I was surprised to learn that thyroid urine testing which assesses thyroid levels over 24hr period gives a more representative pic of your situation over the day(rather than blood test which is a 'snapshot' test.Thyroid levels fluctuate freq during the day,so levels may be temporarily normal when having blood test).Urine test also gives u an idea of amount if hormones actually used by your cells rather than the amount just swilling around waiting to be used;in ur blood.
How come i never read about this anywhere else;or heard it mentioned on here even?!
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I am not sure whether it tells you what is happening at cellular level though, but it seems it is more sensitive than other tests. It is certainly expensive at £146.
I really cannot say if it will be beneficial to someone whose GP refuses to diagnose on the basis of blood tests, though, since he/she would likely reject a 24hr urine test.
Sorry, but I think it's bunkum. Not only is output dependent on kidney function but the excreted substances aren't T4 or T3 alone, but a collection of products of all sorts. The body is very good at both preserving T4 and T3 and recycles the iodine from breakdown products back to the thyroid to produce more T4 and T3. Also T4 does not fluctuate significantly over the day and T3 only slightly.
Whatever you take if it is in "quick response" form whether it is T4 alone, NDT or T3, you will have a fluctuation in your blood values. The penalty for taking Armour or and T3 in any form is that the short halflife of the T3 part (half of a dose gone in 24 hours) makes you more likely to have bigger T3 peaks and troughs rather than T4 ones. This means that your average through the day should be made correct for you, but the potential problem encourages taking smaller doses at regular intervals to minimize the variations. T3 is a dangerous potent hormone and must be treated with respect, otherwise things like heart fibrillation and the danger of stroke/heart attack are increased. Ideally I'd like NDT to be in a slow release format if it is to be used at all. But do realize that whatever you take, T4 alone or NDT, it's by definition a "one size fits all" dosage as regards trying to find the ratio of T4 and T3 that is uniquely right for you. Extra T4 or T3 might be needed to make up your unique situation. Going on to the problem of urinary measurement. There are lots of papers showing it is not a good measure of T4/3 content in the blood - if only because your output of T4/3 in urine fluctuates a lot throughout the day, whereas the underlying FT4/3 in your blood is virtually constant. There's no guarantee that the 24 hour urine output is a realistic measure of the blood levels if they themselves are not changing. There's also the problem of kidney function - someone with a weaker system may pour out lots more T4/3. Another indication of problems is that pregnant womens' urinary T4/3 output is quite different from nonpregnant, even if they are well. The pill can have an effect through the oestrogen content. I have a good number of publications to demonstrate the problems.
Why do you say T3 is dangerous? I can not tolerate T4 in any form, so it has to be T3 on it's own. I am aware that it is very strong and like any medication can have problems if not used correctly. However saying that Dr John C Lowe had the opposite opinion saying that T4 is a no no. I have also read that the Urine test is better than the blood tests, I will be doing one next week, so I will no if it shows up more than the blood test.. We are all desparately trying to get better, their is too much difference in opinion in what is good and what isn't. Things are miserable as they are without Docs filling our heads with T3 or HC is dangerous.
T3 is a dangerous hormone to take lightly because of its fast powerful action and its short lifetime. In nature, humans with normal function produce 5 times as much T4 as T3 from their thyroids. The T4 is then converted to more T3 in the tissues. We have developed this safeguard of producing a rather inactive prohormone T4 to avoid overproducing T3 – T4/T3 conversion only happens as fast as the cells need it and no faster. There must be a genetically selective reason for this arrangement. When you take T3 alone you are theoretically opening yourself to rapid and for some people unpleasant (and life threatening) effects because you are NOT controlling your T3 uptake like the normal body and thyroid gland does. You don’t have the milder T4 reserve to control T3 production. This does not mean you can’t use T3, but the obligations on you to be more careful than when taking T4 are clear. I do not agree with Dr Lowe about T4 monotherapy – for the majority of people it works well, but by no means all. Sheer facts on the ground refute his position if that is what it is. I’d like as I say slow release T3 to be used because at least you aren’t then getting regular ups and downs in blood levels nad there’s more control. Regarding urinary T4/3: here are a selection of paper references casting doubt on its value:
1) J. F. Finucane Random urine tests in the assessment of thyroid function
Irish Journal of Medical Science December 1976, Volume 145, Issue 1, pp 195-200.
