Talk:Desiccated thyroid extract/Archive 1

Aargh

Aargh. Desperately needs sourcing and WP:NPOV. The historical material is good, though, and can be moved to hypothyroidism where it belongs. JFW | T@lk 07:30, 23 June 2006 (UTC)

I have edited this for NPOV now. The original author is encouraged to link his statements to his sources, as I do not own these books and cannot verify which statement is made where. JFW | T@lk 10:17, 23 June 2006 (UTC)

Natural

I would like to know how pooled animal glands, acetone de-fatted, then dried can be considered as "natural"? In the era of mad cow disease, I'm not sure you can justify the use of any pooled animal product.Pustelnik 15:34, 15 June 2007 (UTC)

Natural means 'not synthetic or artificial.' The word natural says nothing about safety, desirability, what you've since done to the original materials, or anything else. WhatamIdoing (talk) 05:22, 13 January 2008 (UTC)

NPOV

What is NPOV?? Also, I know that references can include websites, but am unsure how to put them in the article. After the sentence "Yet, the experience of patients reported on various interactive thyroid groups.........and many other positive results", the references would be http://www.altsupportthyroid.org/dt/dtexp2pr.php and http://www.stopthethyroidmadness.com/stories-of-others/.

Under treatment protocol, and after the sentence about suglingual would be this: http://www.positivehealth.com/permit/Articles/Colon%20Health/lea13.htm. As far as the statement about multi-dosing, that comes from reading patients comments on the Yahoo group Natural Thyroid Hormones Users. How is that cited?? It is http://health.groups.yahoo.com/group/NaturalThyroidHormones/

The same is true for the comment about generic thyroid being reported by patients as weaker than Armour and others--that comes from the comments of patients on the Natural Thyroid Hormones Users group mentioned above.

The comment from Forest Labs about T2, T1, and calcitonin not being removed come from talking to Daryl R. Wesche of the Forest Pharmaceutical Professional Affairs Department. How is that cited?

NPOV is the most important Wikipedia policy. It bears reading that article closely, as most discussions about appropriateness of content revolve around that policy and WP:NOR/WP:V.

If you have a quick look at the article you will see that I've embraced my references with <ref> and </ref> tags. Wikipedia:Footnotes contains more details.

On the whole I would avoid making generalising statements. "The experience of patients reported on various interactive thyroid groups" needs further support. Citing webpages is a bit troublesome, because one never knows whom the author of that webpage represents (himself, 100 of 10,000 people). That dilemma improves if the page is of an official organisation or there are clear indications that the views expressed are the aggregate of a representative group (e.g. a working party, a poll).

This is an interesting article. Are you sure natural desiccated thyroid hormones is a good title? Wouldn't thyroid extract be a more accessible title? JFW | T@lk 09:54, 25 June 2006 (UTC)

Actually, for most patients, no one would know what you were talking about if "thyroid extract" was used, even though it's a legitimate medical description. Now, the common term is "natural thyroid hormones", thus the title here being Natural Desiccated Thyroid Hormones.

As far as the "experience of patients reported on various interactive groups...." under the Controversies heading needing further support---citations to support that sentence can only come from citing these groups, I fear. Why? Because there is a huge movement going on with patients talking to each other about their experiences ON these internet groups: Yahoo Groups like the popular Natural Thyroid Hormones Users, the Hypothyroidism group sponsored by Cure Zone, the Thyroid group of Mary Shoman, and many other smaller but active groups. They are not reporting their experiences in books; they are reporting it in the huge amount of conversation going on in these groups, which can be viewed.

Also, they are reporting their experience (which is contrary to what doctors say about natural thyroid hormones) on the www.stopthethyroidmadness.com website, plus the thyroid.about.com thyroid website, and the www.altsupportthyroid.org website, and many other smaller sites.

Granted, it's a new phenomena, but it's real to our modern society with the abounding use of web groups and websites to communicate.

You state: "Citing webpages is a bit troublesome, because one never knows whom the author of that webpage represents (himself, 100 of 10,000 people). That dilemma improves if the page is of an official organisation or there are clear indications that the views expressed are the aggregate of a representative group." The websites definitely do appear to be the views of a representative group--thyroid patients on natural thyroid hormones--even if there are no clear-cut authorized 'officialdom'. The authors appear to have brought these views and 'stated experiences' together to form the 'website'. I think the Stop the Thyroid Madness is a good example of that. Plus, the websites themselves have their forums to continue the talk.

I will read the NPOV article, plus the one on footnotes. Thank you for steering me. I'm still unclear how to add them to what you've already done (and thank you for that), but will hopefully figure it out! I am new to this. Doodlebug1 (talk · contribs)

I understand your point about the naming issue. Is this the official generic name of all Armour-like products?

As I am not an endocrinologist I have no way of knowing how "popular" the use of natural desiccated thyroid hormones is. But I very frequently encounter patients who are hypothyroid, and most are doing just fine on 50-75 μg/24h of levothyroxine. In fact, I wasn't aware of a large support base for natural thyroid supplements until I'd read your contributions. This makes me wonder about the currency of the view that levothyroxine is inadequate and that TSH is not a useful blood test.

I'll have a stab at converting your references to footnotes. JFW | T@lk 18:59, 25 June 2006 (UTC)

reply: Thank you for all you assistance (and I'm bolding this to get it to stand out). Yes, patients are calling all Armour-like products Natural Thyroid Hormones. Not sure where it started, unless it was with Mary Shoman, a thyroid advocate, or Janie, the owner of the Natural Thyroid Hormone site on Yahoo and another thyroid patient advocate on the Stop the Thyroid Madness site. Yes, the use of Natural Thyroid Hormones is becoming quite popular, apparently, because patients are stating that they never got resolution of symptoms on levothyroxine, and have gotten it on Armour. When they informed their doctors of their continued symptoms while on levothyroxine, they have consistently been put on anti-depressants, statins, and numerous other medications which only masked the inferior treatment of levothyroxine. On dessicated thyroid, they are stating that have gotten resolution of those symptoms, plus others. In fact, when you say that most of your patients are doing fine on levothyroxine, you might want to see what patients are saying on these sites. They are also stating that going by the TSH has kept them sick, and that even includes on the Armour-like products. When they say they are rid of all their former hypo symptoms, they have a suppressed TSH, yet no hyper symptoms whatsoever.

Removal of T2/T1/calcitonin

Referring to a company spokesperson without a verifiable source makes it impossible for any other reader to verify this statement. If Forest Labs says Armour contains T2/T1/calcitonin doesn't that imply that it does indeed contain these hormones? JFW | T@lk 19:13, 25 June 2006 (UTC)

reply: JFW, I'm unclear what you mean about the company spokesman. I included the Armour Contact page so anyone can call and verify from Daryl what he stated. So, it's not "impossible" to verify it! The reason I included that info is because of what you removed---that there is an ongoing rumor that desiccated thyroid like Armour ONLY contains T4 and T3 (i.e. that the T2, T1 and calcitonin are removed. Doodlebug1 (talk · contribs)

Doodlebug1, this is an encyclopedia. Encyclopedias refer to other sources, but they never instruct their readers to go ahead and phone/email someone for confirmation. Please provide a reliable source. JFW | T@lk 22:01, 25 June 2006 (UTC)

Need help on the following

In the paragraph titled Controversies and in the first sentence "It has been said by medical professionals that natural desiccated thyroid like Armour is inconsistent from dose-to-dose, dangerous, unstable, hard to dose, unreliable, and outdated.", these are again reports made by patients about their doctors on these patient-to-patient talk groups. These are very common reports by patients about how their doctors described desiccated thyroid. Perhaps I can state "Patients report their doctors as saying that natural desiccated thyroid like Armour is...." and then cite the group. In fact, I would say that most everything stated under the Controversies heading comes from the discussions between patients on most of the groups on the net, including the Yahoo groups, the About.com forums, and many others.

By the way, you added that the Yahoo Natural Thyroid Hormones group is related to the Stop the Thyroid Madness group. It is not. The STTM group has it's own forum, which is not the Yahoo group. It's the same subject, but they are two totally different groups, just as the other thyroid groups on the net are.

Also, I am trying to add the same #6 as a reference to information under Controversies, but all I get is a #7 which ends up repeating #6 in the References below. I think I remember there is a way to avoid that??

I think the Controversies is a good reality to the Encylopedic discussion about Natural Desiccated Thyroid Hormones, and am doing it from a "Neutral Point Of View", but am forced to cite the groups where patients talk about this over and over, since there appears to be no book to verify what they are talking about.

The references are to different URLs, so they should not be merged. If you want to make multiple references to one footnote, please consult Wikipedia:Footnotes, which explains it clearer than I ever could. JFW | T@lk 22:17, 25 June 2006 (UTC)

Reasons for changes and some removed material

I am moving some of the references here as they do not belong in this article. Note that the trials cited did not use desiccated thyroid but synthetic preparations, and are tests of the T4 vs T4+T3 controversy, and used different ratios of T4 and T3. These studies were not tests of thyroxine versus desiccated thyroid, and used T4:T3 ratios higher than those of desiccated thyroid preparations (about 5:1 and about 12:1 by quick look). I will try to find an example of a study of thyroxine versus desiccated thyroid.

I would recommend we move the T4 vs T4+T3 controversy to the hypothyroidism article.

The article should do justice to both perspectives and I will make a couple more changes to the latter part but don't have time to finish right now. I plan to leave the current pointers and references to the pro-armour websites and books, but will find some balancing studies showing no difference, and will try to add some material on the T4 vs T4+T3 controversy to the hypothyroidism article where it better belongs.

