Iodine, Supplement Reactions, Hormones And More - KMUD, 2016-02-19

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    Iodine, Supplement Reactions, Hormones and More KMUD - Ask Your Herb Doctor - 2016

    https://dl.dropboxusercontent.com/u/22195338/kmud_FPS160219_FPS190002fritalk.mp3

    HD1 – Andrew Murray
    HD2 – Sarah Johannesen Murray RP – Ray Peat

    Transcribed by moss, verified by Sheila
    HD intro not transcribed


    _____________________


    HD 1: So brain development, aging and the hormones involved in that gradual decline in good health. So just for people listening to the show, we will be taking calls from 7.30 to the end of the show either related or unrelated to this month’s continuing topic of Nitric Oxide (NO) and wanted to get into a little bit of the subject of Iodine as an opener for the show for people thinking about supplementing with iodine and also open up a little bit about the Zika virus that’s really catching media attention here. I know there’s certain authoritative reasons for it and there are other supposedly conspiracy theories, if you can call them conspiracies, I think some of the merits of conspiracies are worth picking up and exploring. Anyway, if you live in the area, the number here is 1800 568 3723 or 9233911.

    HD1: So Dr Peat, I was looking today and I guess what prompted it was hearing advice of people touting a product called nascent iodine and I know that you specialized in thyroid hormone and that iodine is definitely a key component of thyroid hormone. And I think we’ve always been led to believe that there has been adequate supply of iodine in the diet and then they produced iodized salt back in the 50s or 60s, perhaps earlier or not, I’m not too sure, but iodized salt has been around and seafood also contains a lot of iodine in its own right. So when I heard about this product called nascent iodine they were saying that it was essentially not the stable, so stable ionic form and was more available and it’s more readily taken up by the thyroid gland and then I read some other articles about nascent iodine and how reactive it was and I just wanted to feel you out, what you know about the thyroid’s natural need for iodine, whether or not we are deficient and whether or not we need supplementation and if in fact, this is something that actually may not be necessary.

    RP: In the 1980s, I was looking into the iodine nutrition question because I saw some women with breast disease who recovered quickly when they took supplements of kelp or thyroid hormone and the safest thing, I think, is to correct the thyroid problem directly rather than counting on big doses of iodine because the large doses over many years, for example, there are about 70 or more publications looking at iodine intake around the world, over a period of decades, and they see that over half a mg or even especially over 1mg of iodine per day over a population is closely connected with increased risk of thyroiditis and thyroid cancer. One of the theories of why that happens is that iodine spontaneously reacts, or in the presence of white blood cells their enzymes can cause iodine to react with fatty acids that are unsaturated. And if you’ve heard about the iodine number to describe the degree of unsaturation of the fats - for example, the food oils that are highly unsaturated have a high iodine number. That means the number of molecules of iodine that will be spontaneously absorbed by a certain quantity of the oil, because the iodine attacks the double bonds in the fats and where they lack hydrogen saturation, the iodine fills in like an analogue to the saturated hydrogen content. So there is this tendency of unsaturated fats to react with iodine and when that happens the body can then interpret that as a signal to the thyroid gland, possibly imitating the thyroid-stimulating hormone (TSH).

    HD 1: Really?

    HD2: So it doesn’t cause an increase of thyroid hormone?

    RP: It can fill the site where TSH should be acting and it can interfere with that, so it can probably go either way, forcing too much activity, or more likely blocking the effect of TSH. The polyunsaturated fats (PUFAs) by themselves interfere with the enzyme which releases thyroid hormone from the glands, so too much of the unsaturated fats with or without iodine will have an anti-thyroid effect. But potentially the iodine reaction could cause overstimulation by TSH or in its place could imitate the action.

    HD1: Dr Peat, you mentioned the iodine binding to the double bonds producing this product and in it’s own right that could stimulate an inflammatory thyroiditis and/or a cancer?

    RP: Yeah. I think that’s why the high iodine intake around the world statistically associated with greater risk of thyroid cancer and if there really were a product that contained a more reactive form of iodine, that would just mean that it would attack more molecules, but I looked up the sources of that product and one of the products started about 10 years ago. A man in Texas filed a patent that is just completely goofy. If you look at the diagram, it shows things that just can’t happen and so it was filed 10 years ago and I think it still hasn’t been and probably never will be actually approved as a patent. But you can apply for a patent on any goofy idea and then publish the application and impress a lot of people!

    HD1: But maybe not bring the product to the market.

    HD2: So iodine supplementation is very risky and basically you should get your trace minerals from seafood sources, rather than from isolated iodine supplements and especially not in combination with any kind of vegetable polyunsaturated oils.

    RP: Yeah I think that’s true.

    HD 1: So, just to quickly wrap up this nascent iodine, I think the reason that it caught my attention was that the media spin on was that it because it didn’t have, any chemistry people hearing this will understand what I’m saying and can go and elaborate it more simply perhaps, but it doesn’t have a stable octet so its outer electron shell isn’t filled. And they were saying that because of this, it was much more suitable in some way to occupying these sites in the thyroid to produce thyroid hormone, but its very reactivity is counterproductive, because surely, if you keep it as unreactive as that in a bottle waiting for to be ingested, wouldn’t it surely react with one of the first things it came into contact with when you ingested it - just to fill its octet and become stable again?

    RP: Oh yeah. The whole idea of a “newly born” nascent molecule, when I was in junior high, in high school, the chemistry people talked about nascent oxygen which for a few seconds after it’s formed in a certain way is highly reactive but that’s because the electrons are simply in an excited state, like it had been sitting in the sunlight too long. That’s an electronic excitation which quickly passes as it gives off a little bit of energy but in certain short term situations a few seconds, that kind of excited electron state can make a molecule useful for certain reactions but isn’t something you’d want to put your body through.

    HD 1: So, not for in vivo use, but maybe in vitro experimentations, it might have some kind of a use?

    HD2: So it’s basically a more dangerous form of iodine that can cause a free radical reaction?

    RP: Yeah, that’s what they are talking about but I don’t think it even exists in the product?

    HD1: So, Dr Peat, I was looking at some abstracts here that were going to form the show and the first couple caught my attention just because they were based on isoflavones and I know from our studying herbal medicine, soy and isoflavones were all the rage and were touted as being very health beneficial, reducing cholesterol and all this other ridiculously unscientific information that was purported. So from the basis of soy, they mentioned that there was an alcohol soluble fraction that had been shown essentially to basically cause female cancers, that these things were taken up by the thyroid or rather they inhibited the uptake of iodide by the gland and that this increased the oestrodial in females and that this was, I know that we’ve heard about soy and now we definitely are aware of soy being very pro-carcinogenic because it’s an oestrogen mimic. What do you think about this whole industry push that was producing, and probably still is producing, soy infant formula, which is one of the main foods that was generated from it?

    RP: I think it has seriously harmed lots of kids by partly the oestrogenic effect. The oil itself has a pro-oestrogen effect, anti-thyroid effect. Apart from those little molecules, the isoflavones, the category of flavones or flavonoids, it’s very similar to the isoflavones, the phenyl group or benzene group is just located slightly closer to the keto oxygen in the isoflavones and that group seems to be the oestrogenic group. The other orientation of the benzene group makes it more likely to be anti-oestrogenic and lots of fruits and vegetables contain the anti-oestrogenic forms of those, but the oestrogen industry as a background, led to a lot of the sales talk about the effects of soy chemicals.

    HD1: And of course there is a hugely cultivated GMO products patents owned for its propagation and its use again no doubt another spawned product from big corporations who essentially want to own the product.

    HD2: But don’t all legumes have a certain percentage of these isoflavones? [RP: Aha] But just soy is particularly high?

    RP: No. I think the main problem with soy besides it basically being inedible; I think the main problem is that it’s almost all from grown in the genetically modified form that takes large amounts of toxic pesticides.

    HD2: Which are oestrogenic too, right? RP: Yeah.

    HD2: And again, just for the guys out there, I think it is very important to make you aware that guys have oestrogen. It’s not just a female-dominated situation and soy consumption in males has also been positively associated with gynecomastia, which is another side effect if you like of oestrogen activity within males. The very same thing, Dr Peat, isn’t it with alcohol and drinking alcohol excessively can produce that symptom of male breasts that is an oestrogenic type reaction?

    RP: When I was a kid, just before the Second World War, we knew some of the very poorest immigrants to California and there was one couple in which the wife got a job but the father could nurse the baby because his oestrogen had become so high from malnutrition and at the end of the Second World War when soldiers got out of the prison camps, lots of them had breasts from the effects of prolonged starvation.

    HD1: Are we talking lactation too?

    RP: Well, in the case of this man in California, the wife said, “Pa’s milk ain’t got much strength”.
    Yeah, they can lactate if they have a baby nursing.

    HD: Wow! So there’s enough positive feedback in the physiological mechanism, inherently to produce that?

    HD2: So I guess that high oestrogen stimulation raised their prolactin?

    RP: Yeah.

    HD2: And with the suckling it produced milk?

    RP: Yeah.

    HD2: Wow, that is just absolutely incredible.

    HD1: OK - so again just for people that are listening, it just begs the question again where things like soy and soy products, all we ever hear.... We don’t have a television, we don’t have a TV at all, but we don’t listen to broadcasts from mainstream media. But what I was going to say was that most people have a TV or they listen to a regular radio station, getting the same spin put on things and the same sales pitch and so I just find it hard to believe that for a long time the whole soy thing could exist and it could do what it did - when actually it’s more like a waste product and people really shouldn’t be eating soy because it’s so dangerous in terms of its oestrogenic effects on females and males and those oestrogenic effects are very pro-inflammatory. Dr Peat, you have pointed that out many, many occasions and I am currently on board with that same feeling that the irritation and the inflammation that oestrogen promotes is nothing but a dangerous process in the body.

    HD2: And also Dr Peat, how would you compare oestrogen levels with menopausal women and men?

    RP: With aging, a man’s oestrogen pretty steadily increases but if he has a heart attack it goes up sharply or if he has a traumatic injury it goes up during the recovery time - but generally there’s a trend upward in men and in women when the ovaries stop cycling and up until about the age of 38–40 there is an actual steady increase in the oestrogen and when the ovaries stop cycling, they stop suddenly producing progesterone but they continue producing a considerable amount of oestrogen until the body can adjust it downward. So there are a few years in the 40s or early 50s usually, when oestrogen is extremely excessive relative to the anti-oestrogen effect of progesterone. But then again after the ovaries have pretty much stopped functioning, the rest of the body, as the progesterone fails, all the other tissues begin, similarly it happens in men, all of a woman’s tissues tend to start increasing their production of oestrogen so that after menopause, the fatter a woman is, the more oestrogen she’s producing because the fat tissue is a good source of it. But any tissue after menopause to the degree that it’s stressed, will begin producing oestrogen.

