Some of the most common questions that I get from people who reach out to me are about antibodies.
There seems to be a good deal of confusion about them and also a good deal of emotion and expectation attached to these numbers going up or down.
In this post, we examine thyroid antibodies and, hopefully, dispel some of the myths around them.
First of all, what are antibodies, exactly? I like to use military analogies when describing the immune system. And antibodies are like military intelligence (hold the oxymoron jokes).
They are the part of the immune system that gathers information on the bad guys (bacteria, viruses, fungus, parasites, etc.) and then they label those bad guys. Kind of like putting a red flag on them.
The invader is called an antigen. Antibodies bind to these antigens like a lock and a key. Every cell has antigens and these are what the immune system recognizes. And every cell in our body has a self-antigen which are supposed to let the immune system know that our own tissue isn’t a bad guy.
Once the bad guys have been labeled, other parts of the immune system are signaled and they attack and, in most cases, kill the bad guys. In some cases these antibodies can neutralize the bad guys all by themselves and not have to wait for reinforcements.
With autoimmune disease these antigen signals get confused and the immune system ends up attacking our own tissue.
Over the last 50 years there has been a lot of research in this area.
There is a region on cells located on some of our genes called the HLA (or Human Leucocyte Antigen) System. Many of these are located on chromosome 6 (for those of you keeping count).
Mutations or defects of HLA has been linked to many different autoimmune diseases. Exactly what happens is not known, there are numerous theories, but the end result is that our own tissue gets attacked and destroyed by the immune system.
There is a specific class of HLA (class II) that has been linked to autoimmune thyroid diseases like Hashimoto’s and there are also specific antibodies that are important in the disease.
There are 2 autoantibodies that are important:
Thyroid Peroxidase Antibody (TPO Ab): This antibody is the one that is usually high in autoimmune thyroid conditions like Hashimoto’s. It is also known as microsomal antibody.
Thyroglobulin Antibodies (TgAb): These aren’t seen high as often as TPO Ab. They are usually ordered when thyroid lab results seem strange because these antibodies can interfere with thyroid hormone production.
TgAb is also used to monitor progress after surgery for removing the thyroid in thyroid cancer.
In Hashimoto’s, TPOAbs are present in nearly all (>90 %) patients, while TgAbs can be seen in approximately 80%.
Antibodies against TPO (TPOAbs) and Tg (TgAbs) are of immunoglobulin G class, (IgG) and both are really good buddies with their antigens.
For TPO, it is for the enzyme thyroid peroxidase, which frees iodine and helps in the production of T4 and T3.
And for TgAb it is for Thyroglobulin, which is also used by the thyroid to produce T3 and T4.
When these 2 things get destroyed, over time, the body can’t make enough thyroid hormone.
This results in hypothyroidism and all the familiar problems of Hashimoto’s: fatigue, constipation, depression, hair loss, cold hands and feet, brain fog, memory issues and lots more.
Unlike TgAbs, TPOAbs can activate certain parts of the immune system (complement) and are able to cause damage to thyroid cells.
However, there isn’t much evidence that both antibodies have a major role in the formation of Hashimoto’s or in the destruction of thyroid cells.
It seems a lot more likely that other parts of the immune system are signaled and that they bring in the Navy Seals of the immune system which attack and kill thyroid cells.
TPO and TgAb antibodies, however, are considered the definitive test for whether or not you have Hashimoto’s. Basically, if either one or both of these are found to be above the lab range values, then you are positive for the disease.
Most labs have the high end at about 25 to 35. Numbers vary considerably, but it is not unusual for people who have been diagnosed to have antibodies above 1,000.
As I stated above, in most cases these antibodies, themselves, do not attack and kill thyroid cells.
What’s also important to understand is that there are various stages of autoimmune disease and depending on where you are in the progression, you will have different degrees of thyroid tissue destruction and, therefore, different symptoms.
According to Dr. Datis Kharrazian, there are 3 stages of autoimmune disease. While these stages are not recognized by conventional doctors, they are very useful in determining exactly where you are in the progression of the disease.
And realizing that there are stages and that the stages get worse and worse, is also helpful for motivating you to do as much as you can to stop the progression. (Hopefully!)
You can read more about these stages here.
The antibodies are really involved in signaling the immune system and in setting off a series of events that results in the attack and destruction of the thyroid.
I have written extensively about what happens in this previous post.
The important thing to understand here is that the amount of antibodies don’t necessarily directly correspond to how severe the Hashimoto’s is.
There are many reasons for this, but one simple way to look at it is this: The amount of destruction that is done by the army (the immune system) depends on the strength and number of the soldiers.
As I said earlier, the antibodies are really like the CIA or some intelligence gathering part of the army. The front line soldiers are the killers. If you have lots of soldiers and they are all revved up and ready to dance, then you get more destruction.
If your army is weak and there aren’t that many soldiers, then the CIA tells them to kill, kill, kill, but they can only do so much damage.
On the other hand, even if there are only a few CIA agents and there is a large, aggressive army, you will still have massive destruction (and loss of thyroid function).
