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“A Little” natural desiccated thyroid if you’re “a Little” Hypothyroid? Don’t Make the Same Mistake We Did!

photo Moriah with butterfliesThe following Guest Blog Post is written by Jill, who has a B.S. in Combined Sciences and is the mother six, including 22-month-old Moriah, a thyroid and adrenal patient who has Down syndrome.

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I had gone to several doctors to investigate thyroid treatment for our infant daughter Moriah, who was born with Down syndrome (Ds). From my research, I knew thyroid issues to be quite common in those with Ds, but also frequently overlooked since many of the characteristics associated with Ds are the same as those seen in congenital hypothyroidism.

Also, because many doctors do not order all the appropriate labwork but rely too heavily on the TSH, many of these children remain untreated.

I was determined not to fail my girl on thyroid, so imagine my joy to finally find a doctor willing to prescribe NDT. I happily filled our prescription for 15 mg/day of natural desiccated thyroid and scheduled a follow-up appointment for 6 weeks. What I did not know at the time is that one cannot remain on a low dose of natural desiccated thyroid. (Patient Mistake #1)

The solution to being “a little” hypothyroid is not to take “a little” NDT. As I learned from a new friend and confirmed on the STTM website, that will cause you to become even more hypothyroid than you were to begin with due to the suppression of the feedback loop.

And that is exactly what happened to Moriah.

My friend clued me in, and I felt sick to my stomach, realizing this doctor must not be aware of that since she had not mentioned anything about ever raising Moriah’s dose. Long story short, even with labwork showing a big drop in the free T3, along with multiple new-onset hypothyroid symptoms, the doctor wanted to keep Moriah on just 15 mg/day. Why? Because, she stated “The TSH is by far the most important of the thyroid levels, and her TSH is really good!”

Ugh!

Sadly, the mistaken notion about how to dose NDT is all too common, even among caring, integrative doctors such as the one I had. I read many stories of doctors prescribing “low dose” NDT or adding “just a little” to be “on the safe side” and treat “borderline” hypothyroidism. But this is not how it works with NDT! This “treatment” only makes things worse! There is even pediatric dosing information on the NDT websites, but it is meaningless to a doctor who doses according to the TSH.

What a tragedy that these caring doctors are actually making their young patients even sicker!

Thankfully, we are now working with a new doctor who understands the necessity of evaluating symptoms and all the labwork and understands that, like adults, children cannot be left on “low dose” NDT. I wish there were more doctors like her.

The STTM website has been a Godsend, and I refer everyone to it, especially to check out “Mistakes Patients Make“” so they do not make the same one I did.

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– See why going by the TSH is the WORST way to diagnose or treat hypothyroidism, here.

– For adults, here’s what we have learned about using Natural Desiccated Thyroid.

– Having what seem like bad reactions to NDT? Learn why. It’s not about NDT, but what it’s revealing!

– Have you Liked the STTM Facebook page?? Come on over for daily inspiration and information based on shared patient experiences!

A hopeful new article proposing that adding T3 to thyroid treatment is the way to go!

Screen Shot 2014-03-19 at 5.48.52 PM(This post was updated in 2015. Enjoy!)

In a recent article by thyroid patient Mary Shomon, there was mention of an interesting article by Dr. Wilmar Wiersinga that came out this year in the journal Nature Reviews Endocrinology titled “Paradigm shifts in thyroid hormone replacement therapies for hypothyroidism.” And I find this article fascinating.

I’m going to break it down a bit and add more important observations that I’ve not seen expressed elsewhere and which are important, because the truth stands out about T4-only and decades of patient experiences.

In the abstract summary of his article, he states:

Evidence is mounting that levothyroxine monotherapy cannot assure a euthyroid state in all tissues simultaneously, and that normal serum TSH levels in patients receiving levothyroxine reflect pituitary euthyroidism alone.

Informed thyroid patients can only shout Hallelujah!!

But actually, the evidence has been there all along…and the medical profession has not been listening!

For over 50 years since T4-only was pushed upon thyroid patients in the early 1960’s (not the 1970’s mentioned in the actual article), we haven’t done well on levothyroxine. But when we came into our doctors offices and complained of those pesky symptoms of continued hypothyroidism while on levothyroxine, the replies from our doctors have ranged from “You need to exercise more and eat less”, to “it’s just your age”, to “It’s part of being a busy mother” to  “Here’s a prescription for an anti-depressant/statin/BP med”….on and on.