    HD2: So is that about the same level between men and women, after the menopausal period?

    RP: Yeah, I think woman tend to be fatter in old age and so they are more likely to have a higher level of oestrogen. But just measuring the blood oestrogen gives a misleading impression because when progesterone is deficient, the oestrogen receptor as well as the aromatase enzyme that makes oestrogen, the receptors binded in cells and there’s no progesterone to destroy the oestrogen receptor so it just stays in the cell and some of the enzymes that are no longer inactivated by progesterone, other enzymes capture circulating oestrogen that should have been excreted, cause it to be deposited in cells still other enzymes shift any oestrogen away from the oestrone form to the oestriol form which is the most active, intense oestrogen. So everything that happens when progesterone is deficient tends to load up various cells all through the body with more and more oestrogenic stimulation, even though, it isn’t being released to be measured in the blood.

    HD2: Right, so the blood test could appear that it’s fine but if you have a large amount of fat cells it could be stored in that and other tissues. And what about weight loss for woman who are in the menopause state, to lose that weight do they then poison themselves with that oestrogen as it comes out of the cells?

    RP: Just temporarily, but it’s better to get rid of it than have it local because inside the cells because it produces things such as breast cancer, lung cancer, uterine cancer, ovarian cancer, all of the tissues that no longer have enough progesterone are subject to cancer infestation.

    HD2: So what about the women that continue to menstruate, like I heard from this lady the other day, that she had this friend who was 70 and was still menstruating?

    RP: I talked to a gynaecologist, who was giving his wife progesterone and she was still menstruating at 60. And if you happened to have a very good system for producing progesterone there’s no reason why it should stop at 55.

    HD2: So there’s no reason to stop at 55 then, right?

    RP: No.

    HD2: So basically do you think it would be beneficial that woman to continue to menstruate until the day they die?

    RP: I think so.

    HD2: Like the flamingos.

    RP: Yeah the flamingos have no life limitation according to ordinary mortality curves cause they seem to only die by accidents.

    HD2: Or starvation.

    HD1: Dr Peat, I wanted to pick up on the point that you mentioned during your last discourse there. I’ve not heard that before: Progesterone destroys the oestrogen receptor? Does anything similarly happen with oestrogen doing the same thing to progesterone receptors or is it just that way around?

    RP: Well, oestrogen activates its own receptor in most tissues and it will activate inflammatory things, which tend to turn off the progesterone receptor, if you have excess. Generally, the normal function would be for progesterone to rise as soon as the oestrogen has had its surge and then knock it out. The oestrogen is fine if it is active only for 12-24hrs every month.

    HD2: It does its job and then it’s finished.

    HD1: But like you said the tissues will carry on producing oestrogen in tissues especially in
    obese individuals and menopausal or even postmenopausal women.

    HD1: OK, so just another call for all the ladies out there that there really is nothing, and I know it is a personal thing, but nothing wrong with continuing your menstrual cycle as long as you possibly can Progesterone is your friend, oestrogen is your enemy and the only thing really that oestrogen is any good for is the implantation and so we have our first caller, so let’s get this first caller. Caller, where are you from?

    Caller: Kansas City. Hi Dr Peat, what do you think is happening if someone experiences digestive cramps and bloating within 30 minutes when using vitamin E orally and which still occurs even when switching to a few different products as well as when using several drops of Progest-E which also contains vitamin it E.

    RP: I think it’s the viscous oily quality that is irritating if you are... some people have that reaction, for example, if they try to use it in their armpits where the skin is very sensitive, the highly viscous oil can be very irritating and so I think it should be taken with food so that it doesn’t hit any of the membranes in the concentrated form.

    Caller: Do you think it is possible to develop a soy allergy somewhere along the way?

    RP: Yeah. Many people do have soy allergies but the oil doesn’t contain any of the proteins that people are allergic to, so I haven’t heard of any documented allergies to the oily soy products such as soy oil.

    Caller: OK, do you think it’s possible for that person to have something like 400 IU alpha tocopherol, with 300mg of gamma, delta, beta tocopherol receptors is excessive and possibly be excreted mostly in bile, which is alkaline and possibly irritating to an already irritated intestine which would be the cause of cramps and bloating?

    RP: I doubt it because the effect of vitamin E on many cell processes is anti-inflammatory - for example, it inhibits prostaglandin formation similar to aspirin and its range of anti-inflammatory effects.

    Caller: OK. That’s great, thank you.

    HD1: First caller from Mexico! Welcome to the show. What’s your question?

    Caller: Thanks. Hi, if I understood correctly, earlier you were talking about how taking extra iodine can interact with PUFAs to cause problems and I know someone who took a few mgs of extra iodine and she went into some kind of thyroid, hyperthyroid-like crisis state where she couldn’t tolerate any physical exertion. Her muscles were really weak and her pulse was very high and years later she still gets that reaction from thyroid and I was wondering if that’s related to iodine?

    RP: Back in the years when many people were in certain regions, for example, in Southern Mexico, Western China, Ohio and Eastern Europe, those areas were very deficient in iodine and they would develop an enlargement of the thyroid gland and then when they ate iodine even a fairly normal amount, suddenly their gland would start forming thyroid hormone and if the goiter was very big they could have serious hyperthyroidism that could last for years but, if the gland was just slightly swollen, it would pass in about two months.

    HD1: So that’s a very real sequelae of using iodine in that particular individual that they would have that increased thyroid production that would result in what the caller’s just mentioned?

    RP: Yes if they took their iodine in the form of thyroid hormone they could normalize their body functions and be replacing iodine in a limited graded fashion and so they wouldn’t go into those hyperthyroid states and getting the required amount of hormone would cause their pituitary to settle down and let the gland gradually shrink.

    HD2: And so that is treatment for goiter, is that you supplement with thyroid hormone?

    RP: Yes to treat hyperthyroidism the safest thing is to supplement usually with thyroid hormone.

    HD1: OK, and so again just to expand on the very first question to Dr Peat about the nascent iodine - not a good idea and also many other forms of iodine supplementation are not necessary - and if you need iodine and you have any kind of low thyroid actually thyroid hormone is the best way to get bound iodine. And did you have anything else you would like to bring up, Caller?

    Caller: Well, thanks for that and I was just wondering if you know if it would be a good idea to do anything specific to try to rectify this problem or if there’s any tips on tolerating thyroid, would avoiding iodine help in a situation like that?

    RP: The people who have trouble with the actual thyroid hormone they can be either deficient in magnesium because hypothyroidism makes all of your tissues fail to retain a normal amount of magnesium and then when you supplement it, suddenly you experience an extreme magnesium deficiency in your heart, for example, and your brain, and so taking some magnesium at the same time as the thyroid will help those people. Others, if they are deficient in adrenal or ovarian or gonadal steroids, will suffer stress symptoms when they take thyroid and so using a supplement such as pregnenolone will make them tolerate adapting to the thyroid hormone more easily.

    HD2: And what about, Dr Peat, how some people if they supplement with T4 thyroxine, they will have those symptoms like our caller mentioned where their muscles are weak and their heart’s
    pounding, and their pulse is high and isn’t that because if they are already low thyroid and they take the T4 then are actually stimulating the adrenalin because they are not converting it?

    RP: Yeah. When people have suffered for a long time with a low thyroid they are likely to have extremely high adrenalin and cortisol levels and that causes them to turn T4 into reverse T3 blocking the actual active T3 hormone and then if they accumulate more and more T4 that will interfere competitively with the little bit of T3 that they do have, so they can exaggerate the state of their hypothyroidism if they’re in that extreme stressed state.

    HD1: Would you say that T4 perhaps is maybe only 10% as active as the active T3 hormone?

    RP: It really varies. In the 1940s, when they first synthesized it, they tested it on male medical students and it was exactly as effective as Armour natural thyroid and that’s because young men, 20-22 years old, have very good livers that can perfectly convert it, but even at the same age women are more likely to have problems with plain thyroxine.

    HD1: So when you talk about T4 being weakly active, how do you interpret that or how do you see T3 versus T4 in terms of orchestrating metabolic events?

    RP: Well the standard textbook idea is that T3 is 4 times more powerful than T4 but really if your liver is good you can get 100% of the benefit out of T4 and if you are a woman under stress with high oestrogen your liver isn’t going to convert any of it to the right active hormone, and the more you take – I’ve known of one woman who was hospitalized and got more and more hypothyroid the higher they raised her thyroxine dose - and as soon as they gave her T3 she came right out of the myxedema coma, but I have seen people in less extreme states who got more and more depressed or psychotic or whatever when they increased their thyroxine dose.

    HD2: I have one more question for the caller. Do you know if this lady you’re speaking about was taking a T3/T4 combination supplement or were they taking just T4 or just T3? Are you aware of that?

    Caller: Yeah, well, originally she was taking an Armour supplement and when she took the supplemental iodine that caused the problem and since then she has tried different T4/T3 combo products, as well as a couple of different, pure T3 supplements. So I think it’s something to do with this adrenalin or sensitivity to adrenalin that Dr Peat was talking about, where if I understand him correctly, the thyroid sensitizes the tissues to the already high, the already existing adrenalin.

    HD2: But that should only last a couple of days and then it should balance out.

    RP: Well, sometimes it lasts for a couple of weeks. If you’re really extreme, you have to use little bits of supplements and be very careful about your intake of protein, sugar, calcium, everything that is counter to the stress.

    Caller: So when you are in a situation like that she was using very small specks of T3, under 1 mcg sometimes. Is the thing to do to hold that very low dose for a couple of weeks, then increase it in very, very small increments as the adrenalin hopefully comes down?

    RP: Yeah. I’ve known people for a week or two who would stay with 1mcg doses of T3, but you have to make sure your whole diet is very good, having hormone tests, and a vitamin D blood test is helpful because magnesium and calcium work together and vitamin D regulates them.

    HD2: Yeah and making sure that she’s getting plenty of carbohydrates like in the form of fruit juices because that’s like Dr Peat is saying - making sure nutritionally that she is getting at least 75g of protein and - I don’t know the weight and nutritional needs –but at least 150 grams of more sugars and good fats.

    Caller: OK, thanks very much.

    HD2: OK – I think have another caller. Caller, where are you from? Caller: Hi, I’m calling from New York.

    HD1: Welcome to the show what is your question?

    Caller: I have a question for Dr Peat about Buteyko breathing and heart rate. Dr Buteyko noted that as you progress with retaining more and more Co2 with the Buteyko breathing, then the heart rate will decrease and I wondered what you thought about that. I’ve noticed that in my own practice that it does go down but the temperature is still good and I wondered if the metabolism is still good when that happens or what you think about it?

    RP: Yeah, there have been experiments with animals increasing their Co2 and watching what happens to the heart and blood vessels and Co2 relaxes the blood vessels so it decreases peripheral resistance and that makes the heart able to pump more blood more easily with less work. So it usually means a bigger stroke volume.

