Iodine is an essential mineral that is critical for growth and development. Insufficient iodine status leads to goitre in adults and cretinism in infants, and is particularly important for pregnant women. Iodine deficiency is a growing issue in Australia, largely due to depleted soils and recent changes in dairy sanitation practices.
In today's podcast, we welcome back Rachel Arthur who is passionate about separating the facts from the fiction when it comes to the clinical applications of iodine. Rachel shares with us her considered approach to testing, dosages, cautions and contraindications based on over two decades in practice.
Covered in this episode:
[00:52] Welcoming back Rachel Arthur
[02:02] Why is there an iodine deficiency issue in Australia?
[05:24] Changes in dairy sanitation procedures
[06:28] Mandatory bread fortification in Australia
[11:10] Pregnant women: most at risk
[14:00] Fortification risks?
[18:32] How geography influences iodine status
[20:47] Iodine toxicity
[28:54] The Wolff-Chaikoff effect
[35:37] Iodine dosages and exclusion criteria
[42:51] Scope of practice
[48:10] Assessing iodine status
[1:00:26] Rachel Arthur Mentoring
Andrew: This is FX Medicine. I'm Andrew Whitfield-Cook. Joining me on the line today is Rachel Arthur.
She's contributed a decade of teaching naturopathy across SSNT, Endeavour, Monash University, Victoria University, and lastly Southern Cross University.
Rachel's family have a running joke that wherever she goes, she manages to come across her past students. They cover a wide distribution across Australia and New Zealand, and encompass a range of professions including naturopaths, doctors, and allied health professionals.
Whether it's circulating free weekly blogs to her professional peers about important things she's just discovered that can improve the way we practice, or being a key speaker at the major integrative medical conferences, or co-founding the extraordinary Australian Naturopathic Summit. Rachel sees every platform as an opportunity to improve the knowledge base of the naturopathic and integrative professional community. As well as raise the standard of our profession by virtue of, she says hopefully, I say definitely, being a worthy ambassador. And she certainly is that, obviously.
Welcome, Rachel. How are you?
Rachel: I'm good. Thanks, Andrew.
Andrew: Now, Rachel, we're going to be discussing iodine. Why is iodine such an issue in Australia?
Rachel: I think that there's a number of coalescing reasons about why it's such a big issue. One is simply a matter of geography. And a lot of people appreciate this aspect and know that the soils, generally speaking, in Australia, particularly the East Coast, particularly the South East and the southern parts of Western Australia, to some extent as well, are really low in iodine content, and that is just simply a matter of geography. You know, I say to people, we can make vitamins, we can get all sorts of animals to make vitamins for us, and bacteria. Minerals, it comes down to the rocks and the soil. And iodine is profoundly influenced by those sort of factors.
So we know that this is an issue for a lot of regions in Australia. There's low iodine content. We also know one of the other really big players here was the change in sanitising practitioners in the dairy industry. So, previously, the primary source or the biggest contributor to iodine intake in Australians was found to be dairy products, much to people's surprise, but it was, actually, the major contributor. And that was prior to a change in, as we were saying, you know, the use of sanitisers. They were previously iodophors, iodine-based, that were used in milking sheds and that sort of thing, for cleaning milk vats. There was a change in practice around this, and so they are no longer typically used, and this has radically changed the iodine content in dairy.
Some of us might sort of think, "Oh, so what? Why does that matter?" But as I said, prior to this change in practice, dairy actually, was the biggest contributor to iodine intake in the Australian diet. And that change has translated to mean, you know, there have been some studies where they've actually gone back to exactly the same region in Victoria or New South Wales and sampled the milk and checked the iodine content after this change in practice, and they found drops of up to 66% in the iodine content. So it's really quite potent.
So I think, you know, we've got one is geography. Two is this change in the dairy industry. Three is the fact that we don't actually use iodine as part of our fertilising in mass agriculture in Australia. So, you know, your home gardener knows to go and get some kelp off the beach. But unfortunately, it's not used on a large scale in any sort of commercial fertilising products. And, yeah, put those all together along with some good kind of, you know, environmental goitrogen exposure, which we're all unfortunately exposed to, and that's probably the culmination of why iodine is such an issue in Australia.
Andrew: And now, of course, we've changed our practices, as you say, from iodine, so we're now having a chlorine supplement in our milk. Is that what...
Rachel: That's right.
Andrew: Lovely.
Rachel: It's called the double whammy. So, you know, they took out the iodine, they replaced it with chlorine. We know that chlorine blocks iodine uptake to a certain extent. So we're going more...we've lost something, and now, got one hand tied behind our back as well.
So, you know, it's quite interesting to think about what seemingly was a small change in a vaguely related industry that, perhaps, has had quite potent ramifications on the nutrition of a whole population.
Andrew: I remember Professor Creswell Eastman talking about this issue that it'd sort of resurfaced, because it was an issue in the, what, in the 1950s or something, 1940s with goitres. And then there was this iodised salt thing, then salt became bad. So it was just...
Rachel: Yeah, that's right.
Andrew: It's just been this flow on, flow on, flow on, and now, it's resurfacing again.
Has anybody looked at what the mandatory fortification of iodine of all bread, apart from organic, what the effect of that has been in Australian, especially children and pregnant women, I would imagine, but also, the general population?
