If you have Graves’ disease or Hashimoto’s thyroiditis, and if you want to do more than just manage your thyroid symptoms, then you might be interested in joining our 21-Day Overcoming Graves’ Disease and Hashimoto’s Challenge (starts November 2nd!):

The 21-day challenge will include the following…

Component #1: Daily Overcoming Graves’ Disease and Hashimoto’s Video Lesson

During this daily 20-30 minute recorded lesson I will focus on a different topic that is essential to overcoming your autoimmune thyroid condition. There will be one lesson every day for 21 consecutive days (although a few lessons include multiple videos). If you’re interested in the specific topics that will be presented please check out the video where I discuss the 21-day challenge calendar (the website link is below).

Component #2: Daily 30-45 minute live group coaching session

The live group coaching calls will take place on Zoom, which is very easy to use on computers, mobile phones, and tablets. And if you are unable to attend live you’ll have the opportunity to email your questions during the separate Q & A sessions (discussed below). For those who choose to join live, the way it works is that I’ll send you a link to join the call, and if you are using a mobile phone or tablet you’ll need to install the free app. I will record every coaching session and post the recordings in a private membership area for those who are unable to attend live. As for the time of the coaching sessions, I will rotate them to accommodate those in different time zones. Most of the live calls will take place either 1pm or 8:30pm Eastern time (New York time zone).

Component #3: Recording of each coaching call for those who are unable to attend live

I hope most people will be able to attend at least 2 or 3 live sessions per week, although I’ll add that with my last two challenges there were participants who didn’t attend the live calls, but simply watched the recordings and emailed their questions for me to answer during the Q and A sessions (discussed below).

Component #4: Daily priority action step

I want people to take action, but I want the action steps to be attainable, which is why there will be a single priority action step each day, although at times there will be one or two additional action steps that aren’t as urgent.

Component #5: Access to a private members-only group

We want you to build relationships with one another and enjoy this challenge together. One way we accomplished this in previous challenges was through the live coaching calls, but another way was through the private members-only communities we had. Since not everyone wants to be on Facebook we initially hosted the group on a platform called Kajabi, and while we did have a lot of people participate, we realized that there are some limitations to Kajabi. So for second challenge I had two private members-only groups…one in Kajabi, and one in Facebook, and it worked out well. And so you can join either one of these groups, or both if you’d like! In our last challenge we had in June approximately 100 people joined the Facebook group and around 25 people joined the Kajabi group. I’ll pop into these groups every now and then, but I plan on having my nutritional health coaches moderate the groups.

Component #6: Weekly 90 minute live Q & A session

Although I’ll be answering some questions during the daily coaching calls, these will be around 45 minutes, and I will focus on answering live questions. But there will also be three separate live Q & A sessions (one per week) during the 21-day challenge. These will be at least 90 minutes long, although with both of my longer challenges I exceeded two hours with each of the Q & A sessions, as my goal is to answer ALL questions! I’ll once again rotate the day and times to accommodate those in different time zones, and so they will either be at 12pm, 1pm ET or 8pm ET. However, unlike the daily coaching calls, if you are unable to attend any of the Q & A sessions live you can email your questions ahead of time.

You Get All of This For A Single Payment of $49

If you watch the video on top of the registration page (the link is below) you’ll see dozens of people rave about my challenges, and I think it’s safe to say that just about everyone easily got back their investment.  I do want to mention that this past summer I had a 5-day challenge, but the testimonials on the website are from participants of my two longer challenges.

Optional Upgrade: 45-minute one-on-one diet and lifestyle call with a certified nutritional health coach

Both of my nutritional health coaches are excellent, and I thought it was important to include an option for affordable one-on-one support with all of the stress everyone is dealing with, although I’m confident the daily group coaching calls will also help with this. You have the option of doing this over the phone or through Skype/Zoom. If you listen to some of the video testimonials from members of the past challenges you’ll hear some rave reviews about the diet and lifestyle call! And so if it’s in your budget I’d highly recommend taking advantage of it for the discounted rate of $50. But if not you still will receive a ton of value from the rest of the challenge.

