Category Archives: 17. Making Thyroid Perfect

N-Acetyl Cysteine Increases Free T3 in NTIS

N-Acetyl Cysteine Increases Free T3 in NTIS

References: Critical Care,

A reference to this article caught my eye when I saw the reference to NTIS which is jargon for Non-Thyroidal Illness Syndrome (NTIS). NTIS is what happens to you when you get critically ill, like with a heart attack. Your free T3 plummets and your reverse T3 rises dramatically. Just when you need it, your body goes into a perverse “antagonistic pleiotropy” cycle. Antagonistic pleiotropy is the concept that what is good for you in one environment, isn’t good for you in another. I suspect you can make the reasoned argument that Neolithic humans, when injured or ill, were well served by “hunkering down” and getting through an illness or crisis in medical care by downregulating their metabolism. That allows calories to be shifted to immune function instead of metabolic function. That remains conjecture because we weren’t there to test it. We just see the effect in modern humans.
That’s what NTIS is. Your body “Hunkers Down” in response to a crisis. In this study, the crisis was 67 patients with heart attacks. In the ICU their Free T3 and Reverse T3 were measured, and predictably they changed dramatically, shifting from regular T3 to reverse T3. NAC reversed that and improved T3.

Reverse T3 reverses T3. It blocks the action of the free T3 on your body. (Remember, T3 is the active thyroid hormone your body actually runs on. You convert it from T4, made by your thyroid. T4 is not biologically active. It’s simple the precursor template.) You feel the effect of low T3 when you get sick. You feel exhausted and can’t get out of bed. A heart attack patient can hardly lift their head off the pillow. Folks in an ICU are sick. Really sick. Can hardly move. That is the nugget of Non-Thyroidal Illness Syndrome. You get a physiological stress and your body goes into “hunker down”, or NTIS.

In this study, N-acetyl cysteine was given to the study folks in a randomized, placebo-controlled fashion. The folks who got the NAC got better and had higher free T3. What is NAC? Very simple. It is the key building block to make glutathione. Glutathione is your body’s key anti-oxidant. At age 20 you make tons of it, naturally. At age 50, dramatically less. Older, less, older, less.

Now, let’s switch to the modern era of day-to-day 24-hour stress, media, artificial light, sugar, deadlines, jerks at work – have I named enough of your stressors? Ok, add in-laws and teenagers. You feel tired all the time. Your free T3 is just too low. Could you be low in glutathione, your natural anti-oxidant? Well, NAC is the natural building block for making more of it. It is simply two amino acids plugged together, waiting for a third to be attached and presto, you have glutathione. Your stress may not be as dramatic as a heart attack, but it’s nevertheless real. Could NAC help you? I bet it could.
WWW.What will work for me. Simple. I take NAC myself. Every day. It’s on Bredesen’s lists of suggested supplements for brain health. That’s good enough for me to pull the trigger and add it to my list. I remember back when NAC was a precious, rare ICU drug to reverse Tylenol overdoses. Worked like a charm. Then it became an ER drug. Then it became a take-home drug. Then it became an OTC supplement. You can buy it yourself. This incredibly powerful building block for you to make your own glutathione is available for you over the counter. Gives you back the vital T3 for your own energy system. Isn’t that a unique cross synergy of metabolic systems?

Pop Quiz
1. Free T3 is the hormone your body naturally runs on. T or F Answer: True
2. You make less free T3 when you are under stress. T or F Answer: True. Probably a result of “antagonistic pleiotropy” which means it was good for us in one environment, but not the one we are in now.
3. NAC boosts our ability to make free T3 when we are under stress. T or F Answer. Bingo. Either you guessed right or you actually read and understood the article above.
4. We make less glutathione as we age. T or F Answer: Double bingo.
5. The right way to fix our low Free T3? (Bonus question) Answer: Get rid of the stress, add selenium and zinc, make sure you have enough iodine, avoid PCBs and dioxins, and take a break from the teenager.