Rachel: They have. We're only just starting to look at it now. I mean, this rollout of this public health initiative of commercial bread fortification. So, basically, what it meant is that commercial breads now rather than using standard salt, had to use an iodised salt instead. As you said, there were a few breads that were exempt from that. That included not just organic, but also salt-free breads and bread mixers. So people making their own bread at home didn't, you know, have to have iodised salt in there.
So the whole kind of premise behind this was, here we go, we're going to fix this iodine deficit that Australians suffer from, and we're going to fix it by putting it into breads that everybody eats, you know, in inverted commas. The modelling for this, so, of course, there was extensive kind of scientific modelling behind the public health initiative and mathematical modelling was based on the idea that every individual would consume roughly three slices of this bread per day, and that that would contribute about 54 micrograms of iodine to people's daily intake.
One of the things that you heard me say at a conference, Andrew, and I often say this, is I say, "Hands up who eats three slices of commercial non-organic, you know, blah, blah, blah, breads per day." And, usually, there's no one that puts up their hand at those conferences, or maybe, one or two random people. Now that's a skewed sample but, we do know that the follow-up studies about the impact, about the degree to which this has actually addressed and resolved iodine deficiency in the community is not looking that good. The data from that is not really looking that convincing.
So, you know, there's been, you know, a number of studies, in particular, by Charlton that was published in 2016, and also a study by Condo et al that was published the same year. They've looked at different kind of groups. We know that there's been a shift in the right direction. So we know that, for example, individuals that do eat these particular fortified bread products at 100 grams per day, they absolutely were showing, you know, 5 times the rate of achieving adequate iodine as measured by their urinary iodine concentration. This is shown in women, and I think it's 12 times the rate of iodine adequacy for those kids that were eating 100 grams of commercial bread every day.
But we know that studies, generally, when we look at the shift in median UIC values, they're moving in the right direction. There has been a general positive shift. But we know that the proportion of the individuals that remain deficient in iodine post-fortification, is still strikingly high. And, in particular, Condo's study in 2016 said that, or showed that, post bread fortification, there was still over 50% of pregnant women that were iodine-deficient. So we're still left going, "Hmm, how effective has that public health initiative been?"
I think, also, one of the problems, and Condo talks about this, those researchers talk about this in the study, was they've actually interviewed pregnant women and said, “What do you know about iodine? And what are you doing about iodine?” And, certainly, one of the comments they came across fairly commonly was women saying, "I don't need to take iodine because it's in my bread." And so there's this kind of backflip or, you know, counterintuitive thing that's going on where rather than necessarily giving us the results that we wanted, in terms of reducing iodine deficiency, we've almost got a reverse psychology going on where at particular at-risk groups are going, "I don't need to do anything about iodine anymore because apparently the government's got it sorted."
Andrew: Despite there being a public health recommendation from the NHMRC that pregnant and breastfeeding women have a supplement of 150 micrograms, even though there's bread fortification. So, in other words, the bread fortification is not enough, and even though there's a NHMRC guideline for this. I remember Creswell Eastman screaming to GPs because the message was not getting through.
This is the first time that the National Medical Health and Research Council has recommended a supplement. It wasn't folate. Folate, they said, "Get it from your green leafy vegetables, and if you need to, take a supplement." But this is, "You need a supplement even though we've fortified the bread."
Rachel: Yeah. Look, it's really interesting, isn't it? It's kind of, we know that this is always the risk with, let's call it, public health nutrition prescribing. We know that, and this is always, you know, one of the primary concerns that's raised in the proposal phase of public health nutrition fortification programs. Is, the concern that's raised is, some people will still be deficient and not be getting enough, and yet they've been reassured at some level that the government's got this covered. And then there'll always be some people who are overdosing. And the data that's coming out is showing exactly that.
So you've got the study by Condo which found that even women, they were looking at a pregnant cohort. Even women who were taking at least the recommended 150 micrograms of iodine as a supplement per day during their pregnancy. Even out of that group, it was 27% who were still iodine deficient, according to their measure. And then you've got the new data coming out as well, looking at, you know, there’s some evidence that, particularly, in WA and in Queensland, and as I said, because of geography, there are differences in iodine intake across Australia, just because of geography.
So in WA and in Queensland, there is some suggestion that there is a little bit of overdosing going on just because of the introduction of bread fortification, particularly in children. So, you know, you go, yeah, it's this kind of crude… you know, it comes from a good place, where we're trying to resolve this really marked issue for Australians. But anything that follows that kind of one-size-fits-all model is pretty crude. And you're going to see people who fall short and people who get overdosed.
Andrew: Yeah. But can I ask though, what was their determination of overdose? Were they talking about levels of iodine, or were they talking about effects of iodine on, for instance, thyroid-stimulating hormone?
Rachel: So in these particular studies, as I said it's early days, you know, they were just coming out in the last two years. And these studied have just been measuring urinary iodine concentration. And they're looking at median values. So they're not looking at individuals and saying, "Little Johnny's got a problem here." They're looking at a trend in age groups and at-risk groups and things like that. And I know that, the trend has been across, you know, the ages in WA and Northern Territory, that the median UIC has actually jumped up to, I think, it's over 150 micrograms now, and I think it's quite a bit over 150 micrograms.
