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An Open Letter to All Physicians from a Nurse about thyroid treatment

pen-writing

A Thyroid patient who is also an RN was shocked to see the contents of a letter that a patient’s doctor had sent out to this patient. It was filled with terrible inaccuracies about thyroid treatment, she exclaimed, and she was horrified. No wonder so many thyroid patients are exasperated with their doctors!

So she compiled this excellent letter, refuting several comments made by this doctor, but directing it to ANY doctor who holds these false views.

Take the time to share this on your Facebook pages, your blogs, to your doctor, you name it. Spread the word as we work to Stop the Thyroid Treatment Madness!!

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An Open letter to physicians regarding the use of “Pig Thyroid Hormones”

I am writing this letter in response to any physician’s stance against the use of any forms of Natural Desiccated Thyroid (NDT) hormones as replacement for inadequate thyroid hormone levels. I will attempt to include links to medical-journal/peer-reviewed/scientific-based information to help you catch up on the latest in thyroid treatment and information.

I know that you, as a physician, have very limited time when it comes to researching various information on treatment protocols. I acknowledge that you were given limited training on thyroid diagnosis and treatments during your medical school programs, as well as in internship and residency programs, and have likely had to rely on the information provided by Pharmaceutical sales reps.

As such, I believe that your views are unfairly skewed and not fully fleshed out towards the use of T4-only medications such as Synthroid, Levoxyl, and others.

1) Regarding your assertion that Synthroid/T4 only medications are “bio-identical” in structure and thus, are an “adequate replacement” for a thyroid that makes 5 hormones (T4, T3, T2, T1 and calcitonin)

Please review the following photos, showing the chemical structure of human thyroxine (T4) and the chemical structures of T4-only medications such as Tirosint and Synthroid: (source: Synthroid Manufacturer’s Full prescribing information). As you can see below, there is a great difference between the molecular structure of Synthroid and human thyroxine.

Screen Shot 2014-02-17 at 11.55.23 AM

 

 

 

 

 

 

 

 

 

 

And below, in the top photo, is the human thyroxine (T4) molecule (Source: Chemical and Engineering news: https://pubs.acs.org/cen/coverstory/83/8325/8325thyroxine.html)  Compared that to the T4 molecule found in Nature-throid, bottom photo, which is one of several commonly-prescribed forms of Natural Desiccated Thyroid (NDT) medication.  (source: Nature-throid prescribing information http://www.nature-throid.com/images/Nature-Throid-PI-Rev041121-03.pdf)

As you can see, the molecules are identically formed, and therefore are the ones which are truly “bio-identical in structure”.

Screen Shot 2014-02-17 at 12.00.13 PM

 

 

 

 

 

 

 

 

 

 

2) Regarding your assertion that the TSH is a stable and reliable test which should be looked at first, while T4 and T3 levels fluctuate frequently and are not stable enough to be considered. 

Here are several medical journal articles which should make anyone rethink the use of the TSH lab test:

http://www.sciencedaily.com/releases/2010/03/100315230910.htm

http://jcem.endojournals.org/cgi/content/abstract/90/9/5483

http://www.thyroid-info.com/articles/david-derry.htm

http://thyroid.about.com/od/thyroiddrugstreatments/l/blderryb.htm

And not only the above, but there are a large body of thyroid patients who, for decades, have reported having a very “normal” TSH lab test while having very obvious symptoms of hypothyroidism, including a low temperature, fatigue, exercise intolerance, feeling cold, dry skin, depression, hair loss and more.

3) Regarding your idea as to what amount of T4 or T3 a human thyroid produces in a day (such as 100 mcg T4 and about 6 mcg T3 daily).

That information will vary. For example, another source states that a human thyroid makes on average between 3-5 grains of thyroid hormone per day:  “Estimates of average normal secretion for euthyroid humans are 94-110 µg T4 and 10-22 µg T3 daily (300).  If  you need more, it can be due to exogenous desiccated thyroid (giving it to yourself) vs. the superior absorption of natural release of thyroid hormones.” 

Source: http://www.thyroidmanager.org/chapter/thyroid-hormone-synthesis-and-secretion/

Either way, it varies according to each individual as to what amount of NDT will remove all symptoms.

