Autoimmune conditions are characterized by the presence of autoantibodies. It’s no exception with Graves’ disease and Hashimoto’s thyroiditis. While most endocrinologists focus on improving the thyroid panel (TSH and thyroid hormones), very few conventional medical doctors will do anything to improve the health of the person’s immune system, and thus normalize thyroid antibodies. The main reason for this comes down to their training in medical school, as they aren’t taught how to address the autoimmune component of these conditions. And it admittedly can be very challenging to normalize thyroid antibodies, which I’ll talk more about later this blog post.
Before discussing how to lower autoantibodies, I’d like to briefly discuss what antibodies are. Antibodies, also known as immunoglobulins, are Y-shaped molecules that help to protect the body against foreign substances called antigens. Examples of antigens include bacteria, viruses, fungi, chemicals, and there can even be dietary antigens. Essentially antigens lead to the formation of antibodies, and each antibody is manufactured to match a specific antigen. In autoimmunity, autoantibodies are produced against self-antigens, or against the cells of your own body.
I mentioned that antibodies are also known as immunoglobulins, and there are five immunoglobulin classes found in the serum:
Immunoglobulin A (IgA)
Immunoglobulin D (IgD)
Immunoglobulin E (IgE)
Immunoglobulin G (IgG)
Immunoglobulin M (IgM)
When discussing autoantibodies, we’re mostly referring to IgG. This includes the antibodies associated with Graves’ disease and Hashimoto’s. IgG is further divided into four subclasses, and the majority of known antibody-mediated autoimmune diseases are caused by IgG1 and IgG3 autoantibodies, although IgG4 plays a prominent role in the pathogenesis of at least 13 autoimmune diseases. (1) [1].
With Graves’ disease, unique IgG antibodies bind to and activate the TSH receptor on the surface of thyroid follicular cells, which leads to an increased production of thyroid hormones (1) [1]. Antithyroglobulin antibodies and antithyroperoxidase antibodies are also predominantly of the IgG class (2) [2]. It has been reported that Hashimoto’s thyroiditis can be divided into IgG4 and non-IgG4 thyroiditis (2) [2].
The 3 Main Types of Thyroid Antibodies
Let’s briefly take a look at the three most common types of thyroid antibodies [3]:
Thyroid peroxidase (TPO) antibodies. Thyroid peroxidase (TPO) is an enzyme that plays a role in the production of thyroid hormone. TPO antibodies [4] are the most common type of thyroid antibody. Although they are more closely associated with Hashimoto’s thyroiditis, many people with Graves’ disease have elevated TPO antibodies.
Thyroglobulin antibodies. Thyroglobulin is a glycoprotein that is secreted by thyroid follicular cells, and when someone has anti-thyroglobulin antibodies this means that the immune system is attacking and damaging thyroglobulin. These antibodies are associated with Hashimoto’s.
Thyroid stimulating immunoglobulins. Thyroid stimulating immunoglobulins are associated with Graves’ disease, and they bind to the thyroid stimulating hormone receptor, which causes the excess production of thyroid hormone.
As I’ve discussed in other blog posts, it’s common for people to have multiple types of thyroid antibodies. So for example, some people will have both TPO antibodies and thyroid stimulating immunoglobulins, while some will have all three of these autoantibodies. And since people with Graves’ disease and Hashimoto’s commonly develop other autoimmune conditions it’s also possible to have other types of autoantibodies as well.
What Causes Elevated Thyroid Antibodies?
I’ve spoken about the triad of autoimmunity [5] in the past, as there are three factors which are necessary for autoimmunity to develop, and thus lead to elevated autoantibodies. These three factors include 1) a genetic predisposition, 2) an environmental trigger, and 3) a leaky gut. The triad of autoimmunity applies to all autoimmune conditions, and not just Graves’ disease and Hashimoto’s.
A loss of self tolerance [6] is also necessary, and this is when the immune system doesn’t recognize our tissues and organs as being “self”. I discussed how people develop a loss of self tolerance in a past article, but I’ll list some of the different ways below:
- Exposure to an environmental trigger
- Having certain genetic polymorphisms
- Decrease in regulatory T cells
- Low selenium levels
- Low vitamin A levels
- Intestinal dysbiosis (imbalance of the gut flora)
Can Thyroid Antibodies Be Normalized?
It is possible to normalize thyroid autoantibodies. However, there are a few things you need to understand. First of all, different labs will commonly have different reference ranges for the same autoantibodies. As a result, you might test positive for a specific autoantibody with one lab, but test negative for the same autoantibody with a different lab. So how do you know which lab reference range is accurate? First of all, you do need to keep in mind that everyone is different, and we can make the argument that some people might be fine even if their thyroid antibodies are slightly elevated according to the lab reference range.
For example, the Labcorp reference range for TPO antibodies is currently 0-34 IU/mL. The Quest Diagnostics reference range for TPO antibodies is <9 IU/mL. I don’t know which reference range is more accurate, and we need to keep in mind that although the units are the same with these two labs, the methodologies can differ between labs, and there are other reasons why different labs have different ranges for the same marker.
In any case, if someone has TPO antibodies that are well above the reference range (i.e. 2,000 IU/mL), then we can conclude that this is abnormal. On the other hand, if someone has TPO antibodies that are consistently around 50 IU/mL does this mean that the autoimmune response isn’t as big of a concern? There’s some debate here, as some well known practitioners will say that a lower number doesn’t necessarily correlate with the severity of the autoimmune response, but I think it’s safe to say that most practitioners would still like to see the antibodies on the low side.