Here is the removed paragraph to preserve the references for use elsewhere.

than regained popularity due to experiential reports of success, as compared to their former thyroxine-only treatment, by thyroid patients on numerous interactive websites, in spite of the lack of "medical" evidence that adding T3 to the treatment is beneficial.

The references are in the copied block but do not show up above until you switch to edit mode.

alteripse 15:40, 29 June 2006 (UTC)

I left a brief allusion to the T4+T3 issue and replaced the references. alteripse 16:51, 2 July 2006 (UTC)

reason for page move and title change

"Desiccated thyroid extract" is the briefest accurate title. The preparation is not "desiccated thyroid hormones" but desiccated thyroid gland. Natural is simply a marketing adjective like "organic" or "new and improved" and is not the name it has been known by for most of the last century or in most current publications. We can leave a redirect for readers looking for the other terms and can include them in the first paragraph.

The other additions are to balance a one-sided article: a reader would have had almost no clue as to the reasons nearly all thyroid doctors prefer thyroxine for most patients. I am not done yet and have no intention of deleting either the pro-thyroid extract POV and arguments, nor the websites and books cited, but I am providing a broader perspective for the reader who is interested in more background, both sides of the controversy, and a more accurate delineation of strength of evidence. alteripse 22:02, 1 July 2006 (UTC)

npov the other way?

I believe this to be factually inaccurate...

"Attempts to objectively demonstrate the superiority of desiccated thyroid pills over synthetic thyroxine by controlled clinical trials have generally shown no advantage, and many physicians remain unconvinced that the superiority is anything other than a placebo effect or an overtreatment effect."

I know of no clinically controlled trials comparing natural thyroid products to levothyroxine. Suggest it is removed and replaced with a statement that "no clinical trials were ever done" to demonstrate the adequacy of levothyroxine as a replacement when it was introduced, unless a reference can be provided. These days an introduced drug would have to go head to head with the best current treatment - this was never done (and has never been done to my knowledge).

There have been trials of levothyroxine against combined T4/T3 medications. And these show a consistent patient preference for the combined medications (even when the mean TSH in the combined group rose slightly (Weston study) - suggesting it isn't just an increase in dose that causes this preference), suggesting patients (in double blind trials) strongly prefer combined medications, even if doctors don't understand why (no other medically significant results were found - although that suggests the doctors were measuring the wrong things to me). However I think it would be foolish to assume these results can readily be applied to natural thyroid extracts, as natural thyroid have a much higher ratio of T3 to T4 and other components (for better or worse).

Similarly the article overstates the case for thyroxine as effective treatment, and fails to reference papers that demonstrate experimentally that levothyroxine replacement doesn't result in normal levels of thyroid hormones in all tissues. There are also studies showing obesity levels in people on levothyroxine treatment with normal TSH being higher than the population average, which contradicts the claim that levothyroxine treated patients have normal levels of symptoms of hypothyroidism. Indeed such a claim is I think indefensible -- if taking one dose of levothyroxine a day was a complete treatment, why would the body have such elaborate feedback mechanisms to adjust and control these levels so precisely, evolution doesn't tend to favour unnecessary over engineering. As such it is likely inevitable that those treated for hypothyroidism will exhibit more symptoms of both over and under activity of the thyroid, until a full replacement of the thyroid (and any faults in the control mechanism) is possible.

My understanding is that dessicated thyroid products are now assayed in the same manner as synthetic thyroid medications. Whether the USP requires this I haven't ascertained. The assay by Iodine content was merely because when it was introduced, this was the only test that was possible. Levothyroxine Sodium was also assayed by Iodine content, and possibly in the early days that gave it an advantage in consistency of potency. There is evidence now that the dessicated products are as good or better in consistency than the synthetics (note that the synthetics had to undergo a NDA (new drug application) in the US -- i.e. lost their grandfather right to be consider "general safe and effective" - due to issues surrounding their potency, and most were reformulated at this point). --ANON

Thanks for taking the trouble to respond. To facilitate constructive discussion, the custom here is to add a comment like this either in a new section or at the bottom of the page so it can be more easily recognized as new, and to sign it so it becomes possible to recognize the parts of a discussion. I moved your comment and added ANON, but strongly request you take 30 seconds and make an account, which will be free and more anonymous than your Shrewsbury IP number. You sign with 4 tildes and it will add your username and a date stamp.

Some of your detailed points are substantive and evaluatable. Some can and perhaps should be included but need sourcing. Here are four of your specific assertions and replies:

• No clinical trial compared thyroxine and extract head to head. Not true, see the Surks reference, and I will find some more. Your comment is only supportable if you are specifying the type of rigorously constrolled and monitored tests that the FDA would require now. The fact that you cannot readily find a well-controlled study from the 1950s demonstrating that penicillin treated syphilis more effectively than mercury is pretty weak support for continuing to prefer mercury. One can certainly find descriptions by endocrinologists caring for large numbers of patients and seeing no disadvantage. It is fairly strong evidence that virtually none of the doctors with the most experience with thyroid patients stopped switching patients or published concerns about the switch-- you would have to concoct a mass conspiracy theory to explain this as one can readily find all sorts of dissenting opinion articles in medical journals of the last 60 years against many other conventionally preferred treatments. Before you reject this argument, you have to recognize that nearly all of the evidence of thyroid extract proponents is no better and most is even weaker (smaller numbers with larger possible sources of personal bias). Why do you think none of the proponents of thyroid extract have conducted the type of controlled study that would satisfy you?

• The T4 vs T4+T3 issue is an interesting one and is certainly a live controversy as mentioned in the article. I just heard an excellent detailed review of the ten published controlled studies (incl the 2 cited here) by Wilmar Wiersinga at the 2006 Endocrine Society meeting in Boston. The audience was packed and interested. The evidence of superiority of the mixture is weak and inconsistent. Every study that attempted to blind the recipients as to the preparation they were receiving and to track objectively the key symptoms for more than a few months revealed inconsistent short term differences and long term differences diminishing to undetectable. I will try to find a more recent overview. And as you admit, trials of T4+T3 mixtures are not trials of thyroid extract for a number of reasons and I think a more detailed discussion of this controversy belongs in the hypothyroidism article.

• Your assertion that newer preparations of thyroid extract are better standardized and controlled for hormone content might be true, but needs sourcing. It was demonstrated in 1980 that the first 2 decades of criticism of unevenness and unreliability did not result in improved thyroid extract products. If there is evidence of improvement since then, I agree it should be added. I think your specific claim that current thyroid extracts are "as good or better than synthetics in consistency" is doubtful but please offer evidence if you have it.

• The issue of normalcy of hormone levels in blood and tissue during treatment may be a valid issue and worth mentioning. What the article says is true: T4 alone produces normal T4, T3, and TSH blood levels in most patients. Can you cite the studies you had in mind that show demonstrable differences at the tissue level? I won't even ask you for a study showing that tissue levels are closer to normal in patients on thyroid extract.

• And a citation please for the one showing higher obesity rates in properly treated thyroxine patients? And how about a study showing lower obesity rates in patients on thyroid extract with similar blood hormone levels? In other words, there is a difference between showing that a treatment is less than perfect for some patients and showing that treatment A is better than treatment B in reversing those same imperfections. Most of us suspect that no matter how much money the thyroid extract companies make from patients looking for further improvement, they will never fund a relatively inexpensive head-to-head blinded trial against standard treatment (similar to the best of the T4 vs T4+T3 trials).

Thanks for the constructive criticism. I will change one of the sentences and await your evidence for the other points. I am trying to make this article accurately descriptive of the controversy. alteripse 16:04, 2 July 2006 (UTC)

reversion of misleading and inaccurate material

All of the alterations of the last 24 hours either removed accurate statements or introduced inaccurate statements or reduced the precision of the statement. Please no more anonymous drive-by editing. Please produce documentation for any more alterations. alteripse 21:36, 3 July 2006 (UTC)

As above. Specifically, no matter how Good our anonymous contributors think dried pork thyroid is, and how Evil endocrinologists are, it is accurate to say that there are numerous studies and references documenting that the majority of people with hypothyroidism treated with thyroxine have relief of signs and symptoms. No one has claimed that all patients get relief from all symptoms. alteripse 12:34, 20 July 2006 (UTC)

Concerning this entire page--looks good, but.....

I am the one who originally started the Natural Desiccated Thyroid article here, but have had to be out of town so much that I haven't been back. It's greatly increased it's information--good job, though I see some of the information is suspect in accuracy and needs sourcing itself, as was asked of me. By the way, what "drive-by editing" is going on? Also, in reference to the above comment about "evil" endocrinologists"...laughing...I don't see that these patients are calling them evil but "uninformed and rigid", which looks valid when you take the time to open-mindedly read their arguments against Endocrinologists.

Additionally, you stated that "there are numerous studies and references documenting that the majority of people with hypothyroidism treated with thyroxine have relief of signs and symptoms": THAT is exactly what I see needs citing. Because these patients are strongly claiming that if you interview the majority if not all of thyroid patients on thyroxine meds, they do not get total relief or are even close, and are instead "bandaided" (their words) with anti-depressants, statins and "other" meds which only cover up the obvious "signs and symptoms" of undertreatment.