For more information on the 21-day challenge visit the link below:

www.ThyroidHealthChallenge.com/Enroll2020

Since 2009 I have had a practice that focuses on thyroid and autoimmune thyroid conditions, and while I do work with people who have non-autoimmune thyroid conditions (i.e. toxic multinodular goiter), most people I work with have Graves’ disease or Hashimoto’s thyroiditis.  Some people have the antibodies for both Graves’ disease and Hashimoto’s.  Every now and then someone will ask what the difference is between these two conditions, and so I figured I’d put together a blog post that discusses the similarities and difference between Graves’ disease and Hashimoto’s.

Let’s first start out by discussing the differences between these two conditions:

What Are The Differences Between Graves’ Disease and Hashimoto’s?

1. They involve different autoantibodies.  Those with Graves’ disease have elevated thyroid stimulating immunoglobulins, which is a type of TSH receptor antibody.  Hashimoto’s thyroiditis is usually diagnosed when someone has an elevated thyroid stimulating hormone (TSH) in the presence of thyroid peroxidase and/or anti-thyroglobulin antibodies.  However, it’s worth mentioning that many people with Graves’ disease also have elevated TPO antibodies, and some people have all three of these thyroid antibodies.

2. Hashimoto’s involves damage to the thyroid gland.  Whereas Graves’ disease involves the thyroid stimulating immunoglobulins binding to the TSH receptors without causing permanent damage, this isn’t the case with Hashimoto’s.  In Hashimoto’s there is damage to the thyroid gland.  And while the thyroid gland can regenerate, it does so slowly, and sometimes the damage is so extensive that the person needs to remain on thyroid hormone replacement.  Keep in mind that it can take many years before there is sufficient damage to the thyroid gland that results in an elevated TSH and thyroid hormones that are out of range.

3. Graves’ disease involves hyperthyroidism, and Hashimoto’s involves hypothyroidism.  The truth is that not everyone with Hashimoto’s experiences overt hypothyroidism, as many times it’s subclinical.  In other words, they might have an elevated TSH with the thyroid hormone levels within the lab reference range.  It’s also important to mention that some people with Hashimoto’s experience hyperthyroidism due to Hashitoxicosis.  On the other hand, most people with Graves’ disease will experience overt hyperthyroidism, although there are exceptions.

4. The symptom management differs.  Because most people with Graves’ disease experience overt hyperthyroidism, most endocrinologists will recommend antithyroid medication (i.e. methimazole, PTU) to their patients.  Of course many will recommend radioactive iodine or thyroid surgery.  With Hashimoto’s, thyroid hormone replacement is commonly recommended.  This is true even if the thyroid hormone levels are looking good, as many medical doctors will go by the TSH alone.

5. Unmanaged hyperthyroidism is arguably a greater risk than unmanaged hypothyroidism.  The truth is that there are risks of both unmanaged hyperthyroidism and hypothyroidism.  But arguably unmanaged hyperthyroidism is a greater risk, as it can lead to heart arrhythmias, decreased bone density, and in rare cases thyroid storm, which is a life threatening situation.  On the other hand, myxedema is a severe form of hypothyroidism that can be life threatening, although it’s very rare.

6. The autoimmune triggers can differ.  While there is an overlap of certain triggers, there can also be different triggers for different autoimmune condition.  For example, while stress can be a factor with both Graves’ disease and Hashimoto’s, in the research it shows that it’s a greater factor with Graves’ disease.  And while there is a case report suggesting that Blastocystis Hominis might be a trigger of Hashimoto’s, nothing in the research suggests that it’s a potential trigger of Graves’ disease.

What Are The Similarities Between Graves’ Disease and Hashimoto’s?

So now that you know some of the differences between Graves’ disease and Hashimoto’s, let’s take a look at some of the differences:

1. They are both autoimmune thyroid conditions.  Both Graves’ disease and Hashimoto’s are autoimmune conditions that affect the thyroid gland.

2. Most medical doctors don’t do anything to address the underlying cause of either condition.  Every medical doctor knows that Graves’ disease and Hashimoto’s are autoimmune conditions, yet they never do anything to address the autoimmune component.  Of course this comes down to their training in medical school, and fortunately some medical doctors are open minded enough to look into underlying causes, although not nearly enough.

3. It’s possible to reverse the autoimmune component.  Although there are genetic factors behind autoimmune conditions, it still is possible to reverse the autoimmune component of both Graves’ disease and Hashimoto’s.  This admittedly isn’t easy to do, as one needs to find and remove the autoimmune triggers, and since a leaky gut is a factor with autoimmunity it is also necessary to heal the gut.

