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

arrowPlease note this is a OLDER post from 2014, a HYPOTHESIS based on limited information, and not to be taken as gospel. We’re just leaving it here for kicks sake. 

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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Thyroid Patients and their Doctors: all the information you need

DoctorI’m so glad I wasn’t yet into hypothyroidism when I was a child. I had a doctor named Dr. Roach. Yes. Really. And he was quite tall and very serious. Not the kind of guy who should have been a pediatrician. So when my mother took me into the office for my required childhood vaccinations, I was SCARED…TO…DEATH…of him. I would hide behind the chairs as if I could really escape this nightmare. It didn’t work…lol.

So IF I had to see Dr. very-tall-very-serious-Roach for hypothyroidism, I shudder to think how it would have gone. lol.

INEFFECTIVE DOCTORS

As adults, we have somewhat more choices on who we see. And even so, it’s not always an easy issue. Thyroid patients report far too many doctors who they feel are missing the mark in their thyroid disease treatment.

And I get that!! When I was on Synthroid and later Levoxyl and suffering miserably, I remember going to at LEAST 20 doctors over those years, trying desperately to get help for what was debilitating me…and failing!

And boy oh boy, are there some bad memories. One doctor decided to use me for his “experiments” and I was put on a medication which really had nothing to do with what I went in there for. In retrospect, I think he was using me for a medical article he wanted to write, which he did then and still does today.

Another doctor put his foot down in arrogance when I asked if I could please get my potassium, sodium and magnesium tested to see why I was getting blood pressure problems. “That’s not your problem”, he swiftly said. i.e. he came across as “I’m the doctor; you are not. Don’t ask for anything”.

And there were many doctors who, in light of my hypothyroid-caused depression due to being inadequately treated thanks to T4-only, told me I need to see a psychologist or get on anti-depressants. NOT the right answer when natural desiccated thyroid would have ended that depression!

Yes, I finally found a couple of medical professionals who have been wonderful! And that’s because they have started listening to our experiences, and are willing to learn from me, as well.

A better direction

Today, patients have a lot more help and a sense of proactivity in their treatment thanks to the education and support that Stop the Thyroid Madness offers. Here are pages related to doctors that may help:

  • TAKE A SURVEY as to your experiences with the majority of your doctors over the years. This will become important information which STTM will use in the future. Please contribute by answering the five questions!
  • Here’s where you can see how patients find a good doctor. It can take a little work, but the end results will be much better.
  • Don’t know how to say things to your doctor? Here’s a letter to your doctor which can help.
  • And of course, YOU need to become informed somewhat ahead of time, because there will probably be some areas you’ll need to guide your doctor about. Here’s a summary of what patients have learned.
  • Also helpful is to take a copy of the revised STTM book with you. You can have it bookmarked and read to open, if needed, in the discussion with your doctor.
  • What if your doctor is the kind that needs research proof? STTM has a medical research page you can print out and hand to him.
  • And to make you feel empowered, here is a page which outlines the areas doctors need to change in their thinking.
  • Finally, get support from patients.

Bottom line about working with your doctor

Yes, thyroid patients may be disgusted and angry about the lack of good care they’ve received, but it still helps to to interact respectfully and tactfully. And definitely be INFORMED. That will give you the edge and your doctor’s respect in return. If not, move on to much better doctor! Be our OWN best advocate!

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  • Want to talk to Janie and learn about patient experiences and wisdom concerning your issues? Go to the Talk to Others page.
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Three Sleeping Issues you might encounter as a Hypothyroid Patient

Snoopy

(This page has been updated for the present day and time! Enjoy!)

Have trouble sleeping? Here are three scenarios you might identify with, the causes, and the solutions.

1) INSOMNIA or WAKING UP FREQUENTLY SOON AFTER YOU FALL ASLEEP

This is an extremely common problem faced by thyroid patients, and the most common reason is going to bed with high levels of cortisol–the opposite of what healthy adrenals should be doing. With normal adrenal function, your bedtime cortisol levels should be low, or at the bottom of the range of a saliva cortisol test. Symptoms include laying awake for a long time before falling asleep for the night…or if you can fall asleep well, you tend to wake up often within the next hour or two.

