These days, there is a lot of focus on diet and supplements as a solution to autoimmune thyroid problems. The basic idea behind these approaches is to reduce, and ideally stop, any autoimmune response that may be damaging to the thyroid gland. However, in some special cases, this may not always be the right approach.
In most countries, thyroid levels are only tested once a person has become symptomatic. It is rare for routine health screening to contain a complete thyroid hormone assessment, including the most common autoantibodies TPOAb and TgAb (those associated with Hashimoto’s thyroiditis). However, if one is performed and a patient is told that they have raised autoantibodies, they may well want to find out what can be done to stop this response before it does any serious damage to the thyroid gland.
Therefore, if someone discovers that they have Hashimoto’s thyroiditis in its early stages before the thyroid gland is damaged, then reducing the autoimmune response using an Autoimmune Protocol (AIP) can be extremely helpful indeed.
However, by the time some people find out they have Hashi’s, their thyroid gland is often already very damaged. Because the thyroid gland is the most important organ for converting T4 to T3, the loss of thyroid tissue greatly reduces the patient’s ability to convert. Once most of the thyroid gland is destroyed, a thyroid patient typically loses around 25% of their total T4 to T3 conversion capability. Furthermore, the loss of T3 can be far more than this, because for some people the T3 contribution of their thyroid gland through conversion of T4, and through direct production of T3 can be very large. I explain this in more detail in my book, The Thyroid Patient’s Manual.
Losing a significant amount of production and conversion capability can be a huge problem. It can, in some cases, make using an AIP problematic. Let me discuss my own history first, before talking more generally about this.
Paul Robinson’s own history of Hashimoto’s and losing a lot of T4 to T3 conversion capability.
I was diagnosed with Hashimoto’s thyroiditis around the age of thirty. My symptoms were already quite extreme when I went to see my family doctor: severe fatigue, weight gain, dry skin, dry hair, memory issues, slow thinking etc. Surprisingly, she ran a full thyroid panel and found that my TSH was around 70 and my FT4 and FT3 levels were below the bottom of the reference ranges. Hashimoto’s was already advanced. During the previous year or two, I had probably had some more minor symptoms, but my thyroid gland had compensated a great deal even though it was being severely damaged. Thyroid tissue does not recover from this attack and it simply becomes dead non-functional tissue.
Over the last few years, I have tested DIO1 and DIO2 and found that both my parents gave me a copy of the defect in each gene. Hence, I am homozygous for both DIO1 and DIO2. When this is the case and the gene defects have manifested, which I believe mine did when I was in my late twenties, the effect is to have more of the bioavailable FT4 in the blood be converted to Reverse T3 (rT3) and to have less FT4 converted to FT3 (the active thyroid hormone). So, when this happens the person is much more likely to be symptomatic with thyroid hormone issues, even when they are on Levothyroxine (T4) treatment. I will give you a blog post link at the end with more information about these gene defects and how to test for them.
So, because Hashimoto’s had destroyed a lot of my thyroid gland I would already have lost a great deal of my ability to convert from T4 to T3. The DIO1 and DIO2 gene defects would also have been likely to further impair this conversion ability.
It is no surprise that Levothyroxine (T4) medication never worked for me at all and left me with all the symptoms that I had when I was first diagnosed. Even T4/T3 combination therapy failed to resolve my symptoms. T3-Only (T3-monotherapy) did help a great deal. However, for the first few years on T3-Only therapy, I found it hard to get my T3 daily dosage over 35-40 mcg. I felt much better on the T3, but not completely optimal. This was true even though I had created a way of using T3 to correct my low cortisol (the Circadian T3 Method – or CT3M).
The reason that I could not become optimal on the T3 at the beginning was that I still had some thyroid function left. It was impossible for me to shut this production off by taking enough T3 to completely suppress the thyroid gland without becoming hyperthyroid. So, I had some T4 left in my system. It may well have been at the very low end of the reference range (or just below it) but it was there and measurable on blood tests. Reverse T3 (rT3) could not be tested back then, but I imagine that a lot of the T4 my remaining thyroid tissue was making was converting to rT3. This is because my TSH was very low due to T3-Only therapy. We know that low TSH tends to increase the conversion to rT3, because low TSH downregulates the production of the deiodinase enzymes that convert T4 to T3. My autoantibodies were also still present, albeit at a lower level than when first diagnosed.
Over a period of a few years, the ongoing autoimmune attack gradually destroyed my thyroid gland completely. As my thyroid was destroyed, my autoantibodies got lower and my FT4 got closer to zero. I was gradually able to increase my T3 dosing and as it approached 50 mcg per day, my health, energy and wellness began to return to normal.
After a few years, I was able to get my T3 dosage to 60 mcg per day. This slow process of increasing the T3 was not anything about me slowly getting adjusted to it. It was that, whilst my thyroid gland was producing T4, I was simply unable to get the T3 dosing up. Any T4 produced by my thyroid would have given me some small amount of extra FT3 but also enough rT3 that I simply could not cope with.