But they talked, specifically in this study, about, you know, kids, and the really dramatic shift upwards in the median UIC for children. So, you know, we're not as yet able to say, and look at the impact of the issue in terms of thyroid behaviour or anything like that, but we know from other countries that there's a risk there.
Andrew: Okay, so they have seen a suppression of TSH in other countries that have had supplements?
Rachel: It's not that they've seen a suppression of TSH. Probably the biggest trend that has been demonstrated in countries like Greece and Turkey, which all had very similar sort of problems with iodine deficiency and then they introduced fortification programs, not dissimilar to what we've done here.
Is they've found that there was, you know, increases in rates of new diagnoses for autoimmune thyroid disease. A dramatic increase in incidence. I mean, there's been so many studies, Andrew, I'm just sort of cherry-picking, but they have been some of the most current ones. Of course, has been a lot of studies looking at China. Because of regions of China has been fortified with iodine for a long, long time. They see higher incidences of a range of thyroid disease. It could be hypo, hyper, or we also see a very particular type of thyroid cancer that has gone up in some of those Chinese populations as well. So the impact of the overdose is actually, not quite individualistic, but there is huge variability in how that excess will manifest. Yeah.
Andrew: Yeah, yeah. If there has been a rise in the urinary iodine concentration, in children. But if there's no effect on dampening, on suppression of thyroid stimulating hormone, then maybe it's our levels that we need to adjust, not the iodine.
Rachel: I think that that's a… that the data would...because we have a lot of data on iodine, you know. This has been such a well-researched mineral. It's not to say that there aren't gaps in our knowledge. But as you say, I mean, there have been countries subject to endemic goitre since the turn of the, you know, the 19th century. This has been a public conversation not just in Australia, but many countries all over the world for the last 100-plus years. And hence, we have a lot of data on what deficiency looks like, in terms of UIC values. What toxicity looks like in terms of UIC values.
So I don't know that I would support that argument. I think that there is quite strong evidence that a UIC value for an individual, or for a population as an adult, you know, over 300 micrograms per litre is going to start to suggest that people are getting so much that it was going to be problematic for them. There’s big bodies of data that suggests that. And in women, in pregnant women, we know the maximum level we want to see in the UIC is 500. And it's not based on, you know, small data sets. This is based on huge studies from all over the world.
Andrew: I want to ask about toxicity, but before that, I want to try and clear up something in my mind that I just thought of. And that is, I used to say, I, you know, said Australia has an iodine deficiency issue because it's an old continent and all of the minerals are washed away. But then there's an issue in Nepal, which is a new continent, and it's a mountainous area. It doesn't gel?
Rachel: Yeah. Well, again, it's fascinating, isn't it? Because when we talk about geography and we say, well, you know, it's about the soil and the rocks, even that is over-simplifying it. It's about the rate of precipitation or the water exposure of the soil. That's one of the other major determinants of iodine.
Andrew: Gotcha.
Rachel: Because iodine is highly leachable. So if you've got an area that is subject to, you know, a high rainfall, whether it's monsoonal, or just because you're lucky enough to live in Tasmania or whatever it is. Then that, regardless of how your, you know, the iodine content in the rocks and the soil to begin with. That places that region at risk because it is such a leachable mineral.
So, you know, there are all these other kinds of, I guess, factors in the environment. You know, we talk about the kind of the environmental iodine cycle. So, yes, there's what was existing in there in the soil and the rocks in the first place. And I've read some fascinating stuff, Andrew, that says, you know, coastal areas are at risk, but so are inlands. You know, young mountainous areas are at risk, but so are, you know, flat areas. So you realise that it is more complex...
Andrew: There's no hard and fast rule.
Rachel: ...than just saying this is an old continent or this is a new continent or this is mountainous or, yeah. But, certainly, water, the exposure of that landscape to heavy irrigation practices, or heavy rainfall is one of the most detrimental things in terms of the iodine content that remains in that soil for the plants and for the water source for us to consume.
Andrew: So about toxicity. Like I remember an old argument, and you and I have discussed this a bit, about a debate that went on between somebody that used to propose extremely high dosages of iodine versus somebody that was a lot more salient in their dosages, Guy Abrahams versus Dr Alan Gaby. What's the appropriate iodine dose, and just how toxic are we talking with this halide?
Rachel: Look, I think that, like I've just sort of suggested before, I'm not ever going to say we know everything about iodine. We really don’t. I think that our knowledge will continue to build in this area. I think that if we're talking...and that may change, you know, some of our thoughts over time.
But I think if we're talking about that huge contrast in school of thought between Alan Gaby and Guy Abrahams. One is talking about too much iodine is never enough, you know, we need milligram doses, all of us do, every day, to be well. And Alan Gaby, of course, encouraged us to be cautious and to question the level of evidence that that megadose was sort of based on. I certainly sit on the side of Alan Gaby, and think that mega-dosing is problematic.
I think that, again, I can come up with this from so many different angles. Either I can talk about the plethora of studies that have been done. I mentioned some of them before on populations post-fortification programs, and some of the negative health consequences of excesses. And then people will say, "Yeah, but that's because they used, you know, iodide and they didn't use iodine." And equally, I can talk to you about case studies where iodine has been used, and either that has been iodine orally, or iodine topically.
