Thyroid Gland: an endocrine gland located in the anterior neck which consists of two lobes connected by an isthmus. The thyroid tissue within the gland is comprised of spherical structures called " thyroid follicles". "Follicular cells will form the borders of the follicles and a substance called "colloid" is located within the follicles. The follicular cells contain TSH-receptors, which when stimulated will synthesize thyroid hormones (T3 and T4). The thyroid will produce 80% T4 and 20% of T3. Most of the T3 originates from the conversion of T4 to T3 in peripheral tissues in a process called deiodination.
Thyroid Stimulating Hormone (TSH): a hormone released from the anterior pituitary lobe in response to TRH (Thyrotropin Releasing Hormone, which is synthesized and released by the hypothalamus. TSH will stimulate the thyroid cells to synthesize T3 (triiodothyronine) and T4 (thyroxin). TSH is the one of the routine labs I will draw on your first visit, and this hormone is by far the most important one, as it is the most sensitive and specific marker of thyroid function. One important caveat is that TSH will spike in the AM, we call this the "TSH-circadian spike", so if your labs are drawn in the AM, and the TSH is high, I will likely redraw them after 12:00 noon, before initiating any treatment. Oftentimes, the TSH level will be significantly lower in the afternoon and I don't want to start any medicines that are not absolutely necessary.
Thyroxin (T4): a thyroid hormone released from they thyroid gland in response to TSH. Free T4 is the active form of T4 that enters into cells all over the body to regulate your metabolism. Metabolism is measured in calories. Free T4 is one of the routine labs I will draw on your first visit. The half-life of T4 is long, about 4-6 days and for this reason, it is a relatively good marker of your thyroid function.
Triiodothyronine (T3): a thyroid hormone released from they thyroid gland in response to TSH. Free T3 is the active form of T3 that enters into cells all over the body to regulate your metabolism. I will also draw a total T3 as well as a free T3 during your first visit. However, it is important to remember the T3s are not as important markers of thyroid function, as compared to TSH and Free T4, namely because the half-lives are so much shorter (between 6 hrs to one day), so levels of this hormone will be wax and wane much more rapidly as compared to levels of TSH and T4.
Primary HYPOthyroidism: this diagnosis is made when the patient has HIGH blood levels of Thyroid Stimulating Hormone (TSH) and LOW or LOW-normal levels Free T4.
Subclinical HYPOthyroidism: this diagnosis is made when the patient has HIGH or HIGH-normal levels of TSH with normal levels of Free T4.
Central (Secondary) HYPOthyroidism: this diagnosis is made when the patient has LOW or LOW-normal levels of T3 and T4 and the TSH level is not appropriately elevated..
Autoimmune Thyroiditis: a condition in which a person's body makes antibodies against proteins that are part of the person's own thyroid tissue; these are called "auto-antibodies".
Hashimoto's Thyroiditis: a condition were there is inflammation within the thyroid tissue due to auto-antibodies, most often anti-thyroid peroxidase antibodies (anti-TPO Abs) or anti-thyroglobulin antibodies (anti-TG Abs). The inflammation is caused by lymphocytes infiltrating the thyroid tissue, which will eventually cause the thyroid cells to die causing HYPOthyroidism. We don't know why this happens, but most likely there is a combination of environmental factors and a genetic predisposition.
HYPERthyroidism: this diagnosis is made when the patient has LOW blood levels of Thyroid Stimulating Hormone (TSH) and HIGH or HIGH-normal levels Free T4.
Graves' Disease: an autoimmune thyroiditis and the most common cause of HYPERthyroidism. The pt will make Thyroid Stimulating Immunoglobulins (TSIs) also called TSH-receptors antibodies. These autoantibodies will bind to the TSH-receptor sites located on the follicular cells within the thyroid gland and over stimulate the production of T3 and T4.
Thyroid Function Tests (TFTs): laboratory tests that are done to diagnose thyroid conditions. The most common tests I will ask for are: TSH, FT4, T3 (total and Free), anti-TPO antibodies, anti-TG antibodies, and/or Thyroid Stimulating Immunoglobulins (TSIs).
Thyroid-Binding Globulins: proteins that bind T4 and T3 to transport the hormones through the blood. More than 99.95 % of T4 and 99.5 % of T3 are tightly bound to proteins in the blood, a very small percentage of these hormones are "Free"; only free hormones are metabolically active.
Thyroglobulin: is a protein found inside the lumen of the thyroid follicles (circular structures within the thyroid tissue). Follicular cells form the borders of the follicles and contain receptors for TSH. When the TSH-receptors are stimulated by TSH (or at times by TSIs), thyroid hormones (T3 and T4 )will be synthesized within the follicles and then released into the blood stream. The thyroglobulin protein serves a a substrate for the synthesis of T3 and T4.
Thyroid Stimulating Immunoglobulins (TSIs): antibodies made to the TSH-receptors located on the follicular cells within thyroid tissue. TSI's are also called "TSH-receptor antibodies". They are the most common auto-antibodies found in Graves' Disease. The overstimulation of the TSH-receptors and subsequent over-production of thyroid hormones is the underlying cause of Graves' Disease.
