Autoimmune Disease in the U.S.- Part 2 in 6-Part Series

What are the different types of autoimmune disease?  How common is Hashimoto’s hypothyroidism?  What is involved in the development of AI disease?

Main points of this issue:

  • Autoimmune (AI) disease is characterized by an immune response against self-tissue
  • The most common AI disease in the U.S. is Hashimotos autoimmune thyroid
  • 8% of the U.S. population has thyroid antibodies
  • 1 out of 10 females in the U.S. has thyroid antibodies
  • 90% of people that become hypothyroid have AI thyroid
  • The presence of autoantibodies indicates current (or future) AI disease
  • Over 50% of people that have autoimmune thyroid have antibodies against other tissues
  • AI disease is characterized by loss of immune tolerance
  • AI disease is characterized by a dominance in either the TH1 or TH2 system

In the first issue, we discussed the prevalence of autoimmune (AI) disease in the U.S. and how they are diagnosed. We discussed their progressive nature and the fact that patients who develop one AI disease are at high risk of developing others. We also discussed conventional treatment of AI disease being primarily the use of immune-suppressing medication.

In this issue, we will take a deeper look at the nature of autoimmune conditions and their common characteristics. We will look at Hashimotos autoimmune thyroid as an example of one of these AI conditions and its prevalence.

What is autoimmune disease?
Lets first take a look at how AI disease is defined: a condition characterized by a specific humoral or cell-mediated immune response against constituents of the bodys own tissues

In any immune response, antibodies are generated by the immune system to help identify and target foreign invaders or harmful substances. In autoimmune diseases, the immune system generates antibodies against the bodys own tissue (autoantibodies). The bodys own tissue becomes a target of the immune system. There are two general types of autoimmune conditions depending on whether or not they are organ-specific.

Autoimmune disorders can be classified as either organ specific or non-organ specific

In organ-specific AI diseases, the autoantibodies are specifically directed against antigens localized in a particular organ and are often detected in circulation.

Examples of organ-specific autoimmunity include Hashimotos Thyroiditis, Type 1 Diabetes and Myasthenia Gravis.

The non-organ-specific AI disorders are characterized by the presence of autoantibodies directed against ubiquitous antigens (not specific to a particular organ).

This is characterized by the presence of specific circulating immune complexes. Non-organ-specific AI includes diseases such as systemic lupus erythematous (SLE), rheumatoid arthritis (RA), and scleroderma.1

Lets take a look at one example of autoimmune (AI) disease, autoimmune thyroid, which is the most prevalent AI disease in the U.S. today and how it manifests in the affected individual.

Autoimmune Thyroid Disease
The most common AI disease in the U.S. is Hashimotos autoimmune thyroid. The thyroid gland is very vulnerable to autoimmune attack and often times thyroid antibodies are the first sign of the development of an autoimmune disease. 8% of the U.S. population has thyroid antibodies. It is estimated that 1 out of 10 females in the U.S. has thyroid antibodies.

Thyroid Autoimmune Diseases are the most frequent autoimmune diseases in the population being present on average in 7-8% of the general population, (approximately 24 million people) in the U.S.2

90% of hypothyroid patients have AI thyroid
The most common mechanism for thyroid disorders in the U.S. today is autoimmunity, not iodine deficiency. Most hypothyroid patients actually have antibodies against their thyroid, although this is often overlooked and remains undiagnosed in most cases of hypothyroidism. Current research indicates that approximately 90% of people that become hypothyroid have an autoimmune attack against the thyroid gland.3 These hypothyroid patients are put on thyroid hormone to replace the lack of this hormone in the body but nothing is done for the autoimmune condition itself. What you are really seeing in these thyroid patients is the first expression of an autoimmune disease.

Importance of Early Detection of Autoantibodies
The presence of thyroid antibodies indicates future thyroid disease. The literature shows if you have thyroid antibodies, at some point, you will have thyroid failure leading to hypothyroidism. In most cases, thyroid antibodies are only discovered after the patient has been diagnosed as hypothyroid. Almost all autoimmune disorders are associated with circulating antibodies which bind self protein4

These antibodies appear in the blood years before presentation of symptoms in various disorders

Therefore, these antibodies may be used as biomarkers for early detection of various diseases5

Why is early detection of autoantibodies important? Because early detection allows for earlier intervention, possible prevention of the onset of autoimmune disease, potential for slowing down the autoimmune destruction of tissue and better prognosis.

Early identification might result in earlier treatment, better quality of life and an improved prognosis for these patients6

Autoantibodies As Predictors of Disease
Since autoantibodies are markers of disease activity, it follows that, under some circumstances, autoantibodies should be able to predict disease

The practical value of autoantibodies has not been fully realized in the majority of diseases in which they can be detected. Realizing the clinical potential of autoantibodies could be extremely valuable 7

Several studies have shown that autoimmune diseases are preceded by a long preclinical phase, and that many autoantibodies can be detected in the serum of asymptomatic subjects years before the diagnosis. 8

We also know that most people (over 50%) that have autoimmune thyroid have antibodies against other tissues. 9

This is important because as we will see, there are many things we can do to modulate the autoimmune response through diet, lifestyle and nutritional medicine that can decrease your risk of developing other AI diseases. Remember that any tissue is up for grabs for autoimmune destruction in AI disease.

