Dr. Jack Kruse

HYPOXIA #30: EXOGENOUS USE OF I, Cl, Br CAN CAUSE HYPOXIA

Added 2020-12-10 20:41:27 +0000 UTC

Did you know that arterial blood analysis indicates a frequent incidence of hypoxia in cases of hypothyroidism?

Did you know that a greater longevity has been associated with higher TSH and lower TH levels? The mechanisms underlying TSH/TH differences and longevity remain unknown. The HPT axis plays a pivotal role in growth, development and energy metabolism.

During illness, humans experience a fall in serum thyroid hormones termed the nonthyroidal illness syndrome. An inverse relationship between serum thyroxine (T4) and mortality in critically ill patients has previously been observed, but several controlled trials have reported no benefit or even worsened outcome with thyroid hormone supplementation. This has led to the hypothesis that the nonthyroidal illness syndrome is an adaptive process that promotes survival during life-threatening illness by reducing metabolic rate and energy cost.

This is all about Kleiber's power law. Longevity is always linked with a lower basal metabolic state. This means that hypothyroidism in some cases might be a protective mechanism for poor mitochondrial redox power. In this way, hypothyroidism might be like cataract formation in a blue light toxic person: It is protecting the retina from chronic light abuse.

Kleiber Law states that larger animals have relatively slower metabolisms than small ones. A mouse must eat about a third of its body mass every day not to starve whereas a human can survive on only 2%. The relationship follows a power law: basal metabolic rate (R) is proportional to the ¾ power of an animal's mass (M).

It turns out when we get ill, hypoxia is something our colony of mitochondria do by design to keep is alive until we change the environment to foster wellness.

The hypoxia target gene TGF-β3 stimulates DIO3 transcription (deiodinase), this has caused reseachers to investigate hypoxia as a regulator of D3 gene expression.

Researchers have found that hypoxia induced expression of the D3 gene DIO3 by a hypoxia-inducible factor–dependent (HIF-dependent) pathway.

The crux of the issue is that thyroid hormone availability is under strict temporal, circadian timing, and tissue-specific control by these deiodinases. They react boldly to exogenous Iodine, chlorine, or bromine use.

SCIENCE:

Several tissues that express D3 are known to be hypoxic, including the normal tissues of the human fetus and the ischemic tissues of critically ill patients, but a molecular mechanism for this has not been established. Studies have shown that hypoxia increased D3 mRNA and activity in diverse cell types. Hypoxia-inducible factor (HIF) is the central transcriptional mediator of the cellular response to low oxygen, and hypoxia mimetics such as desferrioxamine (DFO) and CoCl2 were also sufficient to induce D3, indicating a HIF-dependent mechanism. This D3 activity was sufficient to inhibit T3-stimulated metabolic rate in isolated cells and to induce anatomically specific reductions in tissue T3 content and action in an in vivo model of RV hypertrophy. This data reveals a role of D3 in the regulation of local as well as systemic thyroid status during hypoxic-ischemic illness.

D3 activity and mRNA were increased both by hypoxia and by hypoxia mimetics that increase HIF-1.

HIF-1α interacted specifically with the DIO3 promoter, indicating that DIO3 may be a direct transcriptional target of HIF-1. Endogenous D3 activity decreased T3-dependent oxygen consumption in both neuronal and hepatocyte cell lines, suggesting that hypoxia-induced D3 may reduce metabolic rate in hypoxic tissues. Using a rat model of cardiac failure due to RV hypertrophy, researchers found that HIF-1α and D3 proteins were induced specifically in the hypertrophic myocardium of the RV, creating an anatomically specific reduction in local T3 content and action. These results suggest a mechanism of metabolic regulation during hypoxic-ischemic injury in which HIF-1 reduces local thyroid hormone signaling through induction of D3.

Sensory nerve conduction was diminished in 6 of 11 hypothyroid patients and motor conduction in 6 of 15 was studied. Many cases of hypothyroidism are found because of peripheral neuropathy like symptoms. Hypoxia symptoms are also present in many of these patients.

In distal segments of sensory nerves, the abnormality frequently appeared before clinical symptoms of polyneuropathy. Visual field defect was detected in 71% of patients suffering of primary hypothyroidism. The most common characteristic sensory change in hypothyroid patients was the defect in the central visual field. In this situation, most cases of visual field defect can be cured by thyroid hormone replacement therapy.

Using exogenous iodine to excess can cause clinical hypothyroidism. The use of chloronated and brominated water or food stuffs can also cause it.

CITES:

Langton J.E., Brent G.A. Nonthyroidal illness syndrome: evaluation of thyroid function in sick patients. Endocrinol. Metab. Clin. North Am. 2002;31:159–172.

Kaptein E.M., Weiner J.M., Robinson W.J., Wheeler W.S., Nicoloff J.T. Relationship of altered thyroid hormone indices to survival in nonthyroidal illnesses. Clin. Endocrinol. (Oxf.). 1982;16:565–574.

Brent G.A., Hershman J.M. Thyroxine therapy in patients with severe nonthyroidal illnesses and low serum thyroxine concentration. J. Clin. Endocrinol. Metab. 1986;63:1–8.

Acker C.G., Singh A.R., Flick R.P., Bernardini J., Greenberg A., Johnson J.P. A trial of thyroxine in acute renal failure. Kidney Int. 2000;57:293–298.

De Groot L.J. Dangerous dogmas in medicine: the nonthyroidal illness syndrome. J. Clin. Endocrinol. Metab. 1999;84:151–164.

Visual field defects and pituitary enlargement in primary hypothyroidism.Yamamoto K, Saito K, Takai T, Naito M, Yoshida S.J Clin Endocrinol Metab. 1983 Aug;57(2):283-7. doi: 10.1210/jcem-57-2-283.PMID: 6408109