Missenger
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- Mar 15, 2018
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The Russia vaccine is also GMO, only China got the 'normal' vaccine.
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Ray Peat Email Advice Depository
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meatbag
Member
- Joined
- Jan 15, 2016
- Messages
- 1,771
Asking about the Covivac vaccine, which is inactivated virus. I sent him the description from wikipedia;
"According to that description, it should be no more harmful than any traditional vaccine using aluminum hydroxide, and obviously safer than the injection of nucleic acids specifying the spike protein—which has no rational basis in science. Intramuscular aluminum hydroxide is always harmful to some degree, and is based on ignorance of the nature of biological disease resistance."
"According to that description, it should be no more harmful than any traditional vaccine using aluminum hydroxide, and obviously safer than the injection of nucleic acids specifying the spike protein—which has no rational basis in science. Intramuscular aluminum hydroxide is always harmful to some degree, and is based on ignorance of the nature of biological disease resistance."
Lightbringer
Member
- Joined
- Jan 24, 2014
- Messages
- 235
Asked Ray about this article defending the spike protein from vaccines:
Spike Protein Behavior
Spike Protein Behavior
Lightbringer
Member
- Joined
- Jan 24, 2014
- Messages
- 235
The guy just says the things that seem reasonable to an organic chemist. Sucharit Bhakdi has pointed out that the spike protein, expressed on the surface of an endothelial cell, activates inflammatory immune and clotting reactions, leading to clotting and bleeding problems, CVT and DIC. The subtleties of the immune system, such as exosomes assimilating viral nucleic acids and disseminating them the way viruses do, or the axonal retrograde transport of intramuscularly injected substances, don’t fit into institutional science.
M
metabolizm
Guest
Q: Ray, is persorption a risk even with well-cooked starches? If not, what is it about starches (after cooking) that makes them hard on the gut?
A: Natural starches are often embedded in other materials that resist digestion as well as cooking; that can cause them to support bacterial growth.
A: Natural starches are often embedded in other materials that resist digestion as well as cooking; that can cause them to support bacterial growth.
Beastmode
Member
- Joined
- Feb 7, 2017
- Messages
- 1,258
Me:
Besides the typical ones like carrot salad, aspirin and vitamin e, I've been interested in trying some form of nettle root tea and/or tincture.
Do you think this can be a safe addition, either daily or a few times per week, a good quality source of either the tincture or homemade tea?
Peat:
The tea is safe.
Besides the typical ones like carrot salad, aspirin and vitamin e, I've been interested in trying some form of nettle root tea and/or tincture.
Do you think this can be a safe addition, either daily or a few times per week, a good quality source of either the tincture or homemade tea?
Peat:
The tea is safe.
meatbag
Member
- Joined
- Jan 15, 2016
- Messages
- 1,771
Asking about Ivermectin;
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"It isn’t something I would use, there are so many protective things without the risks."
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"It isn’t something I would use, there are so many protective things without the risks."
UG Krishnamurti
Member
- Joined
- Sep 28, 2020
- Messages
- 555
Q:
1. Have you ever heard of someone improving their hearing - specifically people who are experiencing hearing loss?
2. Why do the fried/heated fats (no matter which ones - coconut, olive, butter etc) give me eczema, dry skin and scalp as well as some blood sugars dysregulation while "raw" fats have no problems?
EXAMPLE: If I cook steak or meat on a grill or use an oven I have 0 issues and If I add some fats to it, or fry in a pan I get all of these skin issues? Are they harder on the liver or is there something else which I'm missing!
RP:
Do you supplement vitamin D and get enough calcium in your diet relative to phosphate? Heated fats are more irritating, and the intestine is exaggeratedly sensitive if vitamin D, calcium, and thyroid are low.
Some people experience improved hearing when they move to a high altitude; I think it has to do with improved circulation.
People going to a high altitude, e.g., 6500 feet or more, sometimes notice improved hearing. Adapting to altitude increases the CO2 retained in the body, improving capillary circulation. The drug acetazolamide increases CO2, and can have similar effects. Thyroid and vitamin D, caffeine and thiamine can help to maintain CO2 levels.
Am J Otol. 1989 Mar;10(2):142-5.
Long-term effect of acetazolamide and chlorthalidone on the hearing loss of Menière's disease
J Corvera 1, G Corvera
Abstract
A retrospective computerized analysis of the records of patients with Meniere's disease was made to evaluate the effect of acetazolamide and chlorthalidone on the rate of hearing loss. Three groups were compared as follows: (1) 79 patients treated with chlorthalidone for 5 to 13.4 years; (2) 42 patients medicated with acetazolamide between 5 and 7.8 years; and (3) a control group of 71 patients who received only intermittent symptomatic treatment for vertigo, followed for 5 to 24.1 years. In the short term, after 2 to 6 weeks of treatment, a statistically significant decrease of the average hearing loss was observed with both chlorthalidone and acetazolamide. In the long term, more than 5 years, no preventive effect on the deterioration of the hearing loss could be detected. Both acetazolamide and chlorthalidone can be useful for diagnostic purposes by causing a fluctuation of hearing, as well as for the management of the vertigo attacks, but it is not useful for the long-term prevention of the hearing deterioration in Meniere's disease.
Q: Also there is a study stating that higher altitudes and hypoxia states can cause deafness and hearing problems.
www.ncbi.nlm.nih.gov
"Ischemia and hypoxia in the inner ear are the main factors leading to sudden deafness, acute acoustic trauma and presbycusis. An animal experimental study confirmed that cochlear tissues were particularly sensitive to hypoxia, and cochlear compound action potential and endocochlear potential disappeared after only 8 sec of cochlear hypoxia (1). In addition, in vitro experiments on organ cultures of the cochlea found that hypoxia causes cochlear hair cell (HC) loss and neuronal death (2,3). The mechanisms underlying hypoxia-induced inner ear damage are not clear."
RP: That’s when the change is so extreme that adaptation doesn’t happen. When climbers on Mt. Everest were suffering such symptoms, and dementia, breathing CO2 corrected the problem.
_____________________________________________________________
Q:Will breathing in the bag by increasing CO2 also improve circulation? What are the best ways that you know of that can improve one's circulation?
RP:
Yes, the bag breathing can make your skin noticeably pinker, and lower blood pressure. Calcium, vitamin D, thyroid, and progesterone are things that help capillaries.
______________________________________________________________
1. Have you ever heard of someone improving their hearing - specifically people who are experiencing hearing loss?
2. Why do the fried/heated fats (no matter which ones - coconut, olive, butter etc) give me eczema, dry skin and scalp as well as some blood sugars dysregulation while "raw" fats have no problems?
EXAMPLE: If I cook steak or meat on a grill or use an oven I have 0 issues and If I add some fats to it, or fry in a pan I get all of these skin issues? Are they harder on the liver or is there something else which I'm missing!
RP:
Do you supplement vitamin D and get enough calcium in your diet relative to phosphate? Heated fats are more irritating, and the intestine is exaggeratedly sensitive if vitamin D, calcium, and thyroid are low.
Some people experience improved hearing when they move to a high altitude; I think it has to do with improved circulation.
People going to a high altitude, e.g., 6500 feet or more, sometimes notice improved hearing. Adapting to altitude increases the CO2 retained in the body, improving capillary circulation. The drug acetazolamide increases CO2, and can have similar effects. Thyroid and vitamin D, caffeine and thiamine can help to maintain CO2 levels.
Am J Otol. 1989 Mar;10(2):142-5.
Long-term effect of acetazolamide and chlorthalidone on the hearing loss of Menière's disease
J Corvera 1, G Corvera
Abstract
A retrospective computerized analysis of the records of patients with Meniere's disease was made to evaluate the effect of acetazolamide and chlorthalidone on the rate of hearing loss. Three groups were compared as follows: (1) 79 patients treated with chlorthalidone for 5 to 13.4 years; (2) 42 patients medicated with acetazolamide between 5 and 7.8 years; and (3) a control group of 71 patients who received only intermittent symptomatic treatment for vertigo, followed for 5 to 24.1 years. In the short term, after 2 to 6 weeks of treatment, a statistically significant decrease of the average hearing loss was observed with both chlorthalidone and acetazolamide. In the long term, more than 5 years, no preventive effect on the deterioration of the hearing loss could be detected. Both acetazolamide and chlorthalidone can be useful for diagnostic purposes by causing a fluctuation of hearing, as well as for the management of the vertigo attacks, but it is not useful for the long-term prevention of the hearing deterioration in Meniere's disease.
Q: Also there is a study stating that higher altitudes and hypoxia states can cause deafness and hearing problems.
Influence of high-altitude hypoxic environments on the survival of cochlear hair cells and spiral ganglion neurons in rats
The aim of the present study was to observe the histological changes in the peripheral auditory system in rats at different time-points after relocating from low altitude to high altitude (3,600 m). The general physical condition of the rats was observed ...
www.ncbi.nlm.nih.gov
"Ischemia and hypoxia in the inner ear are the main factors leading to sudden deafness, acute acoustic trauma and presbycusis. An animal experimental study confirmed that cochlear tissues were particularly sensitive to hypoxia, and cochlear compound action potential and endocochlear potential disappeared after only 8 sec of cochlear hypoxia (1). In addition, in vitro experiments on organ cultures of the cochlea found that hypoxia causes cochlear hair cell (HC) loss and neuronal death (2,3). The mechanisms underlying hypoxia-induced inner ear damage are not clear."
RP: That’s when the change is so extreme that adaptation doesn’t happen. When climbers on Mt. Everest were suffering such symptoms, and dementia, breathing CO2 corrected the problem.
_____________________________________________________________
Q:Will breathing in the bag by increasing CO2 also improve circulation? What are the best ways that you know of that can improve one's circulation?
RP:
Yes, the bag breathing can make your skin noticeably pinker, and lower blood pressure. Calcium, vitamin D, thyroid, and progesterone are things that help capillaries.
______________________________________________________________
Last edited:
Amazoniac
Member
Magnesium water
Stick figure:
Raj:
Stick figure:
Raj:
Orange peels and pressure cooking
Stick figure:
Raj:
Copper as coprous and cupric
Stick figure:
Raj:
Stick figure:
Raj:
My messages was abbreviated, their complete version can found here, but there's nothing else from Raj.
Stick figure:
"What makes the magnesium water preparation that you usually recommend special?"
Raj:
"I don’t recall recommending that, I usually recommend getting it from food, along with vitamin D and calcium, and making sure that your thyroid function is good, so that your tissues can retain magnesium."
Stick figure:
"In other words: what's the advantage of reacting magnesium hydroxide with carbonated water? It's surprising that people find magnesium bicarbonate more agreeable than hydroxide given that stomach acid being renewed should make the effect of a limited amount of carbonic acid on the powder weak in comparison."
Raj:
"I haven’t used it, but a possible reason that people like it could be that some manufacturing impurity is eliminated in reacting it slowly with carbon dioxide."
Orange peels and pressure cooking
Stick figure:
"If you're not into highly fermentable foods, why not favor the yellow part of orange peel that concentrates the flavonoids and discard the white that's rich in pectins?"
"Do you have something against pressure cooking?"
"Do you have something against pressure cooking?"
Raj:
"I discard most of the white material, my marmalade doesn’t gel. The high temperatures of pressure cookers cause tastes that I don’t like."
Copper as coprous and cupric
Stick figure:
"Do you find copper in its cupric state to be inferior or problematic in relation to cuprous?"
"Also, what about copper cookware and having it leaching into foods? I know that you've tried to prepare eggs in a copper pan in the past, but what's your position now in terms of safety?"
"Also, what about copper cookware and having it leaching into foods? I know that you've tried to prepare eggs in a copper pan in the past, but what's your position now in terms of safety?"
Raj:
"I haven’t cooked anything in copper that didn’t taste bad--that’s enough to discourage its use. A problem with inorganic copper supplements is that they degrade many nutrients in the stomach."
Stick figure:
"Is there validity in the claim that ingesting purified copper in its oxidized state is a cause of concern, even when bound to reliable (and organic) ligands?"
Raj:
"In the form of copper chlorophyllin it doesn’t produce that metallic taste (which is peroxidizing fatty acids)."
My messages was abbreviated, their complete version can found here, but there's nothing else from Raj.
Riesensackteil
Member
- Joined
- Apr 4, 2021
- Messages
- 499
Me: Countries worth to live in?
Ray: I like the combination of high altitude and low latitude. My house is in Coeneo, Michoacan, Mexico.
Me: I will knock on your door tomorrow! Will you open for me? :)
Ray: My room is at the rear, it’s necessary to knock loudly.
Me: Any thoughts on Russia (or similar) though?
Samarkand in Uzbekistan seems nice, as well as the Altai mountain and the whole Red Sea region. Any insights? You have been to Russia I think. I haven't but it is on my planner. Some Minijob as Park Ranger at Altai, that is what I would like to do
Ray: The climate of Almaty seems pleasant, A park ranger job sounds great, I was a park ranger for a while.
Ray: I like the combination of high altitude and low latitude. My house is in Coeneo, Michoacan, Mexico.
Me: I will knock on your door tomorrow! Will you open for me? :)
Ray: My room is at the rear, it’s necessary to knock loudly.
Me: Any thoughts on Russia (or similar) though?
Samarkand in Uzbekistan seems nice, as well as the Altai mountain and the whole Red Sea region. Any insights? You have been to Russia I think. I haven't but it is on my planner. Some Minijob as Park Ranger at Altai, that is what I would like to do
Ray: The climate of Almaty seems pleasant, A park ranger job sounds great, I was a park ranger for a while.
Lizb
Member
I like that exchange.
This thread is reserved for email advice exchanges only. If you would like to discuss anything posted in this thread, feel free to make your own thread, or you can go over the Ray Peat Email Advice Depository Discussion/Comment Thread
Lizb
Member
Oops. Ty
UG Krishnamurti
Member
- Joined
- Sep 28, 2020
- Messages
- 555
Ray responds on making gelatin and bones containing fluoride:
The bone fluoride is very insoluble, so I don’t think there’s a problem. Long bones contain marrow, and prolonged cooking of that produces a lot of fat oxidation products. The tendons and ligaments around joints are the main source of gelatin, rather than the bone itself. -RP
The bone fluoride is very insoluble, so I don’t think there’s a problem. Long bones contain marrow, and prolonged cooking of that produces a lot of fat oxidation products. The tendons and ligaments around joints are the main source of gelatin, rather than the bone itself. -RP
Q: Asked Ray about a random list of supplements
A: Some chemicals that are very important metabolically can be disruptive when they are taken orally in inappropriate forms or combinations or amounts. For example, free ionic copper taken with food can degrade vitamins and amino acids. PQQ is probably safe, but I think much more research is needed to be sure. Most vitamin E products contain small amounts of potentially harmful impurities. The amount of aspartate in a tablet of magnesium aspartate is harmless, but it’s good to be cautious; I knew someone who began having daily seizures when he used large amounts of magnesium and calcium aspartate; his daily seizures continued for four months, and stopped the day after he discontinuted the supplements. I think there’s a risk of methyl imbalance when large amounts of betaine are used chronically.