Characteristic of Autoimmune Disease: Loss of Immune Tolerance
Why would we become allergic to ourselves? Are we really allergic to ourselves? Why would our immune systems attack self-tissue?

One of the things we have to have in order to prevent autoimmune disease is immune tolerance. Immune tolerance is the concept that the immune system tolerates (and does not react to) certain antigens in the body, including self-protein markers, and some types of foreign antigens as well, such as heavy metals or toxins. However, when the immune system loses this ability to tolerate a marker, then it initiates an immune response against this antigen or marker. The production of antibodies occurs as part of the immune response.

TH1/TH2 Balancing = Immune Tolerance
In a healthy immune system, there is a balance between two important aspects of the immune system: TH1 and TH2 responses. When you look at the immune system, there are two types of cells: T cells and B cells. The T cell response is called TH1 response (cell-mediated immunity). The B cell response is called TH2 response (humoral-mediated immunity). When your immune system has to destroy an antigen, it attacks it first (TH1 response), then it makes antibodies so that it can be more efficient in finding it (TH2 response). In a healthy immune response, the TH1 and TH2 systems are somewhat in balance.

Autoimmune Disease is Characterized by Polarity in TH1 and TH2 Systems
In AI disease, there is a polarity in these TH1 and TH2 systems. There is always a dominance in their TH1 or TH2 systems. AI diseases are promoted by imbalances in the TH1 and TH2 systems. Regardless of whether autoimmune diseases are caused by too much or too little exposure to micro organisms, it is now generally believed that adaptive immunity and an imbalance between the TH1 and TH2 immune responses are the key elements underlying the pathogenesis of the autoimmune process10

TH3 System Regulates TH1 and TH2 Response
TH3 is the regulatory system that balances the TH1 and TH2 systems. The TH3 system is made up of regulatory T cells that regulate the immune response between the TH1 and TH2 systems. One of the things we want is to have a TH3 system that is as strong as possible for this reason. We will learn later some important compounds that have a powerful effect on the TH3 system, such as vitamin D and glutathione.

There is a constant state of balanced chronic inflammation present in the gastrointestinal tract. This physiologic inflammation is essential for the maturing of the immune system and development of the normal morphology of the intestinal mucosa. 11

TH 17 System Activity Leads to Greater Tissue Destruction
There is one more important system involved in the immune response: the TH17 system. The TH17 system comes from T helper cells and induces IL-17 production. The more active the TH17 system, the more IL-17 produced and the more tissue destruction you get in the TH1 or TH2 shift. If you have a TH1 system that is dominant and an active TH17 system, then it is more destructive than before. One of our goals is to dampen the TH17 system in order to minimize tissue destruction.

Goals of Autoimmune Management
In order to manage autoimmune disease, you need to:
 Balance TH1 and TH2 systems
 Enhance the TH3 regulatory system
 Decrease the TH-17 response

When we manage the AI patient in functional medicine, we are trying to do 3 things:
1. Decrease the triggers of their AI flare-ups
2. Dampen their AI overzealousness altogether
3. Enhance their recovery

In order to accomplish this, we need to be able to answer the following questions:
 What systems are involved in flaring them up?
 What systems are involved in causing destruction of tissue?
 What systems are involved in their recovery?

If we can answer these questions, then we can start to ask what interventions we can employ to make the biggest change in these patients.

Content provided by Datis Kharrazian, D.C., Autoimmune Regulation of the Nitric Oxide and Glutathione Systems, 11/4/10

In part 3 of this 6-part series, we answer the following questions:

  • What are the mechanisms and mediators involved in autoimmunity?
  • Intestinal permeability promotes autoimmunity.
  • Gluten sensitivity and autoimmunity connection.

Continue to part 3 of series

References:
1. Clin. Diag. Lab. Immunology, July 2001, p. 678685
2. Betterele C and Zanchetta R. Update on autoimmune polyendocrine syndromes (APS). Acta Bio Medica. 2003; 74:9-43
3. Baillieres. Autoimmunity and hypothyroidism. Clin Endocrinol Metab. 1998; Aug 2 (3): 591-617
4. Lupus (2006) 15, 183-190
5. Expert Opin. Med. Diagn. (2008) 2(6):1-13
6. Lupus (2006) 15, 183-190
7. Autoimmunity, June 2004 Vol. 37 (4), pp. 253-256
8. Autoimmunity Review 2007; 6: 325-33
9. Betterele C and Zanchetta R. Update on autoimmune polyendocrine syndromes (APS). Acta Bio Medica. 2003; 74:9-43
10. NAT CLIN PRAC GASTRO & HEP SEPT 2005 VOL 2 NO 9
11. Gut. 2002 Feb;50(2):148-9