2) Shakespear RA, Burke CW.
.
Triiodothyronine and thyroxine in urine. I. Measurement and application
J Clin Endocrinol Metab. 1976 Mar;42(3):494-503
3) Wiersinga WM, Fliers E.
Ned Tijdschr Geneeskd. 2007 Dec 22;151(51):2813-2815.
[Determining the thyroid hormones T3 and T4 in the urine: an unreliable test for hypothyroidism]. [Article in Dutch]
4) Changes in renal tri-iodothyronine and thyroxine handling
during fasting
Edgar J Rolleman1,2, Georg Hennemann1, Hans van Toor1, Christian H H Schoenmakers3, Eric P Krenning1,2 and Marion de Jong2
European Journal of Endocrinology (2000) 142 125–130 ISSN 0804
Perhaps we should take a survey. As you mention, it is fast acting, if you want to call twelve hours fast, but that also makes it easy to recognize and stop or reduce dosing if necessary.
Diogenes,can i just ask,are u a med professional?Also,pointing out that some people dont convert t4 to t3 well and so only feel well on t3 med..of course.
Perhaps the very invention of these tests has caused such a lot of controversy?Perhaps the old fashioned ways of diagnosis by symptoms and appearance of the person, both physical and mental, were the best method! I believe that only time will tell as it seems that each person is so unique that no reference range could possibly suit all.
each to their own, my 180mcg daily dose of T3 works 'wonders' for me, my cholesterol is down to normal, my bone density has improved so much my endo is 'gobsmacked', my ECGs/echocardiography are spotless and healthy, my life is now worth living. On small divided doses of T3 I am as good as a rotten egg and get all sorts of problems creeping up, The Dr Lowe way certainly is the 'only' way for me to be healthy
My endocrinologist realises that some people, like me, need the addition of T3. He did indeed remark that slow release T3 needs to be 'invented'-I believe trials are ongoing in the US for such a tablet.I'm sure all of us on here would rather not be put in a position in which we might have a stroke or heart attack due to our medication. Conversely, inadequately treated hypothyroidism has many dangerous risks.So we have to do the best we can in order to get through life with as few symptoms possible. Are you a sufferer of hypothyroidism ?
Yes I have sympathy for the minority of people who can't tolerate T4 therapy. It's a tricky situation that you have to control much more closely. You would find it difficult to overdose by one big swallow of excess T4, your body would excrete most of it unchanged. Kids have swallowed their mother's pills in large quantity and got away with it. T3 is another matter althogether. Yes I have knowledge of practical hypothyroidism. My wife is a Hashimoto's sufferer from 45 years ago when her thyroid was destroyed. Luckily T4 only has been OK, but it results in high normal FT4 and undetectable TSH. We've educated our GP to admit this does not matter and only now in her 70's are the expected problems of periodic atrial fibrillation kicking in. They were expected and she was told this from the outset. What we don't do is to return hypothyroid people back to their FT4/3 levels when they were OK - simply because we don't know what they were. If only a scheme could be set up to take blood from each healthy 20 year old, get FT4 and FT3 and archive the results for them to be viewed and restored later by suitable therapy when disease strikes.
If I were to take too much T4 I might realise four days later that something was amiss. The effects would last longer. I am on T3 and I can quickly realise that if I am a little overdosed, I rest until the sensation passes and then I make a note and take a little less the next day.
Slow-release T3 has not been shown to be particularly good because much more is passed out through the intestine due to the fact that the tablet has passed the optimal point for absorption.
I am not at my own computer so I will look for that information when I am able.
I suspect that as your wife gets older she may well not be converting the T4 into T3 as efficiently - I notice you speak of high normal T4 and undetectable TSH, yet do not say what her T3 levels are.
Low T3 levels are just as likely to cause AF as high T3 levels. My AF was almost certainly caused by poor conversion leading to low T3 level - now I am on T3, it has not entirely disappeared but is far less frequent and more short-lived when it does occur.