My own mother was the classic example. She as put on Synthroid in the early 1960s in her forties. And from that time on until she died in her early eighties still on Synthroid, she paid continual and growing problems: chronic depression, rising cholesterol, heart problems, weight gain, body stiffness, inability to stand for long periods, poor stamina, dry hair and skin, and problems with her cognitive abilities. And today, informed patients know that all those symptoms are classic symptoms of continued hypothyroidism—all common in far too many patients on T4-only in their own degree and kind…sooner or later.

Stop the Thyroid Madness is the direct result of thyroid patients gathering in groups on the internet by the turn of the 21st century and proclaiming T4-only has only served to make them sicker!

Dr. Wiersinga also states in his abstract:

Levothyroxine plus liothyronine combination therapy is gaining in popularity; although the evidence suggests it is generally not superior to levothyroxine monotherapy, in some of the 14 published trials this combination was definitely preferred by patients and associated with improved metabolic profiles. Disappointing results with combination therapy could be related to use of inappropriate levothyroxine and liothyronine doses, resulting in abnormal serum free T4:free T3 ratios. 

That is a bit confusing to say “evidence suggests it is generally not superior to levothyroxine monotherapy”. What about the clinical presentation of patients shown every day in the offices of doctors over the past 50+ years?  Why have so many thyroid patients on levothyroxine for example, been put on anti-depressants, statins, BP meds, pain meds and more?

The Medical Dictionary defines “clinical presentation” this way: The constellation of physical signs or symptoms associated with a particular morbid process, the interpretation of which leads to a specific diagnosis.

Why has there been such a gap between what a doctor learns in medical school /continuing education vs. the clear clinical presentation by millions that underscores how poorly T4-only really has been?

As far as those “disappointing results” which Dr. Wiersinga mentions, informed thyroid patients have the answer: low iron and cortisol issues–both issues which all-too-many levothyroxine patients acquire due to being a poor treatment, and which either T3 or natural desiccated thyroid will reveal. Or, the patient is held hostage to the TSH lab test, leaving them underdosed, and again, many acquire either low iron and/or a cortisol problem.

Dr. Wiersinga concludes in his abstract:

However, in selected patients, new guidelines suggest that experimental combination therapy might be considered.

We agree and bravo!!

But Informed thyroid patients have a strong reply: why limit a better treatment to only “selected patients”?? Why continue to put each and every thyroid patient on one of five thyroid hormones, which more than 50 years have revealed has been an abject failure in too many, sooner or later?

Why not put the majority of your thyroid patients, not a “selected few”, on a medication which gives back the exact same hormones that one’s thyroid would be making in the first place, aka Natural Desiccated Thyroid Hormones? “Selected patients” should only refer to those who may need T3-only since they could have a conversion problem. 

The full article also describes three paradigm shifts, plus a proposed fourth one:

1)   1891, when the real gland (sheep at the time) was first used to treat hypothyroidism. bottle1

2)   1960 — 1988, when desiccated thyroid use declined and levothyroxine use increased

3)   the 1990s, when it was reported that T3 was needed after thyroid removal (but wasn’t pursued)

(See Chapters 1 and 2  in the revised STTM book for more excellent information)

And the 4th paradigm shift might occur, he explains, when those of us with poorly functioning thyroids could see regeneration from embryonic stem cells, as outlined in a 2012 study. Pretty exciting!

But I think a 4th paradigm shift has already occurred! A growing body of doctors have changed the way they treat hypothyroidism, and it’s by prescribing natural desiccated thyroid. As a southerner would say “Bless their little souls!!”

Until the possibility of stem cell treatment of our hypothyroidism becomes a reality, which may not be soon enough, we all hope to see better understanding by our physicians about what treatment really hasn’t worked well, and what treatment really does.

i.e. doctors need to return to the observation of “clinical presentation” 

Adding T3 to our treatment, and especially with natural desiccated thyroid, has changed lives. And we can at least shout “Bravo” to  Dr. Wiersinga for positively proposing that Endocrinologists consider the fact that perhaps, T4-only is NOT the way to go and adding T3 just might be for very good reasons. And by the way, thyroid patients also know that the TSH lab test is as much a failure as T4-only.  

