Heather said:Hi everyone.
I'm wondering if anyone here knows the best way to approach Hashimoto's disease. In my last blood test my Anti Thyroglobulin antibodies are high, as is Thyroid Peroxidase, TPO. My doctor suggested it's Hashimoto's, and I'm doing more blood work probably next week.
I'm re-reading Brownstein on this but if someone here is experienced in this area I'd appreciate a head's up. I suffer from this cloudy brain syndrome, which makes more technical type research a bit difficult and overwhelming at times.
I did do a 24 hour urine test for iodine and I'm not as deficient in iodine as I would have thought. You want to see 90% of the 50 mg Iodoral tablet returned in the urine and mine was 83%. Not nearly as bad as I thought.
I have taken some Iodoral off and on in the past -- not a great deal though. I'm holding off until I understand better what I need to do.
I just found someone by the name of Dr. Richard Hagmeyer on Youtube. His website states too much iodine can be an underlying cause of Hashimoto's, whereas Brownstein states the opposite.
Anyway, I will continue looking into it, but if anyone here has some experience with this I'd be grateful for some advice.
I am not an expert in this but since I have read Dr Brownstein book before I started iodine, one idea came to my mind.
I dont know if you are supplementing with Selenium. If not , then you should start.
See the articles bellow:
_https://www.ncbi.nlm.nih.gov/pubmed/11932302
In areas with severe selenium deficiency there is a higher incidence of thyroiditis due to a decreased activity of selenium-dependent glutathione peroxidase activity within thyroid cells. Selenium-dependent enzymes also have several modifying effects on the immune system. Therefore, even mild selenium deficiency may contribute to the development and maintenance of autoimmune thyroid diseases. We performed a blinded, placebo-controlled, prospective study in female patients (n = 70; mean age, 47.5 +/- 0.7 yr) with autoimmune thyroiditis and thyroid peroxidase antibodies (TPOAb) and/or Tg antibodies (TgAb) above 350 IU/ml. The primary end point of the study was the change in TPOAb concentrations. Secondary end points were changes in TgAb, TSH, and free thyroid hormone levels as well as ultrasound pattern of the thyroid and quality of life estimation. Patients were randomized into 2 age- and antibody (TPOAb)-matched groups; 36 patients received 200 microg (2.53 micromol) sodium selenite/d, orally, for 3 months, and 34 patients received placebo. All patients were substituted with L-T(4) to maintain TSH within the normal range. TPOAb, TgAb, TSH, and free thyroid hormones were determined by commercial assays. The echogenicity of the thyroid was monitored with high resolution ultrasound. The mean TPOAb concentration decreased significantly to 63.6% (P = 0.013) in the selenium group vs. 88% (P = 0.95) in the placebo group. A subgroup analysis of those patients with TPOAb greater than 1200 IU/ml revealed a mean 40% reduction in the selenium-treated patients compared with a 10% increase in TPOAb in the placebo group. TgAb concentrations were lower in the placebo group at the beginning of the study and significantly further decreased (P = 0.018), but were unchanged in the selenium group. Nine patients in the selenium-treated group had completely normalized antibody concentrations, in contrast to two patients in the placebo group (by chi(2) test, P = 0.01). Ultrasound of the thyroid showed normalized echogenicity in these patients. The mean TSH, free T(4), and free T(3) levels were unchanged in both groups. We conclude that selenium substitution may improve the inflammatory activity in patients with autoimmune thyroiditis, especially in those with high activity. Whether this effect is specific for autoimmune thyroiditis or may also be effective in other endocrine autoimmune diseases has yet to be investigated.
And some more here
_https://academic.oup.com/jcem/article-lookup/doi/10.1210/jcem.87.4.8421