If you talk to any doctor who's worked in a hospital, they will tell you that iodine toxicity, they've all experienced it because of individuals who were painted with Betadine post-burns, or post-surgery, and then they watched their thyroid go berserk. That was one of the unfortunate consequences of, you know, trying to, you know, provide antiseptic on the skin to these individuals.
So, you know, and I have seen so many cases of people taking excessive doses, milligram doses of iodine, that, unfortunately, have gone horribly wrong. So I think that, you know, there is reason to be very cautious, and my position is certainly that micrograms are what are needed for the majority of individuals. Milligrams are needed in a very small number of patients with, extenuating circumstances. But I'm very nervous about the kind of message out there from advocates of mega-dosing who sort of suggest that, there's no harm that can come from this.
Andrew: Yeah. I think I have to agree with you there. I must tell you about an example, and it was a mistake. It was a mistake in dosage, that I made. Where the dosage that I wanted to give was drops, four drops. Because of a communication issue, four mLs was given. Now, four mLs is what we used to give pre-surgery for somebody with thyrotoxicosis, to aid in shutting down their thyroid before thyroid ablation surgery. And yet, in this particular lady...now, I must describe this patient because I think this speaks volumes about the reason that there wasn't an issue.
This lady was a large lady. She was tall. She was, let's say, big boned. She wasn't obese, she was a big lady, and she had fibrocystic breast disease. And we went through all of the issues. Been assessed, not this, not been palpated by a doctor. She'd had mammographies done. She'd had all of the safety issues done where I was concerned about some… covering up some issue or even feeding some tumour-type condition. And what I gave her or what I wanted to give her was four drops of Lugol's solution, two drops twice daily.
But because, as I said, of a communication misinterpretation, four mLs were given. Thankfully, this lady had absolutely no untoward side effects, and indeed, her fibrocystic breast disease resolved totally for a period of months, even upon the short-term dosage. However, I am supremely embarrassed about that communication error, and I would never ever recommend it to anybody, particularly in light of, you know, conditions being flipped like Hashimoto's where you can cause all sorts of issues giving high doses. But what's been your experience?
Rachel: Yeah. My experience has been in terms of seeing iodine excess at play, is I… you know, there's been that ongoing debate about the Wolff-Chaikoff effect, and is it real? Does it apply to humans? Was the original study misinterpreted? That's certainly an argument that's been put forward. I am, confident, that without a doubt, I've see the Wolff-Chaikoff effect in humans. You know, I've actually seen their TSH go up, and we expect that to be the case regardless of, you know, the rest of the story, when people start taking iodine.
But I've actually seen people's T4 levels drop from in-range to completely below range. I've see their T3 drop below range as well in response to excessive doses of iodine. So, the argument, again, put forward these, you know, that after a period of adjustment, these people will escape the Wolff-Chaikoff effect, that the thyroid will, you know, kind of recalibrate to the higher circulating levels of iodine, and will start to normalise. And, you know, I've seen patients where there is no way that that was ever happening. And, in fact, what was...they were getting themselves in more and more trouble with more apparent hypothyroidism symptoms. Their thyroid levels continued to get lower.
And one of the big things that, I think, you know, isn't talked about enough is iodine is quite antigenic. It actually attracts the attention of the immune system. It's iodine, not anywhere in the body, but as part of that thyroglobulin molecule which, of course, is in the follicular cells of the follicle cells of the thyroid. So, you know, one of the classic things that I've seen, and this has been, in many, many cases, is somebody who's over-treated with iodine. They either didn't have thyroglobulin antibodies present at baseline, but they sure as heck do now. Or, they did have levels, but they have jumped dramatically, thanks, again, to iodine.
So as much iodine is so important for the thyroid, it does have a double edge or a dual sort of personality. You know, a deficiency is bad for it, but an excess, I truly believe, is bad for it as well.
Andrew: Yeah. So, firstly, can I just ask you to explain to our listeners what the Wolff-Chaikoff effect is?
Rachel: So the Wolff-Chaikoff effect originally came about with some couple of researchers called Wolff and Chaikoff. Wouldn't you know it? And that they did some animal studies. I think it was rat based. And they were looking at intra-peritoneal injections of high dose iodine and how the gland responded to that.
There has been a lot of criticism of this study, and a lot of different interpretations of it. What they did talk about as a consequence of that high exposure to iodine was some reduction in thyroid hormone levels.
You know, there's been a lot of work on this since Wolff-Chaikoff. I think that’s the problem. You know, we all go “Oh that study on the rats in 19.. you know, whatever, that leaves a lot to be desired”. And I'm like, "Well, keep reading, people, because we've done a lot since then."
We know that when you do overexpose the thyroid to excessive iodine, that we see a shutdown of sodium-iodide symporters. They're the gateways, or the doorways on the surface of the glands that are responsible for taking up iodine and hyper-concentrating it within the gland.
