Selenium and acquired resistance to thyroid hormone

[MEguy]

Has this got anything to do with the DIOdinase 2 genetic defect does anyone know?

sciencedirect.com/science/a...

[jimh111]

I don't think it has anything to do with DIO2 polymorphisms (they are not genetic defects, just natural variations like hair colour).I posted about this earlier this year so you can look at these replies. healthunlocked.com/thyroidu... .

Unfortunately, I have a nasty cold so don't have the energy to look at it again.

[radd]

MEguy,

Your paper is saying selenium transporter auto-Abs disturb selenium’s transportation but also negatively affect the making of thyroid hormone, the conversion to T3 and then to ATP (energy) through intracellular selenium deficiency. This is because the three deiodinases that are enzymes responsible for thyroid hormone activation/deactivation are ‘selenoproteins’ meaning they are selenium dependant for biosynthesis.

The deiodinase type 2 (DIO2) genetic mutation is a separate issue, and a selenium malfunction/deficiency would alter deiodinase behaviours whether the mutation was present or not. The DIO2 mutation is often only a small part of the thyroid puzzle, as does not guarantee whole dysfunction (as other genetics will be compensating) but offers indication of probability, and must be considered in context with symptoms and tolerated thyroid hormone replacement meds.

Your paper also touches on the importance of the selenium:iodine ratio suggesting a selenium issue can cause hypothyroidism from other angles. Also glutathione (master antioxidant) is dependant upon selenium which has its own antioxidant properties, and deficiencies of either may lead to damaged tissues and DNA, risking inflammation and possible autoimmunity. The forum already knows that supplementing selenium has been shown to reduce thyroid antibodies.

We all naturally have auto-antibodies that sometimes never disclose a presence or obviously through symptoms, obscure labs and possibly assay interference. Ab’s by their very nature are a form of inflammation and we know chronic inflammation drives further, hence the tendencies to develop more than one autoimmune condition. Your paper indicates selenium transporter Ab’s also instigate other inflammatory cytokines.

We always want a reason for our hypothyroidism but even with positive Hashi TPOAb and/or TGAb’s this isn’t necessarily the whole cause. An atrophied thyroid gland is now known to evidence blocking TRAb’s and I was shocked by my BH thyroid genetic results which showed multiple impairments within the thyroid hormone/TSH associated genes. My consolation was other members results showed similar indicating these are contributory factors resulting in hypothyroidisms perfect storm, eg inadequate amounts of incorrectly utilised thyroid hormones.

Because thyroid hormones drives metabolism to have a deficiency/dysfunction means it influences every bodily system from iron metabolism, liver function and gut motility. Therefore, I have found my own DIO2 impairments performance to have improved (epigenetics) as once we find the correct med(s) the positive effects become cumulative. The true definition in research circles of thyroid hormone resistance is mutations on the thyroid hormone receptor gene that leads to impaired sensitivity. However, if is often also used to describe thyroid hormones not working well due to other causes.

Great paper! Thank you.

[MEguy in reply to radd]

Thanks radd, I understand now. Thanks