Q: Hello, tocotrienols are unsaturated, but vitamin A is as well. I wonder if they could be helpful?
A: A small amount of tocotrienol contributes to the protective vitamin E action.
Q: Which milk brand do you prefer using Mr Peat? someone said that your favorite milk brand was discontinued. I'm wondering how they even found out your favorite milk brand!
A: At the beginning of the panic, they disappeared, but they all came back to some degree. Kirkland and Lucerne are two good brands in the pacific northwest.
^(Disclaimer on above this was last year before Peat knew about the emulsifiers/fillers in milk. I'm also unsure if he knows about the production processes of the above milks or is going by taste as I think those brands are non organic, not sure if Peat cares about certified organic milk)
Q: Do you think 1mg boron every other day is beneficial. Studies seem to show pro estrogen effects yet some studies show pro testosterone effects and yet some show pro DHT effects... the medical people are deciding whether boron is an essential nutrient but boron and vanadium are already being included in several multivitamin products.
Vanadium supposedly mimics insulin? Also what about ashwaganda? Supposedly boosts thyroid and lowers cortisol. Guggul and coleus forskoli also seem interesting.
A: I don’t think there’s good science supporting boron; vanadium is probably safe in very small amounts. I think forskilin can be dangerous, creating stress reactions.
Q: 50mg of pregnenolone supplementation (capsule form, no ingredients in capsule besides cellulose), caused 12 pounds weight gain in 10 days. This weight gain did not subside or go away even after the pregnenolone was stopped for months. All the symptoms from the pregnenolone supplementation matched high cortisol symptoms. The pregnenolone seemed to be converting entirely to cortisol and estrogen. I believe you mentioned pregnenolone doesn't have side effects but I think the studies you mentioned regarding it were done on healthy younger men, so they would likely be converting pregnenolone into the correct androgenic hormones whereas someone who has poor thyroid function likely converts the pregnenolone directly to stress hormones and estrogen?
A: There is some real junk being sold as pregnenolone, what brand was it? Real pregnenolone protects against increased cortisol, lowers cortisol it it’s abnormally high. It can lower estrogen too.
Q: How does aspirin impact muscle growth and muscle mass? there are lots of bodybuilders who have attempted to use T3 for fat burning/weight loss purposes. Many of them have advised to keep T3 doses extremely low because T3 leads to both muscle burning and wasting and fat loss, apparently T3 does not differentiate between burning muscle or fat.
What about aspirin, does aspirin also target both muscle and fat mass for fuel. since it inhibits lipolysis does that mean aspirin and niacinamide preserve fat mass while burning muscle and sugar?
A: Aspirin and T3 activate oxidative energy production, but they have to be used at a “physiological” level, which varies situationally; it’s usually around 3 mcg/hour, and bodybuilders habitually use crazy amounts.
Q: What are your thoughts on supplementing freeze dried thyroid gland, liver testicle and other beef organs, deer antler velvet extract, freeze dried oyster, krill oil, nigella sativa oil
A: I prefer, for sanitation, standard desiccated thyroid. Other dehydrated substances often contain lipid peroxides and tryptophan decomposition products.
Q: vitamin E stimulates the immune system and triggers autoimmune conditions, should intake be limited?
A: Someone just has the facts mixed up. Injecting foreign material intramuscularly damages the nervous and immune systems; many chemically active lipids have similar effects. Entering the body as a nutrient, vitamin E is antiinflammatory.
Q: these people had autoimmune conditions and said their conditions experienced flareups in response to vitamin E usage. People have had extreme immune flareups from the herb ashwagandha, from dhea, from 7 keto dhea, from pregnenolone, from higher doses of vitamin MK4 ,from iodine, and from things like yohimbe bark, Pau D arco bark, and pine bark extract/pycnogenol.
A: I don’t know of any wheat germ based vitamin E that doesn’t contain toxic amounts of polyunsaturated fats. Bacteria, fungi, and viruses stimulate the immune system; most of the published statements about stimulating the immune system are dangerous nonsense.
Q: You used to use a wheat germ vitamin E, wasnt that with polyunsaturated fats? What source of vitamim C did you use? How do you explain people having severe autoimmune responses in response to consuming some of these substances like pregnenolone or ashwagandha or vitamin e or vitamin K
A: I wrote about the polycosanol in the old vitamin E from wheat germ, but I didn’t use it myself, it had been discontinued for a long time before I got interested in it. My first experience with vitamin C was when it was called cevitamic acid, and the largest tablets available were 50 milligrams. Three years later, a new method for making vitamin C very cheaply led to 500 mg tablets becoming common. Remembering my amazing first experience with 50 mg/day, I took 500 mg, and the next morning had a sore throat and cough. That eventually led to finding, when I was working at a clinic in Eugene, that nearly all the people I saw with chronic “allergy” lost all their symptoms when they stopped their supplements. I think vitamins A and E were the last of the regular supplements that I used, and that was around 1972. I started using pregnenolone from Sigma Chemical, then got it by the kilogram from the Syntex factory in Mexico. When they stopped making it, I got a few kilos from European companies, but when they stopped making it, I found that pregnenolone from other sources produced hormonal effects that shouldn’t be pregnenolone, so I stopped using it; that was some time in the ‘90s. Pure pregnenolone never produced hormonal effects in either human or animal studies. Minor producers don’t have the resources of the giants to produce extreme purity.
Q: Hello Ray! What kind of foods do you like to eat out, which restaurants do you eat out at regularly
A: I haven’t eaten in a restaurant since 1984. Restaurants have always been notoriously unsafe places to eat, but in the age of food chemistry it has become impractical to try to identify trustworthy places.
Q: Do you know what the original 50mg vitamin C was sourced from. Most vitamin C is sourced from corn and fungus or mold. There are some manufacturers selling vitamin C extracted from berries, these capsules come in much smaller sizes of 80mg each and are extracted from amla berry acerola cherry other berries. These berry vitamin Cs are referred to as whole food vitamin C and are much more expensive
A: The vitamin C products “from natural sources” that I’ve seen contained ascorbic acid and dried plant material.
(^Disclaimer I think there are some products which use an actual freeze dried acerola cherry or amla berry mixture, which is very low like 80mg vitamin C per capsule. im not sure Ray is aware of these as theres only a few companies making these)
Q: Do you think bread is harmful in general. Like a burger a few times a week, would there be significant health effects involved due to the bun? Its the typical enriched white flour brioche bun.
A: Most people tolerate it very well.
(^Disclaimer I'm not sure if Ray is aware as there's all kinds of filler ingredients and inflammatory things in many processed bread buns these days)
Q: Mr Peat, I was also wondering, how come you never show your face/video call during your youtube podcasts/interviews?
Also, do you think masturbating to pornography would increase estrogen/cortisol and have harmful physical side effects that you do not get from sex with a live partner? or is masturbation and watching naked women a non factor when it comes to physical health?
A: My computer doesn’t have a camera or microphone; I use a landline phone; the constant technological up-dates and innovations are doing more harm than good. Just thinking about, anticipating, sex increases testosterone, makes the whiskers grow faster; general good health keeps the increased testosterone from increasing estrogen and cortisol.
Q: does milk in the us provide an excess of the nutrients vitamin A, molybdenum, and more
A: No. Occasionally, phobic ideas about nutrients circulate, including places like the raypeatforum, and milk phobia seems to be a chronic cultural problem.
Q: Also, do you think masturbating to pornography would increase estrogen/cortisol and have harmful physical side effects that you do not get from sex with a live partner? or is masturbation and watching naked women a non factor when it comes to physical health?
A: Ordinarily, just thinking about, anticipating, sex increases testosterone and well being, but in a stressed hypothyroid person it’s possible that the testosterone produced by sexual arousal could be converted to estrogen.
(^I asked him this question again as I was hoping to get a more specific answer comparing sex with a partner to masturbation. it seems he did address it)
Q: Does masturbation cause negative hormonal effects that you wouldnt get from sex with a partner? or is it the same hormonally as long as youre thinking about sex while masturbating?
also sir, what are your thoughts on supplementing with amino acids such as creatine, beta alanine, taurine, glycine? some claim beta alanine has anti diabetic effects, that creatine supplementation powerboosts the mitochondria and boosts mitochondrial function, that taurine helps excrete fluoride/maintain thyroid function in presence of fluoride, that glycine reduces tryptophan and serotonin.
but isnt it also risky supplementing individual amino acids as they could cause an imbalance in other amino acids, or other vitamins or minerals? isnt there always a risk to supplementing amino acids
A: It would be more helpful to read some physiology books instead of the internet. Almost everything there is exploitative, insane, stupid, or a blend of those.
Q: Mr Peat how much milk do you drink a day? which brand and style of milk do you use?
do you stick to whole milk only now? apparently the whole milk, has much less additives than other milks. perhaps because most whole milks only have vitamin d3 added instead of vitamin A and D. that synthetic vitamin A may be very harmful compared to natural vitamin A from milk and liver. vitamin D3 supplements are supposedly just made from sheep cholesterol exposed to UV light.
Mr Peat, how does lactose as a sugar compare to glucose and sucrose? do you think lactose is a superior sugar to glucose and sucrose. does it burn off easier etc.
A: I get it directly from farmers who don’t treat it, and then I skim it because I don’t want so much fat. Lactose promotes the absorption of calcium and probably other nutrients.
Q: Thats incredible mr Peat! do you care if the milk from your farmers is grass fed, non gmo, organic etc?
do you pasteurize the milk yourself or do you essentially drink a raw skim milk product?
thats incredible. do you think pasteurized, organic whole milk purchased from a grocery store is not safe?
A: The organic milk I have had from various supermarkets, supposedly reliable brands, has often had an unpleasant taste and soured quickly, even when pasteurized, which I think indicates poor feeding and milking techniques. Sanitary milking practices and good feed—combined hay and pasture—produce clean milk with a good taste that doesn’t need pasteurization. I often heat the milk to speed separation of the cream.
Q: mr Peat how much milk do you drink per day? do you think casein proteins are superior to whey proteins? or are both proteins equally valuable?
A: I have averaged two quarts a day for a long time. The method of separating whey from casein determines how much calcium each has; neither by itself is as good.
Q: So Mr. Peat how do you get in 180 grams of protein per day since that milk only provides 64 grams of protein. why don't you drink 4 quarts of whole milk a day instead of 2 quarts?
A: I don’t eat, or recommend, that much protein. For years I drank a gallon per day. The calorie content of a gallon of whole milk is too much unless you are very active physically.
Q: Interesting, how much protein do you eat? I heard you recommended 150 grams minimum and personally consumed around 170 grams protein a day! shouldnt milk boost the metabolic rate to such a high extent that you can safely consume 3000 calories per day of milk and whey protein, fruit juices etc
A: There are lots of insane proposals on the internet, and that forum seems to be meeting its cuota.
Q: Asked Peat a question about a young bodybuilder dude dying at just 29 years old, died from a cancer of some sort.
A: In the US, the incidence of cancer in young people is increasing; one of the factors is probably increased vaccinations.
Q: how dangerous are these thermometers which can get your temperature without touching you? are we being dosed with radiation right on our brains and foreheads with these new touch free thermometers?
A: The skin on the forehead is a poor indicator of core body temperature. Infrared radiation is safe.
Q: random legal question regarding damages for assault
A: Monetary damages for injury are usually based on amount of disability, sometime with the addition of punitive damages. `
Q: Mr Peat what do you think about androsterone and 11 KETO dht
A: Not sufficient research to know of safety.
Q: Mr Peat I thought you have used DHT in the last year and liked using it a lot? someone was saying you mentioned the purple brand or something... or purple panda... is that all false information
A: Internet silliness.
Q: Mr Peat, next time you do the youtube podcast with Danny can you clarify your experience/thoughts on DHT as I've heard conflicting things
A: I have tried it, and experienced an effect from it, but it isn’t something I use or recommend except for extreme situations such as terminal cancer.
Q: mr Peat apparently you have talked about steroids being safer the higher up in the chain they are and riskier the lower they are. isnt DHT a very far endpoint steroid which comes after pregnenolone, dhea, testosterone, making it unsafe.
And how come youve talked about cholesterol and pregnenolone, but not squalene and lanosterol? apparently, squalene is the most ancient molecule and is the precursor to lanosterol, which is then the precursor to cholesterol. doesnt this mean squalene would be the most safest and beneficial to supplement or consume, followed by lanosterol, followed by cholesterol, and then followed by pregnenolone and dhea which many have experienced negative effects from...
A: No, I said the opposite, that the final steroids, especially cortisol, estrogen, and aldosterone can have toxic harmful effects, and that cholesterol, pregnenolone, and progesterone are safe. Squalene is very susceptible to oxidation, e.g., blackheads. The claims of the cosmetic industry are just as likely to be false as those of the drug industry.
Lipids Health Dis. 2010; 9: 141.
Clinical implications of lipid peroxidation in acne vulgaris: old wine in new bottles
Whitney P Bowecorresponding author1 and Alan C Logan2
Acne vulgaris is a common dermatological disorder, one that is frequently associated with depression, anxiety and other psychological sequelae. In recent years there has been an increasing focus on the extent to which oxidative stress is involved in the pathophysiology of acne. Emerging studies have shown that patients with acne are under increased cutaneous and systemic oxidative stress. Indeed, there are indications that lipid peroxidation itself is a match that lights an inflammatory cascade in acne. The notion that lipid peroxidation is a 'starter gun' in acne is not a new one; here we review the nearly 50-year-old lipid peroxidation theory and provide a historical perspective to the contemporary investigations and clinical implications.
