Hashimoto\'s Thyroiditis Lifestyle Interventions for Finding and Treating the Root Cause

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Hyperthyroidism


Hyperthyroidism, or an overabundance of thyroid hormone, has a stimula-
tory effect. Classical symptoms include weight loss, palpitations, anxiety, eye
bulging, tremors, irritability, menstrual disturbances, fatigue, heat intoler-
ance, and increased appetite. Patients often experience hair loss.


Hyperthyroidism is usually caused by a related autoimmune condition
called Graves’ disease in which antibodies to the TSH receptor are pres-
ent. Graves’ can sometimes evolve into Hashimoto’s and vice versa, and
the two disorders appear to be closely related.


Hashimoto’s Thyroiditis


Hashimoto’s thyroiditis is an autoimmune condition that results in de-
struction of the thyroid gland. This damage eventually leads to inadequate
thyroid hormone production, or hypothyroidism. As mentioned above,
Hashimoto’s is the most common cause of hypothyroidism in the United
States and accounts for 90 percent of the nation’s hypothyroidism cases.


Hashimoto’s thyroiditis is also known as chronic thyroiditis, lymphocytic
thyroiditis, lymphadenoid goiter, and recently, autoimmune thyroid-
itis. This condition was first described in 1912 by a Japanese physician,
Hakuro Hashimoto, who first called it struma lymphomatosa.


Hashimoto’s usually begins as a gradual enlargement of the thyroid gland,
which is sometimes detectable by the patient on self-examination. It can
be accompanied by hoarseness or breathing difficulty. Occasionally, pa-
tients may experience tenderness or pain.


When damage to the gland is just beginning, the body compensates
and produces more hormone, thus keeping the hormone levels within
“normal” ranges. The person may start noticing symptoms of hypo-
thyroidism, however. Mild hypothyroidism may be noticed in some
patients, while in others, thyrotoxicosis (too much thyroid hormone)
can be present. This beginning stage is described as “subclinical” hypo-
thyroidism, defined as an increased TSH accompanied by “normal” T4
and T3 levels.


Progressively, as more thyroid tissue is destroyed, the thyroid loses its
ability to compensate and the person becomes deficient in thyroid hor-
mone. Eventually, this results in the gland’s complete loss of ability to
produce thyroid hormone (atrophic thyroiditis), considered the end
stage of Hashimoto’s thyroiditis.

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