Another great source of selenium, nuts make a handy snack that you can take anywhere. They also go well in salads or stir-fries. Brazil nuts, macadamia nuts, and hazelnuts are all particularly high in selenium, which helps the thyroid function properly. With Brazil nuts, you only need to eat one or two; with other nuts, a small handful is enough to get your daily nutrients — and be sure to keep an eye on portion size, as nuts are also very high fat.
Giving appropriate doses of T3 is trickier than appropriately dosing T4. T4 is inactive, so if you give too much there is no immediate, direct tissue effect. T3 is a different story, though, as it is the active thyroid hormone. So if you give too much T3, you can produce hyperthyroid effects directly—a risk, for instance, to people with cardiac disease.
As mentioned above, most thyroid conditions are auto-immune diseases. There are tons of lymphocytes and other immune cells in the gut, which protect the body from viruses, bacteria, and other invaders. This is why most people with thyroid conditions also experience frequent bloating, gas, constipation or diarrhea. A diet change will help your gut tremendously. “All disease begins in the gut“, said Hippocrates, the father of modern medicine. I’m not sure why this is not taught in schools today, but it’s an important part of the thyroid diet plan.
Rather than giving Synthroid (T-4) alone, Dr. Weil prefers combinations of the two natural hormones (T-3 and T-4), and often recommends the prescription drug Thyrolar. Under normal conditions, the body can convert T-4 into T-3; however, there is some question whether the body can do this optimally when under extreme physical or emotional stress. Giving a combination seems to elicit a more natural response for the body, and may also have a better effect on mood than T-4 alone.
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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.
Correcting these problems requires an integrative approach. It involves more than simply taking a thyroid pill. As you’ll see, it involves nutritional support, exercise, stress reduction, supplements, reducing inflammation, and sometimes eliminating certain foods and detoxification from heavy metals (such as mercury and lead) and petrochemical toxins (such as pesticides and PCBs).
The symptoms of hypothyroidism are often subtle. They are not specific (which means they can mimic the symptoms of many other conditions) and are often attributed to aging. People with mild hypothyroidism may have no signs or symptoms. The symptoms generally become more obvious as the condition worsens and the majority of these complaints are related to a metabolic slowing of the body. Common symptoms and signs include:
Dr. George Springer has practiced alternative medicine for 31 years with an emphasis on treating chronic disease conditions. He received his undergraduate BA from the University of Missouri in St. Louis and his Doctor of Chiropractic (D.C.) from Logan University where he graduated magna cum laude. He went on to receive his Doctor of Naturopathic Medicine (N.M.D.) from the American Naturopathic Medical Institute a division of Breyer State University in Los Angeles, California.
I suspect that there is actually enough iodine in the environment to go around, and that we actually need less than 150 micrograms per day of iodine. From the above list, you can see that animal foods are much richer in iodine than plant foods—so how do herbivores (animals which eat a plant-based diet, such as rabbits and deer) get enough iodine? I suspect that there is something about the human diet which interferes with our ability to absorb, utilize, and/or retain iodine, and that this is why we appear to be iodine-deficient compared to other animals. So, what might the possible culprits be? Hmmm….
Stress can also be caused by chronic digestive issues. When the small or large intestine is in distress (ywhen you are always constipated, bloated, suffer from gas, pain, loose stool etc.), the body sees it as a state of stress. Cortisol is a potent hormone we won’t function without. However, when in excess, it can have a detrimental impact on the thyroid and the immune system (one of the functions of cortisol is to modulate the immune system).
These clinical trials also began to define the adverse-effect profiles associated with these agents; thyrotoxicosis was frequently encountered. Patients treated with l-triiodothyronine3 (100 to 175 mcg/d) normalized BMR faster than did those receiving desiccated thyroid (120 to 210 mg/d) or l-thyroxine (200 to 350 mcg/d) but were more likely to experience angina (32). Desiccated thyroid was also associated with adverse symptoms in other studies; muscle stiffness, psychosis, and angina all occurred (33). In a crossover study of l-triiodothyronine monotherapy (75 to 100 mcg/d), l-thyroxine monotherapy (200 to 300 mcg/d), and desiccated thyroid (1.5 to 3 grains/d), all of these therapies restored BMR and serum PBI; with l-triiodothyronine, however, angina and heart failure occurred. Dose reduction corrected these adverse effects, but authors concluded that l-thyroxine monotherapy or thyroid extract was preferred (34). In a trial of l-thyroxine monotherapy at doses of 200 to 300 mcg/d versus l-thyroxine (80 mcg) plus l-triiodothyronine (20 mcg) daily, patients receiving the combination had such symptoms as palpitations, nervousness, tremor, and perspiration (35). Some early proponents of l-thyroxine monotherapy emerged because of less frequent thyrotoxic effects (24), but it is difficult to determine whether such adverse effects were related to the agent used or its high dosage. Thyrotoxic adverse effects were typically remediable by simple dose reduction (36), so desiccated thyroid remained the preparation of choice (37).
Those with hypothyroidism may want to consider minimizing their intake of gluten, a protein found in foods processed from wheat, barley, rye, and other grains, says Ruth Frechman, RDN, a dietitian in the Los Angeles area and a spokesperson for the Academy of Nutrition and Dietetics. And if you have been diagnosed with celiac disease, gluten can irritate the small intestine, and may hamper absorption of thyroid hormone replacement medication.
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