    HD2: So the decreased heart rate is a good thing.

    Caller: OK, so even though it’s a lower heart rate you think that you can still get the same benefits as you would if your weren’t restricting your breathing but... I know you recommend a high heart rate typically for people that aren’t practicing that kind of breath control?

    RP: Yeah, but most people are running on adrenalin and I’ve known people, one woman who had a 180 pulse steadily for years, another person had been around a 130 resting pulse for a long time, and both of these people within two weeks got down to a normal under a 100 pulse rate when they supplemented thyroid. And one of the things the thyroid is doing is increasing your Co2 and decreasing the lactic acid and the inflammation so that your capillaries open up, you have less peripheral resistance, so your heart doesn’t have to work so frantically.

    Caller: OK, well thank you very much.

    HD1: OK, so it’s always good to get people all over the States and so we’ve had Mexico so far, New York, Midwest and so let’s keep it up. I wanted to ask you - we haven’t actually got very far through all the questions I wanted to ask you at this point - and this is good news because people have been calling and I may have to carry over this topic to next month if you are available. I saw the article there which again highlights the oestrogenic problem, that the benign and malignant thyroid nodules are far more common in females than males and no doubt a consequence of oestradiol, so given that the mainstream lie is that oestrogen is good for you and healthy, what can be done you think simply to offset the oestrogen, and I now know we’ve mentioned progesterone, which is probably the first that springs into my mind, but in terms of reducing a female’s oestrogenic burden?

    RP: There were some studies of slices of thyroid gland in vitro and they found that added oestrogen caused the cells to keep synthesizing hormone and to keep growing, but failed to secrete any of the hormone. When they added progesterone it began secreting the hormone. And up until the last few decades women, rather than just having nodules in their thyroid, they were the ones most susceptible to growing a very large goiter that sometimes was as big as a cantaloupe - and the nodules are basically the same process of oestrogen activating the cell division and synthesis of colloid - the material that the hormone later will be made from - and desensitizing the cells to the hormone secreting effect of TSH and progesterone by antagonizing oestrogen will reverse those processes, but when you get the cells multiplying and making the protein you will get at least a nodule, maybe if it continues steadily, the whole gland will get bigger and bigger.

    HD1: We actually do have another caller - so let’s hold that thought and take this next caller. Caller, where are you from?

    Caller: I’m from right here in town. I was curious to know - I heard you talking about the vitamin D and the thyroid and the magnesium. I was just wondering if that would have anything to do with what’s called “restless leg syndrome”?

    HD2: Yes, that’s a magnesium deficiency. Dr Peat, how would you explain restless leg syndrome?

    RP: There has been quite a lot of research about it and, for example, they noticed that people taking SSRI antidepressants tended to have episodes of restless legs and so they saw that Nitric Oxide (NO) and serotonin were involved in producing it. Those are produced largely from the intestine. The most intense problem of both serotonin and NO production is from an irritated intestine and hypothyroid people overproduce both NO and serotonin typically and have sluggish digestive systems and often have a tendency to generalized inflammation. And the serotonin seems to be specifically what pushes those motor nerves that cause the leg jumpiness.

    HD1: Does that help you out or explain things to you, Caller?

    Caller: Yeah. So it’s not an adrenalin thing that makes the legs jump - it’s serotonin?

    RP: All of the inflammatory stress things tend to go together.

    HD2: So, would you recommend aspirin for restless leg syndrome?

    RP: Yep, pregnenolone, aspirin, and avoiding irritating foods, especially legumes and raw green salads. Those are very irritating.

    HD2: Those are things that increase the bowel production of serotonin.

    RP: Yeah.

    HD2: Beans and raw vegetables?

    Caller: That’s interesting; cause we just switched to trying to eat better and we had gone to eating more of both of those!

    HD2: Had you noticed that your restless leg syndrome had increased?

    Caller: It’s a female, and my partner, who experiences this and is becoming very extreme and so that may very well be just from the diet, huh? And she has a vitamin D deficiency and she was told to take vitamin d and magnesium.

    HD2: Do you know what her vitamin D level was and how much she is taking? Caller: I don't know exactly in measurement, but it was very low.

    HD1: Well, most drop forms of vitamin D now are 2,000 IU a drop and if she has low vitamin D it’s probably below 20, maybe right around 20, which is very low, and they’ve raised the reference limit now for vitamin D to about 45 - so if you are supplementing with a 2,000 IU per day drop product, she should really be loading up with 6-8 drops a day for about 4 or 5 days and then getting around 4,000 to 6,000 IU and then re-measuring her vitamin D levels.

    HD2: After about 2 months.

    HD1: So, Dr Peat said that bowel irritation/inflammation increases serotonin production and that serotonin production with NO which we have another question for Dr Peat about NO. Both those two compounds there can be predisposing someone to restless leg syndrome. Anyway, thanks for your call.

    HD1: So, Dr Peat I saw, today just in fact - and I was thinking about it myself and started looking at a couple of websites that do blood testing etc. and I couldn’t see any NO blood testing tests done - but I did see salivary tests for – they were salivary nitrite strips to assess the potential NO production in the body. I know it will be formed from nitrate or nitrite. This is the funny thing, this site actually was letting you know how you could increase NO more by eating various foods which I wanted to question you about also - so I know some of the greens here that are promoting the NO production are some of the things that we are actually promoting as being beneficial but there’s obviously a reason for that. So how do you feel about testing your salivary nitrate/nitrite level and how predictive or pre-emptive that would be of NO production systemically?

    RP: A recent article just a couple of weeks ago came out suggesting measuring the NO or its products in the body as a way of diagnosing hypothyroidism because they are so closely connected, but I would guess that the urine might be better than the saliva because for other hormone testing, for example, just thinking of food or being anxious or whatever can really change the composition of your saliva.

    HD1: OK, so because that changes so quickly, your saying, that it is more relative to test something that’s there and it’s stored and probably more representative of a couple of hours of physiology?

    RP: Yeah. I think that the urine will give you a good picture of your level of stress.

    HD2: You wouldn’t want to test it after eating spinach either with your saliva.

    HD1: Here’s the other thing – this was my other question - this website was touting NO as being beneficial and actually spinach was a very good producer of nitrate, and how spinach will increase your NO - and they were touting that - and I know and I want to ask you here just to be realistic and be real for folks - I know we mentioned greens, purporting greens, and boiled greens and drinking the juice as very beneficial and I know that you do say kale can have a thyroid suppressant effect - so not to use to much kale - but spinach I think has been one of those greens that has been portrayed as being relatively healthy - so what do you think about spinach?

    RP: If they are organically grown without intense nitrate fertilization and if it’s well cooked, I think spinach is good food.

    HD1: Let’s take this next caller. Caller, where are you from?

    HD1: You’re on the air, where are you calling from?

    Caller: Hi, I’m from Shelter Cove. My question is for my daughter actually. She wants to take testosterone and I’m wondering what Dr Peat’s take is on it and if he has any experience on that and how she can keep herself healthy?

    HD1: How old is she and what is the indication for taking the testosterone? Caller: Well, she is transgender and wants to be more male and she is 16.

    RP: Wanting to masculinize?

    Caller: Yes.

    RP: I think that’s safe but it should be backed up with pregnenonlone and some progesterone to keep things in balance because the tendency is, if you are under stress of any sort, for the testosterone to turn to oestrogen and the pregnenolone and progesterone will limit that conversion.

    Caller: OK.

    HD1: Do you have access to those? Both of those can be obtained, so progesterone and pregnenolone, typically for a female anyway they would normally be producing them and I don't know the exact details of the case and how the transgender nature of this subject is either affected her adversely or positively and so in terms of their exposure to their own natural progesterone being female and/or supplementing with pregnenolone, then that would offset the potentially negative effects that may occur with using testosterone in a female.

    HD2: Cause it could convert to oestrogen and become dangerously out of balance. RP: And watching thyroid function.

    Caller: OK. Thanks for your help.

    HD1: I don't even know if we have enough time to ask another question without running out of time, but I’ll try here. And I think we will definitely open this up for the next month if you are available cause we hardly got any questions asked cause we had so many callers and that’s a good thing. I wanted to ask you again with the female issue and oestrogen and inflammation and cancers etc., pretty obvious as definite realities here. In terms of the effects of iodine uptake by thyroid cells, and the inhibitory effects oestrogen has on that, in a female, again would you be just typically wanting to lower oestrogen burden by offsetting that with progesterone and pregnenolone and/or thyroid?

    RP: Yeah, thyroid and good adequate nutrition. All the vitamins and minerals are involved in controlling and keeping oestrogen under the safe limit. And when you inhibit the formation of thyroid hormone, either with an iodine deficiency or an oestrogen excess, the TSH fails to make the thyroxin and T3 and so it keeps stimulating not only the thyroid gland, making it grow and get bigger or nodules to form, but it has a related effect on every tissue to some extent - especially the ovaries. Polycystic ovarian syndrome (PCOS) is associated with low thyroid and especially high TSH. TSH drives inflammation so that the so- called autoimmune conditions associated with high oestrogen - women are far more susceptible to all types of autoimmune diseases than males - and that's largely because of the high TSH exposure driving things like tumor necrosis factor and the various cytokines, and interleukins and prostaglandins that are activated.

    HD1: Excellent. I don’t want to cut you short Dr Peat and I really appreciate your knowledge, as do I know all the people that are tuned in and taken the time to listen and to call from all over. A really good show from people all over the country and I really appreciate people calling. Thanks very much, Dr Peat.
    www.raypeat.com
    _______________________
     
  2. lindsay

    lindsay Member

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    I wrote to RP after listening to this episode (because I had been supplementing Nascent Iodine for months and with good effects, along with thyroid hormone) and I didn't think he really explained the negatives of iodine enough.

    Here was his response to my email, in case you are interested:

    Large doses of iodine can be safe when used for a short time therapeutically, but one milligram or more per day, for a long period of time, is likely to harm the thyroid gland. Nascent (“newborn”) iodine can exist in a laboratory set-up, but it’s short-lived, and doesn’t continue in that state when it’s sold as a product. The incidence of thyroid cancer has doubled in the last 30 to 40 years, and it’s the most rapidly increasing cancer in the US.

