Learner1
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Back to the topic of this thread, and studies like @debored13 has been posting:
Replacement therapy with levothyroxine plus triiodothyronine (bioavailable molar ratio 14 : 1) is not superior to thyroxine alone to improve well-being and cognitive performance in hypothyroidism.
Severe TSH Elevation and Pituitary Enlargement After Changing Thyroid Replacement to Compounded T4/T3 Therapy.
I've been going through my GeneDX WES and 23andme chip 4 data using Enlis. What I've learned points out the ridiculousness of these studies.
Turns out there are several genes that affect how thyroid hormones are regulated, and various mutations in each, many of which are pretty common, can be implicated in "thyroid dyshormonogenesis," aka disregulated thyroid hormones.
These include genes that give one normal TSH when one is hypothyroid, genes that give you high T4 and low T3 and vice versa, problems with iodine binding, tyrosine metabolism, TSH resistance, problems in the ER and Golgi apparatus, and those implicated in Hashimotos, Graves disease, and papillary thyroid cancer.
In total, I found I have over 200 altered SNPs, deletions, frame shifts, and missense mutations on 14 different genes, with about 15% of these rare or novel mutations.
I am hard pressed to believe that this is that uncommon, that is, it's highly likely that everyone has a different pattern of these mutations, which could lead to a wide variation in how we assimilate and metabolize iodine and tyrosine, produce and metabolize the various pituitary and thyroid hormones, and develop and experience autoimmune thyroid disease, goiters and thyroid cancers.
The takeaway, therefore, is that, while these studies may be interesting reading to contemplate, unless patients in them are grouped by these genetic factors, iodine and tyrosine status, and beginning and historical rT3, FT3, FT4, TSH, and antibody titers, one cannot deduce whether the data is meaningful or useful to make decisions for any given patient. Its a highly personalized set of variables...
Replacement therapy with levothyroxine plus triiodothyronine (bioavailable molar ratio 14 : 1) is not superior to thyroxine alone to improve well-being and cognitive performance in hypothyroidism.
Severe TSH Elevation and Pituitary Enlargement After Changing Thyroid Replacement to Compounded T4/T3 Therapy.
I've been going through my GeneDX WES and 23andme chip 4 data using Enlis. What I've learned points out the ridiculousness of these studies.
Turns out there are several genes that affect how thyroid hormones are regulated, and various mutations in each, many of which are pretty common, can be implicated in "thyroid dyshormonogenesis," aka disregulated thyroid hormones.
These include genes that give one normal TSH when one is hypothyroid, genes that give you high T4 and low T3 and vice versa, problems with iodine binding, tyrosine metabolism, TSH resistance, problems in the ER and Golgi apparatus, and those implicated in Hashimotos, Graves disease, and papillary thyroid cancer.
In total, I found I have over 200 altered SNPs, deletions, frame shifts, and missense mutations on 14 different genes, with about 15% of these rare or novel mutations.
I am hard pressed to believe that this is that uncommon, that is, it's highly likely that everyone has a different pattern of these mutations, which could lead to a wide variation in how we assimilate and metabolize iodine and tyrosine, produce and metabolize the various pituitary and thyroid hormones, and develop and experience autoimmune thyroid disease, goiters and thyroid cancers.
The takeaway, therefore, is that, while these studies may be interesting reading to contemplate, unless patients in them are grouped by these genetic factors, iodine and tyrosine status, and beginning and historical rT3, FT3, FT4, TSH, and antibody titers, one cannot deduce whether the data is meaningful or useful to make decisions for any given patient. Its a highly personalized set of variables...