Biotin Messes with Your Thyroid Testing

Biotin Messes with your Thyroid Testing

References: NCBIEndocrine News

Everyone needs biotin. It’s been known since the 1920s but only understood since the 1970s. It is used in 4 enzymes in the mitochondria of your cell. You can make some biotin deficient by feeding them a diet of pure raw egg white (high protein) and despite that sounding odd, folks getting IV parenteral nutrition had a lot of egg white protein given IV and thus biotin deficiency was found. Skin rashes and hair loss were prominent symptoms. Hence, the connection with hair loss. The Institute of Medicine recommends some 30 micrograms a day and that’s what’s in most OTC vitamin pills.

Now, menopause is strongly associated with hair loss, as is thyroid disease. Considering how many Americans go through menopause (rumor has it that it’s more than half), the hair loss industry was born. And biotin plunked down in the middle of it. BEST PRODUCTS to prevent hair loss! It is widely “known” that you “need” biotin to prevent hair loss. Well, is it? And are there problems with that? If you look at the ingredients in most of the hair loss products, you will find 500 mcg of biotin and above in them. That’s 20 times the Institute of Medicine guidelines.
Considering that hair loss is associated with dysfunctional thyroid, mostly low, and low progesterone, many many women are caught in this conundrum, and want to fix their hair loss. And they find themselves on biotin, in one form or another.

What’s the problem? Biotin has now been found to conflict with thyroid measurements.
This should come as a relief to many folks who can’t understand why their thyroid tests keep fluctuating wildly. The problem comes in that biotin is used as an anchor to capture antibodies. Biotin sticks nicely to streptavidin, a protein reagent on the capture surface of the test device. That makes a lot of natural biotin floating around. When someone starts taking lots of extra biotin, it’s going to interfere with that testing process. With interference, you can have falsely elevated blood tests of total T4 and T3, with normal other tests making for combinations that don’t make sense.

You see the conundrum? You have hair loss and are trying to normalize your thyroid. But you are also taking biotin, in a form you didn’t even know about because the supplement you were taking for hair loss called it something other than biotin (Vitamin H is a common misnomer).

www. What will work for me. If I didn’t know 5 people with this situation, it wouldn’t be so notable. The upshot is that it takes some 3-5 years for hair to run through its natural cycle, and up to 6 months for anyone to notice that a real change has come about. Once it has fallen out, it takes at least 3 months (the telogen phase) before it starts growing again. It’s not that biotin is bad for you. It’s that it is used as a reagent in testing thyroid, and high blood levels mess up the testing. If that leads to dose changes, you have a problem. If you are on biotin, then don’t completely trust any test about your thyroid.


Pop Quiz:

  1.  Hair loss is affected most by what two hormones?                        Answer: thyroid and progesterone

2.    Biotin is related to vitamin C? T or F                             Oh, get over it and read it again. It’s a B vitamin, B7 to be exact.

3.    The reason biotin messes up your thyroid is?                                  Answer: it doesn’t. It messes up your thyroid test leading you to look like you are in trouble, when you are just peachy.

4.     If you are worried about your hair, how often should you let yourself make dose changes of your thyroid or progesterone?                                                                 Answer: probably at least 3 months before you change anything.

5.    Your thyroid is easily understood with your thyroid tests? T or F                 Oh, my goodness. You haven’t read much about reverse T3 or de-iodinase yet.



Bromine Toxicity: Real or Not?

Bromine: Secret Toxin?

Reference: Endocrine Society, Oncology Letter,


What do you know about bromine? I bet not much. It’s in the halide family, meaning the same family as chlorine and iodine and fluorine. Iodine is the biggest size of the lot, then smaller bromine, then chlorine and finally fluorine. They all share a negative one charge, so act the same chemically. They differ only in size and weight. Bromine is easily extracted from ocean salt brine pools, and is used industrially as a fire retardant. It used to be used as an insecticide in the form of methyl bromide, but that turned out to be a potent ozone depletor, so that got nixed. And once upon a time it was used as an anti-anxiety drug, and hence the term, “Bromides” for trite and trivial soothing answers.

The issue of bromine that I want to explore is that of its competition with iodine. We need iodine. Desparately. It is one of the elements that all of us are just barely getting enough of. The WHO considers iodine deficiency the #1 cause of mental retardation in the world. And Americans are prone to it too. In Milwaukee, in the year 1900, 50% of women had goiter, the result of iodine deficiency. Today, 80% of American women have fibrocystic disease, an iodine deficiency illness. There is considerable research that shows iodine to be an anti cancer drug and a cure for fibrocystic breast disease.

