Hashimoto’s disease is an autoimmune disorder in which your immune system inappropriately attacks your thyroid gland, causing damage to your thyroid cells and upsetting the balance of chemical reactions in your body. The inflammation caused by Hashimoto’s disease, also known as chronic lymphocytic thyroiditis, often leads to an underactive thyroid gland (hypothyroidism). Hashimoto’s disease is the most common cause of hypothyroidism in the United States.
When You Are Diagnosed With Hashimoto’s
By the time you are diagnosed with Hashimoto’s, Hypothyroidism involving just the thyroid is no longer the primary factor. Any support you give for just the thyroid will provoke further attacks. So stop it!!! Look for the other non-thyroid factors and which of the other five patterns of low thyroid are involved. You will respond much quicker in doing this.
Along the way, however, there can be periods where the thyroid sputters back to life, even causing temporary hyperthyroidism, then a return to hypothyroidism. This cycling back and forth between hypothyroidism symptoms and hyperthyroidism is characteristic of Hashimoto’s disease as the other Non-Thyroid Factors and/or conditions that cause the five patterns of hypothyroidism and/or 22 factors of low thyroid function caused by the neuroendocrine transmitters of the NEI Supersystem flare up and/or calm down. Again, the thyroid is NOT directly involved.
So, for example, periods of anxiety/insomnia/diarrhea/weight loss may be followed by periods of depression/fatigue/constipation/weight gain. Did I mention the 22 different factors that can cause low thyroid function that are due to neuroendocrine transmitters of the NEI Supersystem? Again, the thyroid is NOT directly involved.
Hashimoto’s Thyroiditis Treatment Priorities
- Calm and Quite the immune system
- Quench inflammation in the body
- Reset the immune system
- Support the elimination of the other NON-Thyroid factors that provoke immune responses towards the thyroid. (Not mentioned by Kharrazian or Wentz)
- Address the Neuroendocrine transmitters imbalance that can cause 22 patterns of low thyroid function. (Kharrazian D. Why Do I Still Have Thyroid Symptoms. Chapter Ten, page 179; Not mention by Izabella Wentz)
- Support the underlying cause of whichever of the six patterns of low thyroid is present in the body. (Kharrazian D. Why Do I Still Have Thyroid Symptoms. Chapter Four, page 67; Not mention by Izabella Wentz)
The treatment of Hashimoto’s should not focus on the thyroid until the underlying factors provoking the immune attack are resolved. Any support that enhances the thyroid function will provoke aggressive attacks on the thyroid gland itself. Most of the factors involved in low thyroid function do not involve the thyroid gland.
It is like having a coworker that prevents you from doing your job and you have the job that gets all the attention and blame.
Hashimoto’s typically involves a slow but steady destruction of the gland by the immune system and other NON-THYROID Factors that eventually results in the thyroid’s inability to produce sufficient thyroid hormone — the condition known as hypothyroidism. There are other NON-Thyroid factors that provoke immune responses towards the thyroid that take priority over supporting normal thyroid function. There are six patterns of hypothyroidism (Low Thyroid) – five of which do not involve the thyroid that should be addressed.
Hashimoto’s Antibody Testing
The current dogma is that Immune cells are stimulated by Antibodies. They believe as long as antibodies are present, the antibodies are constantly stimulating an immune response. They also are lead to believe the presence of antibodies are from an ongoing infection. Typically, IgG antibodies are produced in the first phase of immune responses. However, the immune response to IgA, IgG, and IgM declines or is terminated along the course of the disease in most patients. IgM antibodies are indicative of an ongoing immune response., Studies have shown the detection of IgA and IgM antibodies in 62% and 61% of IgG antibodies in autoimmune patients, and after 7 years.,
A resolution of the disease is not associated with a decrease in antibodies. Only those with a short disease duration are likely to experience a decrease in antibodies levels. For most autoimmune patients there is no significant change in antibody levels, However, patients with immune calming/quieting treatment, experienced a 20% decline in their antibody levels. Normalization in the levels of antibodies with treatment intervention occurs in less that 7% of patients. The success of clinical interventions in lowering antibody levels (and thus likely minimizing the pathogenic effects of autoantibody binding) appears to be dependent on disease duration. The association of shorter disease duration with greater declines in antibody levels is highly consistent with the growing body of evidence that shows improved clinical outcomes with earlier disease intervention in autoimmunity.,,
Approximately one-half of patients with Rheumatoid Arthritis had positive IgM-RF and/or antibodies on at least 1 occasion, almost 5 years prior to disease onset. More than 50% of autoimmune patients may have positive antibodies upwards of 13 years after disease resolution, regardless of treatment.
Forbidden Cytokines Make Antibody Tests Confusing
Cytokine secretion by helper T cells is particularly important in autoimmunity because chronic autoimmune diseases, such as Hashimoto’s Thyroiditis, multiple sclerosis, diabetes, and rheumatoid arthritis are predominantly caused by Th1 cells. Th2 cells can antagonize Th1 functions and in numerous autoimmune conditions prevent autoimmune diseases from getting established.
After autoimmune conditions, such as those mentioned above, become established. Th2 is not only an inefficient suppressors of Th1, but can provoke and promote the onset of autoimmune conditions. Furthermore, neuropeptides (NPs): (somatostatin, calcitonin gene-related peptide, neuropeptide Y, and substance P), drive distinct Th1 and Th2 populations to a “forbidden” cytokine secretion: secretion of Th2 cytokines from a Th1 T cell line and vice versa. Such a phenomenon cannot be induced by classical antigenic/antibody stimulation.
Some of the NPs are produced by microbes as part of their defense strategy. Thus, focusing on restoring normal thyroid function to an autoimmune thyroid is futile.