Why the high cortisol?

It’s usually a left-over remnant of when you used to have high cortisol all day long, but which has since fallen to low levels of cortisol except for bedtime, or afternoon and bedtime.

And all the above can happen to certain individuals due to a continued hypothyroid state (such as being treated with the inadequate T4-only medications like Synthroid, Eltroxin, Oroxine, and/or Levothyroxine, etc) or due to undiagnosed hypothyroidism (thanks to the use of the TSH lab test).

Another cause is low bedtime cortisol (i.e below the range), which has caused issues with falling or staying asleep at bedtime. Low cortisol seems to cause high adrenaline, and the latter results in a fitful sleep pattern during the night. The solution? First do a 24-hour adrenal saliva test to prove if it’s high or low cortisol, say informed thyroid patients. Guessing can get you into trouble. (And blood cortisol is not the answer, since it’s measuring both bound and unbound cortisol.) Then compare the results to what we’ve learned they mean.

For high bedtime cortisol, patients have had success with cortisol-lowering herbs like Holy Basil, zinc or others, taken a good hour or two before they want to fall asleep. Each dose is given three nights to see if it’s enough to improve sleep. If not it’s raised…and again if needed. Then they wean off after several weeks of better sleep.

For low cortisol (below the range), patients often have to use a small dose of HC or Adrenal Cortex. Even supplementing with sea salt has been reported to help with sleep. Additionally, if bedtime cortisol is below the range, there’s a good chance your cortisol is low most of the day, which saliva testing will reveal. Chapter 6 in the revised STTM book has excellent and important information on the proper use of HC, which would also apply to adrenal cortex.

2) WAKING UP ANYWHERE AROUND 3 – 4 AM

Waking up a good three to four hours before you would normally start your morning is a strong sign of low cortisol, which in turn causes hypoglycemia (low blood sugar). And the latter can push your adrenaline up, causing you to wake up hours before you are supposed to. You might also feel shaky or hungry.

The solution? Besides taking cortisol at bedtime, if needed, patients have reported doing far better with sleep by eating a complex carbohydrate at bedtime (for example, whole wheat cracker with cheese or peanut butter…or if you need to avoid gluten, berries and cream cheese). The same strategy is used if waking up around 3 am or so, which will help raise your blood sugar levels and you might fall back asleep better.

3) WAKING UP FREQUENTLY WITH NO SET PATTERN

Time to check your sex hormones, which can get messed up with hypothyroidism, or made worse because of adrenal sluggishness or cortisol use.

Low estrogen can cause hot flashes, waking you up. A study titled Sex Hormones, Sleep and Core Body Temperature in Post Menopausal Women reveals that low estradiol (E2) and higher luteinizing hormone (LH) levels are strongly related to lessening the quality of your sleep.

Low progesterone is also known to cause insomnia and even anxiety, and may cause sleep apnea (or make you snore, ladies. Gulp). Entry into menopause has caused this, report many women.

Especially in men, low testosterone can negatively affect the quality of your sleep, i.e. you won’t stay in your deep sleep cycle long enough for recuperation of your body and mind.

SLEEPING TIDBITS:

  • Low levels of the neurotransmitter serotonin, which can cause depression, is also implicated with insomnia.
  • High cortisol can also be caused by Lyme or reactivated Epstein Barr Virus–the latter of which at least 95% of adult have dormant in their bodies, but which can reactivate due to stress or illness. .

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  • Here’s an important summary of what patients have learned in getting well again.
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Wall Street Journal’s recent thyroid article: 13 ways it could have been SO MUCH better!

Screen Shot 2013-08-06 at 1.05.29 PM(This post has been updated to the present day and time! Enjoy!)

As usual, informed thyroid patients can only roll their eyes about the latest example of a watered-down, thyroid-themed article in the media. This time, it’s from Wall Street Journal Online and appeared Monday, August 5th, 2013.

Now on the positive side, the title looks good: New Call for More Thyroid Options.

But let’s set it straight: this is NOT new! Informed thyroid patients have been clamoring about better treatment for more than a decade!!