Thanks for commenting & appreciating the humor. If you look at the page history, you will see at least 3 recent instances of anonymous editing primarily pushing some of the points you make but not explaining or discussing on the talk page despite my requests-- this is what I was referring to as "drive-by editing". As to the proportion of hypothyroid patients who have satisfactory resolution of signs and symptoms being the majority, I provided at least one reference at the point the assertion is first made, and can provide many more. It is certainly my experience as an endocrinologist that the vast majority of patients with hypothyroidism are adequately replaced with thyroxine and do not complain of unrelieved symptoms. I ask them that when I see them. I have certainly known a few who continued to have symptoms. I hope I made it abundantly clear in the article that there are plenty of such people but they are certainly not the majority. You will have to offer a bit more evidence than I have hitherto seen that the "majority" of hypothyroid patients are inadequately treated with thyroxine. I am sure you understand that an internet site that solicits those who still feel that they have unrelieved symptoms is unlikely to have lots of postings from those who feel they are adequately treated with thyroxine. No matter how many people log onto it and agree, you cannot claim it is the majority until someone has actually performed an unbiased survey of a representative population. So until then I will continue to remove claims that the majority of hypothyroid people on thyroxine complain of unrelieved symptoms as it contradicts what is amply and repeatedly published as well as my own daily experience. alteripse 22:32, 23 July 2006 (UTC) PS please sign your post.

Sorry about not signing my post--I am new to Wikipedia and thought it would show up automatically since I am signed in. As far as your reference supporting that the majority of patients report satisfactory resolution, I think you're going to need to cite references to the opposite as well to be balanced in this article, which I am not seeing. Because once again, if you really check out these patient websites (and there are many), they are reporting that most patients on thyroxine absolutely do not acquire satisfactory resolution. They are reporting that "satisfactory resolution" is only in the eyes of the doctor who sees an in-range TSH, and from that, make the "dubious" conclusion that the patient is now adequately treated.

The paragraph I am concerned about is this one:

Current status of thyroid extract use

At present, a large majority of people (at least in the English-speaking world) of all ages with hypothyroidism are being replaced with synthetic levothyroxine. When their blood levels of thyroid hormones and TSH are most normal, the majority have no more signs or symptoms of hypothyroidism than similar members of the population.

A significant minority of adult patients feel that current methods of replacement with thyroxine, guided by normalization of TSH, do not completely eradicate all of the symptoms they attribute to their hypothyroidism. Many of them report that thyroid extract gives them better symptom relief, often at doses that produce abnormal levels of TSH.

I think you need to cite or more fully explain "when their TSH is normal"...."the majority have no more signs or symptoms of hypothyroidism than similar members of the population." Because this is exactly opposite what patients are saying on these numerous websites and groups. And since I have been observing them for the past 6 years, the amount of patient websites are growing in leaps and bounds, and their message is being done extremely professionally.

In the next paragraph, you state "A significant minority of adult patients..."--where does this statement come from? How do you know it's a "significant minority"? Because once again, if you listen to thousands of patients who are represented on these growing sites, including the Stop the Thyroid Madness site, Mary Shoman's About website, and many others, it doesn't appear to be a "significant minority". I am concerned that medical professionals aren't aware of or listening to what is going on out there with patients. That is why the Stop the Thyroid Madness site, as well as numerous Yahoo groups, appear to exist.

You stated above "It is certainly my experience as an endocrinologist that the vast majority of patients with hypothyroidism are adequately replaced with thyroxine and do not complain of unrelieved symptoms." Once again, if you really peruse these sites, you will note that patients are screaming that Endocrinologists are the worst to not listen to their continuing hypo symptoms on thyroxine, or you fail to see them because of your reliance on the TSH, which these patients are calling "the holy grail of diagnosis". As you read the words of these patients, they are also stating that they have complained, but the doctor only "bandaided" their symptoms..implying that these symptoms had nothing to do with their treatment, when patients are discovering that they did.

I personally am not claiming it is the "majority". I have no idea. But I am stating here that these websites are making it clear that there is a large and growing body or patients who are not getting relief from hypothyroid symptoms on thyroxine, and it's impressive what they are trying to say. Remember: you stated above: "I will continue to remove claims that the majority of hypothyroid people on thyroxine complain of unrelieved symptoms as it contradicts what is amply and repeatedly published as well as my own daily experience. Experience does count for something, but this paragraph fails to give enough credit to the "experiences" of these patients who are doing a bangup job of trying to spread the word of THEIR experience..that thyroxine hasn't worked well. Because by my observation, they don't look like they are "soliciting". It looks like they are trying to explain to patients why they continue to have symptoms of hypothyroid on thyroxine. And I note that on the Stop the Thyroid Madness site, it also is speaking to doctors, asking them to at least be more open minded that perhaps the TSH is not telling the whole story. Just my opinions and observation. I am doodlebug1.

Sign by typing 4 tildes. The paragraphs you quote are the summary paragraphs. They are not referenced in the summary because they only repeat assertions made in more detail earlier in the article where they were fully referenced. Essentially they are a valid summary of the whole subject. I have no doubt you have seen many well-done websites describing many people who prefer desiccated thyroid, but that is far from evidence that they are the majority and in simple fact they are a relatively small minority. If you are intelligent, you have to realize there is no reason for endocrinologists to lie about this. Thyroid drugs are low-profit drugs, there are no thyroxine companies showering endocrinologists with enough attention or bribes to make it worth ignoring a clear superiority if there were such; there is no orchestrated conspiracy to suppress a superior treatment. Cui bono? Throughout the 1960s, 1970s, and 1980s, the doctors treating the most thyroid patients gradually changed from use of desiccated thyroid to thyroxine and did not see that there were more complaints of inadequate relief. You cannot find any documentation of worsening treatment results because there was none. Surely some would have written, "hey this doesnt work as well," as medical journals are full of opinion letters and disagreements over optimal treatment. Demonstrating this would have been a way to make an academic reputation. There were always people whose symptoms of fatigue, depression, or adiposity were not completely relieved and there is no evidence there are more of them now than in the 1950s when everyone used desiccated thyroid. No endocrinologist claims that thyroxine relieves all the complaints of every adult with hypothyroidism. If some of them feel better with desiccated thyroid, mixtures of T4 and T3, or doses that suppress their TSH, the facts deserve to be acknowledged and the article clearly does so. The presence of websites that profess the opinion that they represent a majority opinion are simply evidence that people can hold mistaken opinions, not evidence that the opinion is correct. Most of them have seen endocrinologists and, believe me, they are a small subset of our patients. alteripse 04:58, 24 July 2006 (UTC)

More....

If the paragraphs I refer to above "repeat assertations made in more detail earlier in the article", they are only repeating assertations made by doctors and not these patients. That is why I am saying this paragraph is not balanced, and thus not valid. Granted, I see good information that represents the other side, but in these summaries, it doesn't represent the whole. It's a biased summary. To say that it's a "small minority" is certainly biased. I am not saying it's a majority, but you are clearly using a biased opinion.

As far as your personal comments above, I don't see these patients saying that Endocrinologists are lying or are being conspirators. There is no chutzpah going on here. Read the sites. They are clearly saying that Endocrinologists are not fully informed, that they consistently make labwork more important than symptoms, and they also fail to be open minded about the subject. That is not being represented by the word "lying" or "conspiratory".

I would say they believe you that doctors "did not see that there were more complaints of inadequate relief." Because patients are making it clear that doctors saw these complaints as unrelated to their thyroid treatment, when in fact, they were. They report that when they switched to desiccated thyroid (and practically NONE of them refer to it as extract), those symptoms which their doctors "did not see" and attributed to other problems...went away.

No documentation of worsening treatment results?? The "documentation" is clearly coming out via these numerous patient websites that tell the story of how thyroxine treatment was never working, as was dosing by the TSH range. Why didn't they tell the doctors? They state they did, but the doctors routinely claimed that it wasn't their thyroid since their TSH was normal and they were "optimally treated."

Yes, many facts of desiccated thyroid have been presented on this page. In much of it, there is a good overview of desiccated thyroid. But in other places, and especially in the summary I am referring to...it stinks with bias. And honestly, for you to state that these websites are simply evidence that "people can hold mistaken opinions" is just more fuel for their fire that doctors aren't listening. Ecce signum. The proof is in the pudding.

Doodlebug1 06:28, 24 July 2006 (UTC) 04:58, 24 July 2006 (UTC)

You are misreading or misunderstanding or misrepresenting my reply. It is not my "opinion" that a minority of patients with hypothyroidism treated with thyroxine have incomplete resolution of symptoms; it is what we see every day and has been reported over and over, and is referenced amply in the article. You missed my point about the changeover: in the years when endocrinologists were changing from thyroid extract to thyroxine no one saw an increase in unrelieved symptoms in the majority of patients. Why not? Nothing in all those websites you cite is convincing evidence that the majority of people with hypothyroidism are inadequately treated with thyroxine, just that some people with hypothyroidism continued to have symptoms, which even the summary of the article clearly states. The summary is exactly and concisely correct and sums up the article. And the article clearly does not say, and I do not believe, that for those people the benefits are imaginary. Don't put words in my mouth. alteripse 11:49, 24 July 2006 (UTC)

I can certainly respect your comment that doctors feel it's 'what they see every day and has been reported over and over'. But the summary represents what you feel doctors 'see and report', and is not representing what these growing body of patients 'see and report'. i.e. the summary is biased and is written in the slant of a medical professional. So perhaps Wikipedia is not an unbiased information center at all, and that needs to be made clear to the unsuspecting public out there.

Something fairly formidible has been going on to propell these patients to form so many interactive thyroid groups, and they aren't just chewing the cud in these groups, nor are the groups little isolated entities. Additionally, for other patients to create the websites as professional as the about.com and Stop the Thyroid Madness site, plus other smaller ones, means we aren't seeing a little piffling phenomena going on that represents the latest fashion of the day. These patients are clearly spelling out what has gone on in remarkable detail, and that precision is making it quite clear that doctors are certainly not getting it if they "see and report" that "a minority have an incomplete resolution of symptoms" on thyroxine.