Seize the Wisdom!

Yours truly,

Janie A. Bowthorpe

Post Script: The full article can’t be found in most places yet, but here is one place where the charge is less than others if you want to see it: http://www.readcube.com/articles/10.1038%2Fnrendo.2013.258

 

 

 

 

Dr. Melnick discusses alarming article from Harvard about the use of the TSH and thyroid treatment!

(Note: if you are reading this via email notification, do NOT reply to the email if you want to comment. Click on the title of the blog post, which will take you directly to the blog post. Scroll down to comment there.)

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P4089852Dear STTM Blog readers, I am so fortunate to talk to many wonderful individuals because of Stop the Thyroid Madness. And recently, I had a conversion with the very insightful Dr. Hugh Melnick of New York City.

Dr. Melnick brought my attention to a very disturbing article titled “For borderline underactive thyroid, drug therapy isn’t always necessary” that came from the Harvard Health Letters in October 2013, You can see it here: http://www.health.harvard.edu/blog/for-borderline-underactive-thyroid-drug-therapy-isnt-always-necessary-201310096740.

This conversation between Dr. Melnick and I may be of great interest to STTM readers, besides alarming once you see what is being stated in this article and suggested as treatment guidelines. It’s simply Thyroid Treatment Dark Ages!

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JANIE: Hello Dr. Melnick. I’m so glad to chat with you! Can you tell our readers a little about yourself?

DR. MELNICK: I am a reproductive endocrinologist who has been in medical practice since 1976. As the medical director of Advanced Fertility Services In Vitro Fertilization Center in New York City, I have always been impressed by the large number of  infertile women that I have seen over the years, who are symptomatically hypothyroid, and who conceive after treatment with thyroid medication.

Although I did my medical training at a point in time when the TSH test and Synthroid were just being introduced into clinical practice, I was trained by one of the most widely respected endocrinologists of that era, Herbert Kupperman, MD, Ph.D. to diagnose and  treat patients with potential thyroid issues according to their symptoms, rather than solely by their blood test results.  His vast clinical experience, and subsequently mine, as well, is that treatment with Natural Desiccated Thyroid (NDT) gives far superior symptomatic improvement for the vast majority of patients. Furthermore, the dosage of thyroid medication should always be based upon a patient’s clinical symptoms and not the TSH level.

JANIE: That greatly impresses me when I learn of doctors like yourself who understand the efficacy of Natural Desiccated Thyroid as well as the problems with using the TSH lab test.  You recently brought my attention to what was written just a few months ago by Heidi Godman, the Executive Editor of Harvard Health Letter (see introduction above). Can you expound on what Ms Godman meant by “borderline underactive thyroid”? 

DR. MELNICK: Actually, Ms. Godman is mistakenly defining hypothyroidism by TSH levels, rather than by a patient’s clinical symptoms. It is obvious that there are many symptomatic and genuinely hypothyroid individuals, who have normal TSH levels, and who experience relief when given a proper dose of the appropriate thyroid medication. The TSH level only diagnoses a type of hypothyroidism that is due to failure of the thyroid gland itself, or a failure of the pituitary gland.

In my experience, the most common form of hypothyroidism is called subclinical because the TSH levels are in the “normal range.” It is a genetic condition, usually passed through the mother and manifests itself later in adulthood. In subclinical hypothyroidism, the individual’s cells need more active thyroid hormone–T3–than their bodies are able to produce in order to function properly. Therefore, supplementation with a thyroid medication containing T3, in the proper dose, will relieve the troubling symptoms and allow the cells to function optimally.

Again, basing the dosage of thyroid medication on TSH levels is incorrect. When treating hypothyroidism, we are not treating a condition like diabetes, in which the insulin dose is based upon the patients’ blood sugar levels. Although they are both endocrine disorders, they are vastly different conditions and cannot be treated in the same fashion, although many endocrinologists still insist on doing so!

JANIE: In the article, Godman quotes that prescriptions for levothyroxine have increased from 50 million in 2006 to about 70 million in 2010, and a similar increase has occurred in England and Wales. She then calls this increase in treatment “pretty risky business”, citing irregular heart rhythms, insomnia, and loss of bone density”. What is she implying there?

