I believe, many thyroid patients are aware that one can do things to bring thyroid antibodies down. And that high levels of antibodies is not a good thing. You can read my post on antiodies and symptoms here. Many know that gluten is not good for us, and that selenium is good and that what we eat matters. In this post I will share with you, what science has shown really works.
It’s important to be aware, that people who have true Hashimotos have higher antibody levels than us with Atrophic Ord’s. Doctors call everything Hashimotos, but there are in reality many different autoimmune thyroiditis. The two most common are Hashimotos and Ord’s. Hashimotos starts with a goiter (one doesn’t need to be aware of it) and Ord’s not. In Hashimotos the gland stays large, only infiltrated by B and T lymphocytes. Whereas in Ord’s, the gland shrivels up over time.
Why do I talk about this? Because all thyroid antibodies are produced inside the gland. By the said B lymphocytes. So as the gland atrophies in Ord’s, less and less antibodies are produced. This means, we with Ord’s will have lower antibody levels. Often people don’t know what kind of AITD they have. But if you find it difficult to reduce your antibodies, you might have Hashimotos. Remember, we can only do our best. I have hardly any antibodies anymore, I have very little thyroid tissue left.
is absolutely necessary for hormone production. Both the TPO enzyme and the deiodinase enzymes are selenium enzymes.
But selenium is also important for the antibody levels. I am not sure where exactely is a good selenium level. There are three Norwegian doctors who argue, that we need much higher selenium levels than what is currently advised (1). Upper reference is often 1.8 or 1.9 umol/L. These doctors argue, that upper reference should be at 3 umol /L. Toxic level is at 3.5 umol/L. I have read somewhere that high levels of Selenium can inhibit the conversion of T4 to T3, but I can’t find that study again. At least, you don’t need to worry about being a little over range.
A safe dose is 200 mcg/day. As much as 400 mcg is considered safe. Some people eat brazil nuts for selenium. But you should be aware, that the selenium content can vary from very little to very much. I have a study on it under odds-and-ends
There is no doubt, that selenium reduces anti-TPO. In this study (2), they divided the participants into two groups. One group was given 200 mcg selenium/day, the other placebo. In the experimental group, one saw a clear reduction in anti-TPO over 6 months. The group was divided into two subgroups, what they called “subclinical” and “overt hypothyroid”. In the “subclinical” group, one saw a reduction at 4,3% after 3 months and 12,6% at 6 months. In the “hypo” group, the reduction was 21,9% at 3 monts and 20,4% after 6 months. That’s a lot.
They look at sub types of anti-TPO, IgG1, IgG3 and IgG4 in the study. That’s above the level in this post, but if it’s something that peaks your interest, have a read.
is bad for us with an AITD. Many are aware of that. And science says that too. I think everybody with our disease should do themselves a favour and at least try living gluten free. And see for themselves, how it feels. I really regeret eating gluten for so long. I went to a functional doctor that tested me for wheat, rye and barley. The test said, intolerant. Then he siad to me, try eating dinkel, spelt. Many tolerate that better. This was in 2007. I grabbed onto that straw. I blame him and I blame myself. Because when I finally dropped it and went gluten free, what a difference ! The chronic pain between my shoulder blades was gone, the thightness, the tiredness. I can’t say if it impacted my anti-TPO. I lived in Denmark and they don’t believe in testing antibodies here. At least, the doctor I had at the time didn’t. The nice doctor I have now will test most things I ask for. Besides, I have a shrunken gland, so my antibodies has decreased anyway. I know now, gluten make me feel bad. Very tired.
I talked to a guy, who claimed, the gluten we have today is much more aggressive than in earlier times. Crops have been bred to yield much more. Where they only had a few aks, today they have many. Maybe this is the reason many don’t tolerate gluten today. I don’t know. We also have a much greater focus on our digestion today. I am sure people had a lot of digestive issues earlier as well, that they just lived with. But they ate much healthier, less sugar, less refined, less toxins.
This study on healthy mice (3), showed that a gluten containing diet led to a more inflammatory cytokine profile. Cytokiner are signal molecules involved in so many processes in the body. They are produced in many differnt cells, including macrophages, B andT lymphocytes and mast cells.
Our data shows that the gluten-containing standard diet modifies the cytokine pattern of both Foxp3 T cells and Foxp3+ regulatory T cells towards a more inflammatory cytokine profile.
There is so much going on in the immune system as an AITD developes. It’s very complicated. But we do know that the T regulator cells play an important role, and that we with AITD often have a dysfunction in these Tregs. They gave one group of mice a standard gluten diet and another group, a gluten free diet. The gluten free diet created an anti inflammatory cytokine profile.