 

One of the most common questions I have received in 2020 is whether or not those with autoimmune thyroid conditions are more susceptible to getting Covid-19. It’s a good question, as both Graves’ disease and Hashimoto’s are immune system conditions, and viruses are more likely to impact those people with a compromised immune system.  Up until this point my response to this question has been that I don’t think having an autoimmune condition itself is the biggest factor, but of greater concern is that many people with thyroid autoimmunity have other things “dragging down” their immune system, which might make them more susceptible to getting Covid-19 (as well as other viruses).

But now that Covid-19 has been around for awhile there have been a few studies evaluating its effects on thyroid health, and whether people with thyroid autoimmunity are more susceptible to contract this virus.  In June of this year a study came out in the United Kingdom showing that there was no data available at that time suggesting that patients with an autoimmune thyroid condition remain at higher risk of getting Covid-19 (1). The study also mentioned that in patients severely affected by Covid-19, changes in thyroid function might be a result of a “sick euthyroid” syndrome, although the authors did mention that there might be specific thyroid-related damage which requires further investigation.

However, in July a journal article was released entitled “Thyroid disease is associated with severe coronavirus disease 2019 (COVID-19) infection” (2).  The article looked to explore the relationship between thyroid conditions and severe cases of Covid-19. Based on the data the authors concluded that thyroid disease seems to be associated with an increased risk of severe Covid-19 infection, and they gave the following three reasons why this may be the case:

1. Thyroid hormones are important in the regulation of the innate immune response. Therefore, an excess or deficiency of thyroid hormones levels observed in thyroid disease will lead to dysregulation of the innate immune response.

2. Increased levels of proinflammatory cytokines such as TNF-α and IL-6 was observed in patients with thyroid disease. Increased levels of these cytokines were also observed in patients with severe Covid-19 and correlates to the development of severe outcomes.

3. Some thyroid patients, especially those with subacute thyroiditis, were taking corticosteroids. Meta-analysis showed that corticosteroid treatment in Covid-19 patients was associated with higher mortality, longer length of hospital stay, and higher rate of bacterial infections. This isn’t surprising since corticosteroids suppress the immune system.

Most of the people I work with aren’t taking corticosteroids, and I think it’s safe to say that “point #3” doesn’t apply to most people with Graves’ disease or Hashimoto’s, although I should mention that some people with moderate to severe thyroid eye disease will take corticosteroids such as Prednisone, thus making them more susceptible to getting Covid-19 (or another viral infection).  The first and second points mentioned above do apply to most of the people I work with.  But as I mentioned earlier, there are other factors that can be having a negative effect on one’s immune system that can make them more susceptible to viruses such as Covid-19, including having weak adrenals, an unhealthy gut (most of the immune cells are located in the gut), an increased toxic load, certain nutrient deficiencies, exposure to toxic mold, etc.

Can Covid-19 Cause Subacute Thyroiditis?

Subacute thyroiditis is an inflammatory condition of the thyroid gland which causes damage to the thyroid follicles, and as a result, large amounts of thyroid hormones are released into the circulation, resulting in overt hyperthyroidism.  However, unlike Graves’ disease, this state usually self resolves after a few months, although many will first experience a transient period of hypothyroidism.  To learn more about this condition you might want to check out my blog post entitled “Graves’ Disease vs. Subacute Thyroiditis: What’s The Difference?“.

A case study in July showed that an 18-year-old woman developed subacute thyroiditis after getting infected with Covid-19 (3). Another study revealed that a substantial proportion of patients with Covid-19, requiring high intensity of care, present with thyrotoxicosis and low serum thyroid stimulating hormone (TSH) concentrations, possibly as a consequence of subacute thyroiditis induced by SARS-CoV-2 (4).  In other words, SARS-Cov-2 can directly infect the thyroid gland, leading to subacute thyroiditis.

Black Cumin and Covid-19

While on the subject of Covid-19, I would like to mention that there are a few studies which show that Nigella Sativa (black cumin) might benefit those with Covid-19.  Black cumin has numerous health benefits, as it has demonstrated antiviral, antioxidant, anti-inflammatory, immunomodulatory, bronchodilatory, and antihistaminic properties (5).  It also shows anti-hypertensive, anti-obesity, anti-diabetic, anti-hyperlipidemic, anti-ulcer, and antineoplastic activities, which can help with comorbidities commonly found in Covid-19 patients (5).  In addition, the active constituents of N. sativa such as nigellidine and α-hederin have been identified as potential inhibitors of SARS CoV-2, and thymoquinone (the chief bioactive constituent of black cumin) suppresses mRNA expression which downregulate interferon genes and other inflammatory responses (5) (6).