DR. MELNICK: I think that the observed increase in the use of the thyroid medication Synthroid is due to the fact that hypothyroidism is a very common condition, affecting at least 35% of the female and 10% male population.  Considering the population estimates for 2013 is 317 million people in the U.S.A. and the population of the United Kingdom is estimated to be 70 million, 28% of the population in the U.S.  and 23% of the population in England, (assuming one prescription per year per individual patient) are being treated for hypothyroidism. This is actually a bit less than the estimated incidence of hypothyroidism in this country. I also believe that more cases of hypothyroidism are being found because people, in general, are more informed about the symptoms of hypothyroidism and seek treatment.

In my opinion, Ms. Godman erroneously categorizes treatment of hypothyroidism a “pretty risky risky business”. The risks of not treating hypothyroidism is, in fact, more potentially injurious to a patient’s health! 

For example, the increased risk of heart disease in untreated hypothyroid individuals is a solid example of why hypothyroidism needs to be treated. The examples that she cites, namely, irregular heart rhythms and insomnia, are found in many people with hypothyroidism before treatment and are cured by adequate thyroid treatment. The symptoms that she mentioned are not exclusively associated with hyperthyroidism. The loss of bone density claim comes from studies of hyperthyroid individuals, who because of their hyperthyroidism and excessively high metabolic rate, may develop osteoporosis.

JANIE: The next part of this article is alarming. It refers to a particular “clinical practice guidelines” authored by Endocrinologist Dr. Jeffrey Garber, an associate professor of medicine at Harvard Medical School. These guidelines come from a task force representing the American Thyroid Association and the American Association of Clinical Endocrinologists. The first guideline is as follows, and goes completely against what informed thyroid patients know to be wise. Can you comment? 

1) The best way to check for hypothyroidism is to look at the level of thyroid stimulating hormone (TSH) in the blood, and when the TSH level is above 10 mIU/L, there’s uniform agreement that treatment with levothyroxine is appropriate. 

DR. MELNICK: Firstly, clinical practice guidelines are merely suggestions that have been developed to help physicians with limited experience diagnose and treat medical issues. Clinical guidelines are like a cook book, which describes a recipe that makes a simple meal, but not necessarily a complex and elaborate feast. That said, it is quite obvious that the way in which I diagnose and treat hypothyroidism is quite different than that which is suggested by the above referenced societies.

Although I do perform a complete battery of blood tests, including antithyroid antibodies, iron, vitamin B12 and vitamin D levels, I believe that a clinical approach – listening to a patient’s symptoms and treating a patient accordingly – is, in some ways, more important in diagnosing and properly treating patients suffering with the symptoms of hypothyroidism. If a physician only looks at a patient’s blood tests, without listening to the patient’s symptoms and asking them appropriate questions, many people who legitimately need thyroid medication will be denied proper treatment. That is precisely the reason that so many people come to me suffering with all the classical symptoms of hypothyroidism and tell me that their doctors have tested their thyroid and found them to be “within normal limits”.

It is not surprising when these very same patients experience symptomatic improvement when treated with adequate doses of NDT. I rarely treat patients initially with Synthroid. The primary reason is that Synthroid, being a synthetic T4 (a weak thyroid hormone- not chemically identical to human T4), must be converted into T3, the potent form of the hormone that enters every cell in the body and makes the cells of the body function normally. Unfortunately, many individuals are unable to successfully convert T4 into T3, so the patients’ symptoms remain, yet the TSH level is normal.

Natural desiccated thyroid (NDT) is made from the thyroid glands of pigs, which produce thyroid hormones chemically similar to that found in humans and does contain T3. Porcine (pig) thyroid gland also contains other thyroid hormones and proteins, which, in my experience are much more effective in relieving the symptoms of hypothyroidism than synthetic T4.  Who can argue that a natural treatment, if availble, is to be preferred over a synthetic one.

JANIE: I loved the analogy above to a cook book, Dr. Melnick! Garber’s second most-emphasized guideline is the following, and I would love for you to comment on this as well, as informed thyroid patients would find this very disturbing, as well: 

2) If the TSH level is between 4mIU/L and 10mIU/L, treatment may still be warranted in various situations:  

  • if the levels of actual thyroid hormones in the blood–known as thyroxine (T4) and triiodothyronine (T3)–are abnormal
  • if the bloodstream contains anti-thyroid antibodies that attack the thyroid. These antibodies would indicate a hypothyroid condition called Hashimoto’s disease, in which the immune system mistakenly attacks the thyroid.
  • if there is evidence of heart disease or risk for it. 