In addition, we present a novel hypothesis in which lipid peroxidation may be priming an increased susceptibility to co-morbid depression and anxiety in those with acne. The emerging research on the systemic burden of oxidative stress in acne sheds further light on the brain-skin axis. The recent findings also suggest potential avenues of approach for the treatment of acne via specific nutrients, dietary modifications, oral and topical interventions.
Lipid Peroxidation and Acne - Early Research
One plausible mechanism driving the early release of inflammatory mediators is that described by the near half-century-old lipid peroxidation theory of acne. In 1965, University of Chicago investigator Allan L. Lorincz postulated that oxidative breakdown of squalene and other skin lipids may not merely be a consequence of the acne process. He suggested that lipid peroxides might be directly 'acnegenic to the skin'. Based on his theory, it was hypothesized that antioxidants would be of value in limiting and preventing the condition via reduction in the formation of peroxides and other oxidation products. In a small controlled pilot study (n = 15) he reported clinical success with topical alpha-tocopherol (0.05%) in acne after one month of evaluation by an independent examiner [14]. While there had been previous reports of clinical success with vitamins A and C [15-19], Lorincz was the first to specifically consider antioxidants to be of value in acne. The previous benefits of what would turn out to be called antioxidant vitamins and flavonoids (including an 800 mg oral vitamin C and hesperidin complex) were largely attributed to support of normal keratinization [17,18].
Further support to the lipid peroxidation hypothesis would come from University of California, Davis, scientist Alloys L. Tappel, who reported in 1975 that lipid peroxidation is evident in acne, and that localized free radical damage and peroxides might be involved in initiating the damaging inflammatory reactions [20]. Following this, other investigators reported that components of sebum, particularly squalene, show enhanced comedogenicity when oxidized [21]. Indeed, squalene was reported to be highly sensitive to oxidation and researchers reported that both squalene and its oxidized metabolites are found at much higher levels in acne vs. healthy controls [13,22-24].
Q: That is what I was saying youre saying as well Mr Peat however isnt DHT and even testosterone part of the end point steroids? pregnenolone turns to progesterone or dhea and progesterone can turn into cortisol or aldosterone while dhea can turn to testosterone which can turn to estrogen or DHT? in a stressed organism it is more likely pregnenolone will go towards cortisol and estrogen?
A: No, it just doesn’t work that way. “Can turn into" has nothing to do with how the organism works. It’s best to assume that everything on the internet is wrong—they are repeated thousands of times, on “reputable” sites, but it isn’t possible to learn anything useful by studying the great trash heap of the internet.
Q: apparently PUFAS also lower bad cholesterol.
i was wondering, what mechanism do PUFAS lower cholesterol by?
and, why is it a good thing when thyroid hormone lowers cholesterol but a bad thing when PUFA lowers cholesterol?
A: Cholesterol is converted to protective hormones in proportion to thyroid function. Cholesterol is bound inside the blood vessels, liver, brain, and other organs as a defense against PUFA toxicity.
Q: why do the PUFA lower cholesterol!
A: They cause tissue damage, and cells combine them with cholesterol (as esters) for protection, but those esters accumulate in all the tissues with aging, and stresses liberate them, causing prion diseases and other protein folding forms of degeneration.
Docosahexaenoic and eicosapentaenoic acids increase prion formation in neuronal cells
Clive Bate, Mourad Tayebi, Luisa Diomede, Mario Salmona & Alun Williams
BMC Biology volume 6, Article number: 39 (2008)
Abstract
Background
The transmissible spongiform encephalopathies, otherwise known as prion diseases, occur following the conversion of the cellular prion protein (PrPC) to an alternatively folded, disease-associated isoform (PrPSc). Recent studies suggest that this conversion occurs via a cholesterol-sensitive process, as cholesterol synthesis inhibitors reduced the formation of PrPSc and delayed the clinical phase of scrapie infection. Since polyunsaturated fatty acids also reduced cellular cholesterol levels we tested their effects on PrPSc formation in three prion-infected neuronal cell lines (ScGT1, ScN2a and SMB cells).
Results
We report that treatment with docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA) or the cholesterol synthesis inhibitor simvastatin reduced the amounts of free cholesterol in membrane extracts from prion-infected neuronal cells. Simvastatin reduced cholesterol production while DHA and EPA promoted the conversion of free cholesterol to cholesterol esters. Crucially, while simvastatin reduced PrPSc formation, both DHA and EPA significantly increased the amounts of PrPSc in these cells. Unlike simvastatin, the effects of DHA and EPA on PrPSc content were not reversed by stimulation of cholesterol synthesis with mevalonate. Treatment of ScGT1 cells with DHA and EPA also increased activation of cytoplasmic phospholipase A2 and prostaglandin E2 production. Finally, treatment of neuronal cells with DHA and EPA increased the amounts of PrPC expressed at the cell surface and significantly increased the half-life of biotinylated PrPC.
Conclusion
We report that although treatment with DHA or EPA significantly reduced the free cholesterol content of prion-infected cells they significantly increased PrPSc formation in three neuronal cell lines. DHA or EPA treatment of infected cells increased activation of phospholipase A2, a key enzyme in PrPSc formation, and altered the trafficking of PrPC. PrPC expression at the cell surface, a putative site for the PrPSc formation, was significantly increased, and the rate at which PrPC was degraded was reduced. Cholesterol depletion is seen as a potential therapeutic strategy for prion diseases. However, these results indicate that a greater understanding of the precise relationship between membrane cholesterol distribution, PrPC trafficking, cell activation and PrPSc formation is required before cholesterol manipulation can be considered as a prion therapeutic.
Bate C, Reid S, Williams A: Phospholipase A2 inhibitors or platelet activating factor antagonists prevent prion replication. J Biol Chem. 2004, 279: 36405-36411.
Am J Pathol. 2007 Dec;171(6):2000-11. doi: 10.2353/ajpath.2007.070373. Epub 2007 Nov 30.
Polyunsaturated fatty acids induce alpha-synuclein-related pathogenic changes in neuronal cells
Karen Assayag 1 , Evgenia Yakunin, Virginie Loeb, Dennis J Selkoe, Ronit Sharon
Q: Mr Peat what kind of honey do you use. do you care if its organic and raw
i heard all liquid honeys have been processed and heated that honey is solid naturally. some say solid raw honey is dangerous
A: Natural honey is liquid, but if it’s exposed to dry air for a long time it dehydrates and crystallizes; that doesn’t lower its quality.
Q: do you know if lighter or darker honey is better? do you know what kind of vitamins/minerals are present in honey? are the benefits of honey related to its sugar and antioxidants or is there something more.
A: Dark honey is more likely to be irritating. The value is mostly the concentrated sugar, but there are small amounts of antioxidant materials.
Q: sir do you think drinking bovine blood is healthy or beneficial? the same way you eat steak or bovine meats, is it good to have a high amount of blood alongside those meats. isnt the iron content of the blood balanced out by other nutrients present in the blood. dont some tribes, cultures, and even rich elites in the modern world, consume animal (or maybe human) blood for its healing and rejuvenating properties? is there some truth or factual basis to this idea of vampires existing, as in humans who feed on animal or human blood and actually remain in a good physical condition due to it despite aging in terms of years
A: The traditional Maasai diet of iron-deficient milk was supplemented by a small amount of iron-rich blood. Most common diets already have excessive iron.
There are a lot of other things I'm curious about and will maybe ask as I haven't emailed Peat for a while. Im curious of his thoughts on creatine/beta alanine supplementation, himalayan pink salt, penis enlargement/if a higher metabolism increases it's size, and a few other things.
A: Some chemicals that are very important metabolically can be disruptive when they are taken orally in inappropriate forms or combinations or amounts. For example, free ionic copper taken with food can degrade vitamins and amino acids. PQQ is probably safe, but I think much more research is needed to be sure. Most vitamin E products contain small amounts of potentially harmful impurities. The amount of aspartate in a tablet of magnesium aspartate is harmless, but it’s good to be cautious; I knew someone who began having daily seizures when he used large amounts of magnesium and calcium aspartate; his daily seizures continued for four months, and stopped the day after he discontinuted the supplements. I think there’s a risk of methyl imbalance when large amounts of betaine are used chronically.
Q: Hello, tocotrienols are unsaturated, but vitamin A is as well. I wonder if they could be helpful?
A: A small amount of tocotrienol contributes to the protective vitamin E action.
Q: Which milk brand do you prefer using Mr Peat? someone said that your favorite milk brand was discontinued. I'm wondering how they even found out your favorite milk brand!
A: At the beginning of the panic, they disappeared, but they all came back to some degree. Kirkland and Lucerne are two good brands in the pacific northwest.
^(Disclaimer on above this was last year before Peat knew about the emulsifiers/fillers in milk. I'm also unsure if he knows about the production processes of the above milks or is going by taste as I think those brands are non organic, not sure if Peat cares about certified organic milk)
Q: Do you think 1mg boron every other day is beneficial. Studies seem to show pro estrogen effects yet some studies show pro testosterone effects and yet some show pro DHT effects... the medical people are deciding whether boron is an essential nutrient but boron and vanadium are already being included in several multivitamin products.
Vanadium supposedly mimics insulin? Also what about ashwaganda? Supposedly boosts thyroid and lowers cortisol. Guggul and coleus forskoli also seem interesting.
A: I don’t think there’s good science supporting boron; vanadium is probably safe in very small amounts. I think forskilin can be dangerous, creating stress reactions.
Q: 50mg of pregnenolone supplementation (capsule form, no ingredients in capsule besides cellulose), caused 12 pounds weight gain in 10 days. This weight gain did not subside or go away even after the pregnenolone was stopped for months. All the symptoms from the pregnenolone supplementation matched high cortisol symptoms. The pregnenolone seemed to be converting entirely to cortisol and estrogen. I believe you mentioned pregnenolone doesn't have side effects but I think the studies you mentioned regarding it were done on healthy younger men, so they would likely be converting pregnenolone into the correct androgenic hormones whereas someone who has poor thyroid function likely converts the pregnenolone directly to stress hormones and estrogen?
A: There is some real junk being sold as pregnenolone, what brand was it? Real pregnenolone protects against increased cortisol, lowers cortisol it it’s abnormally high. It can lower estrogen too.
Q: How does aspirin impact muscle growth and muscle mass? there are lots of bodybuilders who have attempted to use T3 for fat burning/weight loss purposes. Many of them have advised to keep T3 doses extremely low because T3 leads to both muscle burning and wasting and fat loss, apparently T3 does not differentiate between burning muscle or fat.
What about aspirin, does aspirin also target both muscle and fat mass for fuel. since it inhibits lipolysis does that mean aspirin and niacinamide preserve fat mass while burning muscle and sugar?
A: Aspirin and T3 activate oxidative energy production, but they have to be used at a “physiological” level, which varies situationally; it’s usually around 3 mcg/hour, and bodybuilders habitually use crazy amounts.
Q: What are your thoughts on supplementing freeze dried thyroid gland, liver testicle and other beef organs, deer antler velvet extract, freeze dried oyster, krill oil, nigella sativa oil
A: I prefer, for sanitation, standard desiccated thyroid. Other dehydrated substances often contain lipid peroxides and tryptophan decomposition products.
Q: vitamin E stimulates the immune system and triggers autoimmune conditions, should intake be limited?
A: Someone just has the facts mixed up. Injecting foreign material intramuscularly damages the nervous and immune systems; many chemically active lipids have similar effects. Entering the body as a nutrient, vitamin E is antiinflammatory.
Q: these people had autoimmune conditions and said their conditions experienced flareups in response to vitamin E usage. People have had extreme immune flareups from the herb ashwagandha, from dhea, from 7 keto dhea, from pregnenolone, from higher doses of vitamin MK4 ,from iodine, and from things like yohimbe bark, Pau D arco bark, and pine bark extract/pycnogenol.
A: I don’t know of any wheat germ based vitamin E that doesn’t contain toxic amounts of polyunsaturated fats. Bacteria, fungi, and viruses stimulate the immune system; most of the published statements about stimulating the immune system are dangerous nonsense.
Q: You used to use a wheat germ vitamin E, wasnt that with polyunsaturated fats? What source of vitamim C did you use? How do you explain people having severe autoimmune responses in response to consuming some of these substances like pregnenolone or ashwagandha or vitamin e or vitamin K
A: I wrote about the polycosanol in the old vitamin E from wheat germ, but I didn’t use it myself, it had been discontinued for a long time before I got interested in it. My first experience with vitamin C was when it was called cevitamic acid, and the largest tablets available were 50 milligrams. Three years later, a new method for making vitamin C very cheaply led to 500 mg tablets becoming common. Remembering my amazing first experience with 50 mg/day, I took 500 mg, and the next morning had a sore throat and cough. That eventually led to finding, when I was working at a clinic in Eugene, that nearly all the people I saw with chronic “allergy” lost all their symptoms when they stopped their supplements. I think vitamins A and E were the last of the regular supplements that I used, and that was around 1972. I started using pregnenolone from Sigma Chemical, then got it by the kilogram from the Syntex factory in Mexico. When they stopped making it, I got a few kilos from European companies, but when they stopped making it, I found that pregnenolone from other sources produced hormonal effects that shouldn’t be pregnenolone, so I stopped using it; that was some time in the ‘90s. Pure pregnenolone never produced hormonal effects in either human or animal studies. Minor producers don’t have the resources of the giants to produce extreme purity.
Q: Hello Ray! What kind of foods do you like to eat out, which restaurants do you eat out at regularly
A: I haven’t eaten in a restaurant since 1984. Restaurants have always been notoriously unsafe places to eat, but in the age of food chemistry it has become impractical to try to identify trustworthy places.
Q: Do you know what the original 50mg vitamin C was sourced from. Most vitamin C is sourced from corn and fungus or mold. There are some manufacturers selling vitamin C extracted from berries, these capsules come in much smaller sizes of 80mg each and are extracted from amla berry acerola cherry other berries. These berry vitamin Cs are referred to as whole food vitamin C and are much more expensive
A: The vitamin C products “from natural sources” that I’ve seen contained ascorbic acid and dried plant material.
(^Disclaimer I think there are some products which use an actual freeze dried acerola cherry or amla berry mixture, which is very low like 80mg vitamin C per capsule. im not sure Ray is aware of these as theres only a few companies making these)
Q: Do you think bread is harmful in general. Like a burger a few times a week, would there be significant health effects involved due to the bun? Its the typical enriched white flour brioche bun.
A: Most people tolerate it very well.
