Recently, I interviewed Dr. Alan Christianson, and we discussed iodine’s role in thyroid health, the complexities of iodine uptake, genetic influences, potential risks of excessive iodine intake, the significance of thyroid antibodies, the risks and benefits of thyroid medication, and more. If you would prefer to listen to the interview you can access it by Clicking Here.
Dr. Eric Osansky:
I am so excited to chat with Dr. Alan Christianson. This is going to be an amazing conversation. We are going to be talking about his book The Thyroid Reset Diet, iodine, thyroid antibodies. Let me go ahead and dive into Dr. Alan’s bio here.
Dr. Alan Christianson is a board-certified naturopathic endocrinologist focusing on thyroid care. He is a New York Times best-selling author whose recent title is The Thyroid Reset Diet. He is the product formulator for thyroid-specific coformulation supplements. Dr. Christianson has been featured in countless media appearances, including Dr. Oz, The Doctors, and The Today Show. He is the founding president of the Endocrine Association of Naturopathic Physicians. Dr. C, it’s great to have you on the show.
Dr. Alan Christianson:
Hey, Eric. Happy to be with you. Thanks for having me.
Dr. Eric:
I enjoyed reading your book. I forgot if I also listened to it on Audible. Usually, that’s how I read books these days. I definitely have the hard copy as well.
Let’s start off by talking about the book and what motivated you to write The Thyroid Reset Diet. It’s not your first thyroid-related book; you have a few other ones. Why did you decide to take the time to write this book?
Dr. Alan:
There have been a lot of thyroid diets proposed and talked about. I really hadn’t been that engaged in many of them because there hadn’t been a large amount of clinical evidence. There have been some recent clinical trials, saying that diet could make a difference. It wasn’t the kind of dietary approach that was commonly used, so that was really it. This is actually pretty helpful. It’s not what everyone’s doing, so let’s take advantage of a good opportunity here.
Dr. Eric:
Makes sense. Just to make it clear, I know this, but for those who are listening, this is based on research and also your experience with working with patients as well. This isn’t just a bias where you are anti-iodine, correct?
Dr. Alan:
We can talk a lot about iodine, the whole culmination of that. It’s been about 20 years of medical practice focusing on thyroid care with a real big bias, if anything, toward safe, effective outcomes. I don’t care what does what, where it comes from or how it works. If it will work and is shown to be effective, I’m all for it. A safe option is important to me.
Dr. Eric:
I don’t know how to word this. Were you ever on the iodine bandwagon? You’re familiar with Dr. David Brownstein’s work. Before you did your research, were you at any time recommending separate iodine supplements? Were you always on the cautious side when it comes to iodine?
Dr. Alan:
The arc of that as a physician learning in medical school or in nutrition, I was always aware of iodine being relevant for thyroid disease but never thought much more about it than that. A thing I learned as a historical anecdote, so to speak.
Somewhere around the late ‘90s, I started seeing more and more patients who were developing thyroid disease after megadose iodine supplementation. This was the late ‘90s/early 2000s. I was curious about that.
The origin for all of this was a dear man who passed away. Guy Abrams was his name. He wrote a group of books called The Iodine Project. They were published in magazines. He was called the Original Internist. He compiled all that and called that The Iodine Project. That is where all of this came from. Really nice guy. I talked to him in depth. Read all of his work. All of his citations. I found it really intriguing.
It’d be a really cool thing if this massive problem affecting a lot of people could be solved by just giving them nutrients. It was an easy thing to think. There are many examples in natural medicine where people are getting too little of an essential nutrient. RDA amounts may not be enough. Foods may be low in that. It was an easy story for me to get into. It made a lot of sense in a lot of ways.
The tough thing was it was asking to suspend the last century of research on iodine. This is the most studied nutrient on the planet probably. It was the first nutrient known to be correlated with this specific disease. We have tons of data epidemiologically, interventionally, mechanistically. The more I studied about the ideas behind all of this, it was plausible, but it didn’t sync with what we already knew.
To answer the question, I was aware of that approach but not really into it for a while until I did the research on it. Then I saw the megadoses were not safe. The more recent iteration was the idea that taking below a threshold could also be therapeutic. For quite a while, I knew it was relevant. I knew people could have a problem by getting way too much. The more recent thing that inspired The Thyroid Reset Diet was that deliberately going to a lower range short-term could help fix problems as well.
Dr. Eric:
One of the main concerns is it could be a trigger of autoimmunity, Graves’ and Hashimoto’s.
Dr. Alan:
Yeah. Fascinating thing. Iodine is unlike any other nutrient. Most other nutrients, the amount that’s in the bloodstream is the amount the tissues get exposed to. It’s the same concentration. If you were swimming in soup, what the soup has, that’s what you get. That’s how the tissues and glands work in most cases.