So the way that I always describe the Wolff-Chaikoff effect to people is that, you know, it's almost like the gland, in response to detection of supra-physiological concentrations of iodine, literally shuts up shop and says, "You know what? If I kept picking up the 80% of passing iodine, like the gland normally does, if I kept picking up such large proportions of this now, megadose of iodine, I am going to place my human at risk of thyrotoxicosis." And so as a compensatory mechanism, it closes up those doorways. It down-regulates the sodium-iodide symporters, and you see that it stops concentrating or picking up the iodine. As a result of that, we see the whole conveyor belt of thyroid hormone production slow right down. And that corresponds with the dropping T4 and T3 that we see in patients' results who are affected by this.
So that's the Wolff-Chaikoff effect in a nutshell. This happens within 24 hours, and this is the original study suggested that this could...this kind of thyroid response to mega-dosing can start to occur within 24 hours of a megadose. And then there's the possibility that individuals can adjust to this. This is called ‘the escape’ to the Wolff-Chaikoff effect, that that may take some days.
But I would say, you know, I've seen too many cases where practitioners or patients have been encouraged to just keep riding this, so-called, temporary aggravation from high iodine. So low T4 and low T3 levels, massively alleviated TSH. And, you know, they've been doing it for weeks, and I say, well, that's not… the Wolf-Chaikoff effect, if you're going to escape it, you know, then if your thyroid is capable of doing that, then it will do that within a matter of days, or within the week. You shouldn't have stayed on that long-term. You know, the answer is you're not going to escape it.
Andrew: Yeah. Given though that, you know, the production of the thyroid hormones, the thyroglobulin, etc. That there's so many other nutrients involved in that production, could there be an issue with something else furthering the prolonged Wolff-Chaikoff effect? Could there be another reason, like a co-morbid issue?
Rachel: Yeah. Look, I think that it is possible, and, you know, there's always this kind of speculation. Like I said, at the beginning...you know, iodine over-dosage takes various forms in a range of individuals. Anything from hyper to hypo, to malignancy to, you know, nothing. They did great on iodine. And I think that there is a lot of unknowns in there, you know. I think that, you know, could there be nutritional co-factors? Sure, but the sort of situations where I've seen exactly this, the Wolff-Chaikoff effect, and the inability to escape it from megadoses of iodine, those patients had every other nutrient, you know, ticked off the list. They were absolutely, you know, buoyant in their selenium and, you know, everything else. So we couldn't see why there would be particular vulnerability for them.
So I think there are a lot of unknowns, and I think that's the risk. I think when you get someone using a protocol that says, you know, 50 milligrams for everyone or 12 milligrams for everyone, it just really, it doesn't work, you know. It just doesn't work because there is too many individual kind of biochemical or physiological factors in there.
Andrew: So should we be supporting the patient rather than the thyroid? Including looking at, for instance, particularly with Hashimoto's, looking at their levels of stress, their possible exposure to toxins and all that sort of thing?
Rachel: I mean, I think so. I think with this incredible rise in autoimmune thyroid disease, particularly Hashimoto's, in Australia, you know, it's not going to come down just to iodine. You know, iodine may be a pivotal player in some patient's cases, but like everything else, we need to take a broad perspective. And I think that, you know, a lot of practitioners are very good at that. At thinking about, you know, what else is playing with this pathology. I think, you know, iodine is, as I said, part of a solution for some people. But I haven't seen iodine, on its own, fix anything. It's not...
Andrew: Rarely works, unless, of course, it's a bullet.
Rachel: Yes, yeah.
Andrew: What about, you know, dosage issues then? Given that we've already uncovered a conundrum, and that is that we should be supporting the patient rather than the thyroid. Can you help our listeners out with general or broad sort of safe guidelines with dosage, or even variances in dosage with different conditions, particularly, I guess, with how high would you go with Hashimoto's? Where do you go whoa back there?
Rachel: Yeah. Well, I think what I'll start with is probably my, you know, my kind of exclusion criteria. You know, the people that I would have to think long and hard about ever justifying giving them iodine because there is quite a list of people that I think iodine can be contraindicated in. So I'm going to start there because, you know, that sort of sets the scene.
So, you know, iodine should not be used in Graves' disease unless it is being prescribed by basically an endocrinologist or a specialist. The whole idea, many people will know, that it actually can be a very effective strategy to getting Graves' under control, and the mechanism for that is it induces the Wolff-Chaikoff effect, exactly what we were saying before. It shuts the thyroid down, and it shuts it down faster than antithyroid meds. Because as we said, it can happen...it starts to take effect within 24 hours.
But that particular protocol or that prescription of using high-dose iodine to literally shut down a thyroid gland in Graves' disease. That is something that, you know, I certainly wouldn't want that to happen on my watch, on my shift. That needs to be something that is prescribed and monitored by an endocrinologist who really is familiar with that. It's good to know it's an option. In fact, there was a paper just, I think it was this year that has concluded that that strategy is the safest strategy for dealing with Graves' in pregnancy. Which is really kind of interesting to finally hear that conclusion come out. But, as I said, it's not within the scope of our practice. It's pretty dangerous, and there's a lot of risks associated with it. So Graves' for me, I go, is a no-go zone. Don't use iodine because these people are primed, of course, to turn every drop of iodine into more thyroid hormone, and they already have an excess.