4) Regarding your assertion that very few thyroid patients have issues with conversion of T4 to T3: 

As you may or may not know, many situations can cause problems with the conversion of T4 to T3 within the body, including a) mineral deficiencies (particularly low iron – a common issue in hypothyroid patients), b) gastrointestinal problems, c) liver problems, d) adrenal cortisol deficiencies (VERY common in T4 only-treated patients due to the inadequacy of being on nothing more than a storage hormone 5) the use of many commonly-prescribed medications including beta blockers or pharmacological doses of corticosteroids.

Source: http://www.naturalendocrinesolutions.com/articles/do-you-have-a-t4-to-t3-conversion-problem/

See Also:

http://press.endocrine.org/doi/abs/10.1210/jc.2008-1301

http://press.endocrine.org/doi/full/10.1210/jcem.84.2.5534

In addition to all the above, there are many thyroid patients who report that their FT3 “looked right” on T4-only, yet they continued to have symptoms of hypothyroidism while on thyroxine.

5) Regarding your assertion that there is no good way to dose Armour and other Natural Desiccated Thyroid Products

The growing body of thyroid patients around the world have frankly not had any issues with dosing NDT. Most dose it twice a day, such as first thing in the morning, and then the early afternoon. And it’s worked well.

Additionally, there are a variety of different strengths to choose from by the manufacturers of Natural Desiccated Thyroid meds such as Armour, NatureThroid, WP Thyroid, NP Thyroid, Erfa etc. For example….http://www.nature-throid.com/available_strengths.php

http://www.nature-throid.com/images/Nature-Throid-PI-Rev041121-03.pdf

6) Regarding the idea that a supposed “high dose of T3” has a stimulant effect…or is like a large dose of caffeine…or makes you feel good…or is addictive…or doesn’t make much sense physiologically…or may actually be dangerous, especially for the heart. 

I would hope that any doctor who proclaims to be a hormone-balancing “expert” would have a basic working knowledge of the need for T3 hormone in adequate levels for optimal cardiac functioning. Here are some helpful links which demonstrate the need for adequate T3 in order for cardiac functioning to be considered “optimal.”

The Journal of Clinical Endocrinology & Metabolism has reported that long-term levothyroxine replacement therapy in young adults is associated with cardiovascular abnormalities. http://jcem.endojournals.org/cgi/content/abstract/93/7/2486

And from this article: http://www.ncbi.nlm.nih.gov/pubmed/18221125 “Clinical studies have shown that mild forms of thyroid dysfunction, both primary (subclinical hypothyroidism and subclinical hyperthyroidism) and secondary (low T(3) syndrome) have negative prognostic impact in patients with heart failure. In these patients, the administration of synthetic triiodothyronine (T(3)) was well tolerated and induced significant improvement in cardiac function without increased heart rate and metabolic demand “

From this article: http://jcem.endojournals.org/content/93/4/1351.full.pdf  “Altogether, our data indicate that short-term administration of substitutive doses of synthetic L-T3 state reduces activation of the neuroendocrine system and improves LV SV in patients with ventricular dysfunction and low-T3 syndrome”

And this study: http://www.hindawi.com/journals/jtr/2011/958626/abs/ “The potential of TH (thyroid hormones) to regenerate a diseased heart has now been tested in patients with acute myocardial infarction in a phase II, randomized, double blind, placebo-controlled study (the THiRST study)”

And this statement, from this American Heart Association-sponsored study states: http://circ.ahajournals.org/content/107/5/708.long “…low T3 concentrations are a strong independent predictive marker of poor prognosis in cardiac patients and might represent a determinant factor directly implicated in the evolution and prognosis of these patients. “

To the contrary, hypothyroid patients are not seeking “high doses of T3”. Instead, they seek an amount of NDT that removes their symptoms of hypothyroidism, improves their temperature and metabolism, results in a strong heart and good blood pressure. When we achieve all the latter, we’ve noticed our free T3 in the upper quarter of the range, and the Free T4 around mid-range…and we have no symptoms of excess (if iron and cortisol is also corrected).  It’s all the result of adequate, physiologic doses for replacement, not high doses of NDT with its inherent direct T3.

We are NOT stimulant addicts or drug-seekers, and find that offensive. We are only seeking to replace what our thyroids are not giving us, and to regain a non-hypothyroid state as a result.

