Thank you so much… I am grateful for a response… I am doing most if not all of what you suggest with a DC over the past two years…so I believe almost there but still need to find that missing piece of the puzzle.. So still working on it..stopping the cause… Totally have changed my life habits .. So just need to find the next step.. I still have hair loss .. Not as bad …and am able to rejoin my life which has been great.. Also DC doing some genetic testing .. Getting that back soon along with a full panel thyroid blood work to see where I am now …. Taking many things in your thyroid pack ..maybe I need to look to see if yours includes something I am missing.. Thanks again for your reply..I truly consider it a blessing..truly grateful

Once again, if you look to the anatomy, you find the thyroid gland located in the throat, the center of our communication with the world. Andrea has found in her practice that people with hypothyroid tend to “swallow down” what they really want to say. It’s been very healing for them to learn to speak their truth. On the flip side, she has found that people with hyperthyroid are talking too much, and can benefit by listening more.
Caffeine has been found to block absorption of thyroid hormone replacement, says Dr. Lee. "People who were taking their thyroid medication with their morning coffee had uncontrollable thyroid levels, and we couldn't figure it out," she says. "I now have to be very careful to tell people, 'Only take your medication with water.'" You should wait at least 30 minutes after taking your medication before having a cup of joe.
l-Thyroxine was the first synthetic molecule used to treat hypothyroidism (23) and was shown to be efficacious as monotherapy for myxedema (24). Around that time, serum protein-bound iodine (PBI) emerged as a diagnostic test and therapeutic marker; serum PBI quantitation was the only valid way to biochemically assess thyroid hormone status (25). This tool was limited in terms of treatment monitoring because the effect on serum PBI varied by agent (26). For example, l-triiodothyronine corrected BMR without much increase in serum PBI, l-thyroxine increased serum PBI sometimes to above normal, and combination l-thyroxine and l-triiodothyronine and desiccated thyroid had the advantage of normalizing serum PBI (27). In addition to BMR and serum PBI, other surrogates for treatment response included cholesterol levels, symptoms, and deep tendon reflexes, but their lack of sensitivity was always recognized (28).
The development of TSH assays led to a dramatic reduction in thyroid hormone replacement dosage and the ability to diagnose with certainty milder forms of hypothyroidism. Discovery of peripheral T4-to-T3 conversion gave a physiologic means to justify l-thyroxine monotherapy. In combination with the concerns over consistency and safety of natural thyroid preparations, synthetic l-thyroxine was perceived as a more reliable therapy. These findings laid the foundation for the clinical practice trend away from natural thyroid preparations and toward l-thyroxine monotherapy at doses to normalize the serum TSH. Later, a subpopulation of patients with residual symptoms of hypothyroidism was recognized. It remains to be determined whether this is due to a trend of attributing nonspecific symptoms to minimal thyroid dysfunction, relatively low serum T3 levels and/or high T4:T3 ratio, or the role of Thr92AlaD2 polymorphism, and whether combination therapy with l-thyroxine plus l-triiodothyronine will be beneficial.
Although the implementation of sensitive TSH assays resulted in dose reduction, it also fueled the discovery of subclinical states of hypothyroidism (i.e., serum TSH <10 mIU/L and normal serum free T4); this state is 20 times more prevalent than overt hypothyroidism (64). Hence, many patients with vague symptoms, such as depressed mood and fatigue, are commonly screened and found to have subclinical hypothyroidism. In many cases, this finding prompts the conclusion that the subclinical hypothyroidism is the cause of the nonspecific symptoms, and thyroid hormone therapy is initiated. The patients in whom the cause–effect relationship was incorrect contribute to the increasing number of euthyroid but symptomatic patients (57). The marked increase in prescribing of thyroid hormone with decreasing TSH thresholds amplifies this problem (47).
Studies have indicated that individuals with lower selenium levels are at higher risk for low T3 (50). Selenium has been shown to reduce rT3 levels and improve active T3 status (51). It also reduces anti-thyroid anti-body formation (52). Be sure to get selenomethionine which is the most effective form of selenium for reducing anti-body formation and improving thyroid function.
Lifeworks Wellness Center is long recognized as one of the foremost natural health clinics in the US. At our Tampa Bay, Florida alternative medicine office we have been offering treatment for underactive thyroid for a long time and many of our patients have benefitted from it. The patients fly in from all over the world because they simply can’t find clinics offering natural treatments for underactive thyroid and natural medicine for low thyroid where they live.