(^Disclaimer I'm not sure if Ray is aware as there's all kinds of filler ingredients and inflammatory things in many processed bread buns these days)
Q: Mr Peat, I was also wondering, how come you never show your face/video call during your youtube podcasts/interviews?
Also, do you think masturbating to pornography would increase estrogen/cortisol and have harmful physical side effects that you do not get from sex with a live partner? or is masturbation and watching naked women a non factor when it comes to physical health?
A: My computer doesn’t have a camera or microphone; I use a landline phone; the constant technological up-dates and innovations are doing more harm than good. Just thinking about, anticipating, sex increases testosterone, makes the whiskers grow faster; general good health keeps the increased testosterone from increasing estrogen and cortisol.
Q: does milk in the us provide an excess of the nutrients vitamin A, molybdenum, and more
A: No. Occasionally, phobic ideas about nutrients circulate, including places like the raypeatforum, and milk phobia seems to be a chronic cultural problem.
Q: Also, do you think masturbating to pornography would increase estrogen/cortisol and have harmful physical side effects that you do not get from sex with a live partner? or is masturbation and watching naked women a non factor when it comes to physical health?
A: Ordinarily, just thinking about, anticipating, sex increases testosterone and well being, but in a stressed hypothyroid person it’s possible that the testosterone produced by sexual arousal could be converted to estrogen.
(^I asked him this question again as I was hoping to get a more specific answer comparing sex with a partner to masturbation. it seems he did address it)
Q: Does masturbation cause negative hormonal effects that you wouldnt get from sex with a partner? or is it the same hormonally as long as youre thinking about sex while masturbating?
also sir, what are your thoughts on supplementing with amino acids such as creatine, beta alanine, taurine, glycine? some claim beta alanine has anti diabetic effects, that creatine supplementation powerboosts the mitochondria and boosts mitochondrial function, that taurine helps excrete fluoride/maintain thyroid function in presence of fluoride, that glycine reduces tryptophan and serotonin.
but isnt it also risky supplementing individual amino acids as they could cause an imbalance in other amino acids, or other vitamins or minerals? isnt there always a risk to supplementing amino acids
A: It would be more helpful to read some physiology books instead of the internet. Almost everything there is exploitative, insane, stupid, or a blend of those.
Q: Mr Peat how much milk do you drink a day? which brand and style of milk do you use?
do you stick to whole milk only now? apparently the whole milk, has much less additives than other milks. perhaps because most whole milks only have vitamin d3 added instead of vitamin A and D. that synthetic vitamin A may be very harmful compared to natural vitamin A from milk and liver. vitamin D3 supplements are supposedly just made from sheep cholesterol exposed to UV light.
Mr Peat, how does lactose as a sugar compare to glucose and sucrose? do you think lactose is a superior sugar to glucose and sucrose. does it burn off easier etc.
A: I get it directly from farmers who don’t treat it, and then I skim it because I don’t want so much fat. Lactose promotes the absorption of calcium and probably other nutrients.
Q: Thats incredible mr Peat! do you care if the milk from your farmers is grass fed, non gmo, organic etc?
do you pasteurize the milk yourself or do you essentially drink a raw skim milk product?
thats incredible. do you think pasteurized, organic whole milk purchased from a grocery store is not safe?
A: The organic milk I have had from various supermarkets, supposedly reliable brands, has often had an unpleasant taste and soured quickly, even when pasteurized, which I think indicates poor feeding and milking techniques. Sanitary milking practices and good feed—combined hay and pasture—produce clean milk with a good taste that doesn’t need pasteurization. I often heat the milk to speed separation of the cream.
Q: mr Peat how much milk do you drink per day? do you think casein proteins are superior to whey proteins? or are both proteins equally valuable?
A: I have averaged two quarts a day for a long time. The method of separating whey from casein determines how much calcium each has; neither by itself is as good.
Q: So Mr. Peat how do you get in 180 grams of protein per day since that milk only provides 64 grams of protein. why don't you drink 4 quarts of whole milk a day instead of 2 quarts?
A: I don’t eat, or recommend, that much protein. For years I drank a gallon per day. The calorie content of a gallon of whole milk is too much unless you are very active physically.
Q: Interesting, how much protein do you eat? I heard you recommended 150 grams minimum and personally consumed around 170 grams protein a day! shouldnt milk boost the metabolic rate to such a high extent that you can safely consume 3000 calories per day of milk and whey protein, fruit juices etc
A: There are lots of insane proposals on the internet, and that forum seems to be meeting its cuota.
Q: Asked Peat a question about a young bodybuilder dude dying at just 29 years old, died from a cancer of some sort.
A: In the US, the incidence of cancer in young people is increasing; one of the factors is probably increased vaccinations.
Q: how dangerous are these thermometers which can get your temperature without touching you? are we being dosed with radiation right on our brains and foreheads with these new touch free thermometers?
A: The skin on the forehead is a poor indicator of core body temperature. Infrared radiation is safe.
Q: random legal question regarding damages for assault
A: Monetary damages for injury are usually based on amount of disability, sometime with the addition of punitive damages. `
Q: Mr Peat what do you think about androsterone and 11 KETO dht
A: Not sufficient research to know of safety.
Q: Mr Peat I thought you have used DHT in the last year and liked using it a lot? someone was saying you mentioned the purple brand or something... or purple panda... is that all false information
A: Internet silliness.
Q: Mr Peat, next time you do the youtube podcast with Danny can you clarify your experience/thoughts on DHT as I've heard conflicting things
A: I have tried it, and experienced an effect from it, but it isn’t something I use or recommend except for extreme situations such as terminal cancer.
Q: mr Peat apparently you have talked about steroids being safer the higher up in the chain they are and riskier the lower they are. isnt DHT a very far endpoint steroid which comes after pregnenolone, dhea, testosterone, making it unsafe.
And how come youve talked about cholesterol and pregnenolone, but not squalene and lanosterol? apparently, squalene is the most ancient molecule and is the precursor to lanosterol, which is then the precursor to cholesterol. doesnt this mean squalene would be the most safest and beneficial to supplement or consume, followed by lanosterol, followed by cholesterol, and then followed by pregnenolone and dhea which many have experienced negative effects from...
A: No, I said the opposite, that the final steroids, especially cortisol, estrogen, and aldosterone can have toxic harmful effects, and that cholesterol, pregnenolone, and progesterone are safe. Squalene is very susceptible to oxidation, e.g., blackheads. The claims of the cosmetic industry are just as likely to be false as those of the drug industry.
Lipids Health Dis. 2010; 9: 141.
Clinical implications of lipid peroxidation in acne vulgaris: old wine in new bottles
Whitney P Bowecorresponding author1 and Alan C Logan2
Acne vulgaris is a common dermatological disorder, one that is frequently associated with depression, anxiety and other psychological sequelae. In recent years there has been an increasing focus on the extent to which oxidative stress is involved in the pathophysiology of acne. Emerging studies have shown that patients with acne are under increased cutaneous and systemic oxidative stress. Indeed, there are indications that lipid peroxidation itself is a match that lights an inflammatory cascade in acne. The notion that lipid peroxidation is a 'starter gun' in acne is not a new one; here we review the nearly 50-year-old lipid peroxidation theory and provide a historical perspective to the contemporary investigations and clinical implications.
In addition, we present a novel hypothesis in which lipid peroxidation may be priming an increased susceptibility to co-morbid depression and anxiety in those with acne. The emerging research on the systemic burden of oxidative stress in acne sheds further light on the brain-skin axis. The recent findings also suggest potential avenues of approach for the treatment of acne via specific nutrients, dietary modifications, oral and topical interventions.
Lipid Peroxidation and Acne - Early Research
One plausible mechanism driving the early release of inflammatory mediators is that described by the near half-century-old lipid peroxidation theory of acne. In 1965, University of Chicago investigator Allan L. Lorincz postulated that oxidative breakdown of squalene and other skin lipids may not merely be a consequence of the acne process. He suggested that lipid peroxides might be directly 'acnegenic to the skin'. Based on his theory, it was hypothesized that antioxidants would be of value in limiting and preventing the condition via reduction in the formation of peroxides and other oxidation products. In a small controlled pilot study (n = 15) he reported clinical success with topical alpha-tocopherol (0.05%) in acne after one month of evaluation by an independent examiner [14]. While there had been previous reports of clinical success with vitamins A and C [15-19], Lorincz was the first to specifically consider antioxidants to be of value in acne. The previous benefits of what would turn out to be called antioxidant vitamins and flavonoids (including an 800 mg oral vitamin C and hesperidin complex) were largely attributed to support of normal keratinization [17,18].
Further support to the lipid peroxidation hypothesis would come from University of California, Davis, scientist Alloys L. Tappel, who reported in 1975 that lipid peroxidation is evident in acne, and that localized free radical damage and peroxides might be involved in initiating the damaging inflammatory reactions [20]. Following this, other investigators reported that components of sebum, particularly squalene, show enhanced comedogenicity when oxidized [21]. Indeed, squalene was reported to be highly sensitive to oxidation and researchers reported that both squalene and its oxidized metabolites are found at much higher levels in acne vs. healthy controls [13,22-24].
Q: That is what I was saying youre saying as well Mr Peat however isnt DHT and even testosterone part of the end point steroids? pregnenolone turns to progesterone or dhea and progesterone can turn into cortisol or aldosterone while dhea can turn to testosterone which can turn to estrogen or DHT? in a stressed organism it is more likely pregnenolone will go towards cortisol and estrogen?
A: No, it just doesn’t work that way. “Can turn into" has nothing to do with how the organism works. It’s best to assume that everything on the internet is wrong—they are repeated thousands of times, on “reputable” sites, but it isn’t possible to learn anything useful by studying the great trash heap of the internet.
Q: apparently PUFAS also lower bad cholesterol.
i was wondering, what mechanism do PUFAS lower cholesterol by?
and, why is it a good thing when thyroid hormone lowers cholesterol but a bad thing when PUFA lowers cholesterol?
A: Cholesterol is converted to protective hormones in proportion to thyroid function. Cholesterol is bound inside the blood vessels, liver, brain, and other organs as a defense against PUFA toxicity.
Q: why do the PUFA lower cholesterol!
A: They cause tissue damage, and cells combine them with cholesterol (as esters) for protection, but those esters accumulate in all the tissues with aging, and stresses liberate them, causing prion diseases and other protein folding forms of degeneration.
Docosahexaenoic and eicosapentaenoic acids increase prion formation in neuronal cells
Clive Bate, Mourad Tayebi, Luisa Diomede, Mario Salmona & Alun Williams
BMC Biology volume 6, Article number: 39 (2008)
Abstract
Background
The transmissible spongiform encephalopathies, otherwise known as prion diseases, occur following the conversion of the cellular prion protein (PrPC) to an alternatively folded, disease-associated isoform (PrPSc). Recent studies suggest that this conversion occurs via a cholesterol-sensitive process, as cholesterol synthesis inhibitors reduced the formation of PrPSc and delayed the clinical phase of scrapie infection. Since polyunsaturated fatty acids also reduced cellular cholesterol levels we tested their effects on PrPSc formation in three prion-infected neuronal cell lines (ScGT1, ScN2a and SMB cells).
Results
We report that treatment with docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA) or the cholesterol synthesis inhibitor simvastatin reduced the amounts of free cholesterol in membrane extracts from prion-infected neuronal cells. Simvastatin reduced cholesterol production while DHA and EPA promoted the conversion of free cholesterol to cholesterol esters. Crucially, while simvastatin reduced PrPSc formation, both DHA and EPA significantly increased the amounts of PrPSc in these cells. Unlike simvastatin, the effects of DHA and EPA on PrPSc content were not reversed by stimulation of cholesterol synthesis with mevalonate. Treatment of ScGT1 cells with DHA and EPA also increased activation of cytoplasmic phospholipase A2 and prostaglandin E2 production. Finally, treatment of neuronal cells with DHA and EPA increased the amounts of PrPC expressed at the cell surface and significantly increased the half-life of biotinylated PrPC.
Conclusion
We report that although treatment with DHA or EPA significantly reduced the free cholesterol content of prion-infected cells they significantly increased PrPSc formation in three neuronal cell lines. DHA or EPA treatment of infected cells increased activation of phospholipase A2, a key enzyme in PrPSc formation, and altered the trafficking of PrPC. PrPC expression at the cell surface, a putative site for the PrPSc formation, was significantly increased, and the rate at which PrPC was degraded was reduced. Cholesterol depletion is seen as a potential therapeutic strategy for prion diseases. However, these results indicate that a greater understanding of the precise relationship between membrane cholesterol distribution, PrPC trafficking, cell activation and PrPSc formation is required before cholesterol manipulation can be considered as a prion therapeutic.
Bate C, Reid S, Williams A: Phospholipase A2 inhibitors or platelet activating factor antagonists prevent prion replication. J Biol Chem. 2004, 279: 36405-36411.
Am J Pathol. 2007 Dec;171(6):2000-11. doi: 10.2353/ajpath.2007.070373. Epub 2007 Nov 30.
Polyunsaturated fatty acids induce alpha-synuclein-related pathogenic changes in neuronal cells
Karen Assayag 1 , Evgenia Yakunin, Virginie Loeb, Dennis J Selkoe, Ronit Sharon
Q: Mr Peat what kind of honey do you use. do you care if its organic and raw
i heard all liquid honeys have been processed and heated that honey is solid naturally. some say solid raw honey is dangerous
A: Natural honey is liquid, but if it’s exposed to dry air for a long time it dehydrates and crystallizes; that doesn’t lower its quality.
Q: do you know if lighter or darker honey is better? do you know what kind of vitamins/minerals are present in honey? are the benefits of honey related to its sugar and antioxidants or is there something more.
A: Dark honey is more likely to be irritating. The value is mostly the concentrated sugar, but there are small amounts of antioxidant materials.
Q: sir do you think drinking bovine blood is healthy or beneficial? the same way you eat steak or bovine meats, is it good to have a high amount of blood alongside those meats. isnt the iron content of the blood balanced out by other nutrients present in the blood. dont some tribes, cultures, and even rich elites in the modern world, consume animal (or maybe human) blood for its healing and rejuvenating properties? is there some truth or factual basis to this idea of vampires existing, as in humans who feed on animal or human blood and actually remain in a good physical condition due to it despite aging in terms of years
A: The traditional Maasai diet of iron-deficient milk was supplemented by a small amount of iron-rich blood. Most common diets already have excessive iron.
