People with celiac disease—the autoimmune disease that's characterized by an intolerance to the gluten in wheat, barley, and rye—are also more likely to have higher rates of thyroid problems, according to a 2007 report by researchers in the United Kingdom. "Eating a gluten-free diet helps control the symptoms, which may also help protect the thyroid gland," says Ilic. But unless you have celiac disease—and we're not talking an L.A.-aversion to gluten, here — you might not want to avoid breads after all. In fact, thanks to some of the baking processes, bread can actually contain some iodine.
Is there anything suggestion on eliminating the hydrogen peroxide? I read that an over growth of it can cause gray hair and hair loss..so maybe that is what needs to be addresses.. Will mention it to my DC.. This is a new discovery for me…only heard it mentioned recently by Suzy Cohen…. Any suggestions on how to combat it ? In your program or anything nutritionally to eat?
*In the years prior to the discovery of peripheral T4-to-T3 conversion, most groups recommended treatment with natural thyroid preparations, such as desiccated thyroid, thyroid extract, or thyroglobulin, which contain both T4 and T3. However with the discovery of T4-to-T3 conversion and the development of the radioimmunoassay for TSH in the early 1 970s, not only was there a trend toward l-thyroxine monotherapy, but the recommended daily maintenance doses decreased significantly. These trends led to the adoption of the contemporary standard of care: l-thyroxine monotherapy administered at doses to maintain a normal serum TSH level.
Follow a Thyroid Diet: The consumption of sea food, shellfish and organic vegetables and fruits, rich in iodine content has proven beneficial in overcoming iodine deficiency. It is better to eat small meals rather than three large meals. Non-starchy fruits and vegetables and low-fat proteins should be consumed. Sugary and starchy food items like, pasta, desserts, sodas, white bread, rice, etc. must be avoided completely. An intake of at least 64 ounces of non-fluoridated water is necessary.
Radioimmunoassays for measurement of serum T3 (48) and T4 (49) were soon developed, and it was observed that l-thyroxine monotherapy could normalize both T4 and T3 levels at the expense of a high T4:T3 ratio. In contrast, l-triiodothyronine, desiccated thyroid, thyroglobulin, and l-thyroxine/l-triiodothyronine combination all typically resulted in low or low-normal serum T4 values with usually elevated serum T3 levels, and thus a low T4:T3 ratio (28). Desiccated thyroid resulted in a T3 peak about 2 to 5 hours after administration that corresponded to thyrotoxic symptoms in some patients (50). That a single daily dose of l-thyroxine resulted in stable blood levels of T4 and T3 throughout the day (48) was understood to result from a steady rate of conversion of T4 to T3 (51).
4.   Mitochondrial Dysfunction:  The mitochondria are the energy producing organelles in each cell of the body.  They are extremely key in the bodies ability to handle oxidative stress.  Dysfunction in the mitochondria leads to increased free radical and oxidative stress which creates immune alterations.  This is a classic sign in Hashimoto’s autoimmune pathophysiology (22).

Cases of myxedema were reported in the mid–19th century but were not initially connected with a deficiency from the thyroid gland until surgeons identified incident myxedema after thyroidectomy (11). Initial treatment strategies were largely insufficient and primarily symptom directed, including hot baths and institutionalization (12). The significant morbidity and mortality in the absence of efficacious treatment were clear, and thus the need to “replace” the thyroid through surgical transplantation or oral or intravenous routes was established. Thyroid transplant had some early successes, but for many patients symptoms recurred and the procedure even had to be repeated (13). Because of the rapidity and transiency of improvement (12), it was hypothesized that symptoms improved by absorption of the “juice” of the donor gland (14).


I don’t know all your symptoms or health challenges, but if you have thyroid issues and if you are losing hair (alopecia areata?), you may want to consider getting tested for celiac disease. It is quite common for people to have celiac disease and thyroid disease. It’s important not to eliminate gluten from your diet before being tested as it would cause a false-negative test result.
Despite these successes, authors have questioned the efficacy of l-thyroxine monotherapy because about 10% to 15% of patients are dissatisfied as a result of residual symptoms of hypothyroidism (1, 2), including neurocognitive impairment (3), and about 15% of patients do not achieve normal serum triiodothyronine (T3) levels (4). Studies of several animal models indicate that maintaining normal serum T3 levels is a biological priority (5). Although the clinical significance of relatively low serum T3 in humans is not well-defined (1), evidence shows that elevating serum T3 through the administration of both l-thyroxine and l-triiodothyronine has benefited some patients (6, 7). However, this has not been consistently demonstrated across trials (1). Novel findings highlight the molecular mechanisms underlying the inability of l-thyroxine monotherapy to universally normalize measures of thyroid hormone signaling (8, 9), and new evidence may lay the foundation for a role of personalized medicine (10). Understanding the historical rationale for the trend toward l-thyroxine monotherapy allows us to identify scientific and clinical targets for future trials.
An article published in May 2017 in the journal Endocrine Connections noted that hypothyroidism and celiac disease are often present together, and while no research has demonstrated that a gluten-free diet can treat thyroid conditions, you may still want to talk to a doctor about whether it would be worth eliminating gluten, or getting tested for celiac disease.

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