The Hashimoto's debate, whether you use it or you don't, I actually sit on the side of not using it in most cases. The reason is, in Hashimoto's, there's a couple of reasons. One is that you have often an active thyroiditis at play, and iodine tends to make that worse. Particularly, as I said, when these patients have a significant level of thyroglobulin antibodies. Now, thyroglobulin antibodies, normally, people don't pay so much attention to these because they’re not considered as clinically, kind of, correlatable with the disorder. They're more interested in those TPO antibody levels. But it's the thyroglobulin antibodies that really can be made a lot worse by iodine. So when I see a Hashimoto's patient, if they've got some of these already bubbling around, it really cools my heels about addressing any sort of iodine deficiency that I think is present. I have to really kind of weigh up the pros and cons.
Andrew: So do you then sway your support for that patient more towards an anti-inflammatory-type treatment aspect, if you like?
Rachel: Oh, I think that in active thyroiditis, whether it's Hashimoto's, Graves', De Quervain's, which is an unusual type of thyroiditis postpartum. The first thing that often we should be thinking about is protection. You know, how do we protect that gland? And the best way to protect that, you know, the thyroid gland is really through the use of selenium, you know, NAC. These things have been tried and true.
We know that selenium, through its role in the glutathione peroxidases, is effectively the fire extinguisher for the thyroid gland. We know that it has the capacity to lower antibody titres, and that is indicative of it really ramping or reining in the immune system there. So we know that, you know, selenium and NAC are both very hands-on in their role of controlling that active, damaging inflammation going on in the gland, and I think that that's really important. And then we can kind of, you know, start to talk about vitamin D adequacy and, you know, as immunomodulatory, and those sort of things around that as well.
But, yes, when there's active thyroiditis, iodine really, usually isn't the first thought at all. It's more about those protective nutrients and antioxidant control there. Yeah.
Andrew: Yeah. So I got you off topic there. Sorry. So other conditions where you're...
Rachel: That's all right.
Andrew: ...reticent to...
Rachel: Other conditions. Yeah, other conditions are anybody who has multinodular goitre. So multinodular goitre is quite common. The risk is that a multinodular goitre becomes what's called a toxic nodular goitre. That just means, the difference is that those nodules that are present on the thyroid starts to autonomously pick up iodine, and autonomously make thyroid hormone. So, of course, the, you know, unchecked risk, or potential risk here is that you're going to end up with a thyrotoxicosis because of, you know, those nodules being overfed with iodine.
And, you know, one of these interesting ones is, you know, if you go to a lot of, say, pharmacy textbooks, or you ask a group of endocrinologists whether anyone on thyroxine should be taking iodine, the kind of consensus statement is no, they shouldn't. Now, I can see a lot of situations where there would be benefits from taking additional iodine for some people that are on thyroid replacement therapy. But, again, I think we have to acknowledge that there is a degree of risk and that that patient has to be, you know, really well-monitored to make sure that their safety and efficacy, in terms of giving them any iodine, in addition to thyroxine.
Andrew: Yeah, like I know what I'm thinking, and I'm thinking I don't want to see the inside of a courtroom.
So...but I guess the questions have got to be asked, how brave do you get if, say, you did a 24-hour urinary iodine sample, and it did come up as them being on a certain dose of thyroxine, which contains iodine, it is the T4, and still having an iodine deficiency? How brave would you be about supplementing, even judiciously?
Rachel: I do supplement in a situation like you've described, where I have a good level of evidence for an ongoing deficiency. So, yes, thyroxine contains iodine. It's actually a very low level of iodine. I have quantified it, but I can't think of the numbers off the top of my head, but it's pretty low. You'd be surprised. So, you know, if given that the standard dose of thyroxine is about 100 micrograms. So, you know, the idea that somebody who's on thyroid replacement therapy doesn't need any more iodine, that all their iodine needs are met, is kind of pretty bizarre. Because, of course, we know that the thyroid is about one gland that has an iodine requirement.
We know that the gastric mucosa and the breast tissues equally express sodium-iodide symporters at a comparable level with the thyroid gland. Like, they have a major iodine requirement, these two other tissues. And then there's a whole list of other tissues that have sodium-iodine symporters and the capacity to pick up iodine. But not quite, you know, up at that same sort of enormous level. That's things like salivary glands, thymus, the epidermis, you know, they all need iodine as well.
So I think that that sort of, you know, that idea that they're on thyroxine, no more is required, is very flawed. It doesn't match with the science. But I understand from a litigious point of view that we do need to be very careful when we co-supplement, that we are not, you know, upsetting the thyroid management or, you know, contravening the therapy, the other therapy that's been used.
Andrew: Are there any situations where you'd go, "Look, I've done this test. As you say, there is a good level of evidence to show that there is an ongoing iodine deficiency, but I'm not touching it. You can have it?"
Rachel: Yes, I absolutely have. I've got a few patients like that. I've got a few, and it's really come about from having my fingers burnt just a couple of times.
So a couple of times, you know, I went right, level of evidence, right, you know, they definitely have iodine deficiency. What am I going to do? And I thought, "Look, I'll go very cautiously”. Because that certainly is the way I approach all of these situations. So I have one case, actually, you know, that's quite fresh in my mind. Where this patient had thyroglobulin antibodies. I had a good level of evidence that they still had an iodine, that they concurrently had an iodine deficiency. I put it off, said, "No, no. You know, they've got thyroglobulin autobodies. It looks a bit risky. I won't give them iodine.” Put it off, put it off, and then eventually said, "Look, I'll just include 100 micrograms a day in the prescription." And at 100 micrograms per day, we watched those thyroglobulin antibodies go through the roof, from where they were.
