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*Cassava bears special mention here.  You may have heard of it because it is the starchy root vegetable from which tapioca is made, but cassava is also a popular staple food in many Third World countries, where it is eaten boiled, mashed, or ground into flour.  Fresh cassava root contains a harmless substance called linamarin, which can turn into hydrocyanic acid (aka cyanide!) when the plant is damaged or eaten. Flaxseeds also contain linamarin. Cyanide is very toxic, so the human body converts it into thiocyanate (which, although it does interfere with thyroid function, is less toxic than cyanide and easier for the body to eliminate).

Gluten is a protein found in wheat, rye, and barley. Unless you've been diagnosed with celiac disease, it probably won’t affect your thyroid. Gluten can damage the small intestines of people with celiac disease. They can have other autoimmune disorders like Hashimoto’s disease (which leads to an underactive thyroid) and Graves' disease (which leads to an overactive thyroid). If you have celiac disease, a gluten-free diet may help prevent these thyroid diseases.


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:
The purpose of treating hypothyroidism is to maintain normal metabolism by correcting a deficient output of thyroid hormone. Once replacement therapy begins, the thyroid will stop producing hormones all together, and replacement must be continued for life. Most mainstream physicians prescribe the drug Synthroid, also known as levothyroxine, a synthetic analog of thyroxine (T-4) and monitor how much to give based on symptoms and levels of TSH. Physicians will generally check TSH levels after a couple of months of being on the medication and adjust it accordingly. They will often used a more cautious course in patients who have cardiovascular disease. This allows the heart time to adjust to an artificially increased metabolism. Side effects of taking too much thyroid hormone include shakiness, palpitations, insomnia and changes in appetite.
Iodine is an essential ingredient in thyroid hormone, and thyroid hormone is critical to the growth and development of the bodies and brains of all baby vertebrates (animals with backbones).  Since they need iodine just as much as we do, and they do not have access to artificially iodized salt, how do they get their iodine?  Do they have a secret stash somewhere that they’re not sharing with us? I assume they are getting enough iodine because if they weren’t, they would all be born brain-damaged runts, and many would be infertile if they survived to adulthood.  To the best of my knowledge, wild inland animals are not herds of sterile, stupefied miniatures roaming the landscape in search of iodine…
Hypothyroidism Supplements: Your thyroid is impacted greatly by specific nutrients, like Iodine, Selenium, Zinc, Copper, Vitamin B, Vitamin D3, Vitamin A, Iron, and Omega-3 fatty acids. Instead of taking a dozen separate vitamins every day, I recommend finding a thyroid-specific multi-vitamin that already contains optimal levels of these nutrients. Dr. Meyer’s makes my favorite thyroid multi-vitamin, and it contains methylated vitamins to help with absorption and efficacy. Adaptogenic herbs like ashwaghanda and reishi are also really helpful for managing stress and anxiety, which are linked with your thyroid. 
The thyroid peroxidase test measures the level of an antibody that is directed against thyroid peroxidase (TPO). A presence of TPOAb in the blood reflects a prior attack by the body's immune system on thyroid tissue. A positive thyroid peroxidase test may signal chronic thyroiditis. Other autoimmune disorders, however, may have a positive TPOAb test.
l-Thyroxine monotherapy for athyreotic rats results in a high T4:T3 ratio at doses sufficient to normalize serum TSH levels (8). Yet, the brain, liver, and skeletal muscle tissues of these l-thyroxine–treated animals continue to exhibit markers of hypothyroidism (9), probably because of the inability of l-thyroxine monotherapy to restore tissue levels of T3 (8). This is probably a direct consequence of lower serum T3 levels and the relatively high T4 concentration in these tissues, which inactivates the type 2 iodothyronine deiodinase (D2). In the hypothalamus, loss of D2 is minimal in the presence of T4, which increases sensitivity to T4 levels and explains TSH normalization, despite relatively lower levels of serum T3. Only combination therapy with l-thyroxine plus l-triiodothyronine normalized all thyroid hormone–dependent measures (9), including serum and tissue T3 levels (8). Whether tissue-specific markers of hypothyroidism are restored with l-thyroxine monotherapy in humans remains to be determined, as does the ability of l-thyroxine plus l-triiodothyronine combination therapy to normalize the serum T4:T3 ratio without adverse events. The development of a novel drug delivery system for l-triiodothyronine would facilitate these studies (5).
In the 1995 American Thyroid Association (ATA) guidelines, biological and synthetic thyroid hormone preparations containing T4 plus T3 were not recommended out of concern for fluctuating and often elevated serum T3 concentrations (71). In conjunction with the American Association of Clinical Endocrinologists in 2012, the ATA continued to recommend l-thyroxine monotherapy and noted that evidence does not support using synthetic combination therapies; in addition, they stated that “desiccated thyroid hormone should not be used for the treatment of hypothyroidism” (72). In 2014, the ATA recommendations evolved with the recognition that 1) serum T3 levels might not be normalized in all l-thyroxine–treated hypothyroid patients and 2) some patients remain symptomatic while receiving l-thyroxine monotherapy. Titration of l-thyroxine dose to achieve normal TSH concentrations remains a first-line approach, but trials with combination therapy can be considered. In addition, the guidelines recognize that although superiority data are lacking, some patients do experience a clinical response with desiccated thyroid preparations or combination therapy with l-thyroxine plus l-triiodothyronine (1). The European Thyroid Association has similar recommendations (2).
It's not enough for your thyroid levels to be "normal" or fall within the reference range. In many cases, for you to lose weight with hypothyroidism, you need your thyroid levels to be "optimal." That means that your thyroid stimulating hormone (TSH) level would typically fall below 2.0, and your free T4 and free T3 would fall in the upper half of the reference range.
**Note: It’s important to realize that thyroid medication is not one size fits all, and there is no ONE right solution for everybody. Dosage is incredibly important, your specific thyroid labs will impact what type of medication is needed and we all have different needs, budgets, goals, and symptoms. So work with a functional medicine practitioner to find the thyroid medication that makes the most sense for YOU! 
The purpose of treating hypothyroidism is to maintain normal metabolism by correcting a deficient output of thyroid hormone. Once replacement therapy begins, the thyroid will stop producing hormones all together, and replacement must be continued for life. Most mainstream physicians prescribe the drug Synthroid, also known as levothyroxine, a synthetic analog of thyroxine (T-4) and monitor how much to give based on symptoms and levels of TSH. Physicians will generally check TSH levels after a couple of months of being on the medication and adjust it accordingly. They will often used a more cautious course in patients who have cardiovascular disease. This allows the heart time to adjust to an artificially increased metabolism. Side effects of taking too much thyroid hormone include shakiness, palpitations, insomnia and changes in appetite.
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.

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:


Goitrogens are naturally occurring substances in certain foods that interfere with the production of thyroid hormones (the hormones that people with hypothyroidism lack). They include some of the most commonly consumed foods of the health-conscious community: broccoli, cauliflower, kale, spinach, radishes, soybeans, peanuts, pine nuts, peaches and millet. The good news is that many health professionals believe that cooking may inactivate goitrogens.
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.

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