So what’s the problem? Here’s the rub. Bromine competes with iodine. In fact, every halide competes with iodine. But bromine may be the worst, not because it’s obvious, but because it is subtle and pervasive. Bromine acts chemically just like iodine. It has never, ever, ever, been in the human nutrient supply chain, until the 1950s when it was substituted for iodine as a stabilizer in bread. Some states ban it, but not all. Then, we added it to every chair, mattress and couch in our lives as a fire retardant. We sold it in Bromo-Selzer until the bromide was removed in 1975 for “toxicity“. Bromine may not be a perfect fit for iodine in the process of making thyroid hormone, or in normal breast tissue, but it’s plentiful, pervasive and competitive.

And then we got our undies in a bundle over the supposed toxicity of iodine. A bizarre little story of iodine toxicity developed around the so called “Wolf-Chaikoff Effect” that was an experiment in rats, extrapolated to humans but never clinically proven in humans. I’m quite interested in it personally because, as a child up till age 18 in India, I used iodine to purify water, and on many occasions used iodine up to 10 pills a day (at 2.4 mg of iodine per pill). That was not uncommon practice. Made the water taste terrible, but killed all sorts of nasties. I don’t believe the Wolf-Chaikoff effect is real, and if it is, it is very short term and harmless. It’s not the bugaboo we think it is.

What the real danger, I believe, is that lots of us have a burden of bromine from environmental exposure (fluorine too). It’s not super toxic, or immediately toxic, but it shows up in many folks having flakey thyroid findings because they just can’t get their thyroid to function right. There appears to be a whole cottage industry in detoxing from bromine with salt water flushes. This idea has its detractors as well.

Szent-Gyorgyi, the Nobel Laureate for Vitamin C, took 1,000 mg a day of iodine until he was 93, claiming it to be his most useful supplement. He might be our most famous credible advocate for iodine supplementation, but he is not alone.

WWW.What Will Work for me. I take iodine as a supplement. 1 mg a day. I think we all should. Every woman worried about breast cancer and every man worried about prostate cancer should too. I’ve now met three people taking over 25 mg a day in the form of Iodoral pills. They feel great. No toxicity as far as I can tell. Szent-Gyorgyi took 1,000 mg a day. It appears to me there is latitude for higher doses. I’m thinking this may be what is missing in some folks whose thyroids otherwise just doesn’t act right. I would really like to hear from someone who had toxicity from iodine. I don’t there there are really too many. And I do think there are many of us with too much fluoride, bromide and chlorine in our food chain, all competing with iodine. Precautionary principle: we have too many halides in our food chain that were never there before, and are skimming along on the edge of insufficient iodine because of unproven fears. The only way to push those halides out, bromine included, is more iodine. So do it.

Pop Quiz:

‪1. Bromine toxicity is a proven phenomenon. T or F

Well, really false if you look at the standard PubMed literature, except for the obvious high dose poisoning, but enough advocates out there are claiming it. Are they crazy? Or is it all mixed up in our overblown anxiety about iodine?

‪2. Bromine can chemically act like iodine, and compete with it. T or F

‪This seems to be true. How much, we just can’t tell.

‪3. Iodine deficiency is real. T or F

Emphatically true. If you consider fibrocystic breast disease as an iodine deficiency disorder, its ubiquitous. If you listen to WHO, it’s our number one cause of mental retardation. Apparently very common in politicians. (Small joke)

‪4. Iodine toxicity is real. T or F

I’m coming down on the side of probably false. Too many anecdotes of much higher doses. And it will never be studied. Way too cheap.

‪5. There are many folks taking more than 12 mg a day of iodine without trouble. T or F

Well, yes. After Fukushima, many Japanese took 65-130 mg a day of iodine, and we didn’t see a huge epidemic of iodine toxicity from that. Think about that for a couple of minutes. I know of many who have taken 12.4 mg a day for years, with no apparent toxicity. Szent-Gyorgyi took 1,000 mg a day until he stopped working at Woods Hole at age 93.  I know, I know, there may be some issue with Hashimoto’s.  I haven’t seen much of it.

