It is generally accepted that the thyroid autoantibodies thyroglobulin and thyroid peroxidase reflect disease activity and progression and are valuable in disease prediction and the classification of Hashimoto’s and Graves’ disease.
While clinicians rely on antibody levels and elevations in thyroid stimulating hormone, they give little attention to the factors involved in thyroid autoimmunity. Researchers and clinicians should be asking the question, why does the human body react to its own antigens resulting in the production of potential harmful autoantibodies? This event may be cause by environmental factors such as bacterial or viral infections or toxin haptenic chemicals binding to human tissue, causing modification of self-antigens and the subsequent production of autoantibodies.
Let’s say hypothyroidism symptoms describe you perfectly. How you know if your hypothyroidism is due to Hashimoto’s disease? Although a positive serum antibody test is the definitive test, it’s good to be aware of some classic symptoms and scenarios that typically go along with the condition. Most cases of Hashimoto’s unfold as a gradual attack of the immune system against the thyroid, with TSH levels and symptoms of hyperthyroidism slowly escalating. While the person may have normal TSH levels thanks to a thyroid hormone medication, the underlying problem of immune dysregulation goes untreated, as do their symptoms.
• Feeling tired or sluggish
• Feeling cold – hands, feet, all over
• Require excessive amounts of sleep to function well
• Weight gain despite following various diets
• Difficult, infrequent bowel movements
• Depression and lack of motivation
• Morning headaches that wear off as the day progresses
• Thinning of hair on scalp or excessive hair loss
• Dryness of skin
• Mental sluggishness
In addition to classic symptoms, a couple of medical conditions are red flags for Hashimoto’s. If you suffer from the symptoms above and have pernicious anaemia, gluten intolerance or Celiac disease, Hashimoto’s may be responsible for your thyroid condition. Pernicious anaemia is an autoimmune disease in which the person’s body attacks its own intrinsic factor, a substance necessary to absorb B12 that is secreted in the stomach.
Remember, Hashimoto’s is not a thyroid disease but an immune disorder and it is the immune system that must be addressed (even though thyroid replacement hormones may be warranted if enough thyroid tissue has been destroyed). In order to successfully modulate Hashimoto’s and prevent future autoimmune diseases and enjoy a better quality of life, a basic understanding of the immune system is the first step. Another very important factor, therefore, in managing someone with Hashimoto’s disease is to evaluate as to whether they are what’s known as TH-1 dominant or TH-2 dominant. If Hashimoto’s has been triggered by active infection, remove the antigen that supports the TH dominant pathway differently or focus on restoring the immune barrier of the gut and the brain. Because the lining of the digestive tract is an important immune barrier, poor gut health is a significant factor in triggering autoimmune diseases such as Hashimoto’s, as well as functional hypothyroidism.
One of the first things to go in a poor digestive environment is the balance of healthy gut flora in the intestines, and 20% of healthy thyroid activity depends on healthy gut bacteria. Poor digestive function depletes the body of nutrients that support thyroid health, particularly zinc, tyrosine and selenium, and vitamins A and D. Also common, faulty digestion is believed to be a leading cause of autoimmune disorders, including Hashimoto’s, since at least 60% of the immune system is located in the digestive tract.
Low thyroid function is almost always secondary to some other condition, often adrenal stress. Chronic adrenal stress does the following:
• Affects communication between the brain and the hormone glands
• Hypothalamus and pituitary gland direct hormone production, including that of the thyroid. When the hypothalamus and pituitary weaken due to chronic adrenal stress, they are not able to communicate well with the thyroid gland.
• Increases thyroid binding protein activity so that thyroid hormones cannot get into the cells to do their job.
• Hampers the conversion of T4 to active forms of T3 that the body can use.
• Stymies the detoxification pathways through which unnecessary thyroid hormones exit the body, leading to thyroid hormone resistance.
• Causes cells to lose sensitivity to thyroid hormones.
• Weakens the immune barriers of the digestive tract, lungs and brain; weakens the immune system; and promotes poor immune regulation.
The above factors increase the risk of triggering Hashimoto’s or exacerbating it.
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