I started the Yahoo Natural Thyroid Hormones group in 2002 as a way to begin the important discussion about the efficacy of Natural Desiccated Thyroid as a treatment for hypothyroidism over T4-only. The Stop the Thyroid Madness (STTM) site first went up in December 2005–a compilation of worldwide patient experiences which included lives being changed thanks to natural desiccated thyroid (NDT). The STTM book by the same name first appeared in 2008, and the revision in 2011. The STTM II book came out in late 2014. Today, there are numerous thyroid groups all over Facebook which have been extolling the virtues of better treatment.

Let’s break the article down and go into further detail, correction or clarification–all which might have made this a MUCH more informative and accurate article:

1) Grass roots patient-activist organizations….and the doctor-founded National Academy of Hypothyroidism, say that the current screening test for hypothyroidism leaves out some symptomatic patients and that the main medication used to treat patients, doesn’t always alleviate many symptoms.

True! And let’s be more specific about that so-called “screening test”: it’s the inane use of the TSH lab test which has been a monstrous screening failure! The TSH is a pituitary hormone, NOT a thyroid hormone! And it can consistently look “normal” for years (according to the parameter of an erroneous man-made “normal” range), yet we have raging hypothyroid symptoms…all the while the patient has to hear his or her doctor state they need to “exercise more and eat less”. The “main medication” is the all-too-often lousy T4-only medication like Synthroid, Levoxyl, Levothyroxine, Eltoxin, etc. Yet, a healthy thyroid makes FIVE hormones, not just one.

2) They are calling for doctors to be open to other therapies, including a combination of synthetic hormones and the use of natural, animal-based ones.

True. But though adding synthetic T3 to synthetic T4 is a huge step in a much better direction and can be applauded (and so can being on T3-only), a multitude of worldwide patient experience has found that Natural Desiccated Thyroid has given these patients even better results (in the presence of good iron and cortisol levels). Doctors need to listen to that!

3) Hashimoto’s Disease: A Primer (box on the left side of the article)

What a perfect way to lower the quality of an article. As usual, it contains the dark ages information about the use of the TSH, and mentions the “common” treatment of T4-only. They might as well have inserted a primal on blood-letting.

4) [In reference to Dr. Ridha Arem’s correct comment that “There are so many unhappy thyroid patients,”] : Many of his mainstream medical counterparts disagree. “The vast majority of people are fine on the standard therapy,” says Jeffrey Garber, an associate professor of medicine at Harvard Medical Center and chair of the American Association of Clinical Endocrinologists Thyroid Scientific Committee. Still, he says, “there’s a whole group out there who just thinks we’re clueless.

Yup, millions of informed thyroid patients worldwide would definitely put you in that clueless category, Dr. Garber.

5) The wide range of symptoms, so similar to those of many other diseases, can make diagnosis tough.

Totally untrue, say thyroid patients! Thyroid disease has a common cluster of symptoms in patients, which can include one or more of depression, fatigue, the need to nap, rising cholesterol, rising blood pressure, achiness, hair loss, weight gain, inability to lose weight, dry skin, dry hair, achiness, a low mid-afternoon temperature (below 98.6F/37C) and so many more symptoms.

Additionally, we have noted that if our free T3 is mid-range or lower, or our Free T4 is low, along with the above symptoms, it’s a sure sign that we are hypothyroid. Finally, family history underscores it for others, as can an ultrasound. It’s not that difficult when you understand the clinical presentation of hypothyroidism over an ink spot on a piece of paper!

6) Newborns and pregnant woman are routinely tested. Experts recommend screening all women over the age of 35 every five years.

And how does that help when the testing/screening is with the inadequate TSH lab test, which we, as patients, already know leaves millions of us undiagnosed for years.

7) For treatment, guidelines generally call for the prescription of levothyroxine, a synthetic version of a hormone called thyroxine, or T4, which is produced by the thyroid. The gland also produces one other hormone, Triiodothyronine, or T3.

A healthy thyroid gland produces FIVE known thyroid hormones: T4, T3, T2, T1 and calcitonin. So what’s the motive to prescribe only a storage thyroid hormone???

8) Most doctors, says Dr. Arem, generally prescribe T4-only medications. But such medications may leave some patients with lingering symptoms such as fatigue and depression and, in some cases, low T3 levels.