You stated that no one saw an increase in unrelieved symptoms when patients were switched to thyroxine. No one?? Then who are these numerous older patients who come on these sites and say that when they were switched from desiccated thyroid to thyroxine, they got worse and give numerous examples of how they got worse?? The patients saw the increase! Is the only true opinion that of the doctors and not these patients? Who is Dr. David Derry who stated that he definitely saw the increase in symptoms, and especially when the TSH was introduced? And who are all these patients who, though they were never on desiccated thyroid at the beginning, state they noticed a huge difference in the resolution of symptoms when they switched to desiccated thyroid? Does the average doctor just cop out and say it's a placebo effect of thousands of patients?

Additionally, perhaps doctors didn't see the increase in symptoms because it was decided that instead, a series of "new" and mysterious conditions were popping up, aka "Chronic Fatigue Syndrome". If you haven't already, check out the time frame between patients going on thyoxine, and the sudden appearance of CFS. Additionally, chronic low grade depression became rampant when patients were moved onto thyroxine. Low free T3, which is common on thyroxine, has a strong connection with chronic depression. Also, note the rise in high cholesterol in patients on thyroxine. That is not a simple coincidence of a MacDonalds society.

And frankly, even I can identify with the frustration of these patients when you state that nothing on these websites is 'convincing evidence'. Since when is the repeated experience of patients not evidence! Evidence is not just found in written reports! There are thousands of patients right now reporting the exact same experience--that switching to desiccated thyroid has rid them of the irritating if not debilitating symptoms they had while on thyroxine, and that their doctors have never been listening. Experience is evidence!! These websites are not manned by a plethera of looney tunes reporting their senseless illusions.

Overall, the page is well done and presents a wide variety of information. But in some spots and most expecially in this summary, it's "exactly and consisely correct" only in the eyes of someone who wrote it and his medical colleagues, and definitely does not represent the opinion of a large and growing body of patients who are consisely reporting what they have experienced, and appear to know what they are talking about when they state that doctors aren't listening, and never have.

Doodlebug1 16:32, 24 July 2006 (UTC)

Calm down. Our only disagreement is whether the patients you describe are the majority or minority of hypothyroid people on replacement. You and those websites do not offer a shred of evidence that they represent the majority. Everything else, from published trials, to the experience of the doctors who treat the most thyroid patients, to the sales figures, says that the majority of people with hypothyroidism taking thyroxine are satisfied that it works. This is a simple matter of fact, not my opinion or bias. How about if we add a sentence that some thyroid extract advocates think everyone with hypothyroidism would prefer thyroid extract? Would that satisfy you? alteripse 19:29, 24 July 2006 (UTC)

Another reply, and a hopeful win-win summary

Calm down? Laughing. If I was currently any more calm, I'd be snoring. I ate too much at dinner, and got too little sleep last night.

I think you may be getting it. But do note that I never proposed that it was a "majority", as you were hard bent on saying it was a minority, What I have been trying to communicate to you is that this summary represents ONLY the viewpoint of doctors, and not this strong, well-versed and growing body of patients, who have a very opposite opinion based on their experiences.

You even confirmed my concern when you stated "from published trials, to the experience of doctors, to sales figures". Since when is evidence ONLY found in trials, doctors and sales figures, and not also in the experience of patients??? Oh how I am chuckling. I'm sorry for the sarcasm, but it really does besmirch the intelligence and experiential accounts of a growing body of patients out there who are spreading the word of their experience. It reminds me of the patient who comes in saying they have a stomach ache after eating four Milky Ways, and the doctor saying there are no "trial, observations, or sales figures" to support the claim of a stomach ache, so the stomach is dismissed while the patient walks out in agony with her sample anti-depressants in hand. (smile)

Frankly, I think the best way to remedy the bias of the summary is something like this, with my additions in italics. It incorporates your opinion, with the opinion of these patients:

At present, a large majority of people (at least in the English-speaking world) of all ages with hypothyroidism are being replaced with synthetic levothyroxine. When their blood levels of thyroid hormones and TSH are within range, doctors report that the patients have no more signs and symptoms of hypothyroidism than similar members of the population.

On the other hand, there is a growing body of thyroid patients who feel that current methods of replacement with thyroxine, guided by normalization of TSH, do not completely eradicate all of the symptoms they attribute to their hypothyroidism. Many of them report that thyroid extract gives them better symptom relief, often at doses that produce suppressed, below range levels of TSH, and a free T3 towards the top of the range.

I added the "below range levels" to appeal to the lay person who may have no idea what is meant by a 'suppressed' TSH. And most patients will have no idea what you mean by "thyroid extract" but I left it anyway in case they read the rest of the article.

Doodlebug1 00:49, 25 July 2006 (UTC)

Closer. But the only thing you were mentioning in your previous objections was the majority/minority descriptions. Look again at the evidence business: I was not proposing evidence that some people dont think they are better off with thyroid extract but simply that they are in the minority. The only thing your websites cannot do is offer statistical evidence about what is majority and what view is minority. All the other pieces of evidence that I mentioned support that thyroxine works well for most people with hypothyroidism. Whether you like it or not, it is the simple truth, supported by many types of evidence. Second, your version is too complex for a summary and especially should avoid mixing in the separable issues of whether TSH should guide dosing and whether mixtures of T4+T3 are better than T4 alone. Those are relevant to the controversy, need to be mentioned in the article (as I did), but it is confusing to include them in the summary. Look again at the summary: it says most people are satisfactorily treated with thyroxine and a minority of people prefer thyroid extract because it provides better relief of their symptoms. Those are the basic unbiased facts most supported by the preponderance of the evidence, aren't they? alteripse 01:04, 25 July 2006 (UTC)

Response

Well, I thought we were coming to a more win-win agreement on this summary, which I find in my life to be a mature way of dealing with disagreements. But I see you are holding fast to your way of thinking rather than finding the win in both.

Yup, I have no qualms with you that "all the other pieces of evidence that I mentioned support that thyroxine works well for most people with hypothyroidism". Trials, doctors and sales. LOL. But, as I've said numerous times above, if you leave off the evidence of "patients experience", and not be open to the fact that it may not be a "significant minority", this summary continues to thumb the nose at these growing body of patients whose EXPERIENCE is saying otherwise. If you fail to at the very least CONSIDER that evidence, you are no better than the doctors these patients strongly lament about.

And I can only repeat once again: If the summary continues to state that "the majority" have no more signs and symptoms while on thyroxine, it's ridiculously biased. Because a SIGNIFICANT BODY OF PATIENTS (i.e. no matter what size it is) are saying exactly the opposite. Without mentioning that, and leaving out the biased judgement that it's a 'signficant minority', the summary is biased.

I chuckle at the way you state "it's the simple truth." Because nothing in life, my friend, is the "simple truth." And for your last sentence to state "Those are the basic unbiased facts most supported by the preponderance of the evidence, aren't they? ", you once again reveal that you plan to continue to ignore the evidence of these patient's experience---the experience they are doing a bangup job describing, and which has been growing in leaps and bounds the past 6 years.

I could keep going in and changing the summary to what I feel incorporates both our thoughts, and you can keep going in and changing it to only YOUR biased opinion. But I have better things to do with my energy that that. lol. And now I certainly understand the sentiments of these brave patients concerning doctors!! They make "trials, doctors opinion, and sales reports far more important evidence than "experience"--the very experiences which are being expressed all over the place, and by quite a large and growing body of patients. Fere libenter homines id quod volunt credunt. And a good evening to you. Doodlebug1 02:33, 26 July 2006 (UTC)

I am exasperated. You have offered NO evidence that the majority of people do better with thyroid extract than thyroxine, only the opinions of a minority. You can insult me all you want, but that is not evidence either. It is entirely reasonable for me to say that some people prefer thyroid and most do well with thyroxine because it is exactly the state of affairs. Go back and look at the biased mess of propaganda this article was before I worked on it; a reader could not even understand what the history and controversy was-- there was not a SINGLE attempt to represent any other perspective on the issue than the Armour thyroid propaganda. If you were largely responsible for it, you have no business accusing me of bias, as I have included every single factual point you wanted included. I draw the line at complete fantasy. alteripse 02:49, 26 July 2006 (UTC)

Reference for Armour Thyroid Usage

You are missing the very first book I read on hypothyroidism (I've read 10 or so now). This book saved my life. Doctors just ignored my symptoms for 20 years.

Feeling Fat, Fuzzy or Frazzled?: A 3-Step Program to: Beat Hormone Havoc, Restore Thyroid, Adrenal, and Reproductive Balance, and Feel Better Fast! by Karilee Shames, Richard Shames, Hudson Street Press (July 7, 2005), ISBN: 159463002X

It seems the author(s) spent time on the groups I am on but only picked up our general talk and not the serious research behind our discussion. Like the TSH test. It tests the feedback of the pituitary and the thyroid, not thryoid function. Most endos live for this test and left me sick for over twenty years because of numbers. T3 and T4 test for only the hormones that are bound to protein in the blood. That's the hormones that aren't useable by the body. To get an accurate view of the thyroid , you need the Free T3 and Free T4 tested. This is the hormone levels of freely circulating hormone that is useable by the body.

If you want a truly un-biased article you need to read your references to find the research that the endos ignore. The endos don't even follow the new guidelines for TSH values. Most won't treat if you test 5.0 or less when their own organization (American Association of Clinical Endocrinologists) uses 3.0 as the upper range. http://www.aace.com/newsroom/press/2003/index.php?r=20030118 - Over 13 Million Americans with Thyroid Disease Remain Undiagnosed.

Aswafford 16:31, 20 August 2006 (UTC)

So how about some citations to your "serious research"? alteripse 00:26, 21 August 2006 (UTC)

Armour versus Synthroid

The following is incorrect. "Despite claims of proponents that desiccated thyroid pills are superior to thyroxine or combinations of T4 and T3 for most people with hypothyroidism, no controlled clinical trials have been published, and many physicians remain unconvinced that the superiority is anything other than a placebo effect or an overtreatment effect."