    Endocr Pathol. 2002 Fall;13(3):175-81.
    Thyroid cancer and thyroiditis in Salta, Argentina: a 40-yr study in relation to iodine prophylaxis.
    Harach HR, Escalante DA, Day ES.
    Services of Pathology, Dr A Oñativia Endocrinology and Metabolism Hospital,
    Salta, Argentina. rubenharach@ciudad.com.ar
    The natural history of thyroid cancer and thyroiditis in relation to iodine
    prophylaxis in the region of Salta, Argentina, where goiter is common was
    investigated over a time span of 40 yr. For analysis of thyroid cancer, the
    specimens were divided into two periods. The first 15 yr (59 cases), including 5
    yr before prophylaxis, was compared with the second 25 yr (182 cases), a period
    well after salt iodination. Papillary carcinomas formed the largest group of
    tumors in both periods, with a significant increase in their proportion in the
    second period (44 vs 60%, chi(2): p < 0.05), while the percentage of follicular
    and undifferentiated carcinomas decreased and medullary carcinoma remained about
    the same. The ratio of papillary to follicular carcinoma rose from 1.7:1 in the
    first period to 3.1:1 in the second. Four thyroid lymphomas of non-Hodgkin's
    B-cell type occurred in the second period in females over age 50. A severe
    lymphoid thyroiditis was present in the two cases with assessable background
    thyroid tissue. The frequency of moderate to severe lymphoid infiltrate in
    females rose from 2 of 12 (16.6%) in the preprophylaxis period to 34 of 114
    (28.0%) in the last 25 yr after prophylaxis. After salt prophylaxis, thyroiditis
    was more frequent in patients with papillary carcinoma (36.2%) than in those with
    nonpapillary tumors (14.7%) (chi(2), p < 0.02). These observations indicate that
    a high dietary intake of iodine may be associated with a high frequency of
    papillary carcinoma and thyroiditis, and that thyroiditis is more commonly
    associated with papillary carcinoma than with other thyroid tumors. The
    occurrence of non-Hodgkin's lymphomas only in the postprophylaxis period may be
    linked to an increase in thyroiditis.

    Saudi Med J. 2007 Jul;28(7):1034-8.
    The effect of iodine prophylaxis on the frequency of thyroiditis and thyroid
    tumors in Southwest Iran.
    Soveid M, Monabbati A, Sooratchi L, Dahti S.
    Department of Internal Medicine, Shiraz University of Medical Sciences, Nemazee
    Hospital, Shiraz, Iran. msoveid@sums.ac.ir
    OBJECTIVE: To investigate the effect of the salt iodization program, which was
    initiated in 1989 on frequencies of thyroiditis and papillary carcinoma in Fars
    province of Iran, which was previously an iodine deficient area. METHODS: Four
    hundred and eighty-two thyroidectomy specimens belonging to the pre-iodization
    period from 1983 to 1988, and 466 post iodization specimens from 1998 to 2003
    were re-examined for presence of lymphocytic infiltration and types of thyroid
    tumors. This study was carried out in Shiraz University of Medical Sciences,
    Iran. RESULTS: The frequency of lymphocytic infiltration in non-neoplastic
    specimens increased from 30-60.5% after salt iodization (p<0.001). Background of
    lymphocytic infiltration in neoplastic specimens also increased from 18.5-61%
    after iodine prophylaxis (p<0.001). The frequency of papillary carcinoma in
    neoplastic specimens increased from 15-43% (p=0.01) and that of follicular
    adenoma decreased from 69-32.5% (p<0.0001). CONCLUSION: Salt iodization is
    associated with an increased occurrence of histologic thyroiditis and papillary
    carcinoma.

    Biol Trace Elem Res. 2007 Oct 20 [Epub ahead of print]
    Safe Range of Iodine Intake Levels: A Comparative Study of Thyroid Diseases in
    Three Women Population Cohorts with Slightly Different Iodine Intake Levels.
    Teng X, Shi X, Shan Z, Jin Y, Guan H, Li Y, Yang F, Wang W, Tong Y, Teng W.
    Department of Endocrinology and Metabolism, The First Affiliated Hospital, China
    Medical University, No. 155 Nanjing Bei Street, Heping District, Shenyang,
    Liaoning Province, 110001, People's Republic of China, tengxiaochun@126.com.
    Iodine excess may lead to thyroid diseases. Our previous 5-year prospective
    survey showed that the prevalence and incidence of hypothyroidism or autoimmune
    thyroiditis increased with iodine intake. The aim of the present study was to
    investigate the optimal range of iodine intake by comparing the prevalence of
    thyroid diseases in three areas with slightly different levels of iodine intake.
    In 2005, 778 unselected women subjects from three areas with different iodine
    intake levels were enrolled. Levels of serum thyroid hormones, thyroid
    autoantibodies, and urinary iodine were measured, and thyroid B ultrasounds were
    performed. Among the subjects with mildly deficient iodine intake, those with
    adequate intake, and those with more than adequate intake, the prevalence of
    clinical and subclinical hypothyroidism was 0, 1.13, and 2.84%, respectively (P =
    0.014); that of thyroid goiter was 24.88, 5.65, and 11.37%, respectively (P <
    0.001); that of serum thyrotropin values was1.01, 1.25, and 1.39 mIU/l,
    respectively; and that of serum thyrotropin/thyroglobulin ratio was 7.98, 6.84,
    and 5.11, respectively (P < 0.001). In conclusion, median urinary iodine 100~200
    mug/l may reflect the safe range of iodine intake levels. Serum
    thyrotropin/thyroglobulin ratio might be a better index of evaluating iodine
    status.

    Endocrinology. 2007 Jun;148(6):2747-52. Epub 2007 Mar 8.
    Induction of goitrous hypothyroidism by dietary iodide in SJL mice.
    Li HS, Carayanniotis G.
    Faculty of Medicine, Memorial University of Newfoundland, St. John's,
    Newfoundland, Canada.
    Prolonged intake of large amounts of iodide has been reported to increase the
    incidence of goiter and/or hypothyroidism in humans as well as animals prone to
    spontaneous autoimmune thyroiditis. In the current study, we investigated the
    role of dietary iodide on the development of hypothyroidism, as well as
    thyroiditis, in strains of mice that do not develop spontaneous autoimmune
    thyroiditis. Intake of 0.05% NaI via drinking water for 10 wk induced
    hypothyroidism in SJL/J mice as indicated by elevated TSH and depressed total
    T(4) values in serum and formation of colloidal goiter with an inactive flattened
    thyroid epithelium. Hypothyroidism did not appear to have an autoimmune basis
    because only focal mononuclear cell infiltrates were found intrathyroidally, and
    antithyroglobulin antibodies or increased organification of iodide were not
    detected. These phenomena were not observed in similarly treated CBA/J mice,
    suggesting polymorphisms in genes controlling events downstream of iodide uptake
    by thyrocytes. Interestingly, RT-PCR analysis indicated that unlike CBA/J, SJL/J
    mice could not down-regulate Na/I symporter gene expression during the NaI
    treatment. No significant temporal or strain differences were observed regarding
    the expression of thyroglobulin, pendrin, thyroid peroxidase, and DUOX1 and DUOX2
    genes after NaI intake. Our results point to the generation of a mouse model for
    the study of iodine-induced hypothyroidism, which does not seem to have an
    autoimmune basis.

    J Endocrinol Invest. 2003;26(2 Suppl):49-56.
    Iodine excess and thyroid autoimmunity.
    Bournaud C, Orgiazzi JJ.
    Service d'Endocrinologie, Diabétologie et Maladies Métaboliques, Centre
    Hospitalier Lyon-Sud, 69495 Pierre-Bénite Cedex, France.
    Epidemiological studies, as well as animal models, indicate that iodine might be
    an immunogenic agent for the thyroid gland, at least in subjects predisposed to
    thyroid autoimmunity. This review presents data, either epidemiological or
    experimental, obtained in different conditions: constant and stable iodine
    status, either deficient, sufficient or excessive; long-term iodine prophylaxis;
    temporary supplementation with iodide (6-12 months) or iodised oil. Moreover, we
    also discuss data obtained in the general population, among subjects with
    euthyroid goiter, or autoimmune goiter, or even in women prone to post-partum
    thyroid diseases. It is concluded that the significant increase in the prevalence
    of autoimmune thyroid diseases in populations living in iodine sufficient areas
    should not prevent the implementation of the iodine prophylaxis.

    J Immunol. 2002 Jun 1;168(11):5907-11.
    Enhanced iodination of thyroglobulin facilitates processing and presentation of a
    cryptic pathogenic peptide.
    Dai YD, Rao VP, Carayanniotis G.
    Division of Endocrinology, Faculty of Medicine, Memorial University of
    Newfoundland, St. John's, Newfoundland, Canada.
    Increased iodine intake has been associated with the development of experimental
    autoimmune thyroiditis (EAT), but the biological basis for this association
    remains poorly understood. One hypothesis has been that enhanced incorporation of
    iodine in thyroglobulin (Tg) promotes the generation of pathogenic T cell
    determinants. In this study we sought to test this by using the pathogenic
    nondominant A(s)-binding Tg peptides p2495 and p2694 as model Ags. SJL mice
    challenged with highly iodinated Tg (I-Tg) developed EAT of higher severity than
    Tg-primed controls, and lymph node cells (LNC) from I-Tg-primed hosts showed a
    higher proliferation in response to I-Tg in vitro than Tg-primed LNC reacting to
    Tg. Interestingly, I-Tg-primed LNC proliferated strongly in vitro against p2495,
    but not p2694, indicating efficient and selective priming with p2495 following
    processing of I-Tg in vivo. Tg-primed LNC did not respond to either peptide.
    Similarly, the p2495-specific, IL-2-secreting T cell hybridoma clone 5E8 was
    activated when I-Tg-pulsed, but not Tg-pulsed, splenocytes were used as APC,
    whereas the p2694-specific T cell hybridoma clone 6E10 remained unresponsive to
    splenic APC pulsed with Tg or I-Tg. The selective in vitro generation of p2495
    was observed in macrophages or dendritic cells, but not in B cells, suggesting
    differential processing of I-Tg among various APC. These data demonstrate that
    enhanced iodination of Tg facilitates the selective processing and presentation
    of a cryptic pathogenic peptide in vivo or in vitro and suggest a mechanism that
    can at least in part account for the association of high iodine intake and the
    development of EAT.