Not with iodine. It’s gated. The parts of the body that use iodine, they selectively uptake it. It’s by a mechanism called the sodium iodide symporter, or NIS for short. The basic idea is if there is sparse amounts, you pull more in. If there is way too much, you block it from coming in. That creates what’s called the iodine paradox.
If you get way too much iodine, you block the uptake of it, and you can create something that seems like an iodine deficiency. Too much is just like too little. If someone goes above the requirements, they can have the same problems as if they were deficient. It’s like if you blew a fuse. There’s plenty of power there, but there’s none getting in because your body shut off the safety mechanism. It’s the exact same thing for iodine in your thyroid. A little more variation.
There are two main human genotypes. There are those who are well adapted to being in coastal environments, where you pretty much never have no iodine or very little. Sometimes, you would get a lot. There are adaptations for people who can dump out iodine or block it when they need it.
Then there are those who are adapted to being inland, so they weren’t coastal. They were adapted to be in a lower iodine environment. They were good at operating on small amounts. You don’t get both superpowers. The coastal people couldn’t do great if they were really deficient, and the inland people couldn’t do great if they got a lot of excess.
The problem is that thyroid disease is primarily genetic. We look at the genes involved in that. They are all the genes involved in regulating iodine. Those who are better adapted to being in lower iodine environments, if they are exposed to amounts that are not always harmful for all people, that can be problematic for them.
Dr. Eric:
You answered one question I had, which is why some people can tolerate higher amounts of iodine, whether that’s ioderal or another type of supplement. It is dependent on the genotype, according to what you just mentioned.
Dr. Alan:
That’s one part. The tolerance varies a lot per genotype. There has been so much data on this epidemiologically. If populations stay between 50-200mcg per day for adults, that’s received the lowest rates of adult thyroid disease. When you get above 200mcg per day, that’s when those with the lower tolerance start to have problems. Those who don’t really have problems, who are not intolerant, they’re probably safe to occasionally get to about 1,100mcg per day. They can tolerate a bit more. That’s the tolerance side.
There is also toxicology, which is not genetically variable.
Then there are requirements. The requirements are pretty much based upon body size. There is not a lot of genetic variation with that and not a lot of differences in absorption or assimilation of it. We absorb it really well. It’s quite different from iron or B12. The tolerance is quite variable based upon one’s genetics.
Dr. Eric:
Does it matter the source of iodine? Meaning if someone has the inland genotype, so they can’t tolerate high amounts of iodine, does it make a difference if they are getting that iodine from supplementation versus sea vegetables, such as kelp for example?
Dr. Alan:
That’s a really good question. I have heard you say iodide. We could differentiate a lot of subtypes, to be really precise. Most forms we are exposed to are iodide. They are chemically already reacted with something. Iodine is formed when it’s now in a highly reactive state. That’s what happens within the thyroid. We’ll talk more about thyroid peroxidase (TPO). That’s what oxidizes it.
In terms of what it does, there are many compounds that can form with iodides. That can be relevant in terms of when they are in supplements or sea vegetables. Ultimately, the biological properties are of the actual element. Once it’s in a concentration, where it’s freed from the bond, and it becomes an active iodine, that’s when it does what it does.
It’s a chemical element. As such, it’s irreducible. Unless you have a particle accelerator, you can’t change an element. It does what it does, whether it’s from one supplement or another, or in a nanoparticle or a raw state. It’s labeled a lot of different ways. But it’s a chemical element. That’s where its properties come from. It doesn’t differ if it’s in a food source or supplement or different compound.
Dr. Eric:
Thanks for explaining that. You’re familiar with Dr. Brownstein’s work. He and others will say that the problem is the oxidative stress is caused by iodine, so if you take antioxidants such as selenium, Vitamin C, others, that will minimize the potential risk associated with iodine. What are your thoughts on that?
Dr. Alan:
There is total truth to that, but this is a matter of degree. There are a couple of people who have taken Guy Abrams’ work. They were collaborators of his. They were transparent about sharing his work. They have not innovated it. Those are the same things Guy Abrams said many years ago.
The short version of the story was that Guy Abrams was a gynecologist. He saw clinical trials showing that iodine could lower the pain from fibrocystic breast disease. Not having a nutrition background, nutrients can act like drugs or like nutrients. They can do a drug-like effect, or they can fill the role of a nutrient. For example, if I got a cut or scratch from working on a yard recently, if you put iodine on your skin, you can kill bacteria. They’re separate things.
The same is true with viruses. It’s not an iodine deficiency. It’s more a matter of an excess uptake of it. Not seeing that distinction, he thought, oh wow, that high dose helped. That must mean they required that much. That spawned all this same work from these same people.