He’s right! But there’s more to the story. Even those T4-only treated patients who see a removal of those lingering symptoms still end up seeing them crop up the longer they stay on T4! T4-only treatment is NOT a pretty picture.

9) Some patients go to alternative health professionals to get prescriptions for drugs such as desiccated thyroid extract (DTE) prepared from animal thyroid glands, which include a combination of T4 and T3.

Thyroid patients are NOT just getting their natural desiccated thyroid (NDT is the common term, not DTE) from alternative health professionals. They are also getting it from open-minded and progressive regular doctors who LISTEN to their patients experiences!

10) The danger here, Dr. Arem says, is such patients could end up with an excessive amount of T3, resulting in symptoms of overactive thyroids, such as anxiety and a fast or irregular heart rate. He advocates a combination approach with amounts tailored to the individual.

With all due respect to Dr. Arem, who is light years ahead of his colleagues in many areas, an excessive amount of T3 is not because of the use of NDT. It’s because NDT will reveal the problems of inadequate iron or inadequate cortisol–either of which can cause T3 to pool high in the blood and not make it to the cells. When patients correct those, they eventually soar on NDT. A newer page on STTM explains why NDT appears to cause problems.

11) Most studies looking at combination approaches show conflicting results.

This is because those doing the studies made several key mistakes!! a) they dosed by the TSH, which leaves patients underdosed, b) they had no clue about the problem of inadequate levels of iron or cortisol, either which will leave a patient hypothyroid! Learn from patients!

12) The study’s authors said in a news release that it showed DTE may be a good alternative therapy for a limited number of patients. Harvard’s Dr. Garber says there may be certain subsets who are genetically programmed to respond to such combination therapies.

That’s like saying a “limited number” of human beings and only those “who are genetically programmed” will do well with a healthy thyroid (NDT gives the exact same hormones as a healthy thyroid!! T4, T3, T2, T1 and calcitonin).

13) Dr. Garber, like many endocrinologists, uses T4 medications with the vast majority of his patients. Occasionally he’ll also use conservative doses of a synthetic T3 drug, but he virtually never prescribes the animal-derived form, he says, because of complications that could arise for women trying to get pregnant or in early pregnancy, as well as individuals with heart disease.

And this is why most thyroid patients, when they report about their doctor experiences, find Endocrinologists to be the worst doctor they ever went to, using descriptive words such as arrogant, close-minded, blind. And by the way, even some heart surgeons know that T3 SUPPORTS healthy heart function, not hurts it! See the Medical Research page on STTM which supports what we already know by our experiences!

See the actual Wall Street Journal article here.

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* Did you know that the original and revised Stop the Thyroid Madness book is in four languages?? English, Spanish, German and Swedish. Wooo hoooo!! And now, there’s a STTM II book with each chapter written by medical practitioners!

* The STTM Facebook page is very active and informative about successful thyroid patient treatment! Come join us! Discussion groups listed on the Talk to Others page.

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Thyroid Patient Experiences vs Medical Research: do they jive or not?

Lightning2There was a long time in my life – more than 20 years in fact – that I suffered immensely, in spite of managing to live my life. I paid hefty prices….and suffered constantly. You can read my story on STTM, and read even more details in the Introduction of the revised Stop the Thyroid Madness book.

Ultimately, science-based, mainstream medicine failed me…and others.

During those 20 years, and more so during the final ten years, I went from doctor to doctor. Thank the good Lord for insurance!! I visited premier medical centers and was subjected to numerous tests and medical procedures. One in particular resulted in a scar on my left bicep that I still carry today – an attempt to see if my extreme fatigue and weakness had an answer in a muscle biopsy.

But I got NO answers, and no relief. There was no pharmacological drug, nor any physical intervention, or a lab result analysis, or any medical diagnosis that changed my misery. I was left to deteriorate on my own. And that pushed me to apply for Social Security Disability. It was only through my own drive in discovering a better treatment I finally got well.

And turns out my experience, both the negative and positive, has similarities with millions of others, to their own degree and kind, as we discovered in patient groups all over the internet.