Hepcidin, Weight Loss, Thyroid, Ferritin and Iron

Hepcidin, Weight Loss, Thyroid, Ferritin and Iron

References: Nemeth Annual Review of Nutrition, Ahmed WJG, Paoletti

Are you trying to lose weight and can’t? Think it might be your thyroid?   You feel tired all the time.   Your doctor doesn’t measure your ferritin or your iron.   Is there a link and connection you should know about? Yes!

Hepcidin is the link. Ever heard of it? It was discovered in about 2000. It is a peptide hormone that is used to regulate iron. It’s output is increased in inflammatory states.   When you are overweight, you start out behind the eight ball because fat cells spew out inflammatory markers 24/7.   Serum iron falls due to iron trapping in macrophages and decreased gut absorption.   The protein ferroportin is present in gut cells and it is turned off by hepcidin.

If you have severe enough inflammation, you can even become anemic because your body will simply reject any iron.   It’s hard to measure hepcidin, but a C-reactive protein is a pretty good surrogate marker.   Your ferritin is lower in your blood because you just don’t have any iron absorbtion.   And what is ferritin? It’s your storage form of iron that in inside cells and in blood.   It reflects your total body iron. But it’s function is more basic, it converts the Fe+2 ferrous ion into the F3+3 form which protects your body from the dangerous “Fenton” reaction that creates hydroxyl ions.

How does all this fit together? Pretty elegantly.   Iron deficiency promotes fat storage. And the effect of that on your thyroid is slightly indirect, but perverse.   Low ferritin and your thyroid doesn’t function like it should. There are some 80 proteins inside the cell that need iron in part of their structure to process the gene signaling that T3 starts.   When you have low ferritin, your iron is low, and your gene signaling will be disrupted.

Ironically, if there is severe inflammation, ferritin can be elevated as an “acute phase reactant”, but that would be a red herring in this case. Most of the time, folks with normal TSH and T4 but with all the symptoms of hypothyroidism like being cold, weight gain, lousy hair will have a low ferritin and a modestly high CRP (as a stand-in for the unmeasurable hepcidin.)

Does that sound too confusing?   Read Byron Richards summary. He adds some insight into inflammatory diets and yeast overgrowth setting off inflammation. That’s another topic for another day.

WWW. What will work for me.   If you want to lose weight, your first step might be to get off of carbs and have lower nutrition for the yeast in your gut. Then, get your ferritin, iron and CRP checked.   The picture will emerge that you really did need a bit more thyroid.   It may not be any more complicated than that.   And if your doctor won’t allow it, you can always just but the test at “AnyLabTestNow”.


Pop Quiz

  1. Hepcidin is your iron controlling hormone. T or F

That’s it

  1. It regulates the amount of iron your absorb, store, tuck away or activate? T or F

If this is all you learned, I’m happy.

  1. In response to inflammation, hepcidin goes up, and iron goes down? T or

True. Now you are on a roll

  1. When iron (ferritin) goes down, your thyroid can’t work right. T or F

Bingo. Ready for the bonus round?

  1. So, once you are overweight, your first step should be to turn off inflammation, which tones down hepcidin, which allows iron to rise, which allows your thyroid to work.   T or F

Whew. Now you have got it perfectly.

Why is My Thyroid Still Not Normal?

Why Is My Thyroid Still Abnormal?

Reference Kent Holtorf Journal of Restorative Medicine 2014

Jan 19th, 2015

Standard medical practice measures two simple tests with your thyroid.   Your TSH (thyroid stimulating hormone) and your T4 (the circulating precursor to the active hormone T3).   Your doctor says, “You’re fine.”   You still feel crummy.   What’s going on?

Your doctor made the assumption that your blood test shows “normal” so you must be ok.   That assumption is based on the premise that if blood levels are ok, intracellular levels are also ok.   Aha!   Therein is the glitch. Transport of T4 into cells is not a passive subject.   There is much recent evidence that insulin resistance, diabetes, depression, chronic fatigue, high blood lipids, anxiety, dieting and plain old aging all contribute to reduced T4 transport into cells, while the pituitary is unaffected. In fact, the pituitary can continue to concentrate T4 up to as much as 600 times higher than peripheral tissues. The pituitary/hypothalamus combination is thereby not the best indicator of peripheral tissue function.   That’s what your doctor measures when she/he draws a TSH test. The TSH is what your pitutitary thinks you need. If it’s level is higher, it’s your pituitary saying you need more. If it’s lower, your pituitary says you have enough.