When I was at 60 mcg of T3, I felt extremely well. I could function as I could before I had become ill. At that point, I had no thyroid tissue left at all.
What is the point of my story? Well, here is the important bit.
I did try a number of autoimmune protocols e.g. using selenium supplements, adopting a gluten-free and dairy-free diet for over two years. They failed to make any difference to me. However, if these approaches have been successful in stopping the autoantibodies earlier on, the consequence would have been to permanently leave me with ill health! I will explain why this would have been the case.
I had a major T4 to T3 conversion issue that had nothing to do with the ongoing autoimmune response. It was everything to do with the gene defects and the loss of thyroid gland tissue. Basically, I had lost too much T4 to T3 conversion ability already. I actually NEEDED to get my T4 totally out of my system. The only way I could do that effectively was to have the Hashimoto’s run its course and destroy my thyroid gland completely. Once my thyroid could no longer make T4 I could get my T3 higher and feel well. The fact that my autoantibodies, fell to zero had little or no benefit – that was just a side effect of having no more thyroid tissue.
I did try several times to raise my T3 beyond 50 mcg when I had some thyroid tissue left because I wanted to get the T3 dose up and to shut down my thyroid but it just made me feel hyper and ill. I was simply unable to completely shut the thyroid gland down, whilst I still had some thyroid tissue left.
The above is also backed up by the fact that even today I am unable to add even 5 mcg of T4 medication per day without feeling ill within a week. I just cannot cope with the T4 and the rT3 it produces.
I now consider myself lucky that my Hashi’s ran to completion and destroyed my thyroid gland utterly. When I was first diagnosed it was already too late to ever regain decent T4 to T3 conversion – the thyroid tissue loss combined with the gene defects had already made it impossible for me to deal with T4 properly.
I never wrote about this aspect of my own health issue in my Recovering with T3 book, as I felt it was far too complex and would have made the book too long. I also did not know when I first wrote it that I had the DIO1 and DIO2 gene defects.
What are the implications for other Hashimoto’s patients considering using an AIP?
The dietary and supplement approaches that are currently popular in terms of reducing and stopping the thyroid autoimmune response are excellent if the person finds out they have Hashimoto’s thyroiditis early in the process. There is no doubt of this. I think these approaches are excellent early on before there is significant thyroid tissue damage.
However they do suffer from a couple of problems:
1) Often, it is too late to avoid thyroid tissue damage and the lost conversion ability that comes with it. The diagnosis of Hashimoto’s frequently comes at the point when much of the thyroid gland has already been destroyed.
2) There are often many other problems that cause T4 to T3 conversion issues that no amount of working with diet or supplements is going to help, e.g. DIO2, DIO1 gene defects don’t go away, lost thyroid tissue doesn’t come back etc.
Let me be very clear if the autoimmune issue is found early enough before very much thyroid damage is caused and if the autoimmune response can quickly be stopped in its tracks, then this is extremely helpful. In addition, if the thyroid patient is unlikely to lose a significant amount of their conversion ability, then an AIP can also help. AIP can avoid years of problems and the need to go on lifelong thyroid medication.
However, for those with a severe T4 to T3 conversion issue caused by either lost thyroid tissue or gene defects or both, AIP could be a total and utter disaster. For these people, stopping the autoimmune response could prevent them from ever getting on the right level of T3 that resolves all their symptoms. Thyroid patients in this category could be left with no autoimmune reaction, a partially working thyroid gland but very poor conversion. They would then potentially find it difficult to take the right balance of T4 and T3 hormones to make them feel well.
For some people, it may be better to let the autoimmune attack run its course and do what it needs to do! I bet you’ve not heard anyone say that before – but in some circumstances, it can be true.
Those that have a severe T4 to T3 conversion issue (through lost thyroid tissue, gene defects or both) need to be careful what they wish for regarding stopping any autoimmune response using an autoimmune protocol (via diet or supplements).
I also believe that the most important thing with thyroid problems, especially if they are not caught early, is to get people on the right balance of thyroid hormones for them. People need to get well fast. This is the single best approach to avoid all the other dreadful consequences to jobs, relationships etc. Life is too short to spend years trying other approaches out. The kind of collateral damage that can come with being unwell for a prolonged period really needs to be avoided.
Trying to fix Hashimoto’s with dietary or supplement approaches can be effective if the issue is caught very early on before significant thyroid damage occurs and if the person responds well to the AIP approach. However, if the thyroid patient already has serious conversion issues, the AIP approach needs careful consideration.
Here is a blog post on these gene defects that you may wish to read:
To find out more about AIP you can visit Dr Westin Child’s website, one of his links is here:
Izabella Wentz also has some very good books on the subject of AIPs.
I hope this quite complex article has been informative and helpful to you.