    Autoimmunity 1995;20(3):201-6
    Excess iodine induces the expression of thyroid solid cell nests in lymphocytic thyroiditis-prone BB/W rats. Zhu YP, Bilous M, Boyages SC. Department of Clinical Endocrinology, Westmead Hospital, Sydney, Australia. Previous epidemiological studies have suggested that lymphocytic thyroiditis and/or an increased iodine intake may be risk factors for the development of thyroid cancer. We previously reported that excess iodine accelerated the development of thyroid lymphocytic infiltration (LI) in the autoimmune BB/W rat model. We also found that excess iodine increased thyroid cell proliferation in a disordered manner. The present study was designed to further explore these observations and to address the question as to whether excess iodine under certain conditions predisposes the thyroid gland to neoplasia. To test this hypothesis, the lymphocytic thyroiditis-prone BB/W rat was exposed to excess iodine in drinking water. Ten BB/W rats at 4 weeks of age were given iodine water (NaI 0.05%) for 10 weeks, whilst another 10 BB/W rats were given tap water and served as controls. Eighteen normal Wistar rats were also divided into excess iodine and control groups, served as a comparison to the BB/W rats. We found that an excess iodine intake accelerated the development of LI in the BB/W rat. Severe LI was usually accompanied by prominent thyroid cell proliferation, evident as numerous microfollicles and cell masses, not forming normal thyroid follicles. Numerous lymphocytes and plasma cells often encroached on these areas of increased cellular proliferation. The surprising feature, and a possible indicator of activated thyroid cell proliferation, was the high incidence of thyroid solid cell nest-like lesions (SCN) in the iodine treated BB/W rats.(ABSTRACT TRUNCATED AT 250 WORDS)

    Clin Endocrinol (Oxf) 1989 Oct;31(4):453-65
    Thyroid autoimmunity in endemic goitre caused by excessive iodine intake.
    Boyages SC, Bloot AM, Maberly GF, Eastman CJ, Li M, Qian QD, Liu DR, van der
    Gaag RD, Drexhage HA.
    Department of Medicine, Westmead Hospital, Sydney, Australia.
    The pathophysiology of endemic goitre caused by excessive iodine intake is not
    well defined. By interacting with the immune system, iodine excess may trigger
    the development of autoimmune thyroid disease such as lymphocytic Hashimoto's
    thyroiditis (LT). In an attempt to examine this further, we compared the
    presence of thyroid autoantibodies in 29 goitrous children, from an iodine
    excess area, and in 26 healthy children, from an iodine sufficient area, of
    north central China. Serum was tested for antimicrosomal (MAb),
    anti-thyroglobulin (TgAb), second colloid antigen antibodies (CA2-Ab) and TSH
    binding inhibitory immunoglobulins (TBII). Affinity chromatographically purified
    IgG was tested for thyroid growth-stimulating activity (TGI) by two different
    methods: a sensitive cytochemical bioassay (CBA) using guinea-pig thyroid
    explants and a mitotic arrest assay (MAA) employing a continuous rat thyroid
    cell line (FRTL-5). We found no increased prevalence of LT in patients with
    endemic iodine goitre. The levels of MAb, TgAb and CA2-Ab did not differ
    significantly between the two groups of children. Further, TBII were not present
    in either group. Thyroid growth-stimulating immunoglobulins (TGI) were the major
    autoantibodies found in children with goitres caused by iodine excess. In the
    CBA, 12 of 20 (60%) goitrous children and 0 of 12 (0% P less than 0.05) healthy
    children were positive for TGI. Similar results were found in the MAA, and a
    good correlation between results of the CBA and MAA was found (P = 0.003).
    Maximal TGI activity in dose-response CBA showed a good relation with clinical
    goitre size (r = 0.63; P less than 0.05) indicating a possible
    pathophysiological role for these antibodies. We conclude that endemic iodine
    goitre is not associated with Hashimoto's lymphocytic thyroiditis. Nevertheless,
    autoimmune growth factors such as TGI may play a primary role in the
    pathogenesis of thyroid growth in this condition.

    Science 1985 Oct 18;230(4723):325-7
    Induction of autoimmune thyroiditis in chickens by dietary iodine.
    Bagchi N, Brown TR, Urdanivia E, Sundick RS. Clinical studies have suggested that excess dietary iodine promotes autoimmune
    thyroiditis; however, the lack of a suitable animal model has hampered
    investigation of the phenomenon. In this study, different amounts of potassium
    iodide were added to the diets of chicken strains known to be genetically
    susceptible to autoimmune thyroiditis. Administration of iodine during the first
    10 weeks of life increased the incidence of the disease, as determined by
    histology and the measurement of autoantibodies to triiodothyronine, thyroxine,
    and thyroglobulin. Further support for the relation between iodine and
    autoimmune thyroiditis was provided by an experiment in which iodine-deficient
    regimens decreased the incidence of thyroid autoantibodies in a highly
    susceptible strain. These results suggest that excessive consumption of iodine
    in the United States may be responsible for the increased incidence of
    autoimmune thyroiditis.

    Am J Clin Nutr. 2005 Apr;81(4):840-4.
    High thyroid volume in children with excess dietary iodine intakes.
    Zimmermann MB, Ito Y, Hess SY, Fujieda K, Molinari L.
    Human Nutrition Laboratory, Swiss Federal Institute of Technology, Zurich,
    Switzerland. michael.zimmermann@ilw.agrl.ethz.ch
    BACKGROUND: There are few data on the adverse effects of chronic exposure to high iodine intakes, particularly in children. OBJECTIVE: The objective of the study was to ascertain whether high dietary intakes of iodine in children result in high thyroid volume (Tvol), a high risk of goiter, or both. DESIGN: In an international sample of 6-12-y-old children (n = 3319) from 5 continents with iodine intakes ranging from adequate to excessive, Tvol was measured by ultrasound, and the urinary iodine (UI) concentration was measured. Regressions were done on Tvol and goiter including age, body surface area, sex, and UI concentration as covariates. RESULTS: The median UI concentration ranged from 115 microg/L in central Switzerland to 728 microg/L in coastal Hokkaido, Japan. In the entire sample, 31% of children had UI concentrations >300 microg/L, and 11% had UI concentrations >500 microg/L; in coastal Hokkaido, 59% had UI concentrations >500 microg/L, and 39% had UI concentrations >1000 microg/L. In coastal Hokkaido, the mean age- and body surface area-adjusted Tvol was approximately 2-fold the mean Tvol from the other sites combined (P < 0.0001), and there was a positive correlation between log(UI concentration) and log(Tvol) (r = 0.24, P < 0.0001). In the combined sample, after adjustment for age, sex, and body surface area, log(Tvol) began to rise at a log(UI concentration) >2.7, which, when transformed back to the linear scale, corresponded to a UI concentration of approximately 500 microg/L. CONCLUSIONS: Chronic iodine intakes approximately twice those recommended-indicated by UI concentrations in the range of 300-500 microg/L-do not increase Tvol in children. However, UI concentrations >/=500 microg/L are associated with increasing Tvol, which reflects the adverse effects of chronic iodine excess.
    Multicenter Study

    Hokkaido Igaku Zasshi 1994 May;69(3):614-26. [Screening for thyroid dysfunction in adults residing in Hokkaido Japan: in relation to urinary iodide concentration and thyroid autoantibodies]
    [Article in Japanese] Konno N, Iizuka N, Kawasaki K, Taguchi H, Miura K, Taguchi S, Murakami S, Hagiwara K, Noda Y, Ukawa S. Department of Internal Medicine, Hokkaido Central Hospital for Social Health Insurance, Sapporo, Japan. The prevalence of thyroid dysfunction and its relation to thyroid autoantibodies (TAA) and urinary iodide concentration (UI) was studied in apparently healthy adults in Sapporo (n = 4110) (Sapporo group), and in five coastal areas of Hokkaido (n = 1061) (coastal group) which produce iodine-rich seaweed (kelp). The frequency of above normal UI (high UI) in the morning urinary samples of coastal group was 10.8%, significantly higher than that of Sapporo group (6.4%) (p < 0.001). Frequency of positive TAA in both groups were similar. In Sapporo group TAA was positive in 6.4% of males and 13.8% of females with an age-related increase. The overall prevalence of hyperthyroidism (TSH < 0.15 mU/L) in coastal group (0.6%) was similar to that in Sapporo group (1.1%), while that of hypothyroidism (TSH > 5.0 mU/L) in coastal group (3.8%) was significantly higher than that in Sapporo group (1.3%) (P < 0.001). The frequency of high UI correlated significantly with that of hypothyroidism with negative TAA (r = 0.829, P < 0.05), but not with positive TAA, or with that of hyperthyroidism. Hypothyroidism was more prevalent in TAA negative subjects with high UI than with normal UI. Moreover, serum TSH and thyroglobulin levels were higher and free T4 level was lower in former than in latter group. These results indicate that 1) the prevalence of TAA negative hypothyroidism in iodine sufficient areas may be associated with the amount of iodine ingested, 2) this hypothyroidism is more prevalent and marked in subjects consuming further excess amounts of iodine, and 3) excessive intake of iodine should be considered an etiology of hypothyroidism in addition to chronic thyroiditis in these areas.

    Endocrinol Metab Clin North Am 1987 Jun;16(2):327-42
    Environmental factors affecting autoimmune thyroid disease.
    Safran M, Paul TL, Roti E, Braverman LE.
    Department of Medicine, University of Massachusetts Medical Center, Worcester.
    A number of environmental factors affect the incidence and progression of
    autoimmune thyroid disease. Exposure to excess iodine, certain drugs, infectious
    agents and pollutants, and stress have all been implicated.

    Acta Endocrinol (Copenh) 1978 Aug;88(4):703-12
    A case of Hashimoto's thyroiditis with thyroid immunological abnormality
    manifested after habitual ingestion of seaweed.
    Okamura K, Inoue K, Omae T.
    An interesting case of iodide induced goitre with immunological abnormalities is
    described. The patient who was sensitive to synthetic penicillin had previously
    been treated for exudative pleuritis, congestive heart failure and acute renal
    failure. Following recovery, he began to ingest large amounts of seaweed after
    which he developed goitrous hypothyroidism. It was of interest that the serum
    level of gamma-globulin increased, and subsequently the antithyroid microsomal
    antibody became strongly positive, suggesting that thyroidal autoimmune
    processes had been precipitated. Biopsy of the thyroid gland revealed chronic
    thyroiditis, with evidence suggesting extreme stimulation by TSH. Hight
    thyroidal uptake of 131I, positive perchlorate discharge test and biochemical
    analysis of the thyroidal soluble protein showed severe impairment of hormone
    synthesis following continuous accumulation of excess iodide. While there is
    evidence suggesting that increased iodide may be an important factor in the
    initiation of Hashimoto's thyroiditis, this may result from the marked increased
    sensitivity of Hashimoto's gland to the effects of iodine. Thus an occult lesion
    could be unmasked in this manner. The mechanism by which iodide mediates this
    effect is not clear.

    Thyroid 2001 May;11(5):427-36
    Iodine and thyroid autoimmune disease in animal models.
    Ruwhof C, Drexhage HA.
    Department of Immunology, Erasmus University, Rotterdam.
    Thyroid autoimmune diseases are complex, polygenic afflictions the penetrance of
    which is heavily dependent on various environmental influences. In their
    pathogenesis, an afferent stage (enhanced autoantigen presentation), a central
    stage (excessive expansion and maturation of autoreactive T and B cells), and an
    efferent stage (effects of autoreactive T cells and B cells on their targets)
    can be discerned. At each stage, a plethora of inborn, endogenous or exogenous
    factors is able to elicit the abnormalities characteristic of that stage, thus
    opening the gateway to thyroid autoimmunity. Iodine is an important exogenous
    modulating factor of the process. In general, iodine deficiency attenuates,
    while iodine excess accelerates autoimmune thyroiditis in autoimmune prone
    individuals. In nonautoimmune prone individuals, the effects of iodine are
    different. Here iodine deficiency precipitates a mild (physiological) form of
    thyroid autoimmune reactivity. Iodine excess stimulates thymus development.
    Iodine probably exerts these effects via interference in the various stages of
    the autoimmune process. In the afferent and efferent stage, iodine-induced
    alterations in thyrocyte metabolism and even necrosis most likely play a role.
    By contrast, in the central phase, iodine has direct effects on thymus
    development, the development and function of various immune cells (T cells, B
    cells macrophages and dendritic cells) and the antigenicity of thyroglobulin.