There are a lot of other things I'm curious about and will maybe ask as I haven't emailed Peat for a while. Im curious of his thoughts on creatine/beta alanine supplementation, himalayan pink salt, penis enlargement/if a higher metabolism increases it's size, and a few other things.
Lyla
Member
- Joined
- Mar 25, 2016
- Messages
- 41
On hypertension, calcium channel blockers, acute psychosis:
Ray: Has his vitamin D been checked? Calcium channel blockers such as nifedipine tend to increase parathyroid hormone, and high PTH is associated with aneurysms. Does he drink milk and eat cheese? Low intake of calcium relative to phosphate increases PTH. High PTH has been associated with psychological changes.
Clin Endocrinol (Oxf). 1995 Jan;42(1):9-15.
Nifedipine, but not verapamil, acutely elevates parathyroid hormone levels in premenopausal women
A G Wynne, S A Romanski, G G Klee, S J Ory, W M O'Fallon, L A Fitzpatrick
Background: Calcium channel antagonist therapy in humans has been associated with changes in anterior pituitary, thyroid and adrenal hormone secretion. Human studies assessing effects of calcium channel antagonists on calciotropic hormones have been few and typically involved small numbers of subjects studied for short periods of time. Few of these previously published studies have included women. The endocrine effects of calcium channel antagonists in women have become increasingly important as more women are taking these agents for diseases such as hypertension, angina, Raynaud's phenomenon and migraine.
Objective: To assess both acute and chronic effects of calcium channel antagonists on calciotropic hormones in women.
Design: A four-week prospective, randomized trial.
Subjects: Twenty-nine premenopausal women, randomly assigned to receive either 240 mg of sustained release verapamil or 30 mg of sustained release nifedipine daily. LABORATORY END-POINTS: Total and ionized serum calcium, phosphate, creatinine, parathyroid hormone (PTH), parathyroid hormone-related protein (PTHrP) and calcitonin, measured at baseline, after 24 hours, and 28 days of treatment.
Results: Total and ionized calcium, phosphate, creatinine, PTHrP and calcitonin levels were not altered significantly after 24 hours or 28 days in any of the subjects, when compared to baseline. There were no significant differences in PTH levels after 24 hours or 28 days of verapamil treatment. There was a significant increase in serum PTH levels after 24 hours of nifedipine therapy; however, these differences were not evident after 28 days of therapy.
Conclusions: The short-term administration of nifedipine results in increased release of parathyroid hormone; however, long-term administration has no significant effect on the concentrations of calciotropic hormones.
World Neurosurg. 2016 Apr;88:15-20.
Increased Incidence of Hypovitaminosis D Among Patients Requiring Treatment for Cerebral Aneurysms
Jian Guan, Michael Karsy 1 , Ilyas Eli 1 , Erica F Bisson 1 , Scott McNally 2 , Philipp Taussky 1 , Min S Park 3
Objective: Aneurysmal subarachnoid hemorrhage management is hampered by our incomplete understanding of what variables promote aneurysm formation, growth, and rupture. Because hypovitaminosis D has been identified as a risk factor for other vascular diseases, we examined its association with cerebral aneurysms requiring treatment.
Methods: We retrospectively reviewed charts of patients with cerebral aneurysms with recorded 25-hydroxy vitamin D levels undergoing treatment at our institution from May 2010 to May 2015. We compared these patients with a group of patients without aneurysms. We used multivariable Poisson regression and backward elimination to identify factors associated with cerebral aneurysms, with a threshold P < 0.20. A propensity-matching algorithm was used, incorporating all factors with P < 0.10 in our regression model.
Results: Patients in the aneurysm group were older than those in the control group (P = 0.001) and more likely to be female (P = 0.004), to be tobacco users (P < 0.001), and to have a diagnosis of hypertension (P = 0.001), but ethnicity, body mass index, and diabetes rates did not differ. Vitamin D levels in the aneurysm group were lower than in the control group (23.3 ± 12.3 vs. 28.7 ± 14.1 ng/mL, P = 0.001), and the patients were more likely to be vitamin D deficient (P = 0.028). Multivariable Poisson regression demonstrated that vitamin D level, tobacco use, age, and sex were significantly associated with aneurysms requiring treatment (P < 0.05). The propensity-matching algorithm confirmed a significant difference in vitamin D levels between the aneurysm and control groups (P = 0.01).
Conclusions: Patients with cerebral aneurysms requiring treatment have a significantly higher incidence of hypovitaminosis D compared with patients in a control group.
Ray: Has his vitamin D been checked? Calcium channel blockers such as nifedipine tend to increase parathyroid hormone, and high PTH is associated with aneurysms. Does he drink milk and eat cheese? Low intake of calcium relative to phosphate increases PTH. High PTH has been associated with psychological changes.
Clin Endocrinol (Oxf). 1995 Jan;42(1):9-15.
Nifedipine, but not verapamil, acutely elevates parathyroid hormone levels in premenopausal women
A G Wynne, S A Romanski, G G Klee, S J Ory, W M O'Fallon, L A Fitzpatrick
Background: Calcium channel antagonist therapy in humans has been associated with changes in anterior pituitary, thyroid and adrenal hormone secretion. Human studies assessing effects of calcium channel antagonists on calciotropic hormones have been few and typically involved small numbers of subjects studied for short periods of time. Few of these previously published studies have included women. The endocrine effects of calcium channel antagonists in women have become increasingly important as more women are taking these agents for diseases such as hypertension, angina, Raynaud's phenomenon and migraine.
Objective: To assess both acute and chronic effects of calcium channel antagonists on calciotropic hormones in women.
Design: A four-week prospective, randomized trial.
Subjects: Twenty-nine premenopausal women, randomly assigned to receive either 240 mg of sustained release verapamil or 30 mg of sustained release nifedipine daily. LABORATORY END-POINTS: Total and ionized serum calcium, phosphate, creatinine, parathyroid hormone (PTH), parathyroid hormone-related protein (PTHrP) and calcitonin, measured at baseline, after 24 hours, and 28 days of treatment.
Results: Total and ionized calcium, phosphate, creatinine, PTHrP and calcitonin levels were not altered significantly after 24 hours or 28 days in any of the subjects, when compared to baseline. There were no significant differences in PTH levels after 24 hours or 28 days of verapamil treatment. There was a significant increase in serum PTH levels after 24 hours of nifedipine therapy; however, these differences were not evident after 28 days of therapy.
Conclusions: The short-term administration of nifedipine results in increased release of parathyroid hormone; however, long-term administration has no significant effect on the concentrations of calciotropic hormones.
World Neurosurg. 2016 Apr;88:15-20.
Increased Incidence of Hypovitaminosis D Among Patients Requiring Treatment for Cerebral Aneurysms
Jian Guan, Michael Karsy 1 , Ilyas Eli 1 , Erica F Bisson 1 , Scott McNally 2 , Philipp Taussky 1 , Min S Park 3
Objective: Aneurysmal subarachnoid hemorrhage management is hampered by our incomplete understanding of what variables promote aneurysm formation, growth, and rupture. Because hypovitaminosis D has been identified as a risk factor for other vascular diseases, we examined its association with cerebral aneurysms requiring treatment.
Methods: We retrospectively reviewed charts of patients with cerebral aneurysms with recorded 25-hydroxy vitamin D levels undergoing treatment at our institution from May 2010 to May 2015. We compared these patients with a group of patients without aneurysms. We used multivariable Poisson regression and backward elimination to identify factors associated with cerebral aneurysms, with a threshold P < 0.20. A propensity-matching algorithm was used, incorporating all factors with P < 0.10 in our regression model.
Results: Patients in the aneurysm group were older than those in the control group (P = 0.001) and more likely to be female (P = 0.004), to be tobacco users (P < 0.001), and to have a diagnosis of hypertension (P = 0.001), but ethnicity, body mass index, and diabetes rates did not differ. Vitamin D levels in the aneurysm group were lower than in the control group (23.3 ± 12.3 vs. 28.7 ± 14.1 ng/mL, P = 0.001), and the patients were more likely to be vitamin D deficient (P = 0.028). Multivariable Poisson regression demonstrated that vitamin D level, tobacco use, age, and sex were significantly associated with aneurysms requiring treatment (P < 0.05). The propensity-matching algorithm confirmed a significant difference in vitamin D levels between the aneurysm and control groups (P = 0.01).
Conclusions: Patients with cerebral aneurysms requiring treatment have a significantly higher incidence of hypovitaminosis D compared with patients in a control group.
Q: Mr Peat, what your thoughts on creatine supplements?
methionine, arginine, glycine, and SAM-e/ and choline are used to make creatine endogenously.
i have heard creatine somehow boosts phosphate levels in the body too.
so im wondering your thoughts on creatine supplements.
what do you think about eating grounded up animal bones for calcium? theres new zealand grass fed bovine, ground up bone powder available online. it has calcium to phosphate in a 2 to 1 ratio and apparently these cows are organic, drug and disease and antibiotic free and purely grass fed.
i think the maasai or maybe other tribes eat bones for calcium sometimes.
what do you think about silver EMF blocking tents as well as high altitude tents? emf tents use silver to block EMF. high altitude tents someghow attempt to replicate a high altitude environment some of them use certain machines to lower the air pressure im not sure if theres side effects associated with those
A: I had a friend who got an expensive “altitude tent”; it smelled so bad she couldn’t use it. I recently heard of a 15 year old boy who was using a creatine supplement, died of heart arrest. Bone meal was a popular supplement, until a published analysis showed very high lead content. Wire nets can provide EMF shielding if they are grounded.
Q: mr Peat someone posted these quotes from your article to attempt to promote iodine/iodide usage please advise on this. Some are claiming you only have negative opinions on iodine supplementation, not on iodide supplementation, similar to how chlorine is toxic whereas chloride is beneficial and necessary.
From "The transparency of life: Cataracts as a model of age-related disease" by Ray Peat.
One of the best-known free radical scavenging substances that has been widely used as a drug is iodide. It has been used to treat asthma, parasites, syphilis, cancer, Graves’ disease, periodontal disease, and arteriosclerosis. Diseases that produce tissue overgrowth associated with inflammation--granulomas--have been treated with iodides, and although the iodide doesn’t necessarily kill the germ, it does help to break down and remove the granuloma. Leprosy and syphilis were among the diseases involving granulomas* that were treated in this way. In the case of tuberculosis, it has been suggested that iodides combine with unsaturated fatty acids which inhibit proteolytic enzymes, and thus allow for the removal of the abnormal tissue.
In experimental animals, iodide clearly delays the appearance of cataracts. (Buchberger, et al., 199l.)
Inflammation, edema, and free radical production are closely linked, and are produced by most things that interfere with energy production.
Endotoxin, produced by bacteria, mainly in the intestine, disrupts energy production, and promotes maladaptive inflammation. The wide spectrum of benefit that iodide has, especially in diseases with an inflammatory component, suggests first that it protects tissue by blocking free radical damage, but it also suggests the possibility that it might specifically protect against endotoxin.
A: If someone had leprosy, scrofula, syphilis or unexplained granulomas and couldn’t get appropriate things such as penicillin, then a short trial of iodine wouldn’t be crazy. Medical use can’t be extrapolated to chronic large doses as a nutritional supplement. Have you seen the many studies of the hamful effects on the thyroid of regular iodide supplementation?
Q: anyway some of the dudes on the forums have mentioned theres studies showing b6 supplements deplete vitamin B1. there is one or two studies claiming pyridoxine HCL inhibits activity of the active form of b6 pyridoxal 5 phosphate so some recommend using the active b6 form.
these studies always seem to come out years after the fact. as far as copper/zinc depleting each other, b6 depleting b1 etc. it seems that when you supplement evern a single vitamin or mineral, it will undoubtedly deplete or affect anothe vitamin or mineral.
in animal thyroid glands, there is T1, T2, T3, T4, calcitonin and parathyroid. when you take T4 and T3 you get something totally different. the animal thyroid gland can probably be eaten infinitely or by the pound with no ill effect. the same goes for progesterone. it probably has to be in balance with other hormones and even nutrients. why do you recommend progesterone and T3? also I have tried T3 and actually gained weight from it and noticed it burning up muscle tissue.
progesterone can apparently convert to cortisol and aldosterone especially in stressed organisms. apparently people have gained weight and had issues with it.
A: John Ioannidis’ article “Why most research findings are false” is worth reading. Things discussed on “forums” aren’t. Ordinary corporate advertising has been supplemented by the much more economical practice of hiring product reviewers to slander competing products, joining multiple forums with their "unhappy experiences."
Specific vitamin and mineral deficiencies were discovered among impoverished people living on foods that were just available sources of energy, and they are rare when people can buy the foods they want. Government agencies serve the industries that they should regulate, and shouldn’t be trusted as reliable sources of information.
In the case of my friend's kid who was dying from diarrhea, appropriate foods weren’t being given in the hospital, and the 10 mg of vitamin B6 obviously served the purpose without depleting anything.
Your sentences "progesterone can apparently convert to cortisol and aldosterone especially in stressed organisms. apparently people have gained weight and had issues with it” wouldn’t be acceptable even in an English composition class, unless “apparently” could be backed up in some way with evidence.
Q: what are your thoughts on the PROP 65 warning label. some whey protein products have that prop 65 warning which is concerning... especially since many whey products dont have that prop 65 warning
A: Have you read my article on Prop 65?
Q: do you disagree with wikipedias statement on pregnenolone "Pregnenolone (P5), or pregn-5-en-3β-ol-20-one, is an endogenous steroid and precursor/metabolic intermediate in the biosynthesis of most of the steroid hormones, including the progestogens, androgens, estrogens, glucocorticoids, and mineralocorticoids.[1] In addition, pregnenolone is biologically active in its own right, acting as a neurosteroid"?
A: Wikipedia isn’t a reliable source, but in that case their statement is accurate.
Q: Mr Peat progesterone is a precursor to aldosterone and cortisol
Mr Peat,i have tried out very high quality pregnenolone capsules from very high end expensive brands like pure encapsulations and life extension
just 50mg pregnenolone, daily for 10 days caused 12 POUNDS of weight gain which did not subside even after stopping. so i do not see how you can say pregnenolone doesnt convert to cortisol/estrogen/aldosterone, how does it cause that weight gain without converting to toxic hormones?
by the way the pregnenolone usage also shrunk my testicles and caused hair loss on the scalp. as well as a bit of a burning sensation in the thyroid. it also caused significant dry eyes.