The gluten-free diet induced an anti-inflammatory cytokine profile with higher proportion of
transforming growth factor-b (TGF-b) + Foxp3 T cells in all tested lymphoid tissues and higher IL-10 expression within non-T cells in spleen, and a tendency towards a mucosal increase in TGF-b+ Foxp3+ regulatory T cells.
I won’t pretend to understand everything they write. I quote here, because the study isn’t open access. So I want to just provide you with the conclusions as the authors present them. But I do understand that gluten created an inflammatory situation. Whereas a gluten free diet created an anti inflammatory situation. And this was in HEALTHY individuals (mice).
Here is a study on human beings, people suffering from AITD (4). Where they looked at gluten and both anti-TPO and anti-TG. They had 34 women who had AITD, but were not on thyroid meds as yet. They were divided in 2 groups, one lived on a gluten containing diet and the other on a gluten free diet. Here are the results:
Variable Gluten-free diet (Group A) Gluten-containing diet (Group B)
TPOAb [U/mL; mean (SD)]
Baseline 925 (265) 891 (242)
After 6 months 705 (206) 920 (280)
Change − 200 (105) 29 (25)
TgAb [U/mL; mean (SD)]
Baseline 832 (311) 792 (274)
After 6 months 629 (240) 845 (324)
Change − 203 (120) 53 (58)
Thyrotropin [mIU/L; mean (SD)]
Baseline 2.7 (1.0) 2.9 (0.8)
After 6 months 2.4 (0.8) 2.6 (0.9)
Change − 0.3 (0.2) − 0.3 (0.2)
Free thyroxine [pmol/L; mean (SD)]
Baseline 14.9 (2.3) 15.3 (2.7)
After 6 months 16(2.4) 15.0 (2.3)
Change 1.2 (1.4) 0.3 (0.6)
Free triiodothyronine [pmol/L; mean (SD)]
Baseline 3.2 (0.6) 3.1 (0.6)
After 6 months 3.6 (0.7) 3.2 (0.7)
Change 0.4 (0.3) 0.1 (0.3)
25-hydroxyvitamin D [ng/mL; mean (SD)]
Baseline 20 (6 ) 21 (5)
After 6 months 25 (6) 20 (5)*
Change 5 (3) − 1 (2)
I have made some changes to this table, taken some numbers out that we don’t need. I apologize for the messy colums. It looks right when I work on it, but turns out like this on the site.
You see that anti-TPO were reduced in the gluten free group, and increased a little in the gluten group. And the same with the anti-thyroglobulin (anti-TG). But the thyroid numbers are really strange. The FT4 is normal, but most of them have a low FT3. Did they suffer from selenium and or zink deficiency ? They have Hashimotos, but do not take meds. Usually in the beginning of Hashimotos disease, the FT4 goes down, but the body manages to keep the FT3 normal for a while. But in this group, we see the reverse. I don’t understand it. But anyway, we are mostly interested in the antibody levels.
Also note, that in the gluten free group, both FT4 and FT3 increased. AND vitamin D.
I think it’s safe to say, that it’s important that people with AITD should not eat gluten. In these studies, they only look at how it affects the immune system. They don’t talk about symptoms. But we do get a poorer quality of life from gluten. But if YOU don’t notice any difference. And you feel it’s a big sacrifice, then I would probably keep eating it. But try for a while , give it a proper chance.
Yes you read right, Levothyroxine. When people start taking Levothyroxine, Synthroid, thyroid antibodies go down. In this study ( 5), they were mostly interested in looking at the positive effect of Levo on the gland itself. And the gland did improve. But they also tested the anti-TPO and anti-TG. And both were considerably reduced.
It’s an open study, so you can check the numbers yourself. They also describe what happens in the immune system when you get an autoimmune thyroid disease in detail.
Before they started Levo treatment, anti-TPO(TPOab)levels were1287(12,6-2000)IU/ml before treatment started . With lowest and highest in brackets. 257(23,9-960) IUml after treatment. So a huge reduction.
Anti-TG (Tgab) also reduced. Before numbers 103 (9,5-386), after 53,5(34-1596)IUml. They also mention that CRP also reduced, but not at a significant level.
I can’t see how long the study lasted, which is a shame. We want to know how long time things take. I can see from the numbers, that many were hypo thyroid despite getting medicine. What’s new? But that isn’t the main thing here. The Levothyroxine treatment reduced thyroid antibodies considerably.