It’s not a matter of a deficiency. Biologically, it has many properties. Someone’s tolerance is largely set by their genotype, but it’s also influenced by other factors, like their nutritional status. If someone is lacking in selenium, that will further narrow their iodine tolerance. That doesn’t mean one can megadose on selenium and suddenly now can take thousands the amount of iodine that is recommended.
It’s a real problem. Anyone can go on PubMed, and there are sad stories about many people who have been hospitalized from a thyroid storm caused by higher doses of iodine. There are many babies who are born with congenital hypothyroidism because their mothers were taking high doses of iodine. These were amounts and products that are recommended verbatim by these sources you mentioned.
These things are not safe. They cause big, dramatic harm in some cases. Most people with thyroid disease, getting too much can slow the thyroid and also trigger the whole autoimmune response.
The slowing effect, that’s the whole tripping the fuse that I mentioned, called the Wolff-Chaikoff effect. The autoimmune response, when you’re forming thyroid hormones, you’re first off oxidizing iodide. That’s TPO. Then you’re attaching it onto the protein thyroglobulin (Tg). That’s where iodine is stored.
Iodine itself is a big source of free radicals. That’s why we can use it as an antiseptic. If you think of bleach or peroxide, those are things that kill stuff by making free radicals. Iodine is no different. It happens to be useful but in very controlled amounts. In the thyroid, when there are amounts there that are not well regulated by the body, that extra free radical damage triggers an immune response, an inflammatory response. Now the lymphocytes treat this enzyme TPO, or this protein Tg, as if they are foreign. That’s the cycle of autoimmunity.
There are so many things that can give rise to thyroid disease. It has been argued that there are only about four factors that are truly causal, that can do it by themselves. That’s age, gender, genetics, and iodine exposure.
A recent researcher argued that of the controllable factors, that’s really just iodine exposure. Age, gender, and genetics are not controllable. Of the many other controllable factors that give rise to thyroid disease, it was argued that all of those together are less relevant than one’s iodine exposure.
Dr. Eric:
How about Graves’? You mentioned TPO, Tg. Any impact on the actual TSH receptor? Can it cause an increase in Graves’ antibodies?
Dr. Alan:
There is less epidemiologic data about iodine exposure triggering Graves’. Once it has started, then it certainly is a big driver of the disease process. All the medications targeting Graves’, all they’re doing is delaying iodine uptake. They are simply slowing that sodium iodide symporter and making less into the thyroid. That’s why they take about 4-6 weeks to do anything. There is already a certain reservoir within the thyroid. The less coming in, the easier that can go.
The iodine paradox comes back here again. If someone is in the emergency room from thyroid storm, the blockers like methimazole or propylthiouracil (PTU), taking 4-6 weeks to work, they can’t help in the acute portions of a thyroid storm. The only thing that can block it that dramatically is megadose iodine. You’re blowing the fuse. When you give a high dose of it, that’s the most powerful way to shut it down.
There have been some clinical trials on using iodine as a longer-term manager for Graves’. The trials look effective. The drawback is none of them were large enough where we could say confidently that it wouldn’t have raised the risk of acute thyroid storm. Theoretically, if there is more substrate there to make hormone, there is more of a chance that the gland could go out of control. It’s possible a subset of people could have more tendencies toward thyroid storm.
You can shut it down in the case of Graves’ with high dose iodine. At the same time, if one is watching their iodine intake, that will make whatever else they do for Graves’ treatment take much less time and require much less medication.
Dr. Eric:
It could potentially be effective, but it’s unpredictable. If they are experiencing a thyroid storm, taking high amounts of iodine might help. But using preventatively, that might backfire in some cases and actually cause a thyroid storm?
Dr. Alan:
Correct. That is the unknown. We know that during an acute storm is when the most effective single treatments are. If someone were doing it chronically, they might be more apt to have a storm form. When an acute storm happens, no treatments are perfect, and it can be life-threatening. It’s something that you wouldn’t want to risk triggering.
Dr. Eric:
Definitely agree. When someone is focused on eating whole, healthy foods- You go into detail in your book, and you list foods like the micrograms of iodine. Would you say it’s easy to exceed the 200-250mcg if you are just relying on food alone and not taking any supplemental sources of iodine? Is it something people still have to monitor on average?
Dr. Alan:
A recent study by the American Heart Association impressed that question: What percent of the population is likely above that 200mcg threshold? This is the thing. You’ll have people argue, “Oh no, Americans are low or high.” Averages are deceiving.
There is a story about a statistician who had his feet in an ice bucket and his head in the oven. He was at an average of 72 degrees. He should have been comfortable. Not all parts of a big thing like America are at a set number.
In this analysis, they broke people down by age, gender, ethnicity. The range of those that were above that safe iodine window varied. About a few of the cohorts were as low as high 20s, and some were as high as low 40s. Ballpark, about a third of the population has been known to be above that threshold by dietary intake. It can happen. One can get there pretty easily by dietary intake. If there is some in supplements, that will go on top of that.