Even though I have written a blog post on black cumin, in the past this is something I’ve mainly given as part of a protocol to those with H. pylori.  And while I’m not suggesting for everyone to take black cumin specifically to reduce their chances of getting Covid-19, keep in mind that it can potentially help to minimize the impact other viruses have on your health as well, and as I listed above, it has numerous other health benefits. So at the very least it might be something to have on hand.  There is one more thing I would like to mention, as the blog post I wrote related to black cumin focused on hypothyroidism and Hashimoto’s, but it’s also fine for most people with hyperthyroidism and Graves’ disease to take black cumin.

In summary, according to the research people with Graves’ disease and Hashimoto’s thyroiditis seem to be more susceptible to getting Covid-19. However, as I mentioned earlier, the reason for this might be related to other imbalances commonly found in people with these conditions that can further compromise the immune system.  Either way the goal should be to do everything you can to improve the health of your immune system, and black cumin might also be something to consider adding to your supplement arsenal when combating viruses.  You also might want to check a blog post I released earlier this year entitled “5 Ways To Improve Your Immune Health Without Taking Supplements”.

I’ve written separate articles on thyroid peroxidase (TPO) antibodies and anti-thyroglobulin antibodies, but I haven’t put together a post on thyroid stimulating immunoglobulins…until now!  These antibodies are associated with Graves’ disease, and it’s unfortunate that some endocrinologists don’t test their hyperthyroid patients for these antibodies, but instead will test the TPO and/or anti-thyroglobulin antibodies.  While it’s common for people to have two or three different thyroid antibodies, everyone with hyperthyroidism should get the thyroid stimulating immunoglobulins tested.

So what are thyroid stimulating immunoglobulins (TSI), and how do they differ from other types of thyroid antibodies?  TSI are a type of thyrotropin (TSH) receptor antibody (TRAB). There are actually two types of TSH receptor antibodies. In addition to thyroid stimulating immunoglobulins, there are also thyroid binding inhibitory immunoglobulins (TBII), which is a type of thyrotropin receptor blocking antibody.  These antibodies bind to the TSH receptor and inhibit the binding of TSH, thus blocking the synthesis and secretion of thyroid hormones.  These aren’t commonly tested, and one reason is because not all labs offer this.

What Do Elevated TSI Levels Indicate?

Elevated TSI levels are associated with Graves’ disease.  What happens is that the TSI bind to the TSH receptors, which results in the excessive production of thyroid hormone.  This is why most people with Graves’ disease have hyperthyroidism, although some people have subclinical Graves’ disease, which is when the TSI are elevated, the TSH is depressed, but the thyroid hormone levels are within the lab reference range.

What Causes Elevated Thyroid Stimulating Immunoglobulins?

As I have mentioned, elevated TSI levels are associated with Graves’ disease, which is an autoimmune condition.  In the past I’ve discussed the triad of autoimmunity, and according to this, in order for autoimmunity to develop the following three factors need to be present: 1) genetic predisposition, 2) exposure to an environmental trigger, 3) a leaky gut.  So just as is the case with any autoimmune condition, someone with elevated TSI levels has a genetic predisposition for Graves’ disease, but having the genetics alone doesn’t mean they will develop thyroid autoimmunity, as they will need to be exposed to an environmental trigger and have a leaky gut.

What Is The Lab Reference Range?

Unfortunately different labs will use different units of measurements, and you can’t compare them with one another.  For example, the Labcorp reference range is 0.00-0.55 IU/L, whereas the reference range for Quest Diagnostics is <140%.  As for the thyrotropin (TSH) receptor antibody test, Labcorp has a reference range of 0.0−1.75 IU/L, while Quest Diagnostics has a range of ≤2.00 IU/L.  If at all possible I recommend getting the thyroid stimulating immunoglobulins tested, although it of course is fine to get both the TSI and TRAB tested.

