How the Immune System Works
If we understand Hashimoto’s Disease, we can understand every autoimmune reaction. So what is autoimmune thyroid? Autoimmune thyroid disease is typically classified into two groups, Hashimoto and Graves’. Both Hashimoto’s and Graves’ can cause a hyper, or an overactive thyroid response, but it is Graves Disease that is dangerously overactive thyroid and Hashimoto’s that hovers low.
When someone has an overactive thyroid their blood testing will indicate a low Thyroid Stimulating Hormone (TSH) and a high T4 and/or T3. These people typically have increased metabolic rates, symptoms like high anxiety, nervousness, insomnia, and heart palpitations, racing heart, and inward trembling. Though these symptoms may also be similar to a hyperactive adrenal state, both a Graves and a Hashimoto patient may experience these symptoms.
The difference between Hashimoto’s and Graves’ is that Graves Disease always expresses itself as hyperthyroidism and Hashimoto’s patients are more typically hypothyroid; though they can experience some hyperthyroid symptoms like those listed above, more often those symptoms stem from subsequent adrenal dysfunction happening concurrently. Hashimoto’s patients ultimately experience hypothyroid symptoms which we have and will discuss in more detail.
Unfortunately, in the current healthcare system, these people typically don’t get evaluated from an autoimmune perspective, which may be a hidden blessing since the traditional medical approach to autoimmune disorders is currently quite barbaric. Hashimoto’s disease is far more common than Graves but both are autoimmune, i.e., caused by an immune attack against the tissue; they just have different outcomes. If you can understand the mechanism of the Hashimoto’s immune attack, then you can equate much of it to all autoimmune disorders.
Hashimoto’s is the most common cause for hypothyroidism in the United States and has been published and well accepted in the endocrinology literature, but often overlooked in traditional and alternative healthcare models as far as applications. In the alternative medicine model, hypothyroidism is blamed on things like iodine and tyrosine deficiencies and need for thyroid glandulars and though this has been our approach for quite some time, we really have not seen much success in this treatment. The traditional medical approach is hormone replacement. Neither of the above models address the attack on the thyroid tissue and both are destined for disaster.
As in all autoimmune conditions, there is tissue destruction in Hashimoto’s; the reason their thyroid is not working is because their immune system is attacking the gland.
We first need to address the mechanism involved. All autoimmune diseases may have some type of genotypic component, i.e., there may be a latent gene that the individual has carried in an unexpressed state for a period of years until some ‘event’ that triggered a immune response suddenly ‘turned on’ the gene. If this exists, and the autoimmune disease truly has genetic components, the practitioner’s job is to rightly manage the patient to diminish the immune response and calming the attack. Once a gene is expressed, it will always stay ‘turned on’. We will walk you through procedures to keep it ‘calmed down’ to stop the destruction mode. Other processes can ‘turn on’ an autoimmune attack like environmental compounds, some types of endocrine imbalance, toxic chemical exposures, abnormal stress responses, antigen responses, as well as the person’s preexisting genotype. So, the combination of all these things and some genetic susceptibility leads to an autoimmune disorder.
Usually the immune system is slowly attacking the tissue over several years. And then, the person eventually has a great enough destruction that brings about symptoms that lead them to seek some type of doctor. In the case of Hashimoto’s, they often get diagnosed with hypothyroidism because their TSH is high. And then, the TSH is managed by replacement but no management for the immune response is initiated because it was never assessed. In the case of other autoimmune disorders, the patient is often misdiagnosed for years, even decades; and they are left laden with multitudes of drugs attempting to suppress their symptoms.
The autoimmune response is an inflammatory response, which produces chemicals called cytokines, which are part of the body’s natural defense system against outside invaders. The body’s immune system may be separated into a Th1 and a Th2 response. The Th1 response may be thought of as the police force, the body’s initial strike force against an invader or what is called an antigen. When an antigen is present, the Th1 system fires and kills the virus; should the bug be of a nasty persuasion and strong enough to resist the Th1 response, the Th2 system kicks in, creates antibodies against the virus, tagging them so appropriate white blood cells can finish them off. A person with an autoimmune disease has this process stuck in the ‘on’ position, either hyper-Th1 or hyper-Th2, which prolonged, destroys the tissue where the antigen is recognized.
In Hashimoto’s, if the autoimmune disorder is hyper-Th1, certain types of lymphocytes and cytokines become ‘dominant’. This is an inflammatory, destructive response. These cytokines also block thyroid receptor sites from creating a proteomic response thereby making the hormone that is present, unresponsive; well, that stinks, even the hormone that IS present works worse! So, even when thyroid hormones bind to the receptor site, the actual proteins that impact metabolic rates are not produced rendering it inactive. This is why Hashimoto’s patients, despite the fact they go on replacement, don’t necessarily feel better after the ‘honeymoon’ period of a few weeks to several years because there’s a defect created from the inflammatory immune response blocking the ability for the replacement hormones to have an effect on the receptor sites. This is why simply replacing the absent hormone doesn’t work!
Hence, both the traditional medical and the traditional alternative models of care are doomed to failure. The most important battle to fight is to calm down their immune response and stop the destruction.
The “new model” we are proposing is simply to be more specific. If an autoimmune disease is a hyper-Th1 or hyper-Th2 attack against an antigen, doesn’t it make sense to do everything possible to find out what the antigen is, attempt to remove it and calm down the Th1 or Th2 dominance? I’m no rocket scientist, but this makes sense to me. It’s logical and possible to find the specific biochemical pattern perpetrating the response so we can determine how we treat them.