So, you know, I think that there are situations where I say, and this is kind of like a, you know, this is not something… this is not a position that I can say is supported by the research. This is a little Rachel Arthur kind of, position, that after 20 years of practice. Where I would say that, for some people, perhaps the problem with their thyroid, to some extent, was caused by an iodine deficiency. Perhaps they present to you and they still have one. The problem is, when you're faced with a real conundrum like this, is, in some of those patients, I have to say, even though I can see there is still some iodine deficiency going on, the pros and cons just don't weigh up, and I feel that the damage has already been done to your gland.
Now, that doesn't sound very uplifting, but what I'm saying is when patients really do have marked thyroglobulin antibodies, it's a bit of a "wrong way, go back" sign for iodine. You have to come about it from a different angle. You have to resolve those antibody levels from a different angle before you can bring in any iodine. That's my personal experience after years of dealing with this. And yes, so there will be people who will say, "Just make sure you eat iodine in your diet," but we're not going to do any more than that, you know, at this point.
Andrew: Yeah, err on the side of caution. So I guess this leads in to if, you know, as we've said before, in that last example, you know, sure that there was an iodine deficiency going on, but what do you do? How should we be assessing iodine status?
Rachel: A highly contentious issue, of course, and I love nothing more than a good bit of conjecture…
Andrew: That's why I'm asking you.
Rachel: That's right. Look, there are so many, you know, ideas put forward about how to assess the iodine level of an individual. You know, some of them are things like the patch test, where you paint somebody's skin with Betadine, and you see, you know, how quickly that colour disappears. That's completely a furfy. It doesn't actually reflect the iodine status of the individual. What it actually reflects is, the rate of evaporation off your skin. Which comes down to things like the temperature and the moisture of the air, and things like that. So, actually, when we paint our skin with Betadine or something like that, about 88% of the iodine will evaporate. It's just a question of how quickly it does that, and that has nothing to do with your iodine requirements, or your iodine status. And the other reason why the colour disappears is we also have iodine being reduced back to iodide. So iodine has a colour, iodide doesn't. So, you know, that’s again, got nothing to do with your, you know, iodine kind of a nutriture. So the patch test is out. Sorry to break the news, but it is. It's out. It's not got any scientific...
Andrew: Don't be apologising to me, I'm glad you covered it.
Rachel: Yes, that's right. You know, then if you go to...you know, as I say, I mean, iodine is, you know, so extensively researched all over the world. You'd think we'd have an answer, wouldn't you, Andrew? You'd think we'd know by now how to determine the iodine status of an individual, and yet, out of all these studies which say, “we know how to quantify the iodine intake of a population and the iodine status of a population”, just about every research paper will tell you that these tests and these assessments are only accurate in populations, and we can't use them on the one individual sitting in front of you. That they lose their accuracy and validity once we try and do an N equals one sort of, sample.
So what I'm referring to here, of course, is urinary iodine assessment. It is absolutely the gold standard in terms of knowing whether Bangladeshi’s need, you know, more iodine or Australians need more iodine. But if I'm looking at one Australian, the researchers and the, you know, ‘powers that be’, would say, "Sorry, we don't have a test that can tell you that," and you go, "Really?"
Andrew: So is it more appropriate to test for deficiency rather than adequacy?
Rachel: No, they would still say the test alone, that the test is not a reliable marker of status, full stop. In an individual.
Andrew: Wow.
Rachel: So they would say there are two main mitigating factors. They are, because, of course, the amount of iodine in the urine is really reflective of the intake of iodine over the last 24 to 48 hours. So if you had a big nori fest yesterday, then your iodine is going to look fab today, and if you didn't, if you had a big kale juice extravaganza, it's going to look like a shocker today.
Andrew: Eew.
Rachel: That's right. So, you know, that's their argument, is it's unreliable even in the one individual. I, you know, you've heard me say, Andrew, getting iodine adequacy in a patient or trying to achieve iodine adequacy, which I think is a good goal, right? I think it's an important goal, particularly in a country like Australia. I think it's hard enough without being told, "Now, you have to do it blindfolded because we don't have a test." I go, "Really?"
So I still use urinary...what's called a random urinary iodine concentration, but I have a few caveats around it, to try and control for those sort of limitations of the test itself. So one of the things that I say is, you know, don't have a nori fest or a kale juice extravaganza the day before. I want you to eat a representative diet. Like, what do you normally eat? Stick with that. Don't vary from that in the three days leading up to the test.
The second thing is the test has to be taken fasting. So let's make sure that it is your...I'm sorry, not just fasting, it needs to be the first-morning urination. So let's make sure that, you know, you go in and you wee in the jar at the collection centre first thing in the morning. Because there is, actually, diurnal variation in urinary iodine levels, okay? So, you know, I started to put these, kind of, protocols in place to increase the reliability and the accuracy of the result we get.