    Clin Immunol Immunopathol 1996 Dec;81(3):287-92
    Iodine-induced autoimmune thyroiditis in NOD-H-2h4 mice.
    Rasooly L, Burek CL, Rose NR.
    Department of Molecular Microbiology and Immunology, School of Hygiene and Public Health, Johns Hopkins University, Baltimore, Maryland 21205, USA.
    Excess iodine ingestion has been implicated in induction and exacerbation of autoimmune thyroiditis in human populations and animal models. We studied the time course and sex-related differences in iodine-induced autoimmune thyroiditis in NOD-H-2h4 mice. This strain, derived from a cross of NOD with B10.A(4R), spontaneously develops autoimmune thyroiditis but not diabetes. NOD-H-2h4 mice were given either plain water or water with 0.05% iodine for 8 weeks. Approximately 54% of female and 70% of male iodine-treated mice developed thyroid lesions, whereas only 1 of 20 control animals had thyroiditis at this time. Levels of serum thyroxin (T4) were similar in the treatment and control groups. Thyroglobulin-specific antibodies were present in the iodine-treated group after 8 weeks of treatment but antibodies to thyroid peroxidase were not apparent in the serum of any of the animals. Levels of thyroglobulin antibodies increased throughout the 8-week iodine ingestion period; however, no correlation was seen between the levels of total thyroglobulin antibodies and the degree of thyroid infiltration at the time of autopsy. The thyroglobulin antibodies consisted primarily of IgG2a, IgG2b, and IgM antibodies with no detectable IgA, IgG1, or IgG3 thyroglobulin-specific antibodies. The presence of IgG2b thyroglobulin-specific antibodies correlated well with the presence of thyroid lesions.

    Verh Dtsch Ges Pathol 1996;80:297-301
    [Spontaneous Hashimoto-like thyroiditis in cats] [Article in German] Schumm-Draeger PM, Langer F, Caspar G, Rippegather K, Herrmann G, Fortmeyer HP, Usadel KH, Hubner K.
    Medizinische Klinik I, Johann Wolfgang Goethe-Universitat, Frankfurt/M.
    A breeding line of domestic cats spontaneously developing symptoms of hypothyroidism between the 40th and 60th day of life (fur changes, loss of appetite, growth retardation), elevated levels of antibodies against microsomal structures and thyroglobulin, and lymphocytic thyroid infiltration has been recently established at our facility. Aim of our studies was to examine the effect of high iodine ingestion or prophylactic thyroid hormone therapy on functional and morphological characteristics of this Hashimoto-like thyroiditis in cat. From birth to day 80 of life cats were treated with iodine (n = 9; 0.1 mg/l) or thyroxin (n = 13; 2.0 micrograms/ kg/d) respectively. Untreated animals served as controls (n = 12). Cat-serum was tested for thyroid function (TT3, TT4). After 8 weeks the thyroid tissue was submitted to routine histological processing (H&E) and the inflammatory activity was scored. Additionally immunohistological staining was performed for MIB-1, IgG, IgM and MHCII expression. Both untreated hypothyroid (UHC) as well as iodine-treated (IC) cats revealed a significantly higher degree of thyroid inflammation and higher tissue levels of IgM as the thyroxin-substituted animals (TC). Epithelial proliferation decreased significantly in the IC and TC groups as compared to the untreated controls. No significant differences regarding IgG production and HLAII expression were detectable. Early thyroid hormone therapy significantly decreases both incidence and activity of autoimmune thyroiditis in cats as measured by inflammatory infiltration, IgM production and epithelial proliferation. Animals with excess iodide intake, however, show an aggravation of the autoimmune inflammatory activity.

    Autoimmunity 1994;18(1):31-40
    Iodide induced lymphocytic thyroiditis in the BB/W rat: evidence of direct toxic effects of iodide on thyroid subcellular structure.
    Li M, Boyages SC.
    Department of Clinical Endocrinology, Westmead Hospital, NSW, Australia.
    A high dietary iodine intake accelerates the development of lymphocytic
    thyroiditis (LT) in the BB/W rat. Our previous studies have defined the temporal
    sequence of the immunological events triggered by excess iodide intake in these
    animals. It was still not clear, however, whether these observed immunological
    changes were a direct effect on immune effector cells, or whether they
    represented a secondary response to a toxic effect of iodine on thyroid tissue.
    In the present study, the effect of excessive iodine intake on the subcellular
    structure of the BB/W rat thyroid gland, particularly, whether iodide had a
    toxic effect independent of its immune response has been examined. BB/W rats
    were exposed, prenatally through maternal drinking water, to excessive iodide at
    two doses (Moderate 3 x 10(-6) M iodide/l; High 3 x 10(-3) M iodide/l); a third
    group of BB/W rats was given tap water; till 12 weeks postnatal age. Two groups
    of Wistar rats received high dose iodide water or tap water for the same period
    of time and served as controls. Thyroid gland ultrastructure was determined by
    electron microscopic (EM) examination. Thyroid 125I uptake and perchlorate
    discharge tests were also performed in separate experiments. We found that
    thyroid glands of non-iodine supplemented Wistar rats were morphlogically normal
    under EM. There were no overt changes in the iodide treated Wistar rats. By
    contrast, iodide treated BB/W rats exhibited marked accumulation of secondary
    lysosomes and lipid droplets; markedly swollen and disrupted mitochondria and
    extreme dilatation of rough endoplasmic reticulum (RER).(ABSTRACT TRUNCATED AT
    250 WORDS)

    Clin Immunol Immunopathol 1993 Nov;69(2):189-98
    An excess of dietary iodine accelerates the development of a thyroid-associated lymphoid tissue in autoimmune prone BB rats.
    Mooij P, de Wit HJ, Drexhage HA.
    Department of Immunology, Erasmus University, Rotterdam, The Netherlands.
    Previous studies have shown that dietary iodine enhances the severity and
    incidence of focal thyroiditis in autoimmune BB rats and OS chickens. However,
    which lymphoid cells are involved in the development of the iodine-induced focal
    thyroiditis and what the consequences are for the anticolloid antibody
    production have not been studied in detail. We therefore performed a study in
    which 3-week-old female BB rats were kept on either an enriched iodine diet
    (EID; iodine intake, 100 micrograms iodine/day) or a normal iodine diet (NID;
    iodine intake, 7 micrograms iodine/day) for a period of 18 weeks. The
    development of the focal thyroiditis was immunohistologically studied.
    Immunohistological data were compared to the thyroid hormone status and
    anti-colloid antibody production. Our data confirm that a high dietary iodine
    intake results in an accelerated development of the focal lymphoid cell
    infiltrates in the thyroid of the BB rat. After 12-18 weeks of an EID 50% of the
    BB rats developed these infiltrates. Our data additionally show that: (a) the
    process starts with increases in the number of infiltrating MHC class
    II-positive dendritic cells and a clustering of these cells with T cells, B
    cells, and some macrophages and (b) the focal infiltrates are highly organized
    and consist of central B cell follicle-like structures surrounded by rims and
    areas of T cells. The architecture of the focal thyroiditis is hence very
    similar to mucosa-associated lymphoid tissue and secondary lymphoid organs
    (spleen and lymph node). Only minor signs of thyrocyte destruction were
    observed. We therefore consider the term "thyroiditis" as inappropriate and
    prefer the term "thyroid-associated lymphoid tissue." Since the thyroiditis
    component was small, it is also not surprising that the BB rats on the EID
    remained euthyroid. The presence of the thyroid-associated lymphoid tissue in
    the BB rats was positively correlated to the presence of anti-colloid antibody
    in the serum of the BB rats. We speculate that the dietary iodine might have
    direct effects on cells of the immune system or on cells forming the
    microenvironment of lymphoid tissue (reticulum cells). A role for highly
    iodinated thyroglobulin in the accelerated development of thyroid-associated
    lymphoid tissue is also possible.

    Autoimmunity 1993;14(3):181-7
    Iodine induced lymphocytic thyroiditis in the BB/W rat: early and late immune phenomena.
    Li M, Eastman CJ, Boyages SC.
    Department of Clinical Endocrinology, Westmead Hospital, NSW, Australia.
    The effect of iodine excess on thyroid function and on the immunological
    sequence of events leading to lymphocytic thyroiditis (LT) was studied in the NB
    subline of BB/W rats to determine the mechanisms by which the level of iodine
    intake influences the development of LT in this animal model. Iodine
    supplemented water (500 micrograms/l, Group 1 or 500 mg/l, Group 2) or
    non-iodine supplemented tap water (Group 3) was given to breeding pairs and
    their offspring ad libitum. A Wistar rat group, also given tap water (Group 4)
    served as controls. To determine the immunological sequence of events, the
    phenotypic nature of the infiltrating thyroid lymphocytes was examined by
    specific immunoperoxidase staining in BB/W and Wistar rats at 6, 9, 12, and 15
    weeks. Antigen-presenting cells and class II (Ia) antigen expression on
    thyrocytes were also examined. The first immunological event apparent in the
    iodine-treated BB/W rats was a sharp increase in the number of Ia positive
    dendritic cells at 9 weeks compared with control BB/W and Wistar rats. In the
    iodine excess groups dendritic cells were associated with scattered areas of
    lymphocytic infiltration, comprising predominantly T helper cells (W3/25). T
    suppressor cells (OX 8) and IL-2 receptor positive activated T-cells (OX 39)
    were both present in small numbers. B-cells (OX 12) were absent. In addition,
    thyrocytes did not exhibit Ia antigen expression. By contrast, lymphocytic
    infiltration was not found at 9 weeks in control BB/W rats.(ABSTRACT TRUNCATED
    AT 250 WORDS)

    J Clin Endocrinol Metab 1992 Nov;75(5):1273-7
    Iodine-induced subclinical hypothyroidism in euthyroid subjects with a previous episode of amiodarone-induced thyrotoxicosis.
    Roti E, Minelli R, Gardini E, Bianconi L, Gavaruzzi G, Ugolotti G, Neri TM,
    Braverman LE.
    Centro per lo Studio, Prevenzione, Diagnosi e Cura delle Tireopatie, Universita di Parma, Italy.
    Amiodarone-induced thyrotoxicosis (AIT) occurs most frequently in patients with
    underlying thyroid disease and is generally believed to be due to the iodine
    contamination of amiodarone and iodine released by the metabolism of the drug.
    We and others have suggested that the thyrotoxicosis may also be secondary to
    amiodarone-induced thyroiditis. To further determine the etiology of AIT, we
    administered large doses of iodides [10 drops saturated solution of potassium
    iodide (SSKI) daily] to 10 euthyroid patients long after an episode of AIT
    believed to be due at least in part to amiodarone-induced thyroiditis. Six of
    these 10 patients had an abnormal iodide-perchlorate discharge test before SSKI
    administration, indicating a subtle defect in the thyroidal organification of
    iodide. During SSKI administration, 6 patients developed marked iodine-induced
    basal and/or TRH-stimulated serum TSH elevations, 2 had suppressed basal and
    TRH-stimulated TSH values, and 2 had normal TSH responses compared to
    SSKI-treated euthyroid subjects with no history of amiodarone ingestion or
    thyroid disease. Serum T4 and T3 concentrations remained normal and unchanged
    during SSKI administration in both the AIT patients and control subjects. These
    results strongly suggest that excess iodine may not be the cause of the
    hyperthyroidism associated with amiodarone therapy, especially in those patients
    with probable amiodarone-induced thyroiditis. Furthermore, like patients with a
    previous history of subacute thyroiditis and postpartum thyroiditis, the present
    results suggest that some patients with a previous history of AIT may be at risk
    to develop hypothyroidism when given excess iodine.