Some reading this might wonder what the “optimal” reference range is for these markers, and whether the goal should be to have a level of zero.  While you want the levels to be well below the lab reference range, I wouldn’t say that they have to be zero in order for someone to be in a state of remission.  As for the optimal reference range, I like to see the TSI less than 80% or less than 0.30 IU/L, although this is just what I look for, as I haven’t seen any other practitioners list optimal reference ranges.  It’s also important to mention that some labs don’t reveal a numerical value below the reference range.  For example, if the TSI is below the reference range it might show up on the report as <0.55 IU/L or <120%.

The Relationship Between Thyroid Stimulating Immunoglobulins and Thyroid Eye Disease

Because a higher TSI level usually indicates a more vigorous immune system response, typically the higher the TSI, the more likely someone is to have thyroid eye disease.  For example, if someone has a TSI greater than 300% they are more likely to have thyroid eye disease symptoms when compared to someone with a TSI less than 300%.  Of course there are always exceptions, as I’ve had patients with very high TSI levels who didn’t experience any signs or symptoms of thyroid eye disease.

How Can You Decrease Thyroid Stimulating Immunoglobulins?

As for how to decrease and normalize thyroid stimulating immunoglobulins, the approach is similar to lowering other autoantibodies:

1. Find and remove your triggers. I mentioned the triad of autoimmunity earlier, and exposure to an environmental trigger is one of the factors that causes the development of an autoimmune condition.  As a result, it makes sense that in order to reverse the autoimmune component and lower thyroid stimulating immunoglobulins you will need to find and remove any immune system triggers.

2. Heal the gut. Another component of the triad of autoimmunity is a leaky gut, and so you of course need to heal the gut.  Check out the blog post I wrote on the “5R protocol” for more information on how to heal your gut.  But I’ll say here that you usually need to do more than take probiotics and gut healing agents, as these won’t be effective if you don’t address the factor that is compromising the gut.  For example, if someone has a gut infection that is causing a leaky gut, this needs to be addressed. Similarly, if someone is eating gluten and this is causing a leaky gut, you can’t fix this problem by taking digestive enzymes, probiotics, and drinking bone broth.  In this situation you would need to eradicate the gut infection.

3. Correct other imbalances.  Other imbalances can also be a contributing factor.  For example, having certain nutrient deficiencies can make someone more susceptible to developing an autoimmune condition, such as selenium.  In fact, the research shows that selenium can potentially lower both TSH receptor antibodies and TPO antibodies (1), although you still need to remove the trigger and heal the gut.

4. Break the chronic inflammatory cycle.  While removing the triggers and healing the gut will usually resolve the inflammation, this isn’t always the case.  Sometimes additional measures need to be taken in order to break this cycle, such as taking high doses of natural anti-inflammatory agents (vitamin D, EPA and DHA, curcumin, resveratrol).  Low dose naltrexone might also help to break the chronic inflammatory cycle, and thus is something to consider, although I would first try the natural anti-inflammatory agents.

Do You Have Elevated Thyroid Stimulating Immunoglobulins?

If you have elevated TSI levels, I’d love to hear if you have done anything to try to lower them.  Perhaps you took a natural treatment approach, natural anti-inflammatory agents, low dose naltrexone, or did something else to modulate your immune system.  Either way, please feel free to share your experience in the comments section below.

I think it’s safe to say that many people reading this hope to achieve a state of remission…and remain in remission! Many of you know that I was diagnosed with Graves’ disease, and I’ve been in remission since 2009. It wasn’t easy getting into remission, and I face the same challenge with helping my patients restore their health, but of course it beats the alternative. While achieving a state of remission isn’t easy, it can also be challenging to maintain a state of wellness. I’ll discuss both of these in this blog post.

When Is Someone Considered To Be In Remission?

In the past I’ve discussed the difference between remission and cure, and at least with regards to Graves’ disease and Hashimoto’s thyroiditis, I’m not a big fan of using the word “cure”.  And the reason for this is because genetics do play a role in the development of thyroid autoimmunity, and might even play a role in some non-autoimmune thyroid conditions. So while I would love to say that “my Graves’ disease condition has been cured”, because there is a genetic component there is always a chance that a relapse can occur.