Reference a clinical study published in the New England Jornal of Medicine: Toft AD. “Thyroid hormone replacement—one hormone or two?” N Engl J Med 1999 Feb 11;340(6):469-70.

An article in the New England Journal of Medicine described a study in which patients with hypothyroidism showed greater improvements in mood and brain function if they received treatment with Armour thyroid rather than Synthroid (thyroxine). The authors also detected biochemical evidence that thyroid hormone action was greater after treatment with Armour thyroid.

More useful information is found here: http://search.lef.org/cgi-src-bin/MsmGo.exe?grab_id=0&page_id=1322&query=hypothyroid&hiword=HYPOTHYROIDIC%20hypothyroid%20

Aswafford

Not a single patient in that study took desiccated thyroid. Your citation describes a comparison of synthetic thyroxine versus T4+T3, not desiccated thyroid. The statement is absolutely correct and in fact was written with exactly this type of study in mind. You are being intellectually dishonest or very sloppy at offering this study as supporting desiccated thyroid when not a single patient in the study took desiccated thyroid. Come back when you have something better. alteripse 17:13, 9 September 2006 (UTC)

I get my information from doctors who quote the study. Dr. Mercola mentions the study here www.mercola.com/1999/archive/armour_thyroid.htm and Dr Kellman mentions it in his article here http://search.lef.org/cgi-src-bin/MsmGo.exe?grab_id=0&page_id=4787&query=new%20england%20journal%20armour&hiword=ARMOURY%20ENGLANDS%20JOURNALISM%20JOURNALIST%20JOURNALS%20armour%20england%20journal%20new%20. Another doctor here http://www.weeksmd.com/articles/weight_loss/at_syn.php. So I guess you have issues with their intellectual dishonesty and/or sloppiness. Aswafford

Toft's article is an editorial comment PMID 9971874 that describes the famous Bunevicius study PMID 9971866 link to full text already mentioned that compared synthetic t4 with synthetic t4 + synthetic t3. It did not involve Armour thyroid. Not a single patient took desiccated thyroid. Read my words: NOT A SINGLE PATIENT. You can draw your own conclusions about the intellectual honesty of your sources but I have already drawn mine. They have made a fool of you. alteripse 02:28, 13 September 2006 (UTC) Look, I dont blame you after looking at your sources, but you need to recognize that intellectual honesty is not valued among the Armour proponents: this type of bait and switch is typical and it works because naive people can't believe they would deliberately mispresent a study like that. You need to learn to rely on credible, honest sources. alteripse 03:09, 13 September 2006 (UTC)

testimonial

I am a member on the Yahoo boards that are cited in some of the above references. I won't be citing any studies here; just giving my patient experience. While I have read many articles, both anecdotal and scientific, it is interesting to me that doctors should only be relying on blood tests, which don't always reflect what is really in the tissues, to treat patients. I was diagnosed 20+ years ago as hypothyroid and treated with Levoxyl. I never felt well, gained weight while eating no differently than I had prior to the onset, had terribly dry skin, even in the summer, when the air here in Chicago itself is quite moist, my energy level plummeted, plus many other symptoms. Doctors, and I have seen a few, brush off symptoms and go by tests only, at least the ones I have seen. I'm sorry, but I am NOT a lab value, I am a patient, a person, who needed help, and not one doctor caught on to that - as long as my labs looked good, I was "normal"! I'm sorry, but the state I was in was not normal, and I am angry that it was not recognized by even one so-called professional! The whole patient should be treated, not just the lab values, but also the symptoms. I am now using Armour, 1.5 grains, backed up with adrenal support given to me by my Chiro/Kinesiologist, who knows my situation and tested me for adrenal function and found it wanting. I have also added iodine. I am feeling better than I have in years, and while I have a ways to go to feel normal again, what is happening here is an improvement, definitely. And, no I am not imagining it, nor do I believe that it is due to the "placebo effect" but to my body finally getting what it needed for proper function. I am done with synthetics, I don't believe that they are for every one. Some do quite well on them, but others need more than synthetics can give them. We are all different, and that is what is not being recognized. cccquilter@sbcglobal.net

Thanks for contributing your experience. Your experience is typical of many people and the article attempts to accurately reflect it. As you say, different people need different treatments. I am not against Armour thyroid, but against dishonest claims, as in the section above. I assume you are not defending those. alteripse 02:52, 14 September 2006 (UTC)

Another testimonial

I have been hypothyroid for 3 years now. I have used Synthroid mostly, and Armour for 2 months. Synthroid doesn't treat me 100%, or even 90%. I feel depressed and anxious most of the time, and usually have low energy. When I used Armour, I became another man, it pulled the depression off in 2 weeks, incredibly. But I had fatigue, and I was afraid of the TSH test results. So I went back to Synthroid. I am depressed again and having anxiety. I will probably go back to Armour. The article is not right when it says Armour has no better effect.

That is not what the article says. The article says some people feel better on Armour. alteripse 23:16, 25 January 2007 (UTC)

Merge with Armour Thyroid

• For merge. They are the same substance chemically and legally. An "Armour Thyroid" article borders on commercial use, and the title should be eliminated. Pustelnik (talk) 16:05, 23 December 2008 (UTC)

Dubious

Even if the facts are perfectly true, "a bunch of people chatting on a Yahoo! Groups discussion board" is not a reliable source. WhatamIdoing (talk) 05:04, 13 January 2008 (UTC) Perhaps you would like this article which may clear up some misconceptions about the state of medical treatment and why people feel the way they do about it. It has citations at the end to its sources. Brador1Brador1 (talk) 23:35, 18 May 2008 (UTC)

www.RayPeat.com ©2006-08 Ray Peat All Rights Reserved

A R T I C L E

TSH, temperature, pulse rate, and other indicators in hypothyroidism

Each of the indicators of thyroid function can be useful, but has to be interpreted in relation to the physiological state.

Increasingly, TSH (the pituitary thyroid stimulating hormone) has been treated as if it meant something independently; however, it can be brought down into the normal range, or lower, by substances other than the thyroid hormones.

“Basal” body temperature is influenced by many things besides thyroid. The resting heart rate helps to interpret the temperature. In a cool environment, the temperature of the extremities is sometimes a better indicator than the oral or eardrum temperature.

The “basal” metabolic rate, especially if the rate of carbon dioxide production is measured, is very useful. The amount of water and calories disposed of in a day can give a rough idea of the metabolic rate.

The T wave on the electrocardiogram, and the relaxation rate on the Achilles reflex test are useful.

Blood tests for cholesterol, albumin, glucose, sodium, lactate, total thyroxine and total T3 are useful to know, because they help to evaluate the present thyroid status, and sometimes they can suggest ways to correct the problem.

Less common blood or urine tests (adrenaline, cortisol, ammonium, free fatty acids), if they are available, can help to understand compensatory reactions to hypothyroidism.

A book such as McGavack's The Thyroid, that provides traditional medical knowledge about thyroid physiology, can help to dispel some of the current dogmas about the thyroid.

Using more physiologically relevant methods to diagnose hypothyroidism will contribute to understanding its role in many problems now considered to be unrelated to the thyroid.

==========================

I have spoken to several people who told me that their doctors had diagnosed them as “both hypothyroid and hyperthyroid.” Although physicists can believe in things which are simultaneously both particles and not particles, I think biology (and medicine, as far as it is biologically based) should occupy a world in which things are not simultaneously themselves and their opposites. Those illogical, impossible diagnoses make it clear that the rules for interpreting test results have in some situations lost touch with reality.

Until the 1940s, hypothyroidism was diagnosed on the basis of signs and symptoms, and sometimes the measurement of oxygen consumption (“basal metabolic rate”) was used for confirmation. Besides the introduction of supposedly “scientific” blood tests, such as the measurement of protein-bound iodine (PBI) in the blood, there were other motives for becoming parsimonious with the diagnosis of hypothyroidism. With the introduction of synthetic thyroxine, one of the arguments for increasing its sale was that natural Armour thyroid (which was precisely standardized by biological tests) wasn't properly standardized, and that an overdose could be fatal. A few articles in prestigious journals created a myth of the danger of thyroid, and the synthetic thyroxine was (falsely) said to be precisely standardized, and to be without the dangers of the complete glandular extract.

Between 1940 and about 1950, the estimated percentage of hypothyroid Americans went from 30% or 40% to 5%, on the basis of the PBI test, and it has stayed close to that lower number (many publications claim it to be only 1% or 2%). By the time that the measurement of PBI was shown to be only vaguely related to thyroid hormonal function, it had been in use long enough for a new generation of physicians to be taught to disregard the older ideas about diagnosing and treating hypothyroidism. They were taught to inform their patients that the traditional symptoms that were identified as hypothyroidism before 1950 were the result of the patients' own behavior (sloth and gluttony, for example, which produced fatigue, obesity, and heart disease), or that the problems were imaginary (women's hormonal and neurological problems, especially), or that they were simply mysterious diseases and defects (recurring infections, arthritis, and cancer, for example).

As the newer, more direct tests became available, their meaning was defined in terms of the statistical expectation of hypothyroidism that had become an integral part of medical culture. To make the new TSH measurements fit the medical doctrine, an 8- or 10-fold variation in the hormone was defined as “normal.” With any other biological measurement, such as erythrocyte count, blood pressure, body weight, or serum sodium, calcium, chloride, or glucose, a variation of ten or 20 percent from the mean is considered to be meaningful. If the doctrine regarding the 5% prevalence of hypothyroidism hadn't been so firmly established, there would have been more interest in establishing the meaning of these great variations in TSH.