Studies on slow release tablets of either T3 or T4 are universally badly done and do not stratify patients according to their degree of dysfunction and residual thyroid tissue. Furthermore, slow release + dose can be adjusted so that the supply to the body can be optimized, even if some hormone escapes unused - doses would be adjusted so that the net effect was beneficial. The proper work just hasn't been done. As for adjusting T4 dose at an advanced age, this can be difficult and certainly in my wife's case leads straight to hypothyroid symptoms - dry hair, skin, raised cholesterol even though the TSH is now just detectable. So I don't think she is T4-toxic, but rather that AF and (luckily not in her case) osteoporosis are possible problems for people in her situation in late life.
diogenes, I hope you are paying attention to Marram's message. Your wife could be T4 toxic. If she is very high T4 normal and you don't even know what her free T3 level is at, I suggest you check it out.
I also am in the age range and had lots of heart beat issues and now neuropathy in my toes from very low T3 ranges. Being on T3 only for six months has been excellent although I don't know if I can undo the past 15 years on Synthroid and Armour.
Diogenes, 45 years ago would have been 1968. When Dr. Barnes published his book in 1976 Hashimotos wasn't even mentioned. He did mention it in one of his lectures, to answer a question from the audience, and said it seemed to be more prevalent in the UK and needed Syn T4 and T3 to treat. Do you know when they developed the TPO and TG AB tests? When Dr. Hashimoto first described it in 1912 how did they test for it or recognize it as a unique condition?
What I find curious is that in 45 years it has gone from a fairly rare condition to the most common thyroid condition. Why? PR
For TPO I can give you the following papers which seem to start it off.
Ruf J, Czarnocka B, Ferrand M et al Novel routine assay of thyroperoxidase antibodies (TPO). Clinical Chemistry 1988;34:2231-2234.
Czarnocka B, Ruf J, Ferrand M et al. Purification of the human thyroid peroxidase and its identification as the microsomal antigen involved in autoimmune thyroid diseases. FEBS Letters 1985; 190: 147-152.
TG antibody testing is much older - probably in the early 80's.
good point, if we only knew our levels of when we felt good and were healthy! I have requested a copy of my whole medical records, the only fT3 blood I have found from before hypo diagnosis was when I was 20 years old and felt ok-ish (not great but not rotten like when I got diagnosed). My fT3 level was right at the top of normal range at 6.8, at diagnosis my fT3 was barely in rage. Now I need supra-physiological levels of T3 in my blood (so high doses of T3 only treatment) for my cells to have enough going into them.....
Hi diogenes, I wish you hadn't put it quite that way. Anyone who has been starved of T3 finds it a relief rather than dangerous. I stopped Armour in one day and started with 5 mcg. T3 working up to 25 mcg. in a week or so. I started losing weight so I knew it was working and have had no bad effects whatsoever. When I tried to raise Armour, I had all sorts of effects of over exertion. If people are not doing well on T4, there is a good possibility that a sensible trial of T3 can do wonderfully.
We know that lots of people who are not hypothyroid use it for weight loss only and, of course, that is not recommended.
I agree, When T3 is the only option, saying it is dangerous is very unhelpful and causes stress for us trying to get better on T3. I fully believe T3 is perfectly safe to use, carefully. Any medication can cause nasty effects and that includes T4. Dr John C Lowe took T3 and off course Paul Robinson and Dr P is also a Fan of it. I think what has been missed out is that the underactive Thyroid not being treated properly can result heart problems & Stokes etc. As for the urine test, i will be doing one next week and I will then know whether it is more helpful.
Hi Kitten, I am going back to Diogenes and bring up T4 toxicosis. I have an idea that it may be more of a problem than anyone realizes. In fact, if his wife has palpitations or A-Fib I'm thinking SHE may be T4 toxic at times. Good luck with your test. I'm not sure I care what any of my levels are anymore.
Thats right, Toxicosis is terrible - i have suffered that many times. I agree about the levels they are not helpful, I try to avoid all thyroid blood tests. Good luck & I hope you get well
Thyroid function and thyroid hormone metabolism in elderly people. Low T3-syndrome in old age?
Herrmann J, Heinen E, Kröll HJ, Rudorff KH, Krüskemper HL.