We are seeking human decency, wisdom and open-mindedness from our physicians. You would not deny a diabetic patient replacement with the hormone insulin, so why would you deny a person without adequate thyroid function all the right hormones, including the T3 hormone which is critical for every cell in the body to function properly? This seems cruel and unusual treatment in my book, and does NOT correlate with the “first, do no harm” portion of the Hippocratic oath!

7) Regarding the idea that patients are full of “bitter, angry, contentious discourse.”

Do try to understand how it feels to live in a body with a damaged or under-functioning thyroid and to have a doctor replace your missing thyroid hormones with nothing more than a storage hormone. We do not see healthy thyroids only producing a storage hormone. Living life without adequate thyroid hormones (particularly direct T3- the “active” thyroid hormone which every living cell in your body needs to function properly) leaves patients frustrated.

Additionally, put yourself in our shoes when you proclaim us “normal” based on a pituitary hormone, in spite of the fact that we continue to have hypothyroid symptoms. The latter test has repeatedly failed to correspond with how patients feel and function on a daily basis.

Imagine being held to a medication such as Synthroid, which then leaves you with inadequate thyroid hormones to obtain functional levels of daily living, optimal heart function and optimal hormonal balance. Imagine living your life in pain, depression, and with high blood pressure and cholesterol, with inadequate adrenal function, and all your sex hormones thrown off balance simply because your doctor is not open-minded or educated enough to grant you the use of natural desiccated thyroid which can make those symptoms disappear (in the presence of good iron and cortisol). Imagine being unable to get out of bed in the morning due to severe unrelenting fatigue and being unable to think properly due to brain fog caused by lack of thyroid hormones. Imagine missing out on the joys of life, and family, and being a functional member of society, simply because your doctor would not allow you to try a better form of medication. Would you not be upset with your physician if you knew there was a simple solution, yet you were repeatedly brushed off, symptoms ignored, and told to go on with living your half-life and to just “deal with it?”

8) Regarding the idea that Natural Desiccated Thyroid has not worked for some patients

Janie Bowthorpe has compiled several reasons why NDT doesn’t seem to works based on over a decade of reported patient experiences: //www.stopthethyroidmadness.com/ndt-doesnt-work-for-me Can that many patients and their important experiences be unworthy of your open-mindedness and investigation?

In conclusion, I hope that you will read all the above with a more open-mind and rethink your stance on the use of Natural Desiccated Thyroid hormone. It is a proven safe and effective form of treatment for over 122 years and counting. Your patients are counting on YOU to do what is right!

Sincerely,

A Hashimoto’s and Graves patient for over 28 years, Post Total Thryoidectomy 2012. Happily out of heart failure and OFF BP and Cholesterol meds, OFF Cholesterol meds since June 2013- when my thyroid doctor put me on Natural Desiccated Thyroid.

An hypothesis about RT3 – did you know you might have a hidden pool of it?

arrowPlease note this is a HYPOTHESIS, based on limited information, from 2014, and not to be taken as gospel.

Everyone makes Reverse T3 (RT3)–an inactive thyroid hormone. It’s a way to clear out excess T4 when your body isn’t needing that extra storage hormone. i.e. instead of the T4 converting to the active T3, your body (and specifically your liver), will convert it to RT3. If someone without a thyroid problem gets the flu, up goes the RT3 to conserve energy. If someone has a bodily injury, up goes the RT3 to conserve energy.

And thyroid patients seem to see their RT3 go up in the presence of low iron or a cortisol issue.

But if you think about it, why doesn’t it go down faster when we decrease our T4? T4 has a half life of one week, yet it can take 8 – 14 weeks for RT3 to go down. Hmmmmmm…

Thyroid patient Sebastian from Germany sent me this information about Reverse RT3 that I find fascinating. What do you think?

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I’m studying biology and chemistry and have Hashimoto’s Thyroiditis with high RT3. I just wanted to inform you about an interesting idea/hypothesis I have found.

There seems to be a “hidden pool” of RT3 in the human body. This RT3 pool can increase in size while enough T4 is available, and then secrete RT3 in times where the body needs it but hasn’t got enough T4 to produce it via deodination (the removal of an iodine molecule).