    Endokrynol Pol 1992;43 Suppl 1:53-69
    The relationship between autoimmune thyroid disease and iodine intake: a review.
    Foley TP Jr.
    Division of Endocrinology, Metabolism and Diabetes Mellitus, School of Medicine,
    University of Pittsburgh.
    There is evidence to suggest that elevated levels of iodide in the diet are
    associated with autoimmune thyroid disease (ATD) in susceptible individuals, and
    that autoimmune thyroiditis (Hashimoto's disease) is less common in susceptible
    individuals who live in regions with dietary iodine deficiency. There are
    epidemiologic studies in endemic goiter areas that report an increase in ATD,
    particularly thyroiditis, after the therapeutic administration of iodized salt,
    bread and oil. Lymphocytic infiltration of the thyroid is rarely found in
    patients from severe endemic goiter regions, yet there is a reversal of this
    observation after dietary iodine supplementation. Thyroid antibodies, both
    thyroglobulin (TgAb) and peroxidase (TpAb) or microsomal, were not detected in
    serum from patients with endemic goiter, but became positive in 43% of subjects
    three and six months after therapy with iodized oil, and there developed
    transient hyperthyroidism. Similarly, the addition of iodine to the diet or the
    administration of iodine-containing medications increases the frequency of ATD
    and the severity of existing autoimmune thyroiditis. Furthermore, autoimmune
    thyroiditis has been induced by the administration of excess iodide to strains
    of chickens and rats that are genetically predetermined to develop the disease.
    We are beginning to understand the pathogenesis of ATD. In hyperthyroidism the
    evidence clearly supports the hypothesis that TSH receptor antibodies (TRAb)
    stimulate the TSH receptor to induce excessive and sustained secretion of
    thyroid hormones. Cellmediated immune mechanisms, such as antibody dependent
    cellmediated cytotoxicity (ADCC), initiate the lymphocytic infiltration and
    thyrocytotoxicity in autoimmune thyroiditis. The mechanisms that initiate the
    development of the abnormal immune response and the relationship of ATD with
    excess iodide are poorly understood. There is evidence that an increase in the
    iodination of thyroglobulin (Tg) enhances its immunogenicity. The results of
    clinical and experimental studies support the requirement of a genetic
    predisposition to the development of ATD that may be precipitated by exposure to
    certain environmental factors. Another mechanism supported by experimental data
    is the direct toxic effect of excess iodide on iodide-deficient thyroid glands.
    High concentrations of iodide after oxidation to iodine causes epithelial
    necrosis and inflammation associated with lipofuscin accumulation suggestive of
    toxicity mediated by lipid peroxidation from excessive amounts of free radicals.
    The epithelial damage would initiate inflammatory and immune responses. Although
    these mechanisms would relate to the onset of autoimmune thyroiditis on exposure
    to excessive amounts of iodide, the relationship of iodide intake and autoimmune
    hyperthyroidism is less clear.(ABSTRACT TRUNCATED AT 400 WORDS)

    J Clin Invest 1991 Jul;88(1):106-11
    Uptake and metabolism of iodine is crucial for the development of thyroiditis in
    obese strain chickens.
    Brown TR, Sundick RS, Dhar A, Sheth D, Bagchi N.
    Department of Medicine, Immunology and Microbiology, Wayne State University,
    Detroit, Michigan 48201.
    To assess the importance of the role of thyroidal iodine in the pathogenesis of
    thyroiditis in the obese strain (OS) chicken, a model of spontaneous and severe
    disease, we studied the effect of antithyroid drugs that reduce thyroidal iodine
    or prevent its metabolism. Reduction of thyroidal iodine was achieved with
    KClO4, an inhibitor of iodine transport and mononitrotyrosine (MNT), a drug that
    promotes loss of thyroidal iodine as iodotyrosines. A regimen consisting of
    KClO4 and MNT administration beginning in ovo and continuing after hatching
    reduced thyroidal infiltration to 2% of control values and decreased
    thyroglobulin antibody (TgAb) production for as long as 9 wk. Untreated birds
    had severe disease by 5 wk of age. The suppression of disease was independent of
    TSH, not mediated by generalized immunosuppression and reversed by excess
    dietary iodine. Two drugs that inhibit the metabolism of iodine,
    propylthiouracil (PTU) and aminotriazole, reduced thyroidal infiltration and
    TgAb levels, although to a lesser extent. When splenocytes from OS chickens with
    thyroiditis were transferred to Cornell strain (CS) chickens, a related strain
    that develops late onset mild disease, only the recipients that were iodine
    supplemented developed thyroiditis. In conclusion, autoimmune thyroiditis in an
    animal model can be prevented by reducing thyroidal iodine or its metabolism and
    optimal effects require intervention at the embryonic stage.

    Med Clin North Am 1991 Jan;75(1):169-78
    Iodine and thyroid disease.
    Woeber KA.
    Mount Zion Medical Center, University of California, San Francisco.
    Iodine is a requisite substrate for the synthesis of the thyroid hormones, the
    minimum daily requirement being about 50 micrograms. An autoregulatory mechanism
    within the thyroid serves as the first line of defense against fluctuations in
    the supply of iodine and also permits escape from the inhibition of hormone
    synthesis that a very large quantity of iodine induces (Wolff-Chaikoff effect
    and escape therefrom). Environmental iodine deficiency continues to be a
    significant public health problem worldwide, compounded in some geographic
    regions by the presence of other goitrogens in some staple foods. The pathologic
    consequences of severe iodine deficiency include endemic goiter, endemic
    cretinism, increased fetal and infant mortality, and an increased prevalence in
    the community of cognitive and neuromotor disabilities. The implementation of an
    iodization program prevents endemic cretinism and reduces the frequency of the
    other pathologic consequences of iodine deficiency. Iodine excess results
    principally from the use of iodine-containing medicinal preparations or
    radiographic contrast media. The pathologic consequences of iodine excess will
    ensue only when thyroid autoregulation is defective, in that escape from the
    Wolff-Chaikoff effect cannot occur, or when autoregulation is absent. Defective
    autoregulation characterizes the fetal and neonatal thyroid, Hashimoto's
    thyroiditis, radioiodine or surgically treated Graves' hyperthyroidism, the
    thyroid of patients with cystic fibrosis, and the thyroid that has been exposed
    to weak inhibitors of the organic binding of iodine. In these circumstances, the
    provision of excess iodine may lead to iodide goiter with or without
    hypothyroidism. Absent autoregulation may be a feature of longstanding
    multinodular goiter, and the provision of excess iodine in this circumstance may
    induce thyrotoxicosis (Jod-Basedow disease). The pathologic consequences of
    iodine excess will resolve when the source of iodine has been dissipated. In
    addition to its role in reversing iodine deficiency, iodine is used as
    adjunctive therapy for hyperthyroidism. By inhibiting the proteolytic release of
    iodothyronines from thyroglobulin, it induces a prompt slowing of thyroid
    hormone secretion. This effect is exploited in the treatment of thyrotoxic
    crisis or severe thyrocardiac disease. Iodine also reduces thyroid cellularity
    and vascularity and therefore is used in the preparation of the patient for
    thyroidectomy. Finally, by exploiting the failure of escape from the
    Wolff-Chaikoff effect, iodine may also be used in the early management of
    radioiodine-treated Graves' hyperthyroidism.

    J Endocrinol Invest 1989 Sep;12(8):559-63
    The inhibitory effect of large doses of methimazole on iodine induced
    lymphocytic thyroiditis and serum anti-thyroglobulin antibody titers in BB/Wor rats.
    Reinhardt W, Appel MC, Alex S, Yang YN, Braverman LE.
    Department of Medicine, University of Massachusetts Medical School, Worcester
    01655.
    The BB/Wor rat spontaneously develops autoimmune insulin dependent diabetes
    mellitus and lymphocytic thyroiditis (LT). Excess iodine ingestion enhances and
    low iodine diet decreases the incidence of LT in this rat model but does not
    affect the incidence of diabetes mellitus. The administration of a low dose of
    methimazole (MMI; 870 ng/gm bw ip daily) from 30-90 days of age had no
    significant effect on thyroid function or on the incidence of iodine induced LT
    and serum anti-thyroglobulin (Tg) antibodies measured by an ELISA assay. A large
    dose of MMI (0.05% in the drinking water) induced goiter and hypothyroidism. In
    addition, the incidence of LT was markedly attenuated (76% vs 6%, p less than
    0.001) and reduced titers of serum anti-Tg antibodies (0.59 +/- 0.1 OD vs 0.08
    +/- 0.01, p less than 0.001) were observed. This inhibitory effect of MMI on the
    occurrence of iodine induced LT in the BB/Wor rat may be due to the lower
    antigenicity of the poorly iodinated Tg secondary to MMI therapy and/or to an
    immunosuppressant effect of MMI itself.

    Bull Mem Acad R Med Belg 1989;144(5-7):313-8; discussion 318-20
    [Experimental goiter formation]
    [Article in French]
    Denef JF.
    Nodules formation in goiter is still poorly understood due to the lack of an
    adequate animal model. The key role of iodine in the increased heterogeneity of
    iodine metabolism and in cold follicle formation has been demonstrated.
    Administration of iodide excess to goitrous mice induces follicle cell necrosis
    and thyroiditis. Necrosis and inflammation can be prevented by reducing the
    iodine dose, giving T3 or T4, or combining iodide with antithyroid drugs or
    vitamin E. This suggest that iodide toxicity is related to excessive production
    of free radicals. During inflammation, Ia positive interstitial cells were
    increased in number whereas no Ia expression was seen in follicular cells.
     