Abstract
T4-, T3- and reverse-T3 concentrations were measured in the sera of 365 subjects beyond the age of 65 in order to evaluate if the decrease of serum T3 frequently observed in old age can be attributed to old age per se or to concomitant nonthyroidal disease. The results obtained from a carefully selected healthy group of elderly people show that 1) total and free T3 levels are lower in senescence but well within the range for euthyroidism in younger healty controls;2) the decrease of serum T3 is more pronounced and occurs earlier in healthy old males than in females, so that for subjects over the age of 75, the upper limit for euthyroidism has to be adjusted by 10% in women and by 20% in men; and 3) there is no low T3 syndrome characterized by decreased serum T3 and increased serum reverse T3, solely due to old age. Turnover kinetics have shown the daily production of T4 and T3 in old age to decrease by 20 micrograms and 10 micrograms, respectively, and an increased T3 metabolic clearance not to account for the reduction of serum T3 concentrations. Combined stimulation tests with TSH and TRH showed that the functional reserve of the thyroid gland to produce T3 is maintained in old age. The first step in the sequence of events may be seen in an impairment of TSH secretion leading to an adaptation of the amount of thyroid hormones to a reduced mass of metabolically active body tissue in old age.
I and Reinhold Gruner published a paper in 1985 in Nuklearmedizin (1985 Apr;24(2):57-65.). In it we studied FT4 and FT3 trends in 1548 healthy blood donors aged 18-65, and 5700 ambulatory euthyroid patients presenting to hospitals/clinics but deemed euthyroid - these would then be suffering possibly from mild nonthyroidal illnesses. We found no mean or range change in FT4 or FT3 in the donors, and no change in FT4 of any significance up to 100 years old in the patients. In the patients we found that FT3 declined with age, owing to the increased prevalence of nonthyroidal illnesses in the elderly. This confirmed and added to the results above.
we still go back to the fact that bloods do NOT tell you what is used 'inside' your cells. So ok, we say that if we only knew what levels of fT3 were in our blood when we were young and healthy then we would know what levels to aim for now. I don't think this is right as it still does not tell you what is going on 'in the cells', if your cells receptors are now having a more difficult time in uptaking the T3 then surely you need to throw T3 at them as much as you can until some of it 'gets in' right? that is the only way I can explain why I am only healthy on a once a day dose of 180mcg of T3 and nothing else, levo did not work, NDT did not work for me, blood tests NEVER work for me, they 'never ever' tell me if I am well, only my symptoms do and then some other pin pointers like cholesterol/bone density/heart 24hr holter/ECG/echo/ resting metabolic rate. Sorry am just thinking here when I was young and healthy my cells seemed to take in the T3 and use it properly now they don't, they are half dormant!
I don't agree with your statement that blood FT4/3 tests don't indicate what is happening in the cells of your body. They show how T4 is being converted to T3 (or reverse T3 if you are otherwise ill). But they cannot cope with the rare (possibly in your case) occasion when a form of T3 resistance occurs - ie your receptors and T3-binding proteins in the cells are insensitive to T3 and therefore require more. Why I enter these conversations is my worry that I see people on this site falling into the same trap as they condemn in the doctors who use blood tests as a dictator rather than a guide. That is, by rejecting those tests, they are elevating alternatives into a role they too cannot fulfil. No tests in any field whatever are infallible. I know this only too well because when progressively improving tests for FT4 and FT3 so that more and more unusual people were included in "normality" or excluded as "abnormal" one had to realize it was impossible to include everyone. The diversity chemically of the human race is staggering. I sometimes think there are aliens in our midst. Normality takes many forms.
Ok, so the bloods could show how T4 is being converted into T3, however for people on T3 only the bloods do become pretty useless as this cannot longer be shown... (so yes, forgive me I am on T3 only that is why I keep thinking of how unhelpful thyroid function tests are in those who are on T3 monotherapy)
by the way, thank you for this very interesting discussion/thread
Diogenes, I don't think T3 resistance is actually all that rare, I think it is more common than realized. I also think it occurs from causes other than inherited genetic glitches. Drs. Refetoff, Weiss, DeGroot, and others, have catalogued about 170 glitches so far and the field of Endocrinology tends to think that that is the only way it can occur. Dr. Derry observed that children who have been abused or suffered a great terror or fright exhibited thyroid resistance. I know a person who was bullied as a young lad and that seems to have caused resistance, both thyroid and cortisol. NBD and Paul Robinson are two very different examples of people who have found that only T3 gave them their life back. There are many others that have replied to this and other posts that also only seem to find relief with T3. I don't find much research into this area, it seems to be largely overlooked. The other curious thing is that not all people with resistance need T3, some of us do fine on NDT. The one common thread is that all of us with some form of resistance usually have a devil of a time getting adequate treatment, we have to fight like hell just to survive because the condition is so poorly recognized. This is one area where science has an almost total lack of understanding. PR
A recent discussion I read [somewhere] mentioned the issue of harsh childhood experiences leading to Wilson's Temperature Syndrome.There are websites dealing with this -and Wilson's more acknowledged in the US.