Garber is next quoted as saying “Use thyroid hormone for a brief period of time.”  and “If you feel better, you can continue with treatment. If not, then stop.”  That recommendation is quite alarming as well, as it fails to understand that it may not be about stopping thyroid medication, but moving over to a far better treatment with natural desiccated thyroid, which informed thyroid patients know should have been the first treatment of choice anyway. Can you comment? 

DR. MELNICK: In my clinical experience, 99% of patients with TSH levels over 4.0 are quite symptomatic, if questioned about their symptoms properly. Therefore, treatment is absolutely mandatory, both to relieve “quality of life symptoms” as well as to prevent heart disease, lower blood pressure, normalize blood sugar and cholesterol levels, if they are found to be elevated.

Dr. Garber’s recommendations about using thyroid medicine for a short period of time and continuing it if improvement is noted omits two essential factors. The first is that since he treats his patients only with Synthroid, a significant percentage will show no improvement because their symptoms are not relieved because they cannot convert T4 into T3. The second factor is that by following TSH levels in the blood, a patient may not actually be taking a high enough dose of thyroid medication, yet  will show low TSH levels in the blood. The level of thyroid hormones circulating in the blood-whether they are bound or free- only indicate absorption of the medication and give no indication as to the amount of T3 entering the cells. When an individual gets enough T3 into their cells, their symptoms will improve.

The only way to measure the correct dose of thyroid medication, in addition to noting improvement in symptoms, is by measuring the Basal Body Temperature and by the measurement of nerve conduction velocity (Thyroflex Test). This is a noninvasive test  which gives a good indication of dosage adequacy. The slower the patient’s nerve conduction velocity, the higher the dose of thyroid medication that is required.

One main point that must be noted is that thyroid medicine may take up to twelve weeks in order to experience some degree of symptomatic relief. The other is that the patients’ dosage should be increased gradually and in divided daily doses until symptomatic relief is  experienced. The dose should be reduced if the patient experiences rapid or irregular heartbeat, shakiness or anxiety. These symptoms will resolve in several hours and are not harmful.

Hashimoto’s or autoimmune thyroiditis is a much more complex clinical condition, in that symptoms in many individuals may vary, from hypo to hyper from time to time. Treatment with thyroid hormone is usually needed, but some patients, in the early stages of thyroid autoimmunity, may be fairly asymptomatic.  As the condition progresses, symptoms will eventually be experienced. The levels of antithyroid antibodies do not correlate with the severity of a person’s symptoms.  Antithyroid antibodies never disappear and will always be detectable in the blood.  There may also be gluten sensitivity in some instances, so dietary factors may be important. When an infertility patient is found to have antithyroid antibodies, whether they are symptomatic or not, I always treat them with NDT since it does help them to conceive and seems to reduce the incidence of miscarriages.

JANIE: Heidi Godman then states the following about individualized treatment for hypothyroidism, which informed thyroid patients know by years of experience is a recipe for disaster: That requires measuring TSH four to eight weeks after starting treatment or changing a dose, another TSH test after six months, then every 12 months.”  

DR. MELNICK: I respectfully disagree with both Ms. Godman’s  formula as stated above, as well as with Dr. Garber’s method for diagnosing and treating hypothyroidism. Although the Harvard Medical School is a very prestigious institution, and that the information that they published cited the work of a physician of professorial rank, it is quite contrary to my own clinical experience and that of the many untreated or inadequately treated individuals who suffer with the many debilitating and disturbing symptoms arising from thyroid hormone deficiency.

I say this in jest, but if a patient follows the treatment protocol advocated by Ms. Godwon, they are more like to die of old age before their symptoms of hypothyroidism begin to show signs of clinical improvement .

JANIE: Your last sentence was excellent, Dr. Melnick. Your sage observations and wisdom jive with over a decade of successful patient experiences and wisdom! And we must push AGAINST the guidelines suggested by Dr. Jeffrey Garber. Informed thyroid patients know how disastrous they can be!

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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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