In recent years the “normal range” for TSH has been decreasing. In 2003, the American Association of Clinical Endocrinologists changed their guidelines for the normal range to 0.3 to 3.0 microIU/ml. But even though this lower range is less arbitrary than the older standards, it still isn't based on an understanding of the physiological meaning of TSH.

Over a period of several years, I never saw a person whose TSH was over 2 microIU/ml who was comfortably healthy, and I formed the impression that the normal, or healthy, quantity was probably something less than 1.0.

If a pathologically high TSH is defined as normal, its role in major diseases, such as breast cancer, mastalgia, MS, fibrotic diseases, and epilepsy, will simply be ignored. Even if the possibility is considered, the use of an irrational norm, instead of a proper comparison, such as the statistical difference between the mean TSH levels of cases and controls, leads to denial of an association between hypothyroidism and important diseases, despite evidence that indicates an association.

Some critics have said that most physicians are “treating the TSH,” rather than the patient. If TSH is itself pathogenic, because of its pro-inflammatory actions, then that approach isn't entirely useless, even when they “treat the TSH” with only thyroxine, which often isn't well converted into the active triiodothyronine, T3. But the relief of a few symptoms in a small percentage of the population is serving to blind the medical world to the real possibilities of thyroid therapy.

TSH has direct actions on many cell types other than the thyroid, and probably contributes directly to edema (Wheatley and Edwards, 1983), fibrosis, and mastocytosis. If people are concerned about the effects of a TSH “deficiency,” then I think they have to explain the remarkable longevity of the animals lacking pituitaries in W.D. Denckla's experiments, or of the naturally pituitary deficient dwarf mice that lack TSH, prolactin, and growth hormone, but live about a year longer than normal mice (Heiman, et al., 2003). Until there is evidence that very low TSH is somehow harmful, there is no basis for setting a lower limit to the normal range.

Some types of thyroid cancer can usually be controlled by keeping TSH completely suppressed. Since TSH produces reactions in cells as different as fibroblasts and fat cells, pigment cells in the skin, mast cells and bone marrow cells (Whetsell, et al., 1999), it won't be surprising if it turns out to have a role in the development of a variety of cancers, including melanoma.

Many things, including the liver and the senses, regulate the function of the thyroid system, and the pituitary is just one of the factors affecting the synthesis and secretion of the thyroid hormones.

A few people who had extremely low levels of pituitary hormones, and were told that they must take several hormone supplements for the rest of their life, began producing normal amounts of those hormones within a few days of eating more protein and fruit. Their endocrinologist described them as, effectively, having no pituitary gland. Extreme malnutrition in Africa has been described as creating “. . . a condition resembling hypophysectomy,” (Ingenbleek and Beckers, 1975) but the people I talked to in Oregon were just following what they thought were healthful nutritional policies, avoiding eggs and sugars, and eating soy products.

Occasionally, a small supplement of thyroid in addition to a good diet is needed to quickly escape from the stress-induced “hypophysectomized” condition.

Aging, infection, trauma, prolonged cortisol excess, somatostatin, dopamine or L-dopa, adrenaline (sometimes; Mannisto, et al., 1979), amphetamine, caffeine and fever can lower TSH, apart from the effect of feedback by the thyroid hormones, creating a situation in which TSH can appear normal or low, at the same time that there is a real hypothyroidism.

A disease or its treatment can obscure the presence of hypothyroidism. Parkinson's disease is a clear example of this. (Garcia-Moreno and Chacon, 2002: “... in the same way hypothyroidism can simulate Parkinson's disease, the latter can also conceal hypothyroidism.”)

The stress-induced suppression of TSH and other pituitary hormones is reminiscent of the protective inhibition that occurs in individual nerve fibers during dangerously intense stress, and might involve such a “parabiotic” process in the nerves of the hypothalamus or other brain region. The relative disappearance of the pituitary hormones when the organism is in very good condition (for example, the suppression of ACTH and cortisol by sugar or pregnenolone) is parallel to the high energy quiescence of individual nerve fibers.

These associations between energy state and cellular activity can be used for evaluating the thyroid state, as in measuring nerve and muscle reaction times and relaxation rates. For example, relaxation which is retarded, because of slow restoration of the energy needed for cellular “repolarization,” is the basis for the traditional use of the Achilles tendon reflex relaxation test for diagnosing hypothyroidism. The speed of relaxation of the heart muscle also indicates thyroid status (Mohr-Kahaly, et al., 1996).

Stress, besides suppressing the TSH, acts in other ways to suppress the real thyroid function. Cortisol, for example, inhibits the conversion of T4 to T3, which is responsible for the respiratory production of energy and carbon dioxide. Adrenaline, besides leading to increased production of cortisol, is lipolytic, releasing the fatty acids which, if they are polyunsaturated, inhibit the production and transport of thyroid hormone, and also interfere directly with the respiratory functions of the mitochondria. Adrenaline decreases the conversion to T4 to T3, and increases the formation of the antagonistic reverse T3 (Nauman, et al., 1980, 1984).

During the night, at the time adrenaline and free fatty acids are at their highest, TSH usually reaches its peak. TSH itself can produce lipolysis, raising the level of circulating free fatty acids. This suggests that a high level of TSH could sometimes contribute to functional hypothyroidism, because of the antimetabolic effects of the unsaturated fatty acids.

These are the basic reasons for thinking that the TSH tests should be given only moderate weight in interpreting thyroid function.

The metabolic rate is very closely related to thyroid hormone function, but defining it and measuring it have to be done with awareness of its complexity.

The basal metabolic rate that was commonly used in the 1930s for diagnosing thyroid disorders was usually a measurement of the rate of oxygen consumption, made while lying quietly early in the morning without having eaten anything for several hours. When carbon dioxide production can be measured at the same time as oxygen consumption, it's possible to estimate the proportion of energy that is being derived from glucose, rather than fat or protein, since oxidation of glucose produces more carbon dioxide than oxidation of fat does. Glucose oxidation is efficient, and suggests a state of low stress.

The very high adrenaline that sometimes occurs in hypothyroidism will increase the metabolic rate in several ways, but it tends to increase the oxidation of fat. If the production of carbon dioxide is measured, the adrenaline/stress component of metabolism will be minimized in the measurement. When polyunsaturated fats are mobilized, their spontaneous peroxidation consumes some oxygen, without producing any usable energy or carbon dioxide, so this is another reason that the production of carbon dioxide is a very good indicator of thyroid hormone activity. The measurement of oxygen consumption was usually done for two minutes, and carbon dioxide production could be accurately measured in a similarly short time. Even a measurement of the percentage of carbon dioxide at the end of a single breath can give an indication of the stress-free, thyroid hormone stimulated rate of metabolism (it should approach five or six percent of the expired air).

Increasingly in the last several years, people who have many of the standard symptoms of hypothyroidism have told me that they are hyperthyroid, and that they have to decide whether to have surgery or radiation to destroy their thyroid gland. They have told me that their symptoms of “hyperthyroidism,” according to their physicians, were fatigue, weakness, irritability, poor memory, and insomnia.

They didn't eat very much. They didn't sweat noticeably, and they drank a moderate amount of fluids. Their pulse rates and body temperature were normal, or a little low.

Simply on the basis of some laboratory tests, they were going to have their thyroid gland destroyed. But on the basis of all of the traditional ways of judging thyroid function, they were hypothyroid.

Broda Barnes, who worked mostly in Fort Collins, Colorado, argued that the body temperature, measured before getting out of bed in the morning, was the best basis for diagnosing thyroid function.

Fort Collins, at a high altitude, has a cool climate most of the year. The altitude itself helps the thyroid to function normally. For example, one study (Savourey, et al., 1998) showed an 18% increase in T3 at a high altitude, and mitochondria become more numerous and are more efficient at preventing lactic acid production, capillary leakiness, etc.

In Eugene during a hot and humid summer, I saw several obviously hypothyroid people whose temperature seemed perfectly normal, euthyroid by Barnes' standards. But I noticed that their pulse rates were, in several cases, very low. It takes very little metabolic energy to keep the body at 98.6 degrees when the air temperature is in the nineties. In cooler weather, I began asking people whether they used electric blankets, and ignored their temperature measurements if they did.

The combination of pulse rate and temperature is much better than either one alone. I happened to see two people whose resting pulse rates were chronically extremely high, despite their hypothyroid symptoms. When they took a thyroid supplement, their pulse rates came down to normal. (Healthy and intelligent groups of people have been found to have an average resting pulse rate of 85/minute, while less healthy groups average close to 70/minute.)

The speed of the pulse is partly determined by adrenaline, and many hypothyroid people compensate with very high adrenaline production. Knowing that hypothyroid people are susceptible to hypoglycemia, and that hypoglycemia increases adrenaline, I found that many people had normal (and sometimes faster than average) pulse rates when they woke up in the morning, and when they got hungry. Salt, which helps to maintain blood sugar, also tends to lower adrenalin, and hypothyroid people often lose salt too easily in their urine and sweat. Measuring the pulse rate before and after breakfast, and in the afternoon, can give a good impression of the variations in adrenalin. (The blood pressure, too, will show the effects of adrenaline in hypothyroid people. Hypothyroidism is a major cause of hypertension.)

But hypoglycemia also tends to decrease the conversion of T4 to T3, so heat production often decreases when a person is hungry. First, their fingers, toes, and nose will get cold, because adrenalin, or adrenergic sympathetic nervous activity, will increase to keep the brain and heart at a normal temperature, by reducing circulation to the skin and extremities. Despite the temperature-regulating effect of adrenalin, the reduced heat production resulting from decreased T3 will make a person susceptible to hypothermia if the environment is cool.

Since food, especially carbohydrate and protein, will increase blood sugar and T3 production, eating is “thermogenic,” and the oral (or eardrum) temperature is likely to rise after eating.