The problematic compound in soy (for your thyroid) are the isoflavones. In fact, a study in the Journal of Clinical Endocrinology and Metabolism reported that researchers fed some subjects 16 mg of soy isoflavones, which is the amount found in the typical vegetarian's diet,  and others 2 mg soy isoflavones, which is the amount found in most omnivore's diets.
SUBJECT: Your thyroid gland is found just below your voice box or larynx. It wraps around your windpipe or your trachea. Your thyroid affects your metabolism. It makes hormones that affect how fast your whole body works and how it uses energy. Your body uses thyroid hormone to increase your energy and raise your body temperature when needed. For example, that helps replace the heat your body loses when exposed to cold weather.
Hyperthyroidism, or overactive thyroid gland, is another common thyroid condition. The most prevalent form is Graves’ disease in which the body’s autoimmune response causes the thyroid gland to produce too much T3 and T4. Symptoms of hyperthyroidism can include weight loss, high blood pressure, diarrhea, and a rapid heartbeat. Graves’ disease also disproportionately affects women and typically presents before the age of 40.4

Goiter - Goiter is a condition in which a gland is larger than it should be. This occurs in the thyroid gland when the gland is being overstimulated because it is receiving constant signals to produce more hormones. Hashimoto’s thyroiditis is one of the more common causes of a goiter. It may not be uncomfortable, but a large goiter can affect appearances and interfere with swallowing or breathing if left untreated.
Goiter - Goiter is a condition in which a gland is larger than it should be. This occurs in the thyroid gland when the gland is being overstimulated because it is receiving constant signals to produce more hormones. Hashimoto’s thyroiditis is one of the more common causes of a goiter. It may not be uncomfortable, but a large goiter can affect appearances and interfere with swallowing or breathing if left untreated.
THIS TOOL DOES NOT PROVIDE MEDICAL ADVICE. It is intended for general informational purposes only and does not address individual circumstances. It is not a substitute for professional medical advice, diagnosis or treatment and should not be relied on to make decisions about your health. Never ignore professional medical advice in seeking treatment because of something you have read on the WebMD Site. If you think you may have a medical emergency, immediately call your doctor or dial 911.
The thyroid gland, situated just below the Adam’s apple on the low part of the neck, produces the thyroid hormones in the body. The thyroid gland is shaped like a butterfly and wraps itself around the trachea with two lobes attached to a central isthmus. When you eat foods containing iodine such as salt and seafood, this thyroid gland uses the idodine to produce the thyroid hormones. There are two important types of thyroid hormones produced which would be T4 or Thyrozine and T3 or Triiodothyronine (T3). These account for most of the thyroid hormones present in the bloodstream. T3 is the more active of the hormones and it affects cellular metabolism.
Studies have indicated that individuals with lower selenium levels are at higher risk for low T3 (50). Selenium has been shown to reduce rT3 levels and improve active T3 status (51). It also reduces anti-thyroid anti-body formation (52). Be sure to get selenomethionine which is the most effective form of selenium for reducing anti-body formation and improving thyroid function.
Thyroid hormone replacement has been used for more than a century to treat hypothyroidism. Natural thyroid preparations (thyroid extract, desiccated thyroid, or thyroglobulin), which contain both thyroxine (T4) and triiodothyronine (T3), were the first pharmacologic treatments available and dominated the market for the better part of the 20th century. Dosages were adjusted to resolve symptoms and to normalize the basal metabolic rate and/or serum protein-bound iodine level, but thyrotoxic adverse effects were not uncommon. Two major developments in the 1970s led to a transition in clinical practice: 1) The development of the serum thyroid-stimulating hormone (TSH) radioimmunoassay led to the discovery that many patients were overtreated, resulting in a dramatic reduction in thyroid hormone replacement dosage, and 2) the identification of peripheral deiodinase-mediated T4-to-T3 conversion provided a physiologic means to justify l-thyroxine monotherapy, obviating concerns about inconsistencies with desiccated thyroid. Thereafter, l-thyroxine mono-therapy at doses to normalize the serum TSH became the standard of care. Since then, a subgroup of thyroid hormone–treated patients with residual symptoms of hypothyroidism despite normalization of the serum TSH has been identified. This has brought into question the inability of l-thyroxine monotherapy to universally normalize serum T3 levels. New research suggests mechanisms for the inadequacies of l-thyroxine monotherapy and highlights the possible role for personalized medicine based on deiodinase polymorphisms. Understanding the historical events that affected clinical practice trends provides invaluable insight into formulation of an approach to help all patients achieve clinical and biochemical euthyroidism.