“It is concluded that a hidden pool of RT3 production exists in vivo in man.”
“It would appear that hypertrophy of this hidden pool of rT3 production occurs in high T4 states […]”

Source: LoPresti et al., “Does a hidden pool of reverse triiodothyronine (rT3) production contribute to total thyroxine (T4) disposal in high T4 states in man.”, J Clin Endocrinol Metab. 1990 May;70(5):1479-84. http://www.ncbi.nlm.nih.gov/pubmed/2335581

I have made observations regarding  my own thyroid blood tests and the blood tests of other patients that seem to support this hypothesis. I have been on T3-only for 6 weeks now, started with an RT3 of 330 pg/mL at approx. day 0, and now have measured a RT3 of 685 pg/mL (twice as much!), even though my TSH is low, FT4 has fallen rapidly to 0.5 ng/dL, and no T4 medication has been taken for full 6 weeks.
Another patient I know has also made interesting correlations between FT4 and RT3. He isn’t on T3-only, but observed a time-delayed (!) correlation between both values – which could be interpreted as an indicator for the presence of an RT3 storage pool in the body, that grows when enough T4 is available, and sets RT3 free in times when there is less T4 available.

I also found studies which found that RT3 has a 1000 times less feedback on the TSH than T3 has, and 100 times less than T4. This could explain any differences between TSH and symptoms, as the “RT3-system” seems to be almost completely isolated from the thyrotropic regulation system (the latter is that which directly influences the secretory activity of the thyroid gland).  RT3 can obviously rise and fall without having (almost) any effect on the TSH.

Source: Cettour-Rose et al.: “Inhibition of pituitary type 2 deiodinase by reverse triiodothyronine does not alter thyroxine-induced inhibition of thyrotropin secretion in hypothyroid rats”, European Journal of Endocrinology (2005) 153 429?434.

In combination, this could explain why the clearing process of RT3 takes approx. 8-14 weeks, although T4 has a plasma half-time of only 8 days, and rT3 only 4.5 hours!

The intracellular T3 receptors aren’t “clogged”, and then suddenly become free after that period of time has elapsed. Instead, RT3 is a competitive inhibitor of T3, meaning it constantly goes in and out of the T3 receptor. You probably know that already.

Patients report feeling well with T3 only dosages of approx. 80-120 µg T3 per day. According to Celi et al., 2010, this would be equal to 240-360 µg of T4. I always wondered why they don’t end up feeling hyper.

This all makes sense now under the assumption that a hidden RT3 storage pool exists somewhere in the body. Although there is no new T4 being produced or taken in, and although the remaining T4 and RT3 have both decayed rapidly after one starts with the T3 only method, there is still alot of RT3 being set free by the storage pool all the time. This storage pool might be big enough to last for several weeks to months. Since RT3 is the competitive inhibitor of T3, this might be why patients are able to tolerate (and even need) so very large amounts of T3.

Then, after the storage pool has been emptied, the remaining RT3 rapidly decays because of its short half-time and no new RT3 can be produced because no T4 is available in the body. Therefore, RT3 concentrations within blood and cells drop. Thus, the competitive inhibition gets a lot weaker at that point, and patients start feeling hyper because the same amount of thyroid hormones (T3) is now significantly increased in its effect, since it can stay much longer in the T3 receptors without being competitively inhibited (kicked out of the receptors) by RT3.

This process of totally emptying the RT3 storage might occur very quickly, therefore the drop in RT3 concentrations is very suddenly, all of which might happen within several days. And this is why patients then get hyper and have to reduce their dosage to half or less of what they’ve taken previously over the 8-14 weeks.

“Clogged receptors” don’t make sense because RT3 is a competitive inhibitor, capable of traveling in and out of the T3 receptor all the time.

“Clearance” occurring after 8-14 weeks, although both educt (T4) and product (RT3) have significantly (!) shorter lifetimes, doesn’t make sense either.  Neither does a totally defective TSH lab test, because in principle, it worked fine for all the patient’s lifetime before they got their thyroid disease; and because significant correlations between TSH and FT3 and FT4 can be observed.

This all makes sense to me now, based on two assumptions:

1. While T3 and T4 have a strong negative feedback effect on TSH secretion, RT3’s effect on the TSH secretion is minimal, being about a thousand times smaller in effect than that of T3, and about a hundred times smaller in effect than that of T4….as described in the study of Cettour-Rose et al., 2005, mentioned above.

2. The body has a large, previously unknown storage for RT3. This storage can grow while enough T4 is available, and the storage’s content can be set free when needed. As described in the study of LoPresti et al., 1990, mentioned above.

I hope you can use this information for further research. Thanks for reading.

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