Reported patient experiences became the gold, NOT medical science

When I started the Natural Thyroid Hormones (NTH) group on Yahoo in 2002, oh did we learn!! (See STTM’s Talk to Others page). It was NOT science that helped us get better. It was learning from each other!! And all of that reported patient experience and wisdom birthed the STTM website, the STTM book, and many more groups. Because we were now getting WELL thanks to all those reported experiences. And others still are getting well–NOT because of “medical science”, but because we have been listening to each other’s experiences and wisdom!

Does “science” support the success we have achieved?

At first, there was little science to support what we knew to be true by our combined and growing experiences in getting well. And we didn’t care. We were FINALLY getting well!

And as we’ve been getting well, we simply roll our eyes when we occasionally run into a “science snob” who looks down his or her intellectual stuffy nose with ignorant criticism like “It’s nothing more than “anecdotal BS”!! i.e. you can’t POSSIBLY know what you are talking about if there’s no rigorous scientific analysis, debate, or documentation.

**crickets chirping**

But it turns out there ARE medical scientific studies which support some of what we already know by our experiences. Many readers of Stop the Thyroid Madness may not have discovered this yet, but STTM has a page which lists medical studies which support what we already know. So take a peek.

On the other side of the coin, how science can be completely flawed

One 1993 scientific study titled “Levothyroxine Therapy in Patients with Thyroid Disease” is one of MANY studies that informed patients came to realize was faulty. The concluding paragraph stated:

With proper patient monitoring, levothyroxine replacement therapy should be effective, inexpensive, and free of complications. Recommendations for thyroid-stimulating hormone suppression with levothyroxine are based on riskbenefit considerations of the biologic characteristics of the thyroid disorder and the individual patient.

Effective? Free of complications? It didn’t take long for a growing body of thyroid patients, who were comparing notes with each other (besides looking back at the experiences of their relatives) to see that this was FAR from the truth for many of us, to our own degree and kind. I started compiling plenty of non-effective results plus complications of being on T4-only medications from the mouths of patients worldwide over the years.

And the longer we’ve been talking to each other, we also discovered that even when some T4-treated patients report good results on these meds at first…or for several years…they were coming into groups to honestly report seeing more and more symptoms of a poor treatment crop up the longer they stayed on their Synthroid or any other T4-only treatment. It’s not a pretty picture overall.

(And by the way, natural desiccated thyroid is CHEAPER.)

Medical school training is just as much the problem as is flawed science

The Carnegie Foundation did a study about medical schools, and in a particular paragraph, concluded (italics mine):

Medical training is inflexible, excessively long and not learner centered. They found that clinical education is overly focused on inpatient clinical experience, supervised by clinical faculty who have less and less time to teach and who have ceded much of their teaching responsibilities to residents, and situated in hospitals with marginal capacity to support their teaching mission. They observed poor connections between formal knowledge and experiential learning and inadequate attention to patient populations, systems of health care delivery, and effectiveness. Learners have inadequate opportunities to work with patients over time and to observe the course of illness and recovery; students and residents often poorly understand non-clinical physician roles. The team observed that medical education does not adequately make use of the learning sciences. Finally, time and again the researchers saw that the pace and commercial nature of health care impede the inculcation of fundamental values of the profession.

And sadly, patients will report problems with their doctors long after they attended medical school. Common descriptions include unteachable, clueless, rigid, narrow-minded, arrogant, and/or blind to the “clinical presentation” of their patients clear symptoms of continued hypothyroidism (for example, depression, anxiety, high cholesterol or other fatty acids, rising blood pressure, aches and pain, and so much more!) These same doctors will then bandaid these symptoms with anti-depressants, statins, pain meds, blood pressure meds and more.

But to be clear: patient reports don’t equal that they feel their doctors are purposely trying to do harm! Instead, thyroid patients clarify that even their most well-liked doctors just aren’t listening, or aren’t willing to learn from patient experiences, or feel threatened if a patient wants to guide part of his or her own care, or are condescending, as if a patient couldn’t possibly have a brain of their own about what they need. So patients leave…and search for a doctor much more willing to listen to patient experiences and wisdom.

Bottom line: some of reported patient experiences and science jive to some degree. For the rest, medical research studies need to catch up with the truth of our successful experiences, or continue to look stupid.

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