Lots of focus on vitamin D these days. Researchers speculate that vitamin D deficiency could contribute to the developement of AITD. Because they find lower levels of vit D in people with thyroid disease. This is one studie (6) where they found this. They compared one group of people with thyroid disease (group II) with one of thyroid healthy (group I).
The healthy ones, group I, did not supplement vitamin D. As you can see, group II were much lower on their vitamin D levels. AND calsium levels. Which makes sence.
This is a study from Saudie Arabia. And we know how women dress there! But there is sun all day long, and they probably enjoy it in the privacy of their own homes. Anyway, there is a big difference between the two groups.
WHY are we low on D?
I don’t think there is a definite answer to this question. In the study, they discuss two things:
- Poor absorption
- Poor ability to activate the vitamin
Importantly, both vitamin D and thyroid hormone bind to similar receptors called steroid hormone receptors. A different gene in the Vitamin D receptor was shown to predispose people to autoimmune thyroid disease including Graves’ disease and Hashimoto’s thyroiditis.
So we can have a genetic predisposition to vitamin D deficiency that sets us off for autoimmune thyroid disease, both hypo and hyper.
They also saw a negative correlation between TSH and vit D levels. That means, the lower the vit D level, the higher the TSH.
Vitamin D and the immune system
Vitamin D affects the immune system in a positive direction. I won’t go into too much detail here, but you find a lot of info on the study. They say:
Vitamin D inhibits the production of Th1 polarizing cytokine (IL-12), thereby indirectly shifting the polarization of T cells from a Th1 toward a Th2 phenotype. In the CD4+ T cell response, vitamin D directly inhibits the production of Th1 cytokines (IL2 and IFN-c), and enhances Th2 cytokine (IL-4) production.
The Th2 fenotype immune system is associated with humoral immunity and anti-inflammatory properties. So very good for us with autoimmunity. And studies have also shown, that supplementation with vitamin D can slow or stop the onset of autoimmune disease.
Vitamin D is very important for us with autoimmune disease. If you are in the beginning of thyroid disease, or genetically predisposed, it would be very improtant to have good vitamin D levels. It’s the Serum 25(OH)D test that is the best way to measure vitamin D apparently. I go for a high level of vitamin D myself. I take vitamin D every day of the year. I have a skin type where I need to wear sunscreen all year round.
In this study from India they looked at how supplementing vit D affected thyroid – and antibody levels (7). They had 100 people who had been diagnosed with Hashimotos within the last 3 months. They were divided in 2 groups, group 1 were given both vit D (cholecalciferol 60 000 U/week for 8 weeks. Plus 1250 mg calsiumcarbonate corresponding to 500 mg elemental calsium/day. Group 2 got just the calsium, and no vit D.
As you can see, anti-TPO almost halved after only 3 months taking vitamin D. BUT there were large individual differences. And anti-TPO went down also in group 2, but much less.
I won’t go into the thyroid levels. These varied a lot, and I see that many were underdosed. But they were just started on medication. A weakness with the study, is that we know that Levothyroxine also reduces antibody levels. And as they were just started on it, the Levo could also have contributed to the large reduction. But that would not explain the differnce between the two groups. In group 2 the 16% reduction might be due to the Levo. I wish they had tested for anti-TG as well.
Where should my vitamin D be?
If you have an AITD, you need your vit D to be quite high. I go for 100 ng/ml myself. Here in Scandinavia, a general advice is 70 ng/ml. But we need to be high, some even say over 100. But 100 is ok, I think.
I have read that LDN reduces thyroid antibodies in many places. I have said it myself, because I have read it . So I am a little surprised when I don’t really find any studies saying it. I see that Izabella Wentz writes, that her clients have a large reduction in antibodies after they start LDN. I don’t know what she means by clients. She is a pharmacist, so I assume she doesen’t have patients. Anyway, she has no documentation. She, and many others, claim that the reason why it hasn’t been studied, is that the pharmaceutical industry doesn’t have anything to profit on studying it. But I don’t buy that. There is a lot of science going on outside of the pharmaceutical industry. You see that even on this post, studies on vitamins and minerals.
But the reason why I include LDN despite of this, is that I know it does people with AITD a lot of good. It certainly has a very positive effect on our immune system. I have included one study on this:
This is a study on LDN and the immune system (8). This is a group of researchers who do a lot of work on LDN. That LDN is not studied, is simply not true.
By increasing the production
of endogenous opioids, LDN could inhibit the proliferation of B lymphocytes , T lymphocytes  and the corresponding immune responses.
could enhance the phagocytic ability of macrophages by influencing
surface marker expression and secretion of various cytokines.