Dr. Eric:
It’s been a while since I read your book. My skincare products could have iodine. Could that be a concern, too?
Dr. Alan:
There used to be quite a bit in hand sanitizers. Pre-pandemic, that was changed, or else it would have been worse. 2018, it was identified healthcare workers were at risk of iodine-induced thyroid disease. They were using hand sanitizers that were iodine-based. That was a common problem. Many were excreting unusually high levels of iodine.
Both thyroid hormones and iodine are not always intuitive. It’s really about micrograms. It’s about microscopic amounts of things. Iodine is a really useful ingredient in personal care products. It makes them not rancid. It makes them stay smooth and not separate out the different constituents. It’s been in a lot of things. It doesn’t take huge amounts.
The most common individual compound used is called polyvinylpyrrolidone or PVP. A lot of natural products can use that and call it a kelp extract or sea vegetable extract. Same thing. It’s a useful stabilizer. It doesn’t take a lot.
It might be a few percent of the product that contains PVP. PVP is about 12% iodine. It sounds like we’re not talking about very much. Again, it’s mcg. If you take a conditioner for example, and you do a couple pumps of that, you have about 20g, or 20 million mcg. Now you take that 1%, and 12% of that. You figured that intact skin might absorb 4% with a couple minutes of exposure. What you’re left with is still about 1,200-2,000mcg that could be entering the bloodstream. That could be another source for people.
Dr. Eric:
Very interesting. I want to talk more about thyroid antibodies. Before we move on, anything else you’d like to chat about related to iodine?
Dr. Alan:
Well, one thing that creates a lot of confusion is iodine testing. Many will hear different views. A super logical approach is let me test my patients or get myself tested to see where I fit in this.
The drawback is iodine is really volatile. It’s the amount in the thyroid and how your immune system responds to it that matters the most. It’s not just how much is in your blood or urine.
The urine does reflect your overall intake but not on a 24-hour cycle. If you’re studying populations, urine tests are fine from a nutritional status, according to groups of 500 or more people. When you’re looking at individuals, they have done a lot of math on this. You have to test someone over 200 times to be within even 80% confidence of their status. One test tells you pretty much zero. There is so much variability. That’s even for a 24-hour urine or a spot urine or a challenge urine. It’s simply not a meaningful thing.
Serum tests are used quite a bit, too. What they exist for is evaluating the effects of iodine in toxicology ranges. Almost the main reason for this, there is a medication for this called amiodarone, which contains a lot of iodine, like 250mg. Now we are talking thousands of mcg per tablet. This medicine can have side effects anywhere in your body, and they might come on six months after usage.
The useful thing about a serum test is someone who has had amiodarone, and they are having kidney failure. You are still wondering if they still have too much iodine, so you test their serum. Th serum levels only elevate when the kidneys can’t clear it anymore. Before then, they might be higher or lower, but there is no correlation with nutritional status of iodine.
Many people get urine tests or blood tests. From there, they think, “I was low or high.” It really means nothing.
The most meaningless is the skin test. You can smear it on your skin, and it will disappear after a while. The story is that it disappears faster if your body wants it. The kernel of truth is that there are some nutrients that our intestinal tracts absorb more quickly if we are lower in them, like iron, for example. The other kernel of truth is a lot of things get in our bloodstream from our skin. Our skin can’t pick and choose. Our skin has no way of preferentially absorbing based on our requirements.
The other big disconnect is iodine disappearing doesn’t correlate with it absorbing. It correlates with it oxidizing after interacting with oxygen. Iodides are dark; iodine is invisible. That one doesn’t mean anything either.
Dr. Eric:
Good to know. No great test for iodine, whether it’s urine, serum…
Dr. Alan:
You can get a good sense of your status by knowing your cellular intake. Do an iodine inventory. Know what’s in your medications, your supplements. What are the main food categories you consume? Because iodine is pretty consistently absorbed, you can know your status based upon what your intake is.
Dr. Eric:
For more information, highly recommend Dr. Alan’s book, The Thyroid Reset Diet. Check that out.
Let’s talk about thyroid antibodies. There is a lot of controversy with thyroid antibodies. If they’re too high, does that at all relate to the severity of the condition? Is it possible to have false negative antibodies? I know the answer to that, but some people don’t. If you could talk a little bit about what people should look for with thyroid antibodies. Are there concerns if their thyroid antibodies are crazy high compared to mildly high?
Dr. Alan:
Great question. This is a fascinating thing. You have done a lot of good work on Graves’. The funny thing is there is discussions now in the medical literature about Graves’ and Hashimoto’s being one disease with a continuum of how it manifests. There is a lot of overlap between the autoimmunity in both of those diseases.