A: Progesterone is an antagonist to aldosterone and cortisol. Experiments have shown clearly that pure pregnenolone, like pure progesterone, lowers cortisol in stressed animals with high cortisol. The price of a supplement, and the claims of its vendor, don’t have anything to do with its quality. Pure pregnenolone just doesn’t cause hormonal effects such as you mention. I haven’t recommended pregnenolone use for several years, since I started hearing about reactions that could only be caused by major impurities.
Q: Mr Peat, how do those experiments show or prove that is always the case? in chemistry charts, pregnenolone is a precursor hormone to aldosterone and cortisol the same way dhea is a precursor to testosterone/estrogen. there have been a variety of people, trying a variety of different brands of pregnenolone experiencing the side effects of hair loss, weight gain, bloating etc. how are you certain that pregnenolone cant cause such effects if even mainstream chemistry charts claim it is a precursor hormone to cortisol. additionally, nearly all pregnenolone supplements on the market are required to carry an FDA warning mentioning they could increase estrogens and cancer risks.
A: For more than 50 years, in animals and people pregnenolone didn’t have those effects. When it became "a product," dozens of little companies, with no experience in steroid production, began making it.
Water and flour are precursors of bread, but they don’t by themselves turn into bread. Chemistry charts aren’t physiology charts.
Just because a vendor puts an absurd statement on their label doesn’t mean either that it’s required or that it’s correct.
Do you consider FDA statements to be based on facts? Where can I find out about the “FDA warning”? It should be assumed that anything on the internet is false.
"Pregnenolone, DHEA, and Estriol are not active ingredients contained in any FDA-approved drug. FDA does not sanction their use in pharmacy compounding and will not exercise enforcement discretion with respect to products that contain Pregnenolone, DHEA, or Estriol." FDA Warning Letter to American Hormones, Inc. | Quackwatch
Q: i think you wrote an article comparing taurine to glycine and people take that and use it to argue that supplementing hundreds of milligrams taurine daily is helpful and recommended.
A: They misquote me. The foods I recommend, such as milk, cheese, eggs and sea foods contain taurine.
Q: Mr Peat do you recommend any foods for chromium and vitamin b6? that seems to be present in no foods at all besides raw broccoli.
whereas molybdenum, manganese, selenium, copper, zinc, and the numerous other vitamins and minerals are found in foods like coconut water, orange juice, milk, eggs, liver.
dont milk and eggs have very little taurine, like a few milligrams per serving? and if you cook or pasteurize them the amount is even less?
sir what are your thoughts on creatine and beta alanine supplementation some people promote creatine usage claiming it boosts mitochondrial function or increases their number
A: Some people promote almost anything. The foods I recommend contain chromium.
Chapter 1 Introduction: A history of chromium studies (1955–1995)John B. Vincent∗and Dontarie StallingsDepartment of Chemistry and Coalition for Biomolecular Products, The University ofAlabama, Tuscaloosa, AL 35487-0336
INTRODUCTION
While the fiftieth anniversary of the proposal that chromium (as the trivalent ion) is anessential trace element for mammals is rapidly approaching, little progress has actuallybeen made in establishing the nutritional requirement for and biochemistry of chromiumover these five decades. This is in stark contrast to the advances in knowledge of thenutritional role and biochemistry of other essential trace elements. The transition metals in the third row of the Periodic Table from vanadium to zinc (V, Cr, Mn, Fe, Co, Ni,Cu, and Zn) and also molybdenum and tungsten are generally considered to be essentialfor some form of life. Currently, for each of these transition elements except chromium,at least one metallobiomolecule has been well characterized in terms of its function, three-dimensional structure, and mode of action. In fact, whether chromium is essentialhas been questioned since it was first proposed to be essential over four decades ago;the question of essentialness is still debated openly (see Chapters 2 and 3). Certainly that such a basic question still remains unanswered is problematic.
Q: what are the amounts of chromium in foods you recommend? Mate the RDA for chromium was 120mcg for many years and recently in 2019 was downgraded to 35mcg. regardless it seems extremely difficult to get the rda. do you think the rda of 120mcg for chromium is correct or 35mcg? how would we get this amount just from liver and milk
A: The book link I sent describes the absence of science behind the claims of essentiality.
Q: mr Peat the weston a price foundation wrote an article about your views on omega 3 and omega 6 and they claim you are flawed and that omega 3/6 are essential in small amounts, as found in WAPF recommended foods... they also promote cod liver oil for its omega 3 and vitamins A D and K
A: That article was published under the name of Mary Enig, a respected lipid researcher, but people told me that she was too sick with cancer at the time to have written it. The article contained such absurdities that it amounted to defamation of Enig; if they have continued to post it, that doesn’t say much for the judgment of the managers of the website.
Q: mr Peat what do you think is a good amount of chromium to take in per day and which foods would you use to obtain it?
A: The book explains that the idea of chromium as an essential nutrient doesn’t have a clear basis in science; it has become a cult to promote the very lucrative industry.
Q: do you think supplementing creatine, beta alaniine and taurine is useful have you tried using them sir! creatine monohydrate
A: The purity of individual amino acids on the market has been a real issue, so their theoretical benefits have to be considered in relation to what’s available.
Q: hi mr Peat
apparently vitamin b6 in pyridoxine hydrochloride depletes b6 and causes issues?
do you recommend not supplementing with zinc and vitamin b6 at all?
what about supplementing magnesium?
A: I don’t recommend supplements generally, because foods can provide them, and the supplements are always contaminated to some extent in the manufacturing process. In extreme cases I have recommended a small dose of pyridoxine hydrochloride which worked immediately and very well.
Q: but theres apparently studies saying pydorizine hydchloride inhibits and depletes activity of pyridoxal 5 phosphate. people say you should only use the active form of supplement. also what cases did you suggest b6 supplementation for what was the purpose/ which foods even contain b6. it seems to not be present in any foods, at least not in high amounts to reach 2 milligrams or more daily
A: People say anything to sell their product. It’s in a wide range of foods. I’ve given small supplements for a variety of problems. The first time was a 2 year old child that had diarrhea that the hospital couldn’t control, and after 3 or 4 days they said she was within a few hours of dying; it was only at that point that the father dared to give her the supplement, and the diarrhea stopped almost immediately. My suggestion, in 1962, was based on old research. It’s effective for many problems related to the distribution of salts and water.
Q: Mr Peat
apparently you have online articles and some lines in nutrition for women where you said positive things about benefits of iodide.
youve talked about the risks of iodine in many online articles and interviews on youtube.
some are claiming you only believe iodine is bad, not iodides. they are supplementing hundreds of milligrams of potassium iodide daily and claiming that you agree with their supplement usage and you believe iodide is very beneficial and only iodine as in lugols iodine is bad.
is this true? do you think iodide can safely and beneficially be used in huge doses daily, while only iodine supplements are bad? i assumed when you used the term iodine you meant both iodine and iodide. most iodine supplements are potassium iodide just like iodized salt
A: Used occasionally as a topical antiseptic, tincture of iodine is safe. Historically iodide has been used to treat a breast infection. That’s very different from the cult of daily use of large amounts of iodide, started by Guy Abraham.
The founder of the current iodine cult, Guy Abraham, was promoting iodine along with their radiation devices to protect against electromagnetic pollution. I couldn’t decide whether he really believed those things, or just used them to sell his product.
1
Case Reports World J Nucl Med. 2012 May;11(2):79-80.
Unilateral breast uptake of tc-99m pertechnetate in a patient with cold nodule of the thyroid
Shankaramurthy Gayana 1 , Anish Bhattacharya, Koramadai Karuppusamy Kamaleshwaran, Bhagwant Rai Mittal
Free PMC article
Abstract
Common causes of unilateral breast uptake of Tc-99m pertechnetate are predominant breast-feeding on one side, mastitis, and breast cancer. Uptake of Tc-99m pertechnetate in the epithelial cells of the breast, like that of iodide, depends on the transmembrane sodium/iodide symporter (NIS), the expression of which is known to be greatly enhanced during lactation and in breast cancer. The authors present an interesting case of predominant left breast uptake of Tc-99m pertechnetate detected incidentally during thyroid scintigraphy, for the evaluation of a nodule in the left lobe of thyroid.
2
Review Rev Med Interne. 1994 Mar;15(3):190-2. doi: 10.1016/s0248-8663(05)82147-2.
[Granulomatous mastitis, erythema nodosa and oligoarthritis. Apropos of a case]
[Article in French]
J C Weber 1 , D Gros, G Blaison, T Martin, D Storck, J L Pasquali
The authors report a case of granulomatous mastitis associated with erythema nodosum and oligoarthritis. The skin and joint symptoms improved with potassium iodide. The breast lesion clinically simulated a tumor of high malignant grade. Granulomatous mastitis is a benign and rare disease. Its interest lies in the possible association with systemic manifestations and in its steroid responsiveness. This condition has been recently described as a distinct entity. When associated with systemic manifestations, sarcoidosis should be considered.
3
Case Reports J Am Vet Med Assoc. 1999 Sep 15;215(6):826-8, 796.
Actinobacillus lignieresii infection in two horses
J L Carmalt 1 , K E Baptiste, J M Chirino-Trejo
Affiliations expand
PMID: 10496138
Abstract
A 10-year-old pregnant Norwegian Fjord horse was examined for gross swelling of the muzzle of 2 years' duration. Examination of biopsy specimens revealed diffuse dermal fibrosis, micropustule formation, and vascular thrombosis; large numbers of Actinobacillus lignieresii were isolated in pure culture. Prolonged treatment with i.v. administration of sodium iodide and oral administration of trimethoprim-sulfamethoxazole caused regression of the swelling and did not induce abortion. A 5-month-old American Paint filly was examined for swelling in the udder region. Bacteriologic culture of purulent material obtained from the left teat revealed A lignieresii. Treatment with oral administration of rifampin and trimethoprim-sulfamethoxazole resulted in complete resolution of clinical signs. To the authors' knowledge, these findings represent the first report of mastitis and chronic nasal cellulitis caused by A lignieresii infection in horses.
Cited by 1 article
4
Vopr Onkol. 1964;10:67-9.
[EXPERIENCE WITH IODINE THERAPY IN MASTOPATHIES]
Q: Mr Peat im wondering if your recommendations regarding supplementation of iodine are the same as for iodide? Many people are aware of your comments regarding IodINE supplementation, but some people are claiming your comments apply only to Iodine and that you believe there are benefits to supplementing large, several milligram doses of IODIDE like potassium iodide. the logic being used is these people claim chlorine is bad chloride is essential, and similarly they claim you believe only iodine is bad whereas you like supplementing with iodide
A: No, I have never recommended several milligram doses of iodide, and I have often pointed out the damage to the thyroid gland that even moderate iodide supplements can cause:
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. [email protected]
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. [email protected]
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, [email protected].
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. [email protected]
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.
methionine, arginine, glycine, and SAM-e/ and choline are used to make creatine endogenously.
i have heard creatine somehow boosts phosphate levels in the body too.
so im wondering your thoughts on creatine supplements.
what do you think about eating grounded up animal bones for calcium? theres new zealand grass fed bovine, ground up bone powder available online. it has calcium to phosphate in a 2 to 1 ratio and apparently these cows are organic, drug and disease and antibiotic free and purely grass fed.
i think the maasai or maybe other tribes eat bones for calcium sometimes.
what do you think about silver EMF blocking tents as well as high altitude tents? emf tents use silver to block EMF. high altitude tents someghow attempt to replicate a high altitude environment some of them use certain machines to lower the air pressure im not sure if theres side effects associated with those
A: I had a friend who got an expensive “altitude tent”; it smelled so bad she couldn’t use it. I recently heard of a 15 year old boy who was using a creatine supplement, died of heart arrest. Bone meal was a popular supplement, until a published analysis showed very high lead content. Wire nets can provide EMF shielding if they are grounded.
Q: mr Peat someone posted these quotes from your article to attempt to promote iodine/iodide usage please advise on this. Some are claiming you only have negative opinions on iodine supplementation, not on iodide supplementation, similar to how chlorine is toxic whereas chloride is beneficial and necessary.
From "The transparency of life: Cataracts as a model of age-related disease" by Ray Peat.
One of the best-known free radical scavenging substances that has been widely used as a drug is iodide. It has been used to treat asthma, parasites, syphilis, cancer, Graves’ disease, periodontal disease, and arteriosclerosis. Diseases that produce tissue overgrowth associated with inflammation--granulomas--have been treated with iodides, and although the iodide doesn’t necessarily kill the germ, it does help to break down and remove the granuloma. Leprosy and syphilis were among the diseases involving granulomas* that were treated in this way. In the case of tuberculosis, it has been suggested that iodides combine with unsaturated fatty acids which inhibit proteolytic enzymes, and thus allow for the removal of the abnormal tissue.
In experimental animals, iodide clearly delays the appearance of cataracts. (Buchberger, et al., 199l.)
Inflammation, edema, and free radical production are closely linked, and are produced by most things that interfere with energy production.
Endotoxin, produced by bacteria, mainly in the intestine, disrupts energy production, and promotes maladaptive inflammation. The wide spectrum of benefit that iodide has, especially in diseases with an inflammatory component, suggests first that it protects tissue by blocking free radical damage, but it also suggests the possibility that it might specifically protect against endotoxin.
A: If someone had leprosy, scrofula, syphilis or unexplained granulomas and couldn’t get appropriate things such as penicillin, then a short trial of iodine wouldn’t be crazy. Medical use can’t be extrapolated to chronic large doses as a nutritional supplement. Have you seen the many studies of the hamful effects on the thyroid of regular iodide supplementation?
Q: anyway some of the dudes on the forums have mentioned theres studies showing b6 supplements deplete vitamin B1. there is one or two studies claiming pyridoxine HCL inhibits activity of the active form of b6 pyridoxal 5 phosphate so some recommend using the active b6 form.
these studies always seem to come out years after the fact. as far as copper/zinc depleting each other, b6 depleting b1 etc. it seems that when you supplement evern a single vitamin or mineral, it will undoubtedly deplete or affect anothe vitamin or mineral.
in animal thyroid glands, there is T1, T2, T3, T4, calcitonin and parathyroid. when you take T4 and T3 you get something totally different. the animal thyroid gland can probably be eaten infinitely or by the pound with no ill effect. the same goes for progesterone. it probably has to be in balance with other hormones and even nutrients. why do you recommend progesterone and T3? also I have tried T3 and actually gained weight from it and noticed it burning up muscle tissue.
progesterone can apparently convert to cortisol and aldosterone especially in stressed organisms. apparently people have gained weight and had issues with it.