Blood sugar falls at night, and the body relies on the glucose stored in the liver as glycogen for energy, and hypothyroid people store very little sugar. As a result, adrenalin and cortisol begin to rise almost as soon as a person goes to bed, and in hypothyroid people, they rise very high, with the adrenalin usually peaking around 1 or 2 A.M., and the cortisol peaking around dawn; the high cortisol raises blood sugar as morning approaches, and allows adrenalin to decline. Some people wake up during the adrenalin peak with a pounding heart, and have trouble getting back to sleep unless they eat something.

If the night-time stress is very high, the adrenalin will still be high until breakfast, increasing both temperature and pulse rate. The cortisol stimulates the breakdown of muscle tissue and its conversion to energy, so it is thermogenic, for some of the same reasons that food is thermogenic.

After eating breakfast, the cortisol (and adrenalin, if it stayed high despite the increased cortisol) will start returning to a more normal, lower level, as the blood sugar is sustained by food, instead of by the stress hormones. In some hypothyroid people, this is a good time to measure the temperature and pulse rate. In a normal person, both temperature and pulse rate rise after breakfast, but in very hypothyroid people either, or both, might fall.

Some hypothyroid people have a very slow pulse, apparently because they aren't compensating with a large production of adrenalin. When they eat, the liver's increased production of T3 is likely to increase both their temperature and their pulse rate.

By watching the temperature and pulse rate at different times of day, especially before and after meals, it's possible to separate some of the effects of stress from the thyroid-dependent, relatively “basal” metabolic rate. When beginning to take a thyroid supplement, it's important to keep a chart of these measurements for at least two weeks, since that's roughly the half-life of thyroxine in the body. When the body has accumulated a steady level of the hormones, and begun to function more fully, the factors such as adrenaline that have been chronically distorted to compensate for hypothyroidism will have begun to normalize, and the early effects of the supplementary thyroid will in many cases seem to disappear, with heart rate and temperature declining. The daily dose of thyroid often has to be increased several times, as the state of stress and the adrenaline and cortisol production decrease.

Counting calories achieves approximately the same thing as measuring oxygen consumption, and is something that will allow people to evaluate the various thyroid tests they may be given by their doctor. Although food intake and metabolic rate vary from day to day, an approximate calorie count for several days can often make it clear that a diagnosis of hyperthyroidism is mistaken. If a person is eating only about 1800 calories per day, and has a steady and normal body weight, any “hyperthyroidism” is strictly metaphysical, or as they say, “clinical.”

When the humidity and temperature are normal, a person evaporates about a liter of water for every 1000 calories metabolized. Eating 2000 calories per day, a normal person will take in about four liters of liquid, and form about two liters of urine. A hyperthyroid person will invisibly lose several quarts of water in a day, and a hypothyroid person may evaporate a quart or less.

When cells, because of a low metabolic rate, don't easily return to their thoroughly energized state after they have been stimulated, they tend to take up water, or, in the case of blood vessels, to become excessively permeable. Fatigued muscles swell noticeably, and chronically fatigued nerves can swell enough to cause them to be compressed by the surrounding connective tissues. The energy and hydration state of cells can be detected in various ways, including magnetic resonance, and electrical impedance, but functional tests are easy and practical.

With suitable measuring instruments, the effects of hypothyroidism can be seen as slowed conduction along nerves, and slowed recovery and readiness for new responses. Slow reaction time is associated with slowed memory, perception, and other mental processes. Some of these nervous deficits can be remedied slightly just by raising the core temperature and providing suitable nutrients, but the active thyroid hormone, T3 is mainly responsible for maintaining the temperature, the nutrients, and the intracellular respiratory energy production.

In nerves, as in other cells, the ability to rest and repair themselves increases with the proper level of thyroid hormone. In some cells, the energized stability produced by the thyroid hormones prevents inflammation or an immunological hyperactivity. In the 1950s, shortly after it was identified as a distinct substance, T3 was found to be anti-inflammatory, and both T4 and T3 have a variety of anti-inflammatory actions, besides the suppression of the pro-inflammatory TSH.

Because the actions of T3 can be inhibited by many factors, including polyunsaturated fatty acids, reverse T3, and excess thyroxine, the absolute level of T3 can't be used by itself for diagnosis. “Free T3” or “free T4” is a laboratory concept, and the biological activity of T3 doesn't necessarily correspond to its “freedom” in the test. T3 bound to its transport proteins can be demonstrated to enter cells, mitochondria, and nuclei. Transthyretin, which carries both vitamin A and thyroid hormones, is sharply decreased by stress, and should probably be regularly measured as part of the thyroid examination.

When T3 is metabolically active, lactic acid won't be produced unnecessarily, so the measurement of lactate in the blood is a useful test for interpreting thyroid function. Cholesterol is used rapidly under the influence of T3, and ever since the 1930s it has been clear that serum cholesterol rises in hypothyroidism, and is very useful diagnostically. Sodium, magnesium, calcium, potassium, creatinine, albumin, glucose, and other components of the serum are regulated by the thyroid hormones, and can be used along with the various functional tests for evaluating thyroid function.

Stereotypes are important. When a very thin person with high blood pressure visits a doctor, hypothyroidism isn't likely to be considered; even high TSH and very low T4 and T3 are likely to be ignored, because of the stereotypes. (And if those tests were in the healthy range, the person would be at risk for the “hyperthyroid” diagnosis.) But remembering some of the common adaptive reactions to a thyroid deficiency, the catabolic effects of high cortisol and the circulatory disturbance caused by high adrenaline should lead to doing some of the appropriate tests, instead of treating the person's hypertension and “under nourished” condition.

REFERENCES

Clin Chem Lab Med. 2002 Dec;40(12):1344-8. Transthyretin: its response to malnutrition and stress injury. Clinical usefulness and economic implications. Bernstein LH, Ingenbleek Y.

Endokrinologie. 1968;53(3):217-21.[Influence of hypophysectomy and pituitary hormones on dextran edema in rats] German. Boeskor A, Gabbiani G.

J Clin Endocrinol Metab. 2001 Nov;86(11):5148-51. Sudden enlargement of local recurrent thyroid tumor after recombinant human TSH administration. Braga M, Ringel MD, Cooper DS.

J Investig Med. 2002 Sep;50(5):350-4; discussion 354-5. The nocturnal serum thyrotropin surge is inhibited in patients with adrenal Incidentaloma. Coiro V, Volpi R, Capretti L, Manfredi G, Magotti MG, Bianconcini M, Cataldo S, Chiodera P.

Rev Neurol (Paris). 1992;148(5):371-3. [Hashimoto's encephalopathy: toxic or autoimmune mechanism?] [Article in French] Ghawche F, Bordet R, Destee A. Service de Clinique Neurologique A, CHU, Lille. A 36-year-old woman presented with partial complex status epilepticus. Magnetic resonance imaging with T2-weighted sequences showed a high-intensity signal in the left posterior frontal area. Hashimoto's thyroiditis was then discovered. The disappearance of the high-intensity signal after corticosteroid therapy was suggestive of an autoimmune mechanism. However, improvement could be obtained only with a hormonal treatment, which supports the hypothesis of a pathogenetic role of the Tyrosine-Releasing Hormone (TRH).

Am J Clin Nutr. 1986 Mar;43(3):406-13. Thyroid hormone and carrier protein interrelationships in children recovering rom kwashiorkor. Kalk WJ, Hofman KJ, Smit AM, van Drimmelen M, van der Walt LA, Moore RE. We have studied 15 infants with severe protein energy malnutrition (PEM) as a model of nutritional nonthyroidal illness. Changes in circulating thyroid hormones, binding proteins, and their interrelationships were assessed before and during recovery. Serum concentrations of total thyroxine and triiodothyronine and of thyroxine-binding proteins were extremely reduced, and increased progressively during 3 wk of refeeding. The T4:TBG molar ratio was initially 0.180 +/- 0.020, and increased progressively, parallel to the increases in TT4, to 0.344 +/- 0.038 after 21 days (p less than 0.025). The changes in free T4 estimates varied according to the methods used--FTI and analogue FT4 increased, dialysis FT4 fraction decreased. Serum TSH levels increased transiently during recovery. It is concluded 1) there is reduced binding of T4 and T3 to TBG in untreated PEM which takes 2-3 wk to recover; 2) there are methodological differences in evaluating free T4 levels in PEM; 3) increased TSH secretion appears to be an integral part of the recovery from PEM.

Neuroendocrinology. 1982;35(2):139-47. Neurotransmitter control of thyrotropin secretion. Krulich L. “The central dopaminergic system seems to have an inhibitory influence on the secretion of thyrotropin (TSH) both in humans and rats.”

Endocrinology 1972 Mar;90(3):795-801. TSH-induced release of 5-hydroxytryptamine and histamine rat thyroid mast cells. Ericson LE, Hakanson R, Melander A, Owman C, Sundler F.