As a generalization, this is something that makes me nuts. So many conventional doctors do not wish to test or entertain the relevance of thyroid antibodies. To their point, the antibodies aren’t big predictors of thyroid disease actually. They really don’t have that strong an effect upon predicting who will develop versions of thyroid disease. That’s why they dismiss it.
The drawback is the antibodies have big effects upon health and symptoms and disease risks independent of thyroid function. No matter how perfect your thyroid is working, if you have marked autoimmunity going on, that by itself can cause a great deal of problems. That’s where they should be taken into account and screened and looked for.
To credit the conventional side again, they don’t have a lot of treatment options for them that they consider useful. You can give high dose steroids like prednisone. You can surgically remove the thyroid. You can do immunosuppressants. That’s all killing flies with a shotgun. The harmful effects would outweigh the benefits. But there is good evidence that diet, lifestyle, and nutraceuticals can be helpful for the antibodies.
Dr. Eric:
You said that just because someone has let’s say TPO and/or Tg antibodies, that doesn’t necessarily mean that they will develop thyroid disease or hypothyroidism.
Dr. Alan:
Let’s put some numbers on that. Our language really lacks the nuance of predictive value. Is there a risk? It is a risk. Here’s the numbers.
One of the recent studies looked at people’s nine-year risks of developing overt hypothyroidism, having their thyroid shut down. It is broken down into people who had no measurable antibodies, moderate elevations, and high elevations.
This cohort had about a 1% annualized risk for developing thyroid disease. We see that in most populations. That is when they had negative thyroid antibodies.
With the highest level, where both antibodies were what is considered the highest elevation per this study, the risk was higher. If you annualize the risk, it went from 1% to about 1.7%. It was higher. In the big scheme of things, you could say it was almost twice as likely. It was, but it was 1.7%.
For someone to be told, or for a doctor to think, “Well, your antibodies are high. Your thyroid is about to shut down,” there is a 98.3% chance it won’t.
Dr. Eric:
That’s really high. You’re talking about long term, not even over the next 6-12 months.
Dr. Alan:
You take that over nine years, and you are talking about an 11-13% risk. 10% over nine years roughly.
Dr. Eric:
The challenge is they don’t test- Maybe not considered a challenge, but they don’t test antibodies typically unless the TSH is out of range. Maybe the thyroid hormones. Some will just look at TSH.
Dr. Alan:
It doesn’t change treatment regardless. There are a few cases of what’s categorized as subclinical hypothyroidism, where some guidelines will take into account marked antibody elevations. In most cases, it doesn’t really inform or influence conventional treatment.
Dr. Eric:
Yeah. My point is that in most cases, you wouldn’t know if you had thyroid antibodies in the absence of thyroid disease because you are usually not testing the thyroid antibodies unless you have thyroid disease. If you were to do the opposite, and do predictive antibody testing, and test the TPO and/or Tg antibodies, maybe even TSI, in the absence of thyroid disease, is there any purpose of doing that, if most people aren’t going to develop thyroid disease to begin with?
Dr. Alan:
The question is irrelevant if they are relevant in every other way. There is so much evidence on this. Normal thyroid function, elevated antibodies has been clearly shown to be correlated with poor quality of life symptoms: hair loss, anxiety, fatigue symptoms. We look at health risks. There is clear data on cardiovascular disease, infertility, certain types of cancers, autism. These are with all perfect thyroid function.
Yes, high antibodies, even in the absence of thyroid abnormalities, they are very clinically relevant. For many people, they are a source of ongoing symptoms.
Dr. Eric:
Okay. You also mentioned genetics are in there, too. If there is a family history, a mother has Hashimoto’s, maybe it’s also not a bad idea to eventually test her children for antibodies, even if the thyroid is seemingly normal, just because there’s a greater likelihood of developing those antibodies.
Dr. Alan:
Certainly if they have any thyroid suspicious symptoms. Knowing a family history, that can justify one taking steps to minimize their risk of developing thyroid disease. Keeping iodine reasonable, making sure that selenium and iron statuses are healthy.
There is this new paper that came out today from the NIH, showing a pretty strong inverse correlation in many populations between serum iron and Hashimoto’s onset. Nutrients are important. The more one can do to cut the risk of things that go wrong that trigger thyroid disease, it’s worth doing, especially when there is a family history.
Dr. Eric:
Agreed. Getting back to negative antibodies. If someone has Hashimoto’s in the presence of negative antibodies, or Graves’ in the presence of negative antibodies, is there a way to determine that they still have Hashimoto’s or Graves’ via an ultrasound or other types of imaging?
Dr. Alan:
Yes. You’re talking about seronegative Hashimoto’s or seronegative Graves’. Hashimoto’s, first off, we know about the numbers mostly from studies that looked at people after they had thyroid biopsies. They had a biopsy done for some other reason. The most definitive way to confirm or rule out Hashimoto’s is the biopsy.