As for when someone is considered to be in remission, here is how I knew I achieved remission when I was dealing with Graves’ disease:

1. My thyroid panel (TSH, free T3, free T4) was optimal without taking anything that influences these markers. In my situation I took the herb bugleweed, but many people with hyperthyroidism take antithyroid medication, and you can’t be in a state of remission if you’re still taking either one to maintain optimal levels. With hypothyroidism/Hashimoto’s it’s a little bit different, and I’ll further elaborate on this shortly.
2. My thyroid stimulating immunoglobulins were negative (I have always tested negative for thyroid peroxidase and anti-thyroglobulin antibodies
3. The above markers remained normal a few months after testing multiple times. In other words, you can’t rely on a single negative reading.
4. Other triggers/imbalances were corrected, such as my adrenals and depressed secretory IgA levels
5. Hyperthyroid symptoms were completely gone

So if you have Graves’ disease or Hashimoto’s, or the antibodies for both of these conditions, then in order to be in a “true” state of remission you need to at the very least have 1) a normal thyroid panel, 2) normal thyroid antibodies, 3) normal markers upon retesting. The reason why I say a “true” state of remission is because most medical doctors consider someone with thyroid autoimmunity to be in remission if their thyroid panel looks good and they are off of any thyroid medications.  As I mentioned earlier, the scenario is a little different with hypothyroidism/Hashimoto’s, and so to make it easier to understand I’d like to separately take a look at Graves’ disease and Hashimoto’s:

Achieving Remission in Graves’ Disease

When is someone with Graves’ disease considered to be in remission?  I briefly discussed how I knew that I was in remission, and so I have already answered the question, but I’ll summarize it below:

1. Optimal thyroid panel (TSH, free T3, free T4)
2. Not taking any antithyroid agents (i.e. methimazole, PTU, carbimazole, bugleweed, etc.)
3. Negative thyroid stimulating immunoglobulins which aren’t a result of taking an immune-modulating agent such as low dose naltrexone (LDN). I discussed LDN in greater detail in a previous blog post entitled “5 Things To Know About LDN and Thyroid Autoimmunity”.
4. The above markers remain normal a few months after testing multiple times. In other words, you can’t rely on a single reading.
5. Other triggers/major imbalances have been corrected.
6. Hyperthyroid symptoms are completely gone

Achieving Remission in Hashimoto’s

With Hashimoto’s it’s a different situation, as while some people are able to avoid taking thyroid hormone replacement or are able to wean off of it, sometimes the damage to the thyroid gland is severe enough where the person needs to take thyroid hormone on a long term basis. So while it’s great when someone is able to reduce the dosage of their thyroid hormone medication and eventually wean off of it completely, not being able to do this doesn’t mean that the person hasn’t achieved remission.

I know this might be confusing to some people, as with Graves’ disease I mentioned how the person needs to be off of antithyroid medication and/or antithyroid herbs before concluding that they’re in remission. So what’s the difference between remission in Graves’ disease and Hashimoto’s? First of all, in Graves’ disease antithyroid agents such as methimazole, PTU, and bugleweed are of course taken to lower thyroid hormone levels, but nobody has a “methimazole deficiency”, or a “bugleweed deficiency”. On the other hand, it is very possible to have a thyroid hormone deficiency, and if this is the case AND the damage to the thyroid gland can’t be reversed then the person will probably need to take thyroid hormone replacement.

So if someone has Hashimoto’s and the autoimmune response has normalized, they still might not have an optimal thyroid panel unless if they take thyroid hormone replacement.

To summarize, in order for someone with Hashimoto’s to be in remission the following need to occur:

1. Optimal thyroid panel (TSH, free T3, free T4) with or without thyroid hormone replacement
2. Negative thyroid peroxidase and/or anti-thyroglobulin antibodies, which aren’t a result of taking an immune-modulating agent such as low dose naltrexone (LDN).
3. The above markers remain normal for at least a few months after retesting multiple times. In other words, you can’t rely on a single negative reading.
4. Other triggers/imbalances have been corrected
5. Hypothyroid symptoms are under control

So with thyroid autoimmunity, while there are a few different things I look at before I consider whether someone is in remission, the number one thing that needs to be normal is the thyroid antibodies. With Graves’ disease, if the thyroid antibodies are negative it’s usually just a matter of time before the thyroid panel normalizes, and thus the person won’t need to take antithyroid agents. On the other hand, if the thyroid antibodies are normal with Hashimoto’s, the person still might need to take thyroid hormone replacement, depending on how much damage to the thyroid gland has taken place.