Where am I going with all this? The amount of destruction, which really is the cause of how crappy you feel, depends on the strength and number of soldiers, not on the number of CIA agents in the field.
This is why antibodies are not a good measure of progress and often don’t correspond with how well people feel.
Antibody numbers don’t correspond, directly, with tissue destruction. As I mentioned above, in some cases TPO antibodies have been linked to tissue destruction, but more often, this is not the case.
Many patients and doctors or practitioners track these numbers and use them as a measure of whether or not what they are doing is working. And many times, they will find that there is no correspondence.
Obviously, getting antibody numbers to drop is not a bad thing. But it is also not necessarily such a good thing, because it may not be an indication that the destruction or the progression of the disease has slowed.
In conventional lab testing there really aren’t tests that are done to look at this. One theory with Hashimoto’s is that the ratio between the CIA and the soldiers is important.
The soldiers are also known as the TH-1 system, the cytokines or immune proteins associated with this part of the immune system are the killers.
The CIA is known as the TH-2 part of the immune system and you can test for ratios between TH-1 and TH-2 cytokines.
If there is a lot more of the soldiers than CIA agents, then the prognosis is not good and the disease tends to be more severe.
With Hashimoto’s there is a tendency towards more TH-1 than Th-2, but this is not always the case.
On the other hand if the CIA is more numerous or more balanced and the control and command part of the immune system (TH-3 or the regulatory part of the immune system- what we can call the General) is also strong, then, usually the prognosis is better and you can calm the attack and slow or stop the progression of the disease.
In reality, the immune system isn’t linear and this is an oversimplification. Testing is available to look at the cytokines that represent these different parts of the immune system, but there are many other factors that make current tests for this unreliable and not that helpful.
However, you can use these ideas to help figure out what you need to do in order to calm the attack, slow the progression of the disease and, most importantly, feel better.
The major cause of thyroid tissue destruction is something called apoptosis. This is programmed cell death.
Lots of crazy things happen on a molecular level (like cytoskeletal disruption, cell shrinkage, chromatin condensation, nuclear fragmentation, membrane blebbing, and DNA fragmentation – membrane blebbing, people!) to make this happen, but the easiest way to grok the root of it is to understand that it is initiated by inflammation.
The best way to slow the progression and minimize destruction is to do everything you can to stop inflammation and to strengthen the regulatory part of the immune system.
2 important anti-inflammatory agents are: Vitamin D and glutathione. These supplements strengthen the regulatory part of the immune system (TH-3 or the General).
(One important thing to note is that some people with Hashimoto’s have a defect with vitamin D receptors and may need to take more than is usually required by normal individuals.)
These are important anti-inflammatories.
Another player in the complicated drama of Hashimoto’s is TH-17. This is like a rouge agent that when numerous and aggressive can do major damage. TH-17 is highly inflammatory.
Natural supplements that reduce TH-17 include Turmeric and Resveratrol. Some Chinese herbs that have been shown to reduce TH-17 are Chang Shan or dichroa root and Huang Lian and Huang Qin whose active compound is berberine.
Also, it is very important to reduce the causes of inflammation in your diet. The three most inflammatory foods in our diet are gluten, dairy and soy.
Gluten has been extensively hybridized and deamidated and has been linked to the initiation and progression of thyroid autoimmunity.
Dairy products when commercially produced are full of antibiotics, hormones and god knows what else. They have also been linked to the initiation of various autoimmune diseases.
Soy is one of the most heavily genetically modified foods in our diet and is also quite difficult to digest.
Some research has indicated that thyroid replacement hormone can reduce TPO antibodies, though there is also some indication that natural desiccated hormone can raise antibodies in some individuals (it seems to be those who have a particularly severe immune reactivity – i.e., they have lots of inflammation).
Selenium has been found to reduce TPO antibodies in a number of studies.
Thyroid antibodies are important for determining whether or not you have Hashimoto’s but are not always a good indicator of how well what you are doing is working.
Do not get too excited if antibody numbers go up or down. It’s not the antibodies that are the problem as much as the other parts of the immune system that are attacking and destroying the thyroid.
Get excited about reducing inflammation. That should be your daily obsession. Really, its that important.
Thyroid replacement hormone and selenium have been shown to reduce TPO antibodies, but this may not work for everyone.
Hashimoto’s is complicated. It is a multi-system disorder that requires a multi-system approach. That’s why created my program: Healing Hashimoto’s: The 5 Elements of Thyroid Health. Click here to learn more.
References:
http://en.wikipedia.org/wiki/Apoptosis
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC555850/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271310/
http://www.thyroidmanager.org/chapter/hashimotos-thyroiditis/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271310/– Technichal, but great info on what happens in Hashimoto’s
http://www.ncbi.nlm.nih.gov/pubmed/15307940
http://www.ncbi.nlm.nih.gov/pubmed/7878464
http://www.ncbi.nlm.nih.gov/pubmed/20477110
http://www.medicalnewstoday.com/releases/241571.php
http://www.jimmunol.org/content/185/3/1855.full
http://www.cambridgemedicine.org/news/1299069648
http://jcem.endojournals.org/content/87/4/1687.long