They would take those who were known to have Hashimoto’s on biopsy and look backward and see if they had measurable thyroid antibodies. Biopsy-proven Hashimoto’s roughly half the time, the antibodies are negative. That’s even those who had it for a larger length of time.
Seronegative Hashimoto’s is a well-known phenomenon. If it’s suspected, a biopsy is not a practical step for that. Ultrasounds can be. That is one way you can often see the tell-tale signs of autoimmunity by the specific changes that occur on ultrasound.
The same thing happens for Graves’. A little more rare. It’s also more time-dependent. The first year someone is manifesting hyperthyroidism that is suspected of being Graves’, there is about a 5% or 10% risk of being seronegative. In most cases, the receptor antibodies or stimulating immunoglobulins are going to be positive when Graves’ is there.
If you go out after that first year, it’s probably 5% or fewer that are seronegative. It does happen that there is false seronegativity with Graves’. It’s more rare than with Hashimoto’s. In those cases, ultrasound or iodine uptake are the main ways you would know about that in a seronegative case.
Dr. Eric:
Do you know the reason why those cases are seronegative? I know they are IgG based. I don’t know if it makes sense to test IgG and see if that’s depressed. Are there other mechanisms involved?
Dr. Alan:
We are going to get pretty weird here. The answer to that in clinical research is that the antibodies we’re aware of are probably not the actual causes of thyroid disease. There is smoke that is often present with a fire but not always. You can have really hot coals that can burn you.
I remember my grandpa, we had a barbecue. He buried the coals in the sand somewhere. I was walking around barefoot and burned myself. There was no smoke, but they were pretty darn hot.
That’s the same way with a lot of autoimmune processes. We know about a dozen immune mediators that are probably relevant for that occurring. Most of us can’t test for it clinically. Your antibodies are like smoke. Generally, you have a hot fire with smoke. Not 100% of the time though. It’s not the smoke doing the damage.
Dr. Eric:
It’s more of a consequence of the autoimmunity, not necessarily the cause of the autoimmunity, those antibodies.
Dr. Alan:
They’re often present when it’s going on, but not always.
Dr. Eric:
How about with Graves’? I agree, it seems that TPO and Tg antibodies are not actually doing any damage whereas the TSIs are not necessarily doing damage, but it seems like, at least according to the research, that they are binding or stimulating the TSH receptor.
Dr. Alan:
For sure. The mechanism and action of hyperthyroidism, it’s probably a big driver. Not necessarily triggering tissue damage.
My favorite analogy there is like a short circuit on a doorbell. When it works right, the doorbell goes off. Somebody opens the door. In the case of Graves’, you’re triggering that response, but there is nobody there. The thyroid thinks it’s being told to work, but it’s not.
That’s a funny quirk of language and acronyms. We have the TSH, and then TSI, that are almost the same thing. Your thyroid can’t tell those apart either. Your thyroid is listening for TSH, waiting when it should be told to work. But it can’t differentiate that from TSI. The errant immune cells can set off a doorbell even though there is no one there.
Dr. Eric:
Okay. I find this conversation fascinating. Seronegative antibodies for someone with Hashimoto’s or Graves’, how would they be able to tell if they are in remission since the antibodies are negative? Are there other ways?
I don’t know your approach. Do you consider someone ever to be in remission? You practice functional medicine, so you’re not just giving thyroid hormone replacement or antithyroid meds. What other factors do you look at before you determine someone might be in a state of remission?
Dr. Alan:
It’s a funny thing. In a lot of the pop health space, so to speak, you put a lot of weight in the idea of being in remission. It’s not a defined term. People can mean they no longer need medication. Some say that means your antibodies are negative. There is no strict definition for that in medical literature.
Many people who are given medications, we could talk about this a lot. That is a big soapbox of mine. Most of them were prescribed medication unnecessarily and never needed them. Many can withdraw and taper and come off very successfully. That is remission of hypothyroidism.
The other paradox about thyroid antibodies is they are also natural mechanisms. Back to primarily TPO and Tg. They are natural mechanisms of killing old cells. Some people have them positive to a low amount, and they are not negative. They are not always causing a problem. Some are concerned about antibodies and levels that are not clinically relevant, and they consider remission when they’re negative.
Another paradox to throw into account is if your immune system is suppressed or weakened, almost all things that are measured that are antibody-based become negative. You could ruin your health in a lot of ways when your antibodies become negative.
Same thing with allergy testing. You could take immunosuppressant medications, and now all your allergy tests are negative. You’re not healthier.
Negative antibodies, as a generalization, when they are extremely high, that’s usually a problem. Lower is better. There are many who will fixate on those things being zero or super bad if they are even up to a high amount, which is not always true.