Rev Neurol. 2002 Oct 16-31;35(8):741-2. [Hypothyroidism concealed by Parkinson's disease][in Spanish] Garcia-Moreno JM, Chacon J. Servicio de Neurologia, Hospital Universitario Virgen Macarena, Sevilla, Espana. Sinue@arrakis.es AIMS: Although it is commonly recognised that diseases of the thyroids can simulate extrapyramidal disorders, a review of the causes of Parkinsonism in the neurology literature shows that they are not usually mentioned or, if so, only very briefly. The development of hypothyroidism in a patient with Parkinson s disease can go undetected, since the course of both diseases can involve similar clinical features. Generally speaking there is always an insistence on the need to conduct a thyroidal hormone study in any patient with symptoms of Parkinson, but no emphasis is put on the need to continue to rule out dysthyroidism throughout the natural course of the disease, in spite of the fact that the concurrence of both pathological conditions can be high and that, in the same way hypothyroidism can simulate Parkinson s disease, the latter can also conceal hypothyroidism. CASE REPORT: We report the case of a female patient who had been suffering from Parkinson s disease for 17 years and started to present on off fluctuations that did not respond to therapy. Hypothyroidism was observed and the hormone replacement therapy used to resolve the problem allowed the Parkinsonian fluctuations to be controlled. CONCLUSIONS: We believe that it is very wise to suspect hypothyroidism in patients known to be suffering from Parkinson s disease, and especially so in cases where the clinical condition worsens and symptoms no longer respond properly to antiparkinsonian treatment. These observations stress the possible role played by thyroid hormones in dopaminergic metabolism and vice versa.

Endocrine. 2003 Feb-Mar;20(1-2):149-54. Body composition of prolactin-, growth hormone, and thyrotropin-deficient Ames dwarf mice. Heiman ML, Tinsley FC, Mattison JA, Hauck S, Bartke A. Lilly Research Labs, Corporate Center, Indianapolis, IN, USA. Ames dwarf mice have primary deficiency of prolactin (PRL), growth hormone (GH), and thyroid-stimulating hormone (TSH), and live considerably longer than normal animals from the same line.

(Lancet. 1975 Nov 1;2(7940):845-8.. Triiodothyronine and thyroid-stimulating hormone in protein-calorie malnutrition in infants. Ingenbleek Y, Beckers C.)

Am J Med Sci. 1995 Nov;310(5):202-5. Case report: thyrotropin-releasing hormone-induced myoclonus and tremor in a patient with Hashimoto's encephalopathy. Ishii K, Hayashi A, Tamaoka A, Usuki S, Mizusawa H, Shoji S.

Rev Neurol (Paris). 1985;141(1):55-8. [Hashimoto's thyroiditis and myoclonic encephalopathy. Pathogenic hypothesis] [Article in French] Latinville D, Bernardi O, Cougoule JP, Bioulac B, Henry P, Loiseau P, Mauriac L. A 49 year old caucasian female with Hashimoto thyroiditis, developed during two years a neurological disorder with tonic-clonic and myoclonic seizures and confusional states. Some attacks were followed by a transient postictal aphasia. Some parallelism was noted between the clinical state and TSH levels. Neurological events disappeared with the normalisation of thyroid functions. This association of Hashimoto thyroiditis and myoclonic encephalopathy has been rarely published. Pathogenesis could be double. Focal signs could be due to an auto-immune mechanism, perhaps through a vasculitis. A non-endocrine central action could explain diffuse signs: tonic-clonic seizures, myoclonus and confusional episodes.

J Clin Endocrinol Metab. 1992 Jun;74(6):1361-5. Fatty acid-induced increase in serum dialyzable free thyroxine after physical exercise: implication for nonthyroidal illness. Liewendahl K, Helenius T, Naveri H, Tikkanen H.

Adv Exp Med Biol. 1990;274:315-29. Role of monokines in control of anterior pituitary hormone release. McCann SM, Rettori V, Milenkovic L, Jurcovicova J, Gonzalez MC.

Acta Endocrinol (Copenh). 1979 Feb;90(2):249-58. Dual action of adrenergic system on the regulation of thyrotrophin secretion in the male rat. Mannisto, Ranta T, Tuomisto J. "....noradrenaline (NA) (1 h), and L-Dopa (1 h) were also effective in decreasing serum TSH levels...."

Endocrinology 1971 Aug;89(2):528-33. TSH-induced appearance and stimulation of amine-containing mast cells in the mouse thyroid. Melander A, Owman C, Sundler F.

Epilepsy Res. 1988 Mar-Apr;2(2):102-10. Evidence of hypothyroidism in the genetically epilepsy-prone rat. Mills SA, Savage DD. Department of Pharmacology, University of New Mexico School of Medicine, Albuquerque 87131. A number of neurochemical and behavioral similarities exist between the genetically epilepsy-prone (GEPR) rat and rats made hypothyroid at birth. These similarities include lower brain monoamine levels, audiogenic seizure susceptibility and lowered electroconvulsive shock seizure threshold. Given these similarities, thyroid hormone status was examined in GEPR rats. Serum samples were collected from GEPR-9 and non-epileptic control rats at 5, 9, 13, 16, 22, 31, 45, 60, 90, 150 and 350 days of age. Serum thyroxine (T4) levels were significantly lower in GEPR-9 rats compared to control until day 22 of age. GEPR-9 thyrotropin (TSH) levels were significantly elevated during the period of diminished serum T4. GEPR-9 triiodothyronine (T3) levels were lower than control throughout the first year of life. The data indicate that the GEPR-9 rat is hypothyroid from at least the second week of life up to 1 year of age. The critical impact of neonatal hypothyroidism on brain function coupled with the development of the audiogenic seizure susceptible trait by the GEPR-9 rat during the third week after birth suggests that neonatal hypothyroidism could be one etiological factor in the development of the seizure-prone state of GEPR-9 rats.

Przegl Lek. 1998;55(5):250-8. [Mastopathy and simple goiter--mutual relationships] [Article in Polish] Mizia-Stec K, Zych F, Widala E. “Non-toxic goitre was found in 80% patients with mastopathy, and the results of palpation examination of thyroid were confirmed by thyroid ultrasonographic examination. Non-toxic goitre was significantly more often in patients with mastopathy in comparison with healthy women, and there was found significantly higher thyroid volume in these patients.” Endocrinology. 1997 Apr;138(4):1434-9. Thyroxine administration prevents streptococcal cell wall-induced inflammatory responses. Rittenhouse PA, Redei E.

Eur J Appl Physiol Occup Physiol. 1998;77(1-2):37-43. Pre-adaptation, adaptation and de-adaptation to high altitude in humans: hormonal and biochemical changes at sea level. Savourey G, Garcia N, Caravel JP, Gharib C, Pouzeratte N, Martin S, Bittel J.

Endocrinol Jpn. 1992 Oct;39(5):445-53. Plasma free fatty acids, inhibitor of extrathyroidal conversion of T4 to T3 and thyroid hormone binding inhibitor in patients with various nonthyroidal illnesses. Suzuki Y, Nanno M, Gemma R, Yoshimi T.

Natl Med J India. 1998 Mar-Apr;11(2):62-5. Neuropsychological impairment and altered thyroid hormone levels in epilepsy. Thomas SV, Alexander A, Padmanabhan V, Sankara Sarma P. Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, Kerala, India. BACKGROUND: Neuropsychological impairment is a common problem in epilepsy which interferes with the quality of life of patients. Similarly, thyroid hormone levels have been observed to be abnormal in patients with epilepsy on various treatments. This study aimed to ascertain any possible correlation between neuropsychological performance and thyroid hormone levels among epilepsy patients. METHODS: Thyroid hormone levels, indices of neuropsychological performance and social adaptation of 43 epilepsy patients were compared with those of age- and sex-matched healthy control subjects. RESULTS: Epilepsy patients exhibited significantly (p < 0.001) lower scores on attention, memory, constructional praxis, finger tapping time, and verbal intelligence quotient (i.q.) when compared with controls. Their T3, T4 and Free T3 levels were significantly lower; and TSH and Free T4 levels were significantly higher than that of controls. There was no statistically significant correlation between the indices of neuropsychological performance and thyroid hormone levels. CONCLUSION: We did not observe any correlation between neuropsychological impairment and thyroid hormone levels among patients with epilepsy.

Crit Care Med. 1994 Nov;22(11):1747-53. Dopamine suppresses pituitary function in infants and children. Van den Berghe G, de Zegher F, Lauwers P.

Ned Tijdschr Geneeskd. 2000 Jan 1;144(1):5-8. [Epilepsy, disturbances of behavior and consciousness in presence of normal thyroxine levels: still, consider the thyroid gland] [Article in Dutch] Vrancken AF, Braun KP, de Valk HW, Rinkel GJ. Afd. Neurologie, Universitair Medisch Centrum Utrecht. Three patients, one man aged 51 years, and two women aged 49 and 52 years, had severe fluctuating and progressive neurological and psychiatric symptoms. All three had normal thyroxine levels but elevated thyroid stimulating hormone levels and positive thyroid antibodies. Based on clinical, laboratory, MRI and EEG findings they were eventually diagnosed with Hashimoto's encephalopathy, associated with Hashimoto thyroiditis. Treatment with prednisone in addition to thyroxine suppletion resulted in a remarkable remission of their neuropsychiatric symptoms. The disease is probably under-recognized.

Cell Immunol. 1999 Mar 15;192(2):159-66. Neuroendocrine-induced synthesis of bone marrow-derived cytokines with inflammatory immunomodulating properties. Whetsell M, Bagriacik EU, Seetharamaiah GS, Prabhakar BS, Klein JR. © Ray Peat Ph.D. 2007. All Rights Reserved. www.RayPeat.com

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T4 & T3 content of desiccated thyroid is not accurate

The Wikipedia article states that each grain (60mg) of desiccated thyroid extract contains T4 100 mcg and T3 25 mcg. The reference listed is Epocrates Essentials.

Epocrates Essentials gives conversion information. For a person taking 60mg of desiccated thyroid, the approximate equivalent is 100 mcg of T4 or 25 mcg of T3. One grain of dessicated thyroid does not contain 100 mcg T4 plus 25 mcg T3

According to numerous references, each grain (60mg) of dessicated thyroid contains 38 mcg T4 and 9 mcg T3

Please update this information

69.12.233.7 (talk) 17:22, 5 February 2009 (UTC) Steve Edgar, Pharmacist edgar9499@comcast.net