LDN had a glial cell modulator effect and thereby improved
the patient’s fibromyalgia symptoms
I have included quotes, as this is not an open access study. It’s a long article with much more info than this. I am just including some things I think is of interest for us with AITD. There is a lot I don’t understand. Our immune system is SO complicated. We as patients don’t need to understand everything. We need to understand something about what happens in our disease. I write about it here. It’s not anti-TPO or anti-TG or TRAb that do the greatest damage to the gland. It’s B and T lymfocytes infiltrating it. AND all thyroid antibodies are produced inside the gland.
That means, if LDN has an inhibitory effect on the proliferation of B and T lymfpcytes, it could have a positive effect on what’s going on in our gland. I believe that would be mostly in the early stages of our disease. Later on, the gland will be totally infiltrated. LDN seems to have a general anti-inflammatory effect.
I think many fatigue states have something to do with imbalances in our immune system. I know, LDN has worked wonders for me. I was absolutely exchausted because of hypothyroidism. This was before I knew where my thyroid levels should be, and I was positively mistreated by my GP in Denmark. He wouldn´t even do labs on me because I was on NDT. I felt incredibly weak. I didn’t know to take my temperature and pulse to follow my levels. You can read more about LDN and my LDN journey here. I didn’t have this blog if it weren’t for LDN.
In this Italian study (9) they looked at how an anti-inflammatory diet affects antibody levels. There is something strange about this study, as they talk about microsomale antibodies AND anti-TPO. But they are the same. One used to call anti-TPO microsomal, one sees that in old studies.
But anyway, they had 180 patients; 84 men and 96 women. They were between 30 and 45 years old. They all had thyroid antibodies. They were divided into two groups. One group (108) ate an anti-inflammatory diet, the other group, ordinary food. They ate a lot of proteins, lots of non fat meat and vegetables. They could not eat goitrogenic food, dairy, beans, bread, eggs, pasta, rice or fruit.
After 3 weeks, the group on an anti-inflammatory diet had a marked reduction in antibodies. And 3 weeks is a very short time. When you look at their thyroid levels (Fig.1), you see that all of them suffered from hypothyroidism. They all had a very low FT4. The mean was 0.5 ng/dl, that’s 6 .5 pmol/L. Way under range. And their TSH was elevated. FT3 wasn’t low. 3.2 pg/ml or 4.9 pmol/L. This is typical for a beginning Hashimotos. FT4 goes down, but the body manages to keep the FT3 level for a time. But eventually that will also come down. But I really don’t understand that FT3 is this close to normal with such a very low FT4. The FT¤ is what I would call critically low. They need thyroid medicine asap. They must all suffer from iodine deficiency to have such low FT4. But the FT4 also increased in the control group after 3 weeks. The people who continued to eat the same diet. There is something strange here. It doesn’t add up.
As you see, antibodies went UP in the control group (Fig.3). While they were quite a bit reduced in the anti-inflammatory group (Fig.4). Anti-TPO was reduced from 140 UI/ml to 70 UI/ml. That’s a LOT. I mean, it’s hard to believe. I have a study here on the blog that says, that it’s anti-TPO over 120 UI/ml where they start seeing damage to the gland.
And anti-TG was reduced from 90 to 60 UI/ml. Very impressive results in only 3 weeks. I wish they had continued the study for 6 months.
And there were also changes on other parameters, like thyroid levels. I really believe low carb is good for us with an autoimmune disease. I know that I feel better on low carb, and I see so many others saying the same. I wish I could live as a vegeterian. I have for long periodes, but I become so tired. Lots of protein and vegetables work best for me.
I won’t include a lot of info on iodine. Iodine can reduce antibodies by a lot. BUT it can also increase antibodies. I have so much info on iodine on the blog. You have to read. I have 4 posts on iodine so far, and there is info on iodine and the particular antibody on each of my 3 antibody posts.
Keep in mind what I wrote at the beginning of this post. Us with Ord’s will see a large decrease in antibodies. If you still have high antibody levels after many years of disease, you probably have Hashimotos. It will be more difficult for you to get antibodies down. It’s also more important that you start supplementing iodine in a careful way. At the very least, read my Iodine for beginners post.
I think this Swedish chiropractor living in LA is very good on diet. Here he talks about fatty liver, which so many of us have. Or at least, a sluggish liver. He calls himself a doctor, as everybody seems to do in the US. Here in Europe, only medical doctors can call themselves that. But he does have a lot of knowledge. And seems very grounded.
I hope this can be an inspiration for you. You probably know some of this already, but maybe not all of it. And it’s always nice to see it in black and white, what works.