Dr. Eric:
Thanks for explaining. You said there is no definition of remission. That being said, at least your definition, can someone with Hashimoto’s still be considered to be in remission if they’re on thyroid hormone replacement? If they’re feeling good, let’s say their antibodies are negative, but the damage is severe where they, at least at the time being, can’t get off the thyroid hormone replacement.
Dr. Alan:
The antibodies have very little correlation to the requirement for thyroid medications. The only thing that correlates with that is overt hypothyroidism, when the gland is really shut down, or being athyreotic, not having a thyroid. There is not a strong correlation between antibody levels and thyroid hormone output. There is some rare variants of Hashimoto’s that are different. The most common types, there is not a strong relationship there.
Being in remission. Take the word out if people have different meanings about it. Let’s talk about getting better. Can someone decrease their antibodies and correlate that to symptoms and problems by a safe natural method? Most can. There is good evidence about that.
One of the clinical trials that inspired The Thyroid Reset Diet took people who had marked elevations of antibodies and overt hypothyroidism, so TSH scores averaging 14-200, quite high. Three months of one simple dietary intervention, 78% had normal thyroid function with no medication. Those who are not on medication, a good chunk can get better.
There has been a lot of focus now on people who have been unnecessarily prescribed thyroid medication. Most of the recent studies have also encouraged iodine reduction as part of the process to help them come off.
Thyroid meds contain a lot of iodine. If you’re consuming an adequate amount already between diet and supplements, and the meds are on top of that, that makes one more barrier for your thyroid to function normally again.
If someone is more deliberate about being lower on iodine to allow room for what’s in the medication, they get better odds of no longer needing the medication. Studies have shown that about 84% of people can decrease their medication and be stable. About half can come off. There is a lot of different cohorts that go into those numbers. Most medications were prescribed unnecessarily, and most can reduce or come off.
Dr. Eric:
That’s great news. Just by reducing their iodine intake?
Dr. Alan:
Well, there is a process of tapering. Some people, if they do that alone, their medicines will suddenly become outgrown. They will move to a hyperthyroid state if they stay on the same dose, but their TSH goes below range. That is a clear sign that your thyroid is getting back online again.
For many, that doesn’t happen, but if they were to taper with a safe, prescribed process and be supervised for that, they could be tracked over time and stay stable. Some just see that they need to reduce. Others now have the potential to reduce.
Dr. Eric:
Could this be true even if someone has been on thyroid hormone replacement for a long time, like 10-15 years?
Dr. Alan:
The stats change. The odds are highest for those who have been on it for four years or fewer. I have seen people who have been on medication for 45 years who are now on none and are doing fine. For someone who has a thyroid, it is not impossible. It doesn’t work for everyone. For many people, it can.
Dr. Eric:
That’s great. You mentioned thyroid hormone replacement is high in iodine. Is that both levothyroxine as well as desiccated thyroid?
Dr. Alan:
A little more so for desiccated thyroid actually. The active hormone, T4 and T3, the 3 and 4 refer to atoms of iodine. Levothyroxine, if you look at the dosage per active ingredient, it’s about a 100mcg dosage of levothyroxine, about 65% iodine. It’s about 65mcg.
The dose equivalency of desiccated thyroid, it’s hard to make dose equivalencies. The best comparison is about 60mg.
The difference here is a lot of the iodine in desiccated thyroid is not in the active hormone. It’s in other iodinated proteins. Per 60mg dose of desiccated thyroid, it’s about .2% iodine. You run the math and get 130mcg of iodine per tablet.
In the big scheme of things, if someone needs thyroid meds, I would not encourage them to choose their medicines based on the iodine content. There are a lot of folks who need meds who can do better on desiccated thyroid. When someone is tapering or deprescribing, it is one more thing to take into account.
Dr. Eric:
Very cool. Do you have a preference when it comes to levothyroxine or desiccated thyroid? Does it depend on the person?
Dr. Alan:
There are populations where desiccated is not a great option: pregnancy, lactating. Elderly, there is a deficit of data; we are not clear on that as much. But in populations where it is an option, there are many who find it preferential and many who feel better on it, even at the same levels. There are also many who do fine on T4.
Most people who I see on thyroid meds who are not doing well, it’s often not a matter of which medicine. It’s about if they need it in the first place. If you don’t, what happens is when you take it, your body loses a whole lot of homeostasis.
We can measure the tiniest bit of thyroid homeostasis between the things we have access to in our blood tests. There is another dozen levels behind the scenes we know of that we can’t measure. There are unknown unknowns as well. We lose a lot of homeostasis when we take over a big, important job by our bodies. Many people are symptomatic even with optimal perfect blood levels. Those same people do fine when they are now taking care of it on their own again and are not taking external therapy that wasn’t necessary.