The treatment for this is small doses of T3 , I think 3xd- for a few days only. Possibly repeated.
WTS is not a thyroid malfunction, as such, but a systemic glitch in metabolism which is 'locked up' until the T3 unhitches the process in some way.
tegz, from what I can tell WTS is an RT3 problem and T3 is used to clear the RT3 which puts the system back in balance. I have read comments from both patients and doctors that say this works but like so many aspects of the endocrine system we are lacking good bench science to back up the theory. The WTS protocol is practiced by some doctors here in the US but they are definitely a minority. The other thing that is poorly understood is the effect of harsh childhood experiences from a biochemical aspect. Dr. Derry thought the maladaptation of the biochemistry somehow allowed them to survive the experience. He is the only one I've read that put 2 + 2 together. If you happen to find that discussion again I would like to read it. PR
I probably won't readily find the article- but will keep a 'weather eye' open. On the RT3/WTS front- I hope to dialogue with a pituitary expert, ere long!
Your post got me thinking. What you are saying is that sudden and severe stresses can permanently alter a person's metabolism and that this can, among other things, manifest itself in thyroid hormone production and control of T4-T3 conversion. Is there any evidence at all for this in other areas of science? I put on my molecular biologists hat and think I have found a possible link. In rats given severe and constant stress, their offspring also inherit the same stresses even though they have not experienced them themselves. This means that somehow the genetic makeup of the rat parents has been altered and this has passed through to the offspring. What has happened is called epigenetics - where the base sequence of DNA that defines the genes and their output of information has been modified. In this case you get a kind of chemical "furring up" of significant parts of the genome caused by the stress which alters the output and this "furring up" persists into the offspring. In humans the same thing could very well happen and could affect T4-T3 conversion as an anti-stress mechanism. It would then be permanent and not recoverable back to the condition before the stress. This possibly could lead in some cases to poorer T4-T3 conversion as a defence mechanism which persists even after the reason for the stress has passed. This is just a theory unsupported by evidence in humans, but the coincidence of rat and human behaviour to stress is compelling.
Diogenes, this is what Dr. Derry said: "People who have had terrible childhood experiences (sexual abuse, physical abuse, personal tragedies etc) for whatever reason have altered thyroid metabolism. They are more complex to treat. They are different from everyone else biochemically and pharmacologically. The blame for most of their residual difficulties is not with their brains and minds but with their chemistry. I believe also other areas of their biochemistry are not normal. I don't think this has been generally recognized yet."
And it still is not generally recognized!
Dr. Derry is an MD with a PhD in Neurochemistry. In 25 years of reading he is the only one I have found that made the connection between abuse, terror or great fright and altered thyroid chemistry. Later I found out that bullying at a young age can also produce the same effect. Actually you might enjoy reading his interview.
In his book, "Breast Cancer and Iodine" Dr. Derry enlarges the discussion. "In terms of the abuse thesis, it is easier to postulate that the fear reaction of abused people below the age of 12 allows for some adaptive changes in the thyroid hormone receptor system likely as a biochemical survival tactic. They may be a large source of thyroid resistant people in the population."
It is a short book, only about 100 pages. If you would like to read it PM me your address and I will mail you a copy, I have a few extra.
I'm not sure the upper age limit of twelve always applies. If you look at the reactions to war, PTSD and so forth, there are some similarities. What I am sure is that very little is understood about this. I have looked at some of the papers by shrinks but they generally only look at the HPA axis and do not seem to understand the far reaching effects on the biochemistry of the body.
To me this is just another example of how little we actually understand about the greater thyroid and endocrine system. PR
PS I just started into Nessa Carey's book "The Epigenetics Revolution". That is another interesting aspect as I am a quarter Scottish and the Scots also endured many famines. The reaction to abuse or fright is also an epigenetic situation.