A: John Ioannidis’ article “Why most research findings are false” is worth reading. Things discussed on “forums” aren’t. Ordinary corporate advertising has been supplemented by the much more economical practice of hiring product reviewers to slander competing products, joining multiple forums with their "unhappy experiences."
Specific vitamin and mineral deficiencies were discovered among impoverished people living on foods that were just available sources of energy, and they are rare when people can buy the foods they want. Government agencies serve the industries that they should regulate, and shouldn’t be trusted as reliable sources of information.
In the case of my friend's kid who was dying from diarrhea, appropriate foods weren’t being given in the hospital, and the 10 mg of vitamin B6 obviously served the purpose without depleting anything.
Your sentences "progesterone can apparently convert to cortisol and aldosterone especially in stressed organisms. apparently people have gained weight and had issues with it” wouldn’t be acceptable even in an English composition class, unless “apparently” could be backed up in some way with evidence.
Q: what are your thoughts on the PROP 65 warning label. some whey protein products have that prop 65 warning which is concerning... especially since many whey products dont have that prop 65 warning
A: Have you read my article on Prop 65?
Q: do you disagree with wikipedias statement on pregnenolone "Pregnenolone (P5), or pregn-5-en-3β-ol-20-one, is an endogenous steroid and precursor/metabolic intermediate in the biosynthesis of most of the steroid hormones, including the progestogens, androgens, estrogens, glucocorticoids, and mineralocorticoids.[1] In addition, pregnenolone is biologically active in its own right, acting as a neurosteroid"?
A: Wikipedia isn’t a reliable source, but in that case their statement is accurate.
Q: Mr Peat progesterone is a precursor to aldosterone and cortisol
Mr Peat,i have tried out very high quality pregnenolone capsules from very high end expensive brands like pure encapsulations and life extension
just 50mg pregnenolone, daily for 10 days caused 12 POUNDS of weight gain which did not subside even after stopping. so i do not see how you can say pregnenolone doesnt convert to cortisol/estrogen/aldosterone, how does it cause that weight gain without converting to toxic hormones?
by the way the pregnenolone usage also shrunk my testicles and caused hair loss on the scalp. as well as a bit of a burning sensation in the thyroid. it also caused significant dry eyes.
A: Progesterone is an antagonist to aldosterone and cortisol. Experiments have shown clearly that pure pregnenolone, like pure progesterone, lowers cortisol in stressed animals with high cortisol. The price of a supplement, and the claims of its vendor, don’t have anything to do with its quality. Pure pregnenolone just doesn’t cause hormonal effects such as you mention. I haven’t recommended pregnenolone use for several years, since I started hearing about reactions that could only be caused by major impurities.
Q: Mr Peat, how do those experiments show or prove that is always the case? in chemistry charts, pregnenolone is a precursor hormone to aldosterone and cortisol the same way dhea is a precursor to testosterone/estrogen. there have been a variety of people, trying a variety of different brands of pregnenolone experiencing the side effects of hair loss, weight gain, bloating etc. how are you certain that pregnenolone cant cause such effects if even mainstream chemistry charts claim it is a precursor hormone to cortisol. additionally, nearly all pregnenolone supplements on the market are required to carry an FDA warning mentioning they could increase estrogens and cancer risks.
A: For more than 50 years, in animals and people pregnenolone didn’t have those effects. When it became "a product," dozens of little companies, with no experience in steroid production, began making it.
Water and flour are precursors of bread, but they don’t by themselves turn into bread. Chemistry charts aren’t physiology charts.
Just because a vendor puts an absurd statement on their label doesn’t mean either that it’s required or that it’s correct.
Do you consider FDA statements to be based on facts? Where can I find out about the “FDA warning”? It should be assumed that anything on the internet is false.
"Pregnenolone, DHEA, and Estriol are not active ingredients contained in any FDA-approved drug. FDA does not sanction their use in pharmacy compounding and will not exercise enforcement discretion with respect to products that contain Pregnenolone, DHEA, or Estriol." FDA Warning Letter to American Hormones, Inc. | Quackwatch
Q: i think you wrote an article comparing taurine to glycine and people take that and use it to argue that supplementing hundreds of milligrams taurine daily is helpful and recommended.
A: They misquote me. The foods I recommend, such as milk, cheese, eggs and sea foods contain taurine.
Q: Mr Peat do you recommend any foods for chromium and vitamin b6? that seems to be present in no foods at all besides raw broccoli.
whereas molybdenum, manganese, selenium, copper, zinc, and the numerous other vitamins and minerals are found in foods like coconut water, orange juice, milk, eggs, liver.
dont milk and eggs have very little taurine, like a few milligrams per serving? and if you cook or pasteurize them the amount is even less?
sir what are your thoughts on creatine and beta alanine supplementation some people promote creatine usage claiming it boosts mitochondrial function or increases their number
A: Some people promote almost anything. The foods I recommend contain chromium.
Chapter 1 Introduction: A history of chromium studies (1955–1995)John B. Vincent∗and Dontarie StallingsDepartment of Chemistry and Coalition for Biomolecular Products, The University ofAlabama, Tuscaloosa, AL 35487-0336
INTRODUCTION
While the fiftieth anniversary of the proposal that chromium (as the trivalent ion) is anessential trace element for mammals is rapidly approaching, little progress has actuallybeen made in establishing the nutritional requirement for and biochemistry of chromiumover these five decades. This is in stark contrast to the advances in knowledge of thenutritional role and biochemistry of other essential trace elements. The transition metals in the third row of the Periodic Table from vanadium to zinc (V, Cr, Mn, Fe, Co, Ni,Cu, and Zn) and also molybdenum and tungsten are generally considered to be essentialfor some form of life. Currently, for each of these transition elements except chromium,at least one metallobiomolecule has been well characterized in terms of its function, three-dimensional structure, and mode of action. In fact, whether chromium is essentialhas been questioned since it was first proposed to be essential over four decades ago;the question of essentialness is still debated openly (see Chapters 2 and 3). Certainly that such a basic question still remains unanswered is problematic.
Q: what are the amounts of chromium in foods you recommend? Mate the RDA for chromium was 120mcg for many years and recently in 2019 was downgraded to 35mcg. regardless it seems extremely difficult to get the rda. do you think the rda of 120mcg for chromium is correct or 35mcg? how would we get this amount just from liver and milk
A: The book link I sent describes the absence of science behind the claims of essentiality.
Q: mr Peat the weston a price foundation wrote an article about your views on omega 3 and omega 6 and they claim you are flawed and that omega 3/6 are essential in small amounts, as found in WAPF recommended foods... they also promote cod liver oil for its omega 3 and vitamins A D and K
A: That article was published under the name of Mary Enig, a respected lipid researcher, but people told me that she was too sick with cancer at the time to have written it. The article contained such absurdities that it amounted to defamation of Enig; if they have continued to post it, that doesn’t say much for the judgment of the managers of the website.
Q: mr Peat what do you think is a good amount of chromium to take in per day and which foods would you use to obtain it?
A: The book explains that the idea of chromium as an essential nutrient doesn’t have a clear basis in science; it has become a cult to promote the very lucrative industry.
Q: do you think supplementing creatine, beta alaniine and taurine is useful have you tried using them sir! creatine monohydrate
A: The purity of individual amino acids on the market has been a real issue, so their theoretical benefits have to be considered in relation to what’s available.
Q: hi mr Peat
apparently vitamin b6 in pyridoxine hydrochloride depletes b6 and causes issues?
do you recommend not supplementing with zinc and vitamin b6 at all?
what about supplementing magnesium?
A: I don’t recommend supplements generally, because foods can provide them, and the supplements are always contaminated to some extent in the manufacturing process. In extreme cases I have recommended a small dose of pyridoxine hydrochloride which worked immediately and very well.
Q: but theres apparently studies saying pydorizine hydchloride inhibits and depletes activity of pyridoxal 5 phosphate. people say you should only use the active form of supplement. also what cases did you suggest b6 supplementation for what was the purpose/ which foods even contain b6. it seems to not be present in any foods, at least not in high amounts to reach 2 milligrams or more daily
A: People say anything to sell their product. It’s in a wide range of foods. I’ve given small supplements for a variety of problems. The first time was a 2 year old child that had diarrhea that the hospital couldn’t control, and after 3 or 4 days they said she was within a few hours of dying; it was only at that point that the father dared to give her the supplement, and the diarrhea stopped almost immediately. My suggestion, in 1962, was based on old research. It’s effective for many problems related to the distribution of salts and water.
Q: Mr Peat
apparently you have online articles and some lines in nutrition for women where you said positive things about benefits of iodide.
youve talked about the risks of iodine in many online articles and interviews on youtube.
some are claiming you only believe iodine is bad, not iodides. they are supplementing hundreds of milligrams of potassium iodide daily and claiming that you agree with their supplement usage and you believe iodide is very beneficial and only iodine as in lugols iodine is bad.
is this true? do you think iodide can safely and beneficially be used in huge doses daily, while only iodine supplements are bad? i assumed when you used the term iodine you meant both iodine and iodide. most iodine supplements are potassium iodide just like iodized salt
A: Used occasionally as a topical antiseptic, tincture of iodine is safe. Historically iodide has been used to treat a breast infection. That’s very different from the cult of daily use of large amounts of iodide, started by Guy Abraham.
The founder of the current iodine cult, Guy Abraham, was promoting iodine along with their radiation devices to protect against electromagnetic pollution. I couldn’t decide whether he really believed those things, or just used them to sell his product.
1
Case Reports World J Nucl Med. 2012 May;11(2):79-80.
Unilateral breast uptake of tc-99m pertechnetate in a patient with cold nodule of the thyroid
Shankaramurthy Gayana 1 , Anish Bhattacharya, Koramadai Karuppusamy Kamaleshwaran, Bhagwant Rai Mittal
Free PMC article
Abstract
Common causes of unilateral breast uptake of Tc-99m pertechnetate are predominant breast-feeding on one side, mastitis, and breast cancer. Uptake of Tc-99m pertechnetate in the epithelial cells of the breast, like that of iodide, depends on the transmembrane sodium/iodide symporter (NIS), the expression of which is known to be greatly enhanced during lactation and in breast cancer. The authors present an interesting case of predominant left breast uptake of Tc-99m pertechnetate detected incidentally during thyroid scintigraphy, for the evaluation of a nodule in the left lobe of thyroid.
2
Review Rev Med Interne. 1994 Mar;15(3):190-2. doi: 10.1016/s0248-8663(05)82147-2.
[Granulomatous mastitis, erythema nodosa and oligoarthritis. Apropos of a case]
[Article in French]
J C Weber 1 , D Gros, G Blaison, T Martin, D Storck, J L Pasquali
The authors report a case of granulomatous mastitis associated with erythema nodosum and oligoarthritis. The skin and joint symptoms improved with potassium iodide. The breast lesion clinically simulated a tumor of high malignant grade. Granulomatous mastitis is a benign and rare disease. Its interest lies in the possible association with systemic manifestations and in its steroid responsiveness. This condition has been recently described as a distinct entity. When associated with systemic manifestations, sarcoidosis should be considered.
3
Case Reports J Am Vet Med Assoc. 1999 Sep 15;215(6):826-8, 796.
Actinobacillus lignieresii infection in two horses
J L Carmalt 1 , K E Baptiste, J M Chirino-Trejo
Affiliations expand
PMID: 10496138
Abstract
A 10-year-old pregnant Norwegian Fjord horse was examined for gross swelling of the muzzle of 2 years' duration. Examination of biopsy specimens revealed diffuse dermal fibrosis, micropustule formation, and vascular thrombosis; large numbers of Actinobacillus lignieresii were isolated in pure culture. Prolonged treatment with i.v. administration of sodium iodide and oral administration of trimethoprim-sulfamethoxazole caused regression of the swelling and did not induce abortion. A 5-month-old American Paint filly was examined for swelling in the udder region. Bacteriologic culture of purulent material obtained from the left teat revealed A lignieresii. Treatment with oral administration of rifampin and trimethoprim-sulfamethoxazole resulted in complete resolution of clinical signs. To the authors' knowledge, these findings represent the first report of mastitis and chronic nasal cellulitis caused by A lignieresii infection in horses.
Cited by 1 article
4
Vopr Onkol. 1964;10:67-9.
[EXPERIENCE WITH IODINE THERAPY IN MASTOPATHIES]
Q: Mr Peat im wondering if your recommendations regarding supplementation of iodine are the same as for iodide? Many people are aware of your comments regarding IodINE supplementation, but some people are claiming your comments apply only to Iodine and that you believe there are benefits to supplementing large, several milligram doses of IODIDE like potassium iodide. the logic being used is these people claim chlorine is bad chloride is essential, and similarly they claim you believe only iodine is bad whereas you like supplementing with iodide
A: No, I have never recommended several milligram doses of iodide, and I have often pointed out the damage to the thyroid gland that even moderate iodide supplements can cause:
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. [email protected]
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. [email protected]
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, [email protected].
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. [email protected]
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.
Q: One of the bigger milk brands organic brands showed me the ingredients list of the actual vitamin mix they add to the milk... and it contains those vitamins PLUS polyethylene glycol PLUS polysorbate 80. These companies said they dont need to list those filler ingredients in the vitamin mixes because theyre a small amount of the ingredients overall.
A: Thanks, that’s very important to know; I asked several milk organizations about the vitamin solvents and they claimed they weren’t there, or they just didn’t answer
Q: isnt supplementing with niacinamide and taurine not safe? These amino acids and vitamins are often synthesized using dangerous chemicals and solvents, moreover isnt it simply straight up unphysiological to just supplement hundreds of milligrams niacinamide or taurine when there is no food source not even liver which would provide an isolated amino acid like taurine or isolated high doses of b vitamins like niacinamide?
A: Any synthesized nutrient frequently causes problems, that’s why I don’t recommend them as nutrients. Sometimes, for occasional use, the drug effect can outweigh the harm of the impurities.
Q: mr Peat I was wondering how do you deal with drinking 1% or 2% milks in the usa? Considering they all have significant amounts of added vitamin A. Doesnt that provide excessive vitamin A especially when youre drinking a gallon of milk a day, or do you limit your intake of milk in order to avoid the added vitamins?