The third thing, which is something that, you know, I debate feverishly with people, is I think that you have to take into account the concentration of the urine. So if you have a patient who has a very, very dilute urine, that can trick you into thinking that the iodine is very low. Because, of course, it's just a random sample. It's just a kind of, they’re only taking a tiny amount. But if that urine is very dilute, the iodine will also look very, very dilute. And so, you know, you can be tricked into the wrong kind of interpretation with both excessively dilute and excessively concentrated samples. So all that necessitates is when they do their urinary iodine test first thing in the morning. That the pathology company also measures creatinine in that sample because creatinine is really the gold standard in kind of benchmarking the concentration of a urine sample. And then there's a single formula that you use so that you can account for that concentration, or that hydration sort of effect.
So I do still use that. I say that I never use a urinary iodine concentration alone in a patient to conclude anything about their iodine status. It has to be married with, you know, other, what I call secondary markers of iodine nutriture. So that’s things like, you know, have a look at their TSH, have a look at their T4 levels, and start to see if there is congruency, if there's, you know, a shared sort of picture emerging.
So what we're looking for here is, in particular, I think the most important secondary marker is the T4 level. If we see a T4 level that is dropping below 12, that really is kind of my line in the sand, where I start to question, not conclude, but just question, iodine deficiency. If I have a T4 dropping below 12 and a UIC value that looks low, then I'm starting to say, "Okay, you know, we're starting to get, you know, more than one piece of evidence pointing toward this kind of conclusion."
Andrew: There's two things I have to say here. The first thing is it's obvious to me that iodine is such an issue, and this, in particular, it's so controversial. Even though we think we might have it right with a simple health guideline, we haven't got it right. That people need to be joining your mentorship group to be able to discuss this, at depth.
Rachel: I do get a bit excited about iodine. It's true.
Andrew: But it's from a place of responsibility, and this is what I really like about you. You care. You give a damn about your patients. That's the first thing I'll tell our listeners, before we go any further. I did want to ask one quick other question though.
We know that, you know, measuring T4 doesn't tell us how well that thyroid hormone is working. Do you use random urinary iodine concentrations, with creatinine, but also combining it with other assessments, relevant assessments of metabolic rate?
Rachel: Yeah, good question. So first of all, you're right. T4 is the inactive form, and you know, it's only one sort of piece of the thyroid, you know, efficacy or health picture.
The classic thing that I would say though, why I look to T4, is because iodine, the way to think about its relationship to T4, is it's like the rate-limiting ingredient. So what I'm saying is, if you haven't got the iodine, you will not make the T4. It's a chocolate cake without any chocolate. You just go, "Can't do, cant do” So if you've got someone who's got, you know...you're questioning iodine deficiency, and they've got a T4 of 15, forget it, okay? This person has iodine. This person has got plenty of iodine. They wouldn't be making that level of T4 if, in fact, there was really a big deficit.
So the T3 thing, the interesting thing in iodine deficiency, the classic picture is that the T4 drops, because the gland, you know, it's missing the chocolate for the chocolate cake, but can't make as much. But in compensation for that, the T3 levels, relative to the T4, actually rise. So it's a trick. You know, people might, if they don't know that, they might go looking for low T4, low T3. That's not necessarily the classic picture of iodine deficiency.
The other question you asked me is, should we be looking at other markers like basal metabolic rate and temperature and things like that? I think that we can, and sometimes, we should. In fact, I believe that the most...I'm probably going to give it the wrong sort of description. But certainly a well-validated assessment for thyroid is the speed of the Achilles reflex. I'm pretty sure that's still regarded as being one of the most important markers. So, you know, there are certainly people who practice in that way and use, you know, testing that measures reflex speeds and things like that. So I think that there is an interesting aspect.
In terms of basal body temperature, it's very, very hard to get accurate readings. And if you talk to a lot of clinicians who had extensive experience in this area, they will agree, and say, "Yeah, you know, I get a lot of results, but I'm not sure about their validity. I'm not sure about how well that temperature has been taken in the patient." So I think that it's a little bit tricky, the application of that.
But I think, definitely, you know, the more we can take our blinkers off and kind of look around the whole case and say, "Where is the evidence, you know, for iodine deficiency, and how many pieces of evidence can I attribute in this case?” I think the better the job you're doing, and the more likely you are to succeed with, you know, your treatment and your intervention.
Andrew: Rachel Arthur, I truly do admire two things, not just two, but two main things about you. One is that you care. You truly care for your patients, and it's evident after years and years of practice. No offence meant. But the other thing is that you constantly question, and you are never ever satisfied with the status quo. You will always question, and question again what you think. Am I...is this current truth? Is this what's true now? And I truly, truly admire you for that because the people that are under your mentorship now, are truly learning to be better clinicians, safe clinicians, and I really admire you for that. So thank you for taking us through the...
Rachel: Thanks, Andrew.
Andrew: ...the quandary that still exists with the regards to iodine today, on FX Medicine.
Rachel: That's right. Look, I think that, you know, a lot of us, I've said this before, who are in this business, are mavericks by nature, and we're naturally good at questioning things. And I think that a lot of nutrition still, there's a lot of gaps in our knowledge. So we have to keep asking ourselves, you know, what do we understand now? How does it change our opinion now? What have we learnt from our mistakes? You know, how can that change the way we go forward? And I think iodine is a great example of that.
Andrew: This is FX Medicine, and I'm Andrew Whitfield-Cook.
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