Anti-thyroid peroxidase antibodies (anti-TPO Ab): antibodies made against thyroid peroxidase, which is an enzyme that catalyzes the synthesis of the thyroid hormones which takes place within the thyroid tissue. Note: there is a percentage of the normal population (ie: persons without thyroid disease) who have small amounts of anti-TPOs in their blood (generally less than 50 IU/ml) who will never develop thyroid disease at all. Whereas, patients with anti-TPOs greater than 50 IU/ml typically do eventually develop hypo or hyperthyroidism. The presence of more robust anti-thyroid antibodies indicates the pt's immune system is recognizing something in their normal healthy thyroid tissue as "abnormal" and their immune system is mounting a response to attack the tissue
Anti-Thyroglobulin antibodies (anti-TG Ab): antibodies are made against the person's own thyroglobulin protein. Anti-TG Abs are found in about 70% of the time in Hashimoto's thyroiditis, 60% of idiopathic thyroiditis, 30% of Graves' disease, and about 3% of thyroid cancers.
Tidbit: Early on in my NaPro practice, I used to routinely check for anti-TPOs. However, most often after a dialogue, the patients preferred to watch and wait to see if the more important thyroid function tests (TSH/FT4) became abnormal over time. It was exceptionally common to see patients with completely normal TSH/FT4 levels with mildly elevated anti-TPOs. Giving a diagnosis of "Hashimoto's Thyroiditis" in such settings seemed to cause more harm than good. Additionally, giving Synthroid (levothyroxine) even in small doses can have some unwanted side effects, eg: hair loss, insomnia, anxiety, irritability.
Iodine: Iodine is obtained only by diet. It can be found in iodized salt (not sea salt), seafood, seaweed, kelp, dairy products and some vegetables. The easiest way to ensure you have adequate iodine intake is by just using iodized salt.
I do not recommend any iodine drops or supplements. Supplements, in general, are not regulated, and it has been demonstrated numerous times that ingredients do not accurately reflect what the bottles claim the do. I have personally seen iodine 8x the upper limit in a pt who was taking iodine drops recommended by a holistic practitioner. Too much iodine puts the pt at risk of "Iodine-Induced Thyroiditis", which can be life-threatening in some individuals.
- This is an image of what thyroid gland tissue looks like under a microscope.
- Notice the thyroid follicles, which are circular structures.
- Follicular cells form the borders form the follicles. The follicular cells have TSH receptors on them.
- When the TSH receptors are filled, the synthesis of T4 and T3 ensues.
- Thyroglobulin forms the colloid (the pink substance within the follicles), which is the site of thyroid hormone synthesis.
Pathology:
The image to the Left is a surgical specimen from a patient with Hashimoto's thyroiditis. Some areas show normal-appearing follicles with minimal lymphocytic infiltrates, while other areas have complete destruction of follicles with dense lymphocytic infiltrates, in which the lymphocytes form germinal centers.
Ref: image is from From Up-To-Date.
Thyroid function testing is always done during your fist visit.
*Tidbit: anti-TPO antibodies are almost always seen in pts who have anti-TG Abs. Whereas, anti-TG Abs are found only about 35% of the time in pts who have anti-TPO Abs. In other words, Anti-TPO Abs are more common and are often the only thyroid function test abnormality.
Please have your thyroid tests drawn sometime sometime in the afternoon preferably after 3:00 PM, and please do do this lab work NON-Fasting.
***** Do not take unless under medical supervision *****
There have been many studies published indicating there may be a benefit of using naltrexone to help treat various auto-immune diseases and anti-inflammatory diseases including but not limited to: Rheumatoid Arthritis, Multiple Sclerosis, Crohn's Disease, Chronic Fatigue Syndrome, Chronic Pain Syndromes and multiple types of Cancers.
From what I have seen, there has not yet been any studies published that have looked at many patients and/or evaluated data over several years which demonstrate naltrexone or Low Dose Naltrexone (LDN) is effective in mitigating anti-thyroid antibodies and/or improving HYPO or HYPERthyroidism. Rather I have seen studies indicating this is not true (see #1 and #2 below).
As mentioned above, there is a percentage of the normal population (ie: persons without thyroid disease) who have the presence of small amounts of anti-TPOs in their blood, generally less than 50 IU/ml) who will never develop thyroid disease at all.
The theory presented is that LDN at 4-4.5 mg daily will decrease the anti-thyroid antibodies and prolong the time the patient has before she becomes hypothyroid. However, in my opinion, this has not been demonstrated. I am not sure sure there a way to design a quality, evidenced based study to evaluate the effect of LDN on thyroid antibodies, because we also know that these antibodies will naturally wax and wane over time without any treatment. In other words, we cannot prove the LDN is lowering the antibodies, because they may lower completely on their own.
That being said, I do believe naltrexone may have a positive effect in mitigating inflammation which is found in many disease conditions.