Have you looked into whey protein powder? Is whey protein powder made from raw whole milk, or is it made from pasteurized milks with the added vitamins? If the whey protein powder is made from milk that does not have any added vitamins in it, should we look into getting our protein needs mostly from a good grass fed whey protein product, and limiting milk consumption
A: I don’t think there’s a risk of too much vitamin A from a gallon; the emulsifier risk is from allergic reactions. Dehydration causes some oxidative damage to cystein and tryptophane, at least.
Q: But a gallon of milk would contain about 9600 IU vitamin A palmitate? Additional liver, cheese, etc could even add more to that.
A: Very large amounts of vitamin A can interfere with thyroid functions, and with a vitamin E deficiency it can autooxidize, but that only happens with doses of 100s of thousands of units. The allergenicity of things like PEG and polysorbate decreases as their profitability rises, along with industry bribes to the regulatory agencies. This corruption goes back to the 1940s and the rise of the giant “food” industries.
JANUARY 29, 2019
www.advisory.com
To diagnose his near-fatal allergy attacks, this patient became 'Sherlock Holmes.' (And he found the culprit.)
Daily Briefing
To diagnose his near-fatal allergy attacks, this p...
When a man with no known allergies experienced two near-fatal anaphylactic reactions, he turned detective to unearth what caused the allergic reactions that almost killed him, Lisa Sanders writes for the New York Times Magazine.
A near-fatal incident
The man "had never had any allergies—except, according to his parents, some trouble with penicillin when he was a child." But that changed when he was receiving treatment for arthritis in his neck. Physical therapy wasn't helping with the arthritic pain, so the man's doctor suggested a steroid injection into the spinal area to reduce inflammation.
The shot itself was not painful, according to Sanders, but when the man stood up, he felt warm. "His hair was drenched in sweat. He felt pins and needles all over his body ... his arms and hands were covered by angry red welts," Sanders writes. Before the man blacked out, he felt the "quick sting" of an epinephrine shot in his thigh.
In the ED, he was given more epinephrine and IV fluids. Doctors said he was allergic to the steroid medication. But Sanders writes that diagnosis "didn't make sense" because "[t]he body is naturally awash with steroid hormones."
The experience left the man "wary" of unfamiliar medications, Sanders writes. But it wasn't until two years that he experienced his second, nearly fatal reaction: Minutes after swallowing a laxative for a colonoscopy, the man's "mouth started to itch and the strange pins-and-needles feeling that preceded the welts started." He took a dose of Benadryl, which helped subdue his symptoms.
The man contacted his doctor and requested a different laxative to prepare for the colonoscopy. The man was "relieved" to see that the next laxative had a different name and was made by a different manufacturer, Sanders writes. He drank a glass of the medication, and soon felt the sweating, welts, and pins and needles returning—and this time, Benadryl didn't help.
The man's wife heard a loud crash throughout the house, and she discovered her husband on the floor. His "face was swollen ... his eyes were open but unseeing," and "a strange gurgling noise emanated from his open mouth," Sanders writes.
When E.M.T.s arrived, the man's blood pressure was so low it couldn't be detected, and his trachea was "dangerously narrowed" by swollen tissue. "When he opened his eyes, he heard the E.M.T.s discussing whether they would need to cut a hole in his airway," Sanders writes, "But his breathing improved, and he was once again hustled to the [ED] by ambulance." The man was taken to the Williamson Medical Center, where he was given more epinephrine and IV fluids, and was discharged after a few hours.
The sleuthing begins
The man wanted to get to the bottom of his mysterious, life-threatening allergy. "He was allergic to something that nearly killed him," Sanders writes, but he didn't know what it was.
The man scheduled an appointment at Vanderbilt's allergy clinic, but the next available slot was weeks away. So he decided to take matters into his own hands.
His first step was to learn what medications has triggered his allergic reactions. From the first doctor, he learned he'd been given a steroid medicine called Depo-Medrol. Through some internet sleuthing, he learned the name of the laxative that had caused his anaphylaxis, GaviLyte-C, and the one that caused the milder reaction, MoviPrep. All three products had two ingredients in common: sodium chloride and polyethylene glycol (PEG).
The man "ate a lot of salt," so he ruled that out as the culprit causing his allergic reaction, Sanders writes. However, the man was not familiar with PEG, which turned out to be "an inert chemical" used as a filler and lubricant in hand lotions, pills, and gel caps, as well as steroids and laxatives.
At his appointment with Cosby Stone, a physician at Vanderbilt who specializes in allergic reactions to medication, the man said, "I'm not trying to tell you how to do your job or anything ... but I'm pretty sure I'm allergic to PEG."
When the man told the doctor his story, "Stone was amazed," Sanders writes, adding, "Few patients come in linking an allergy to such an obscure product."
Stone discussed the case with an adviser, Elizabeth Phillips, to determine whether PEG could be behind the man's severe allergic reactions.
The doctors found evidence of similar cases when reviewing literature. "They returned to the room and congratulated the man on his sleuthing abilities," Sanders writes.
The mystery is solved
For the next few weeks, the doctors set out to prove that PEG was causing the man's anaphylaxis.
After testing, they found that the man had a "severe allergy to PEG" and polysorbate 80, one of PEG's "chemical cousins," Sanders writes. The allergy most likely developed because the man was often exposed to industrial PEG at his job at the regional power company. For "genetically predisposed individuals, … repeated exposure can lead to an allergic reaction," Sanders writes.
The doctors advised the man to perform a thorough inspection of the ingredients of unfamiliar products or drugs before using them, and told him to get a medical alert bracelet that could alert others of his allergy. The doctors warned him that "the chemical is everywhere," Sanders writes.
A: Thanks, that’s very important to know; I asked several milk organizations about the vitamin solvents and they claimed they weren’t there, or they just didn’t answer
Q: isnt supplementing with niacinamide and taurine not safe? These amino acids and vitamins are often synthesized using dangerous chemicals and solvents, moreover isnt it simply straight up unphysiological to just supplement hundreds of milligrams niacinamide or taurine when there is no food source not even liver which would provide an isolated amino acid like taurine or isolated high doses of b vitamins like niacinamide?
A: Any synthesized nutrient frequently causes problems, that’s why I don’t recommend them as nutrients. Sometimes, for occasional use, the drug effect can outweigh the harm of the impurities.
Q: mr Peat I was wondering how do you deal with drinking 1% or 2% milks in the usa? Considering they all have significant amounts of added vitamin A. Doesnt that provide excessive vitamin A especially when youre drinking a gallon of milk a day, or do you limit your intake of milk in order to avoid the added vitamins?
Have you looked into whey protein powder? Is whey protein powder made from raw whole milk, or is it made from pasteurized milks with the added vitamins? If the whey protein powder is made from milk that does not have any added vitamins in it, should we look into getting our protein needs mostly from a good grass fed whey protein product, and limiting milk consumption
A: I don’t think there’s a risk of too much vitamin A from a gallon; the emulsifier risk is from allergic reactions. Dehydration causes some oxidative damage to cystein and tryptophane, at least.
Q: But a gallon of milk would contain about 9600 IU vitamin A palmitate? Additional liver, cheese, etc could even add more to that.
A: Very large amounts of vitamin A can interfere with thyroid functions, and with a vitamin E deficiency it can autooxidize, but that only happens with doses of 100s of thousands of units. The allergenicity of things like PEG and polysorbate decreases as their profitability rises, along with industry bribes to the regulatory agencies. This corruption goes back to the 1940s and the rise of the giant “food” industries.
JANUARY 29, 2019
To diagnose his near-fatal allergy attacks, this patient became 'Sherlock Holmes.' (And he found the culprit.)
When a man with no known allergies experienced two near-fatal anaphylactic reactions, he turned detective to unearth what caused the allergic reactions that almost killed him, Lisa Sanders writes for the New York Times Magazine.
www.advisory.com
Daily Briefing
To diagnose his near-fatal allergy attacks, this p...
When a man with no known allergies experienced two near-fatal anaphylactic reactions, he turned detective to unearth what caused the allergic reactions that almost killed him, Lisa Sanders writes for the New York Times Magazine.
A near-fatal incident
The man "had never had any allergies—except, according to his parents, some trouble with penicillin when he was a child." But that changed when he was receiving treatment for arthritis in his neck. Physical therapy wasn't helping with the arthritic pain, so the man's doctor suggested a steroid injection into the spinal area to reduce inflammation.
The shot itself was not painful, according to Sanders, but when the man stood up, he felt warm. "His hair was drenched in sweat. He felt pins and needles all over his body ... his arms and hands were covered by angry red welts," Sanders writes. Before the man blacked out, he felt the "quick sting" of an epinephrine shot in his thigh.
In the ED, he was given more epinephrine and IV fluids. Doctors said he was allergic to the steroid medication. But Sanders writes that diagnosis "didn't make sense" because "[t]he body is naturally awash with steroid hormones."
The experience left the man "wary" of unfamiliar medications, Sanders writes. But it wasn't until two years that he experienced his second, nearly fatal reaction: Minutes after swallowing a laxative for a colonoscopy, the man's "mouth started to itch and the strange pins-and-needles feeling that preceded the welts started." He took a dose of Benadryl, which helped subdue his symptoms.
The man contacted his doctor and requested a different laxative to prepare for the colonoscopy. The man was "relieved" to see that the next laxative had a different name and was made by a different manufacturer, Sanders writes. He drank a glass of the medication, and soon felt the sweating, welts, and pins and needles returning—and this time, Benadryl didn't help.
The man's wife heard a loud crash throughout the house, and she discovered her husband on the floor. His "face was swollen ... his eyes were open but unseeing," and "a strange gurgling noise emanated from his open mouth," Sanders writes.
When E.M.T.s arrived, the man's blood pressure was so low it couldn't be detected, and his trachea was "dangerously narrowed" by swollen tissue. "When he opened his eyes, he heard the E.M.T.s discussing whether they would need to cut a hole in his airway," Sanders writes, "But his breathing improved, and he was once again hustled to the [ED] by ambulance." The man was taken to the Williamson Medical Center, where he was given more epinephrine and IV fluids, and was discharged after a few hours.
The sleuthing begins
The man wanted to get to the bottom of his mysterious, life-threatening allergy. "He was allergic to something that nearly killed him," Sanders writes, but he didn't know what it was.
The man scheduled an appointment at Vanderbilt's allergy clinic, but the next available slot was weeks away. So he decided to take matters into his own hands.
His first step was to learn what medications has triggered his allergic reactions. From the first doctor, he learned he'd been given a steroid medicine called Depo-Medrol. Through some internet sleuthing, he learned the name of the laxative that had caused his anaphylaxis, GaviLyte-C, and the one that caused the milder reaction, MoviPrep. All three products had two ingredients in common: sodium chloride and polyethylene glycol (PEG).
The man "ate a lot of salt," so he ruled that out as the culprit causing his allergic reaction, Sanders writes. However, the man was not familiar with PEG, which turned out to be "an inert chemical" used as a filler and lubricant in hand lotions, pills, and gel caps, as well as steroids and laxatives.
At his appointment with Cosby Stone, a physician at Vanderbilt who specializes in allergic reactions to medication, the man said, "I'm not trying to tell you how to do your job or anything ... but I'm pretty sure I'm allergic to PEG."
When the man told the doctor his story, "Stone was amazed," Sanders writes, adding, "Few patients come in linking an allergy to such an obscure product."
Stone discussed the case with an adviser, Elizabeth Phillips, to determine whether PEG could be behind the man's severe allergic reactions.
The doctors found evidence of similar cases when reviewing literature. "They returned to the room and congratulated the man on his sleuthing abilities," Sanders writes.
The mystery is solved
For the next few weeks, the doctors set out to prove that PEG was causing the man's anaphylaxis.
After testing, they found that the man had a "severe allergy to PEG" and polysorbate 80, one of PEG's "chemical cousins," Sanders writes. The allergy most likely developed because the man was often exposed to industrial PEG at his job at the regional power company. For "genetically predisposed individuals, … repeated exposure can lead to an allergic reaction," Sanders writes.
The doctors advised the man to perform a thorough inspection of the ingredients of unfamiliar products or drugs before using them, and told him to get a medical alert bracelet that could alert others of his allergy. The doctors warned him that "the chemical is everywhere," Sanders writes.
joshquintanilla
Member
- Joined
- Oct 13, 2019
- Messages
- 140
Q:
What are your thoughts on the idea of wearing orange lenses the entire day? Would this be more beneficial than just wearing after sunset? Thank you!
A:
It might make a difference in the risk of cataracts and other eye aging effects.
What are your thoughts on the idea of wearing orange lenses the entire day? Would this be more beneficial than just wearing after sunset? Thank you!
A:
It might make a difference in the risk of cataracts and other eye aging effects.
Me: How come the left is so willing to accept mainstream, corporate viewpoints?
Ray:
I think the way to interpret it is that the real left, starting in the 1940s, has been disappeared, and in its absence, the antiwar, anti-imperialist humane issues of the paleoconservatives have become more conspicuous, but without any foundation for effectiveness. In place of the union-based left, the “new left” was created by the agencies that neutered the unions. In the late 1960s there were people like Martin L. King who were reconnecting unionism with antiimperialism, but the outcome was to intensify the promotion of the pseudo-left, new left, issues. Racial “equality," disconnected from the class system and from reality, became a tool of the CIA-FBI. The Democratic party cooperates in keeping potential left activists completely out of the system.
The Pied Piper: Allard K. Lowenstein and the Liberal Dream by Richard Cummings
Ray:
I think the way to interpret it is that the real left, starting in the 1940s, has been disappeared, and in its absence, the antiwar, anti-imperialist humane issues of the paleoconservatives have become more conspicuous, but without any foundation for effectiveness. In place of the union-based left, the “new left” was created by the agencies that neutered the unions. In the late 1960s there were people like Martin L. King who were reconnecting unionism with antiimperialism, but the outcome was to intensify the promotion of the pseudo-left, new left, issues. Racial “equality," disconnected from the class system and from reality, became a tool of the CIA-FBI. The Democratic party cooperates in keeping potential left activists completely out of the system.
The Pied Piper: Allard K. Lowenstein and the Liberal Dream by Richard Cummings
EMF Mitigation - Flush Niacin - Big 5 Minerals