From what you say and what I've uncovered rat-wise, I think I'll contact my partners Hoermann and Dietrich to see if they have any contacts in cell genetics that we can bring on board for a study. There obviously is an available patient base and saliva donations would form the material that would be analysed for DNA sequence and epigenetic modification. Maybe the genes for T4/3 receptors and deiodinases are already identified - I don't know. What might be interesting is to compare the DNA from normals, T4-only therapy (satisfied), NDT and T3-only patients. The expectation would be a lot more epigeneitc modification in the last two groups than the first two, with T4-only a little more modified than normals. Do you think if we kept confidentiality by coding that enough subjects would volunteer to make a good prospective study? Not promising anything, but a query to my colleagues would be useful.
In social work we refer to this as traumatized DNA which we speculate are chemical changes from significant child hood trauma that changes DNA and that these changes are passed on in reproduction. This could account for intergeneration trauma experienced by First Nations residential school survivors. As for disrupting your thyroid I would definately say trauma could alter it. In my own case I think a viral flu infection caused my thyroid to malfunction.
OrangeGirl, thanks for your input. I understand the first sentence, this is what epigenetics has been discovering, that the effects of famine or trauma can be passed on genetically. I'm not familiar with "First Nations residential school survivors", would you mind expanding a little bit on what that refers to. And yes, there is plenty of antidotal evidence that various infections in the body can spill over and have an effect on the thyroid either directly or indirectly. What Dr. Derry was talking about was more to the thyroid receptor or post thyroid receptor, causing a form of thyroid resistance. I have no doubt that there are many possibilities for genetic glitches that we have yet to understand. PR
PR4NOW I live in Canada and work with First Nations peoples in a child welfare setting. The Canadian government operated residential schools for native children for more than one hundred and fifty years with the last school closing in British Columbia in 1996. The treatment of children at these schools is considered to be genocide under the UN convention. Google Truth and Reconciliation hearings for more information. In my town the residential school closed in the early 1980s but we see over and over the effects of the traumatization on these survivirs passed down from generation to generation and no forms of intervention seem to effect any sustainable changes. First Nations people here (at least where I live) also believe that you carry the effects of trauma in your cells.
OrangeGirl, thank you for the insight. I have watched shows on the educational channel about the schools Native American Indians were forced to attend but I did not see or hear clearly exactly what that meant. Your comments have helped me to connect the dots and gain insight that I lacked. PR
OrangeGirl, you wouldn't happen to know of any papers that have been published about 'traumatized DNA' in your field would you? There is absolutely no question, in my mind, that trauma causes biochemical changes but I am having a hard time finding any science that has studied this issue. I've looked at some of the papers by shrinks but they seem to focus on just the HPA axis. In epigenetics they seem to use rats or mice or they study famine as the effects are passed. Any papers that you might be aware of would be of great interest to me. In all my time on the thyroid boards I seem to be the only one aware of this correlation. I'm trying to build up any information I can to see if I can raise awareness. Medical science seems completely unaware of this and we need to get more science done. PR
The best research I have read to date is a paper called "Intergenerational Trauma: Convergence of Multiple Processes among First Nations peoples in Canada" authored by three professors at Carleton University in Ottawa, ON. It was published in 2009. The authors are Amy Bombay, MSc, Kim Matheson, PhD, and Hymie Anisman, PhD. I have read an article by Ruth Hopkins (2011) in Indian County today (United States) called "Epigenetics: Scientific Evidence of Intergenerational Trauma"
Diogenes, I would love to have some science done in regards to this class of thyroid patient, as far as I know nobody has studied this. Given the rapidly expanding knowledge and interest in the field of epigenetics this would be an ideal subject matter for a study. I have a friend that was abused and she tells me the numbers are appalling, studies estimate that upwards of 50-60% of children have experienced some form of abuse. You have had a big flap recently in the UK about a charity celebrity that apparently had been abusing children and others his entire career. Add those that have experienced a great terror or fright or bullying and the subject pool should be ample. The problem is that neither the subjects nor the doctors are aware of the correlation with changed biochemistry. I know, for instance, that Dr. Peatfield has seen members of this class of patient, I don't know if he ever figured out the relationship.
Confidentiality would probably be important for some since it is a sensitive subject matter. For many of us I bet we would just be happy to have someone finally studying the problem so we could increase our understanding of how to successfully recognize and treat this class of patient.