It’s also important to understand that it’s not always easy to decrease and normalize thyroid antibodies. In some people the thyroid antibodies will gradually decrease until they normalize without any setbacks. For others there will be more of a “rollercoaster” pattern, as the antibodies might fluctuate back and forth until they normalize. Then there are people with Graves’ disease and Hashimoto’s who don’t experience any significant decrease in thyroid antibodies, and in some cases their antibodies gradually increase over time. During this latter scenario this usually means that the person’s triggers haven’t been detected and/or removed, the gut hasn’t been healed, and/or there are other underlying imbalances that need to be addressed. I’m about to discuss this further.
4 Steps To Lower Thyroid Antibodies Naturally
Earlier I discussed the triad of autoimmunity, and how this will determine whether someone will develop elevated thyroid antibodies. So for example, if someone has a genetic predisposition for Graves’ disease or Hashimoto’s and they are exposed to a specific environmental trigger and at the same time they have an increase in intestinal permeability (a leaky gut), then autoimmunity is likely to develop. As a result, it shouldn’t be a surprise to learn that in order to lower thyroid antibodies you need to address these factors:
Step #1: Find the triggers. Not finding the triggers is probably the biggest reason why someone’s thyroid antibodies don’t decrease. Finding the triggers can admittedly be challenging at times, and usually involves doing a comprehensive health history, along with the appropriate testing. In 2018 I wrote a book that focuses on triggers, and while the title of the book is “Hashimoto’s Triggers [7]“, a lot of the information in this book can benefit people with Graves’ disease as well. I also discuss triggers in my book “Natural Treatment Solutions for Hyperthyroidism and Graves’ Disease [8]“.
Here are some potential autoimmune triggers:
- Food triggers (gluten, dairy, corn)
- Stress
- Pathogenic bacteria
- Viruses (i.e. Epstein-Barr [9])
- Parasites
- Heavy metals
- Xenoestrogens
- Overtraining
- Estrogen dominance
Step #2: Remove the triggers. Once the triggers have been detected, obviously the next goal should be to remove them. Sometimes this is easier said than done. For example, if someone discovers that a specific food is a trigger, then of course they can remove this food from their diet. On the other hand, if an infection or chemical is the trigger, then it can be challenging to address these at times. Certain infections can be difficult to eradicate, regardless of whether someone takes prescription antibiotics or natural antimicrobials. And some chemicals are more challenging to eliminate from the body than others.
Step #3: Correct underlying imbalances. Sometimes other underlying imbalances can interfere with healing, which can in turn prevent thyroid antibodies from lowering. For example, inflammation is associated with autoimmunity, and while finding and removing the triggers will frequently resolve the inflammation, this isn’t always the case. Sometimes further action is required to resolve the inflammation, such as taking higher doses of natural anti-inflammatory agents (i.e. curcumin, resveratrol, glutathione [10]). Having deficiencies in vitamin D, selenium, and omega-3 fatty acids can make it very challenging to lower thyroid antibodies.
Step #4: Restore the health of the gut microbiome. Having a healthy gut is necessary for a healthy immune system, and in some people, healing the gut can be challenging as well. Although there is a lot of great information on the Internet and in books on gut healing, most people need to do more than just take gut-healing supplements and eat gut-healing foods, as you need to make sure to remove those factors which are interfering with gut healing. This may sound like common sense, but many people only focus on reinoculation (with probiotics) and gut healing, and while these are important, doing these alone many times isn’t sufficient to restore the health of the gut. For more information on this please read my blog post entitled “What Is The 5-R Protocol [11]?”
Can Low Dose Naltrexone (LDN) Lower Thyroid Antibodies?
I spoke about LDN in a past article entitled “Low Dose Naltrexone and Thyroid Autoimmunity [12]“, and so I definitely would check this out for more information on LDN. This is an option for some people with Graves’ disease and Hashimoto’s to consider, as LDN can lower thyroid antibodies in some cases by modulating the immune system. However, while I’m not opposed to my patients taking LDN, you need to keep a couple of things in mind. First of all, LDN doesn’t work for everyone. Second, even when it does work, LDN isn’t doing anything to address the underlying cause of the problem. That being said, I mentioned earlier how sometimes it can be challenging to find and/or remove autoimmune triggers, and when this is the case there’s nothing wrong with taking LDN to modulate the immune system while still trying to address the cause of Graves’ disease or Hashimoto’s.
Is There a Role for IgG Autoantibodies in a Healthy Immune System?
Over the years some of the labs have lowered their reference range for thyroid autoantibodies, which suggests that there should be no autoantibodies found in healthy people. For example, some labs use a reference range of ≤1 IU/mL for thyroglobulin antibodies. But multiple journal articles discuss that small amounts of autoantibodies are present even in healthy individuals (3) [13] (4) [14].
One study found 66 autoantibodies that are common and abundant in the population, regardless of age, gender and disease status (3) [13]. It was suggested that IgG autoantibodies might be necessary and perform some key physiological function, including the clearance of intracellular debris during inflammation. Perhaps some autoantibodies have important physiological functions, and thus should be present in small amounts, while others don’t offer any benefits. Either way I think it’s safe to say that we don’t know everything about autoantibodies, and I’m sure we’ll learn even more about them in the future.
What Have You Done To Lower Thyroid Antibodies?
If you have the antibodies for Graves’ disease or Hashimoto’s (or both), please let me know what you have personally done to try to lower them, and if you were successful in doing so. If you were successful in lowering and/or normalizing them please let me know! And if you were unsuccessful please let me know! Thank you for sharing your experience with everyone.