Achieving Remission in Non-Autoimmune Thyroid Conditions

With non-autoimmune thyroid conditions there of course are no thyroid antibodies, and so the primary goal is to normalize the thyroid hormone levels, while addressing the underlying imbalances responsible for the thyroid condition.  For example, if someone has toxic multinodular goiter, then the goal should be to correct the underlying imbalances responsible for the goiter and nodules, normalize the thyroid panel, etc.  Having problems with estrogen metabolism and/or insulin resistance can lead to multinodular goiter, and so if either of these problems were the cause then they would need to be addressed in order to improve the person’s thyroid health.

Does Every Imbalance Need To Be Corrected In Order To Achieve Remission?

When I was dealing with Graves’ disease I ordered an adrenal saliva test, and I had depressed cortisol levels, a depressed DHEA, a depressed 17-OH progesterone, and a depressed secretory IgA.  I worked on improving my adrenal health and retested the adrenal saliva panel, and eventually all of these markers normalized.  But you need to keep in mind that not every out of range marker necessarily relates to your thyroid or autoimmune thyroid condition.

For example, let’s say someone with Graves’ disease or Hashimoto’s gets a comprehensive stool panel, and it reveals parasites, along with some opportunistic bacteria.  While it would be great to see a perfectly normal test (if one chooses to retest), it’s not uncommon for people to have elevated opportunistic bacteria, but if this were the only positive finding then it wouldn’t mean that the person with Graves’ disease or Hashimoto’s isn’t considered to be in remission.  In other words, in this situation the opportunistic bacteria wouldn’t need to be normal in order to conclude that the person is in remission.

Another example involves Epstein-Barr.  Most people will test positive for Epstein-Barr, and while testing positive for the Epstein-Barr virus viral-capsid antigen (EBV VCA) IgM antibodies indicates that Epstein-Barr is active, having very high values of the IgG antibodies associated with Epstein-Barr (there are three of these) can also mean that Epstein-Barr is causing trouble.  If someone has very high EBV IgG levels but everything else looks great and they’re symptom-free, does this mean that they’re not in remission? If the person was feeling great, the thyroid panel and thyroid antibodies were well within range, and certain other imbalances were corrected then I would say that the person is in remission, although perhaps they still need to work on improving their immune system so that Epstein-Barr (or other infections) won’t cause problems in the future.

How I Have Maintained a State of Wellness Since 2009

Every now and then someone will ask me how I have maintained a state of wellness since achieving remission in 2009.  While I’m sure a certain amount of luck has played a role, without question I’ve also done a lot of things to maintain my health, including the following:

• Eating well most of the time. I definitely haven’t been perfect with the diet since 2009, and while I eat well most of the time, I do occasionally indulge in “bad” foods such as pizza, ice cream, cookies, etc. I’m hoping this will serve as encouragement for those who think they might need to be super-strict on a permanent basis, as this usually isn’t the case. Once again, I do eat well most of the time, usually following a modified-Paleo diet.
• Blocking out time for stress management daily. Stress was a huge factor in the development of my Graves’ disease condition, although I was in denial when I was diagnosed with Graves’ disease, as I greatly overestimated my stress-handling skills.  But once I saw the state of my adrenals I started incorporating stress management on a daily basis, and I recommend for all of my patients to do the same.
• Getting sufficient sleep. I’ve always been an “early bird”, and so staying up super late wasn’t something I ever did on a regular basis.
• Being aggressive with detoxification. This is something that separates me from a lot of people, as I’m always working on reducing my toxic load.  I try to do as much as I can through diet (i.e. cruciferous vegetables, dandelion leaves, cilantro), I go in my infrared sauna at least twice per week for 25-30 minutes, and I usually follow a detoxification program on a quarterly basis. I realize that many people don’t have access to a sauna, but you can accomplish a lot through diet and supplementation, and of course you also want to do as much as you can to avoid chemicals.  So avoid drinking out of plastic water bottles, use natural cleaners and cosmetics, eat organic whenever possible, and do other things to minimize your exposure to environmental toxins.

How Can YOU Achieve Remission?

I’m sure some people are wondering how they specifically can get into remission.  It comes down to finding and removing triggers, correcting other underlying imbalances, and healing the gut.  I’ve written hundreds of articles and blog posts on this website that can help you with this, and I also have two books, one on hyperthyroidism and Graves’ disease, and another on Hashimoto’s thyroiditis.  In addition, if you haven’t yet joined my “Graves’ Disease and Hashimoto’s Natural Solutions Support Group” you can do so by clicking here.