Please let me know what Drs. Hoermann and Dietrich think about the idea of a study. PR
PS Another indicator is that generally, not always, patients don't react to pharmaceuticals normally. Also some patients chase thyroid, they usually need T3 to get well. Dr. Derry told me that generally these patients do better on NDT than Syn T4.
Rod, I would hope so also. There are a couple that have responded to comments I've made about Dr. Derry's thoughts so I know there are some on this forum. PR
Thank you RedApple, let us think positive thoughts for the possibility of actually getting a study started.
I've been spending some time on Dr. Ben Lynch's site,
mthfr.net/ and he suggests 23andMe. Did you find the information useful and did you run the data through one of the sites that will process the data and give you more information? Was this in relation to the MTHFR gene or were you looking for other things? PR
Maybe each person's own iodine (and thyroid) history affects their need for and tolerance of iodine? For example, those who have had periods of iodine deficiency might react differently to those who have always been replete.
The absolutely directly contradictory experiences need to be explained somehow!
Rod, one possible difference is selenium intake. Dr. Tenpenny was doing a study with Hashi's patients where they started them on selenium first for 2 or 3 months to get their levels up and then introduced iodine and the initial results were positive. I need to follow up and see what the current results are. We simply need more good bench science on this subject. PR
There is a problem for people who live in a low iodine area that suddenly get iodine supplementation. The experience is best shown in Germany where there are large areas of iodine deficiency and goitre. You cannot straightaway replace the iodine to immediately try to restore normal levels. The danger of "thyroid storm" is considerable, where the enlarged thyroid is suddenly put into overdrive. It has to be done very gradually to avoid this possibly fatal event.
Diogenes, yes iodine is tricky. You can go all the way back to 'Coindet' in the 1820s and soon after he used burnt ash of seaweed to cure goiter there were tinctures of iodine available, and popular, and a lot of people got into trouble. It has been the same ever since, every time iodine is introduced into a population they expect a spike in thyroid problems. One article I read talked about one country that introduced iodized salt and iodine in bread at the same time and they really got a spike in problems. There is also the relation between iodine deficiency and selenium deficiency which seems common. As you mentioned there is the danger of 'thyroid storm' if too much is introduced too quickly. Rod and I are both fairly conservative about iodine supplementation and feel that you really need to be working with a doc who is very familiar with its use. What we both lament is that there is such an abundance of conflicting information and conflicting approaches by doctors and such a lack of good science about the various problems people encounter and how to prevent them. You would think that after almost 200 years of fooling with this stuff we would have a much more thorough understanding of its potential benefits and pitfalls. Of course, one could say the same about the thyroid world.
If I did not represent Rod's thoughts accurately hopefully he will correct me. PR
I have just been completely fascinated by this whole discussion, because I recognize here many of the terms, or references made from my own independent research into the several conditions, plus early childhood experiences (which don't include any form of physical abuse) just life circumstances. it's been helpful and reassuring to me to realize that there are several professionally involved contributors on this discussion. I reckon I could give you all a pretty through rundown of my health - much of which I've recently put on here, albeit disjointed, which I put down to effects of the brain injury caused spontaneously, not by any form of accident or physical means, other than my own body. If you want a volunteer I am more than willing. Because recent posts have concentrated more on take this take that eat this eat that, I admit I'm lost when it comes to helping anyone on blood tests, I've just tried to relate my own experiences, including coming off all meds, except thyroxin - results of even that self test in changing or stopping for a few days have given me different results. I believe in listening to my body, just wish the Specialists I have seen over last 2 years would listen to me - but no not interested when I mention anything that is not their specialization, except the Haemo did rather leap out his when I mentioned my TB gland neck op when a baby. Re Genetics, I read recently a father can pass to a daughter or son, she as a mother can pass to a son? I can relate 3 generations of infection. Dad TB, me as baby TB gland, more recently tested for Hepatitis, Son at uni viral infection, tested for HIV AIDS. Me and son were both 'cause unknown' I still am to an extent he responded after several trials to some form of antibiotic. Dads TB flared again in 90's a few years before died age 78, it was named as one cause, stress related oesophalgeal ulceration as another. Basically he drowned in his own blood! Let me know if You want more info from me, which I'm happy to give more privately than on a completely open forum. Shirley.
hi hope this helps ,they do a urine collection that is sent to the labs in hospital over 24 hr collection someone explained it to me once but wish i had took it in now ,im sure someone will know.
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