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Thyroid hormone deficiency affects all tissues of the body, including multiple endocrine changes that alter growth hormone, corticotrophin, glucocorticoids, and gonadal function. Primary hypothyroidism is associated with hypogonadotropic hypogonadism, which is reversible with thyroid hormone replacement therapy. In male children follicle-stimulating hormone (FSH) is elevated and associated with testicular enlargement without virilization. Men with primary hypothyroidism have subnormal responses of luteinizing hormone (LH) to gonadotropin-releasing hormone (GnRH) administration and normal response to human chorionic gonadotropin (hCG). Free testosterone concentrations are reduced in men with primary hypothyroidism and thyroid hormone replacement normalizes free testosterone concentrations. In men with primary hypothyroidism, prolactin is not consistently elevated (except in men and children with longstanding severe primary hypothyroidism), but prolactin declines following thyroid hormone replacement therapy. Thyroid hormone is known to affect sex hormone-binding hormonal globulin (SHBG) concentrations. Men with hyperthyroidism have elevated concentrations of testosterone and SHBG. Thyroid hormone therapy in normal men may also duplicate this elevation. In addition estradiol elevations are observed in men with hyperthyroidism, and gynecomastia is common in them as well. In contrast to patients with primary hypothyroidism, men with hyperthyroidism exhibit hyperresponsiveness of LH to GnRH administration and subnormal responses to hCG. Radioactive iodine therapy (RAI) of men treated for thyroid cancer produces a dose-dependent impairment of spermatogenesis and elevation of FSH up to approximately 2 years. Permanent testicular germ cell damage may occur in men treated with high doses of RAI. RAI commonly increases serum concentrations of FSH and LH while reducing inhibin B levels without affecting serum concentrations of testosterone. Thus, radioiodine therapy transiently impairs both germinal and Leydig cell function that usually recover by 18 months posttherapy.
What so many people also fail to realize is theres a direct correlation between optimal thyroid function and just about every other process in the body. Time and time again I see people complain of low T and when I ask about the thyroid they say "my doc said its fine"....bullshit! Fine for the doctor means you are not clinically hypo or hyper (ie you lab results are in range). But that does NOT mean its functioning optimally. Iodine (and essential nutritional partners) are what the body needs for optimal thyroid function.
Think of it like a muscle and how strong you were back when you started lifting. You were healthy and could move around, feed yourself etc, you were FINE! But now after some time in the gym, you are a lot stronger, more athletic. Thats the difference between "clinically fine" and "optimal".
The relationship between thyroid function and sex hormones is fairly well documented. Here is one of many such abstracts on it. Please note that at the end they comment on radioiodine therapy and how its detrimental, and it is, but the negative results that RADIOACTIVE iodine and other improper forms of iodine has on the body is what has the medical community scared off. When I talk about iodine supplementation I am talking about inorganic, non-radioactive iodine supplementation.
Earlier in this thread you mentioned the importance of not only supplementing with Iodine, but also Boron and Selenium.. Are the other two a must have when going through the therapy?
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If you supplement selenium without adequate iodine or iodine without adequate selenium you will have problems so those two should be supplemented together. Boron you can skip but it really is one of the often overlooked supplements.