Subclinical hypothyroidism refers to a state in which people do not have symptoms of hypothyroidism and have a normal amount of thyroid hormone in their blood. The only abnormality is an increased TSH on the person’s blood work. This implies that the pituitary gland is working extra hard to maintain a normal circulating thyroid hormone level and that the thyroid gland requires extra stimulation by the pituitary to produce adequate hormones. Most people with subclinical hypothyroidism can expect the disease to progress to obvious hypothyroidism, in which symptoms and signs occur.
Before you read on, it’s key to know that 90% of hypo- and hyper-thyroidism results from an autoimmune disorder. (Most people do not realize this, as doctors often don’t take time to explain things.) Most hypothyroid conditions are Hashimoto’s and most hyperthyroid conditions are Graves’ Disease, which means that your immune system is attacking your thyroid. Since the immune system resides in the gut or our intestine (Did you know that?!) a lot of what you will read here is about rebuilding the digestive system.
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.
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).
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.
The most common cause of hypothyroidism in the United States is an inherited condition called Hashimoto's thyroiditis. This condition is named after Dr. Hakaru Hashimoto who first described it in 1912. In this condition, the thyroid gland is usually enlarged (goiter) and has a decreased ability to make thyroid hormones. Hashimoto's is an autoimmune disease in which the body's immune system inappropriately attacks the thyroid tissue. In part, this condition is believed to have a genetic basis. This means that the tendency toward developing Hashimoto's thyroiditis can run in families. Hashimoto's is 5 to 10 times more common in women than in men.
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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).
Hypothyroidism Diet: One of the main causes of hypothyroidism is inflammation, so following an anti-inflammatory diet is key to improving your thyroid function. Likewise, ensuring your diet is rich in nutrient-dense foods, particularly iodine and selenium, will also help your thyroid produce sufficient levels of thyroid hormones. Some of the best foods to eat for your thyroid: wild-caught fish, coconut oil and ghee, seaweed, probiotic-rich foods like yogurt, sauerkraut and miso, sprouted whole grains and nuts, fiber-rich fruits and vegetables, bone broth, and plenty of good ole’ H20. Getting plenty of protein, healthy fat and fiber is of utmost importance when you have thyroid dysfunction.
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…
Subacute thyroiditis: This condition may follow a viral infection and is characterized by painful thyroid gland enlargement and inflammation, which results in the release of large amounts of thyroid hormone into the blood. Fortunately, this condition usually resolves spontaneously. The thyroid usually heals itself over several months, but often not before a temporary period of hypothyroidism occurs.
If you do choose to eat gluten, be sure to choose whole-grains varieties of bread, pasta, and rice, which are high in fiber and other nutrients and can help improve bowel irregularity, a common symptom of hypothyroidism. Also be sure to take your hypothyroidism medication several hours before or after eating high-fiber foods, to prevent them from interfering with the absorption of your synthetic thyroid hormone.
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