3 (tertiles) = All-cause mortality
  • Carrero (2007): Low TT3 (<= 78.5ng/dL) = Increased all-cause and cardiovascular mortality with low TT3 but not FT3
  • Fernandez-Reyes (2010): Low FT3 (tertiles) = No association with all-cause mortality
  • Ozen (2010): Low FT3 (tertiles) AND Low FT3 syndrome [FT3 < 1.71 pg/mL + TSH normal (ref. range: 0.35–4.94 μIU/mL) + FT4 level normal or low (ref. range 0.71–1.85 ng/dL)] = Increased all-cause mortality; estimates attenuated to null with concurrent adjustment for serum albumin and CRP
  • Horacek (2012): Low TT3 [< 1.0 nmol/L (ref. range 1.0–3.0 nmol/L)] = Increased all-cause mortality
  • Lin (2012): Subclinical hypothyroidism, Overt hypothyroidism, and Sick euthyroid syndrome = Increased all-cause mortality
  • Meuwese (2012): Low TT3 (< 66th percentile) = Low TT3 and T4 (basal and persistently low) associated with increased all-cause and
    cardiovascular mortality
  • Yang (2012): Low T3 [< 0.60 ng/mL + TSH normal (ref. range 0.35–5.50 μIU/mL)] = Increased all-cause and cardiovascular
    mortality
  • Meuwese (2013): Low FT3 (Increased all-cause mortality

More recent additions to Rhee’s Table:

  • High cholesterol.  As explained by Jaseem, et al (2015), “T3 regulates lipids” by means of enzymes that control metabolism, catabolism, and oxidization of LDL and HDL. Normal levels of T3 “stimulate lipoprotein lipase . . . and hepatic lipase” which increase clearance of TG-rich cholesterol on the one hand, and reduce catabolism of HDL on the other hand. (p. 5) Therefore, lower levels of T3 mean that more LDL cholesterol is produced and less of it is cleared out of the body.
  • Vasoconstriction, decreased cardiac output, endothelium damage, hypertension, diastolic dysfunction, loss of coronary arterioles, bradycardia – “cardiac symptoms connected to … insufficiency of T3” (Potempa & Jonczyk, 2015).

In general, research shows there are serious long-term risks for Low-T3 status regardless of a TSH within range. It is not generally high TSH, but low T3, that creates the tissue hypothyroidism.

References

Jaseem, T., Hegde, A., Manjrekar, P. A., Mahabala, C., Rao, S., & Rukmini, M. S. (2015). Effect of High Normal Thyroid Stimulating Hormone Levels on Lipid Parameters in Non-diabetic Subjects. British Journal of Medicine and Medical Research, 9(10), 1.

Potempa, M., & Jonczyk, P. (2015). Heart Follows Thyroid. Biology and Medicine, 7(5), 1. http://doi.org/10.4172/0974-8369.1000255

Rhee, C. M., Brent, G. A., Kovesdy, C. P., Soldin, O. P., Nguyen, D., Budoff, M. J., … Kalantar-Zadeh, K. (2015). Thyroid functional disease: an under-recognized cardiovascular risk factor in kidney disease patients. Nephrology Dialysis Transplantation, 30(5), 724–737. http://doi.org/10.1093/ndt/gfu024

Tatar, E., Kircelli, F., Asci, G., & Carrero, J. J. (2011). Associations of triiodothyronine levels with carotid atherosclerosis and arterial stiffness in hemodialysis patients. Clinical Journal of the American Society of Nephrology : CJASN, 6(9), 2240.

Tatar, E., Sezis Demirci, M., Kircelli, F., & Gungor, O. (2012). The association between thyroid hormones and arterial stiffness in peritoneal dialysis patients. International Urology and Nephrology, 44(2), 601. http://doi.org/10.1007/s11255-011-0034-7

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