  3. Makrosky

    Makrosky Member

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    @Kasper have a look at this it talks about good temps low pulse.
     
  4. Makrosky

    Makrosky Member

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    Thanks to the transcribers!!! I liked this show a lot.
     
  5. Makrosky

    Makrosky Member

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    Does anybody know which urine NO test is Ray talking about? The one to detect hypothyroidism
     
  6. burtlancast

    burtlancast Member

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    Thanks to Moss and Sheila once again for this great interview.

    I feel better now knowing i can lactate too and feed my babies ! :rolleyes:

    There's one bit in the interview about using T3 when the person is very hypothyroid with high adrenaline and cortisol that caught my eye:
    So, in this situations, one should not give immediately high T3 doses, and instead supplement with pregnenolone, magnesium, etc and only small doses of T3, in order to progressively keep stress hormones down ?
     
  7. OP
    moss

    moss Member

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    Hi Burt, always a pleasure.

    In this context yes that is how I understood it.... the caller states when the woman took extra iodine some time ago she went into come kind of hyperthyroid-crisis like state and now when she takes thyroid she gets a reaction from taking thyroid with similar reactions to the iodine response.

    RP: The people who have trouble with the actual thyroid hormone they can be either deficient in magnesium because hypothyroidism makes all of your tissues fail to retain a normal amount of magnesium and then when you supplement it, suddenly you experience an extreme magnesium deficiency in your heart, for example, and your brain, and so taking some magnesium at the same time as the thyroid will help those people. Others, if they are deficient in adrenal or ovarian or gonadal steroids, will suffer stress symptoms when they take thyroid and so using a supplement such as pregnenolone will make them tolerate adapting to the thyroid hormone more easily.

    Caller: So when you are in a situation like that she was using very small specks of T3, under 1 mcg sometimes. The thing to do is to hold that very low dose for a couple of weeks, then increase it in very, very small increments and the adrenalin hopefully comes down?

    RP: Well, sometimes it lasts for a couple of weeks. If you’re really extreme, you have to use little bits of supplements and be very careful about your intake of protein, sugar, calcium, everything that is counter to the stress.

    RP: Yeah. I’ve known people for a week or two who would stay with 1mcg doses of T3, but you have to make sure your whole diet is very good, having hormone tests, and a vit D blood test is helpful because magnesium and calcium work together and vit D regulates them.



    I think it is good practice and makes sense when dosing with any supplements, to start small. Particularly wrt to T3, Thyroid...... Taking temps and pulse will give so much information, if one bothers to chart regularly, (especially when starting out on thyroid meds) and yet, so often this simple exercise is not performed. :banghead
    And treat your liver well and it will look after you....

    Burt, as well as Transcripts Moderator, are you now offering services as a Wet Nurse? :thumbup
     
  8. tankasnowgod

    tankasnowgod Member

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    I remember hearing a while ago on a radio show about a man who had a pituitary tumor, and it caused him to lactate.

    I decided to do a quick google search, and look what showed up-

    Lactation associated with a pituitary tumour in a man
     
  9. MyUsernameHere

    MyUsernameHere Member

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    [​IMG]

    upload_2017-7-12_10-2-33.png

    That is clearly not the fault of iodine, as you can see here since the rate of thyroid cancer was much lower in the 70's and 80's when urinary iodine excretion was much higher.
    I don't see the point of bringing up thyroid cancer, as if to say that iodine is causing all this increased thyroid cancer? That does not make sense. If anything, it would make sense that iodine was protective against the cancers because of how much the rates have skyrocketed - particularly in women which need more iodine because of breast tissue, where it acts anti-estrogenically.

    :rolleyes:
     
  10. Makrosky

    Makrosky Member

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    @MyUsernameHere try it and then decide for yourself. And tell us your experience.

    Beware Lugol solution is very harsh on the stomach and detox systems. I think it's better to use SSKI. Much more gentler and equally effective.

    And as I said... don't-forget-the-selenomethionine.

    And also beware that it can boost your metabolism a lot so more calories and micronutrients are gonna be needed.
     
  11. MyUsernameHere

    MyUsernameHere Member

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    I will start a log here once I receive my J. Crow's Lugol's solution. I have selenium on the way too. I know that taking selenium without iodine and iodine without selenium is a bad idea.

    The thing about SSKI is that it only contains potassium iodide, when from my research I've concluded that a mixture of both forms is ideal. Certain tissues preferentially uptake iodine, and others iodide. So I believe it's best to use both.

    To be honest if it can give me a bit more energy as I've heard some report that would be very welcome at this point.
     
  12. Makrosky

    Makrosky Member

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    You are correct. Both are preferred BUT SSKI on it's own is also very useful, gives energy and doesn't have nasty detox reactions, whereas Lugols does. Lugol detox can be really nasty. Keep an eye on that.

    Feel free to PM me if you need something it's been many years since I don't use Iodine but I researched it a lot by that time and have lots of practical info.

    Btw you know Peat is not in favour of iodine, right ?

    Good luck and be careful.
     
  13. MyUsernameHere

    MyUsernameHere Member

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    I took it about 4 years ago but only for a quite short time. I did not have any bad reaction to it whatsoever.

    I know Peat is not in favor of it and I'm sure he has his reasons, but the research on the other side seems very convincing and I feel like I have to give it another try, this time properly.
    I don't do well on thyroid hormones of any sort, and I am trying to increase my own thyroid gland's function. Light therapy is one thing that helps somewhat, so I am looking for more.
    Usually so far the things that have helped me feel better have been very unconventional, so I am already used to not taking anyone's recommendations at face value but instead I just
    read about things that various people say, decide if the research is sound or if it sounds like a good idea, and then try to apply it to myself and see if I can benefit from it.

    I will admit I'm not a 100% Peatarian but despite that this forum is still one of the few locations where people have plenty of really interesting non-mainstream ideas, and that aligns
    the most with my views, if not entirely. I don't really feel like going to PaleoHacks or Mark's Daily Apple and getting bombarded with recommendations to chug down Flax Seed oil, or
    being told that I have a linoleic acid deficiency. :rolleyes:
     
  14. Makrosky

    Makrosky Member

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    Cool man. Good luck! Let us know how it goes.
     
  15. Travis

    Travis Member

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    I don't think I₂ gets absorbed systemically. There are too many reducing agents in the body. When you put it on the skin, you can tell that it does not penetrate far by how it stains. The iodine is then slowly reduced by glutahtione and vitamin C to colorless iodide.

    I₂ + 2e⁻→ 2I⁻

    But I₂ can iodinate unsaturated bonds in the intestines. Iodide (I⁻) cannot add to double bonds at normal conditions, only diatomic iodine (I₂) can.

    [​IMG]

    The problem with these halogens is that the elemental name is the same as the diatomic form, so people sometimes say iodine when they probably should really say iodide, and molecular iodine is sometimes called diiodine for clarity.

    I really don't think that I₂ can make it to the breasts without dissociating. I have no idea where the idea that breasts accumulate I₂ came from. It would have to avoid all reducing agents and unsaturated lipids on its way there. The I—I bond is not a very strong bond. In fact, it is the single weakest covalent bond on this chart:
    [​IMG]

    If anyone can find any data on I₂ in the breasts I would love to see it.

    It seems like seaweed is as good as Lugol's. I personally would use SSKI or kelp. The iodinated products formed from Lugol's (I₂) on intestinal lipids and proteins* could have significance.

    *It has also been shown to add to certain amino acids.
     
  16. MyUsernameHere

    MyUsernameHere Member

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  17. Travis

    Travis Member

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    The full study can be found here: http://iodineresearch.com/files/ghent_eskin_1993_iodine_replacement_fibrocystic_disease2.pdf

    Here is part of the abstract:
    By "was the most beneficial" he is comparing 70% to 72%. I don't think this is statistically significant.

    I was hoping for more data, but most of the actual data is comparing I₂ to placebo. You don't get a full exposition of the side effects of the I₂, I⁻, or casein iodide groups.

    No thyroid hormone or urinary iodide levels were given.

    I read a rat study that showed no difference in serum iodide levels or thyroid hormone levels when either I₂ or 2I⁻ was added to the drinking water. I refuse to believe that I₂ dodges so many bullets on the way to the breast and arrives in one piece.

    He also says this:
    This is not true. Lugol's always exists in a 2:1 ratio.

    The authors, William R. Ghent and Bernard A. Eskin, are listed as the filers for US patent Nº 4816255: Treatment of iodine deficiency breast syndrome

    The filing date of the patent was Jul 28, 1986.

    The article you cited was published in Oct, 1993.

    I don't think that article represents honest and unbiased science.
     
  18. MyUsernameHere

    MyUsernameHere Member

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  19. Travis

    Travis Member

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    That's more Eskin and Ghent stuff. Can you find a study by authors that don't have patents in iodine treatment??

    This is a blatant conflict of interest.
     
  20. Travis

    Travis Member

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    Here is the entire study: http://iodineresearch.com/files/eskin_ghent_1995_iodine_iodide_rat_thyroid_mammary_gland2.pdf

    thyroid.png

    These are the only measurements that aren't subjective. The other ones are based on a more-or-less subjective histological grading scale. The histological investigation appears to have been made the authors. Keep in mind that this is a non-blinded judgment call made by people with I₂ patents.
    thyroid2.png
    The I₂ would have to dodge all reductants (electron donors) including vitamin C, which exists in the body in concentrations many orders of magnitude greater than the I₂ you would be ingesting.
    [​IMG]
    This happens spontaneously at room temperature.


    The I₂ molecule would have to completely dodge the mitochondria, as it is a veritable whirlwind of electrons and ROS.

    It would also have to dodge every unsaturated fatty acid in lipoproteins and cell membranes.

    I'm not saying that it's harmful. Maybe having iodinated lipids is a good thing. I just don't think that it's reasonable to assume that swallowed I₂ will make through the intestine, through the blood, and to the breast as I–I.

    And I don't think that anyone has ever demonstrated that it has.

    Any difference can easily be explained by kinetics. Since I₂ can add to lipids and some amino acids, the same amount given as I₂ will probably amount to a slightly lower overall concentration than the same amount given as I⁻. Diiodine is also more hydrophobic, and will partition and associate more with fatty membranes.

    If you think it can hang-out safely on the lipid membrane, keep in mind that it can be reduced by vitamin E:

    Iodine Oxidation of α-Tocopherol and Its Model Compound in Alkaline Methanol: Unexpected Isomerization of the Product Quinone Monoketals.

    thyroid3.png
     
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