I was inspired to eat better. And I have been, since I wrote the Norwegian version. I usually write my posts in Norwegian first, and then translate. I don’t have antibodies anylonger. As my gland has shriveled. But I just feel much better, and look better, on a Paleo diet. You might do better on keto. Or an anti-inflammatory vegeterian diet. Everyone must figure this out for themselves. There is no one size fits all.
It’s in the beginning of our disease, that it’s most important to focus on antibodies. But most people don’t have that knowledge at that time. It’s important also later, we have poorer quality of life when our antibodies are high.
BEST OF LUCK ✌️
J. Alexander et al. Selenium – a trace element of clinical significance. http://Selenium – a trace element of clinical significance
Effects of selenium supplementation on antibodies of autoimmune thyroiditis. Lin Zhu et al. PMID: 23158484. https://pubmed.ncbi.nlm.nih.gov/23158484/
Julie C. Antvorskov,1 Petra
Fundova,1,2,3 Karsten Buschard1
and David P. Funda. Dietary gluten alters the balance of pro-inflammatory and
anti-inflammatory cytokines in T cells of BALB/c mice . https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3533698/pdf/imm0138-0023.pdf
- DOI: 10.1055/a-0653-7108. https://pubmed.ncbi.nlm.nih.gov/30060266/ The Effect of Gluten-Free Diet on Thyroid Autoimmunity in Drug-Naïve Women with Hashimoto’s Thyroiditis: A Pilot Study.
Levothyroxine Replacement Alleviates Thyroid Destruction in Hypothyroid Patients With Autoimmune Thyroiditis: Evidence From a Thyroid MRI Study. doi.org/10.3389/fendo.2019.00138
Dr. Aman Mackawy, Bushra Mohammed Al-ayed, and Bashayer Mater Al-rashidi. Vitamin D Deficiency and Its Association with Thyroid Disease doi: 10.12816/0006054
Chaudhary, Sandeep; Dutta, Deep1; Kumar, Manoj; Saha, Sudipta2; Mondal, Samim Ali3; Kumar, Ashok; Mukhopadhyay, Satinath. Vitamin D supplementation reduces thyroid peroxidase antibody levels in patients with autoimmune thyroid disease.https://pubmed.ncbi.nlm.nih.gov/27186560/
- Zijian Li et al. Low-dose naltrexone (LDN): A promising treatment in immune-related diseases and cancer therapy. http://doi.org/10.1016/j.intimp.2018.05.020
- Esposito T et al . Effects of low-carbohydrate diet therapy in overweight subject with autoimmune thyroiditis: possible synergism with ChREBP. https://doi.org/10.2147/DDDT.S106440
Thank you for sharing this informative post about thyroid antibodies and their relationship with Hashimoto’s and Ord’s. It’s great to hear that you have very little antibodies left now. My question is, how can someone determine what kind of AITD they have if they find it difficult to reduce their antibodies?
It’s only an ultrasound that can tell you the exact size and state of your gland. But a doctor should be able to palpate and estimate the size. You can feel it yourself. If you can feel your gland after many years of disease, you most probably have Hashimotos. I haven’t seen any science on this. But for me, something bad happened at 7 years of being medicated and 9 years after I actually got sick. I got what I call my second myxoedema, that is, very low on my levels, very sick. I was given Lio after a while, and later, NDT. I believe my gland had shriveled a lot by then. I have observered a similar time line in others as well.
I am not sure I am glad that I have a shriveled gland, and therefore, little antibodies. The gland supports the conversion of T4 to T3 in the body tissues. People without a gland are sicker, have lower quality of life than those with AITD that have their gland a normal size. It does not maybe matter that much to me now. I can get the medicine I need in the doses I need. But it’s a huge problem for people around the world who are not so fortunate.
Thank you for sharing this informative post on reducing thyroid antibodies through dietary changes and proper selenium levels. It’s important for thyroid patients to be aware of the different types of autoimmune thyroiditis and their effects on antibody production.
Hi Emily Anthony!
Yes, it is important that we understand the fundamentals of our disease. I think neither doctors nor patients are aware that there are several AITDs. Not only Ord’s and Hashimotos, but also one called serum negative with no thyroid antibodies and another called Ig4 that men can get. I will write a post on this at some point. If you are interested in antibodies, have a look at my antibody series, esp nr 1, Antibodies, part 1, Anti-TPO. There is a study on that post, by Ewa Frölich et al. Lots of interesting things on what happens in the gland.
If only we knew how to reduce antibody levels in the early stages of our disease. You can change the course of events if only doctors and patients had the knowledge.
All the best, Liv