Dr. Eric:
For someone who, let’s say they were just getting a random physical, TSH was elevated, and the medical doctor, because they were just getting a physical, puts the person on thyroid hormone replacement because the TSH was elevated. Especially if that person wasn’t experiencing hypothyroid symptoms, they just had the TSH elevated. It sounds like there is a good chance. We can’t give specific recommendations here. But just saying if maybe they read The Thyroid Reset Diet, minimize their iodine intake, incorporate diet and lifestyle factors, that they might very well be able to reduce or even get off the thyroid hormone replacement.
Dr. Alan:
What you described is what we call subclinical hypothyroidism. There have been massive articles in the last year in the Journal of the American Medical Association and in the British Medical Journal asking the question that you asked: Is someone like that better off taking medication for their TSH being elevated?
There is a movement now afoot to relabel that as a laboratory artifact and not with a name that sounds like a disease. Subclinical hypothyroidism is not hypothyroidism. A thyroid is still functioning just fine. There is this TSH elevation. Some people are certainly possessing thyroid symptoms, but not that many more than are present in the population with normal thyroid function.
The data is totally clear that at a population level when the only variable is thyroid medication, there is no net benefit to symptoms, and there is no net benefit to health. There are a lot of risks created. There are about 15 types of cancers that people are put at risk for when they are unnecessarily put on thyroid medication. That is based upon five pretty big global studies now in the last few years. It’s a huge decision. There is no net benefit.
The difficulty is that when someone is seeing a person in natural or functional medicine, the only variable is not medication. There are a lot of other things. If they are doing better, it’s probably more credit to those other things than just the medication.
Dr. Eric:
Just backtracking. You said that taking hormone replacement can increase the person’s risk of developing five different types of cancer?
Dr. Alan:
Dr. Eric:
- Even worse.
Dr. Alan:
We just counted a couple days ago. I was saying 12, and someone asked which 12. I made a post, and it was 15. I had to recount.
Dr. Eric:
I don’t know if research shows that correlation doesn’t always mean causation. They are pretty sure it’s due to the actual levothyroxine, for example?
Dr. Alan:
Thyroid hormones have a lot of effects that induce tissue turnover and cell activity. That is not different from any other hormone implicated with cancer risks. In fact, even more so than many others. This is true for T4 and T3. There is mechanistic evidence supporting this possible correlation.
You’re right. Correlations do not prove causations. This is how we learned about tobacco, that those populations have higher risks. The studies looked at cohort populations that are not on thyroid meds. They did a pretty maniacally accurate job of lining up the other risks that were present. Same number of smokers, same number of obese, etc. Here is a cohort just like that but on thyroid meds. It’s pretty compelling.
There are five different studies, and each study was done in a different part of the world. They were independent. They saw the exact same cancers at pretty much the exact same degrees of risk. It’s a compelling concern.
The thing about a risk is that it’s not definite. No one is saying this definitely will happen, or it’s definitely a problem. But it’s a risk. People should be informed of risks when they are present.
Dr. Eric:
I agree. It just makes me wonder. Most people who are on thyroid hormone replacement are on levothyroxine. Many are on Synthroid, which also has other ingredients, fillers and other things. It makes me wonder if it is the actual thyroid hormone replacement, or if it is the fillers in the levothyroxine. We don’t have an answer to that right now.
Dr. Alan:
There are not good mechanistic arguments for the fillers in the doses used. There are pretty clear mechanistic arguments to why T4 and T3, even more so T3, could be drivers for those cancers. They are known to do that in cell studies in vitro. We know we take away a certain amount of internal homeostasis when they are given exogenously. It’s a compelling concern.
Dr. Eric:
Very interesting. Before we wrap things up, is there anything else that I should have asked you that I didn’t ask you? Anything else you want to chat about related to iodine, thyroid antibodies, or anything else?
Dr. Alan:
You asked great questions. You’re super knowledgeable about this stuff. I’m happy to have a chance to speak with you about this.
The big thing I’d love people to hear is I’d encourage them to keep listening to what you’re sharing with them and not to give up on their hope. Realize that in my experience from doing this now for about 30 years, more than ever before, I’m hopeful about the capacity for the body to work by itself, for the thyroid to heal, and for the power of simple changes in diet, lifestyle, nutraceuticals. These things are big.
If you learned what Dr. Eric says and apply those and work with good doctors, don’t give up on feeling your best. Don’t give up on your body working well again.
Dr. Eric:
Well said. Thank you so much, Dr. C. Where can people buy your book? Where else can they find out more about you?
Dr. Alan:
Wherever you buy books, your local bookstore or Amazon.
DrChristianson.com. That is my main hub for blogs and articles.
Dr. Eric:
Wonderful. This was an amazing conversation. Thank you so much, Dr. Alan. It was great chatting with you.
Dr. Alan:
Good to be with you, Dr. Eric.