There is little mention of patients who did not respond symptomatically to treatment despite having normalization of their other measured variables, such as BMR or serum PBI, in the early clinical trials in the 1940s through 1960s. After the 1970s (38, 52), a new category of hypothyroid patient was recognized: the patient who received thyroid hormone replacement therapy, had normal serum TSH, and exhibited residual symptoms of hypothyroidism. Initially, such symptoms were largely dismissed as unrelated to the thyroid condition (62). Indeed, hypothyroidism is prevalent, and symptoms overlap with those of other common conditions, including menopause, depression, and chronic fatigue syndrome. Likewise, thyroid hormone had been administered for nonthyroid disorders, including obesity and psychiatric disease, for decades. Thus, it was difficult to assess whether patients with residual symptoms had been misdiagnosed. Residual symptoms were even attributed to nonadherence (63).
Whether it is sports, dancing, or yoga that gets you moving, it is important to engage in movement that does not drain your adrenals or your thyroid yet gives you a sense of accomplishment and joy. If you are suffering from adrenal fatigue, be sure to be very gentle with your body and don’t do excessive cardio work-outs and switch to light weight lifting, yoga, pilates, gentle cycling, hiking, dancing, etc.
The association between hypothyroidism and energy expenditure was suspected clinically, and the discovery of lower O2 consumption in myxedema provided an early diagnostic tool (19). The development of a device to assess energy expenditure through measurement of the basal metabolic rate (BMR) in humans proved to be useful for not only diagnosis but also titration of therapy (20). The scale was calibrated so that a normal BMR reference range would be around 0%, whereas athyreotic individuals could have a BMR of about −40% (21). Because of lack of specificity (for example, low BMR in malnutrition), BMR was used in conjunction with the overall clinical impression; a low BMR in the setting of high clinical suspicion would secure a diagnosis and justify treatment (21, 22).
A clinical trial investigating symptoms found that patients receiving l-thyroxine monotherapy, even with a normal TSH, displayed substantial impairment in psychological well-being compared with controls of similar age and sex (3). Because some hypothesized that this phenomenon came about only after adoption of l-thyroxine monotherapy, a study assessed combination therapy with l-thyroxine and l-triiodothyronine. Remarkably, the latter study showed that psychological measures improve in patients receiving combination therapy until serum TSH level is normal (6). In another study comparing l-thyroxine monotherapy versus desiccated thyroid, in which both groups had a normal TSH, many patients preferred desiccated thyroid and lost weight (60). Unfortunately, the solution to this complex problem is not as simple as reverting to combination therapy; the more than a dozen clinical trials on the subject have not shown benefit of superiority and preference for combination therapy, as previously reviewed (1, 3, 70).
Essential fatty acids found in fish oil are critical for brain and thyroid function. DHA and EPA omega-3s found in fish oil are associated with a lower risk for thyroid symptoms, including anxiety, depression, high cholesterol, inflammatory bowel disease, arthritis, diabetes, a weakened immune system and heightened autoimmune disease. Omega-3 fish oil such as cod liver oil can also help balance levels of omega-6s in the diet, which is important for ongoing health.
You need to reduce the toxins you ingest from additives, preservatives, artificial sweeteners (!), excessive sodium, and trans-fats and try to eliminate toxins hiding around your house. Water toxicity is a HUGE problem in thyroid conditions. Most public water systems in the US have fluoride added, which is now linked to slowing down the thyroid; fluoride is believed to be leaching on to the thyroid cells inhibiting the uptake of iodine, hence the altered production of the thyroid hormone (T4).
In the developed world, where protein is plentiful and many countries add iodine to salt and processed foods, we don’t typically need to worry about protein malnutrition or iodine deficiency.  However, the rest of the world is not so lucky. More than 2 billion people around the world suffer from hypothyroidism due to iodine deficiency.  2 billion!  We are told that the reason for this planetary epidemic is that iodine comes from the ocean, and that the soil of inland areas has had most of its iodine washed away over time by erosion:
For starters, consider the effect that hypothyroidism can have on weight. Hypothyroidism (also called low thyroid or underactive thyroid) is marked by insufficient hormone production in the thyroid — the butterfly-shaped gland located at the bottom-front of your neck. This gland affects the body’s metabolic processes, and often, sudden weight gain is an early sign of low thyroid.

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