Transport of T4 into cells is not passive. That is the assumption your doctor made. It takes energy. Transporting T4 takes more energy than T3. If you are treated with pure T4, you might not be getting enough thyroid effect in your tissue. So, if you are cold, gaining weight, have muscle aches, decreased libido, weakness, water retention, depression, have low basal body temperature, all symptoms of being hypothyroid, you likely need to be treated with T3.

If this sounds like you, you may need to have some unique tests done. A much better assessment of your thyroid comes from testing your REVERSE T3 and calculating a T3 / rT3 ratio.   (Reverse T3 is a mirror image of T3 and basically blocks T3 from working – giving your body a valuable tool to adjust your energy metabolism up and down.)   High levels of rT3 are more likely due to reduced transport into the cell, and not due to increased T4 to rT3 conversion. So, a high rT3 is simply a good marker for lousy intracellular transport of T4. If you can’t transport T4 into the cell, you can’t make T3, and you feel tired, cold and achy.

Then, you should measure your Sex Hormone Binding Globulin (SHBG). SHBG is made in your liver in response to sufficient estrogen and sufficient intracellular T4 in the liver.   If women have a level above 70 nmol/L and men above 25 nmol/L, each has enough intracellular T4.

Read the whole article referenced above. Holtorf is one of your best thyroid educators.   The final kicker you will find is that dieting repeatedly changes the speed at which you transport T4 into the cell. It has been demonstrated that repeated dieting results in weight loss at half the rate, and weight gain at three times the normal rate unless thyroid hormone deficit is addressed. Hmmm.

WWW. What will work for me.   Weight loss is the holy grail of good health. But it messes up our thyroids and then we see our doctors who can’t figure out our problems. We feel cold. I’m checking rT3 and SHBG all the time now, and the light turns on when you see the results. It’s a much better set of tests than the simple TSH and T4.

Pop Quiz

  1. Reverse T3 is the mirror image of T3.   T or F

Perfect. True

  1. Reverse T3 reverses T3.   T or F

Again, on the money

  1. Our body balances T3 and rT3 intracellularly to deal with stress, which boomerangs on us in a highly stressed world, filled with dangerous foods. T or F

That’s about the sum of it

  1. Your pituitary gland reads blood levels of T4 accurately. T or F

Dead wrong. It can concentrate T4 and convert it to T3 many times more efficiently than local tissues

  1. The pituitary makes TSH which accurately reflects your bodies thyroid needs? T or F

T if your are taking the Internal Medicine exam, false if you are a human

  1. Sex Hormone Binding Globulin is an interesting adjunct measure of the accuracy of sufficient intracellular thyroid hormone activity. T or F





The Circadian T3 Method (CT3M) for Adrenal Fatigue

The Circadian T3 Method (CT3M) for Adrenal Fatigue

Reference: Recovering with T3 by Paul Robinson

This is a very simple idea, wrapped up in some complex physiology. To date, we have defined “adrenal fatigue” as someone who is exhausted when they wake up, can’t get out of bed, need three cups of coffee to do anything and don’t feel rested all day long. When you measure their salivary cortisols four times in a day, you see low morning and/or noon cortisol levels. To date, in traditional Internal Medicine, we have said there is nothing particularly wrong with that, and tell you to go to bed on a regular basis and see an endocrine doctor who says, “There is no such thing as adrenal fatigue!%$&!”. Ok, ok. But in traditional anti-aging medicine, we have stated that you have to deal with your adrenals first BEFORE you start to replace thyroid hormone. We acknowledge adrenal fatigue and have lots of relatively slow acting responses to it, mostly using self care methods like extra sleep, laughter, friendship, hobbies and time off from your stressor. A few Chinese herbs and supposedly, you get better. Both thyroid hormone and cortisol affect energy – thyroid sets the idle on your engine, cortisol goes out and mobilizes the fuel to be burned. Both are needed to have good energy.

Cortisol is clearly secreted in circadian fashion, with multiple small bursts of ACTH in the early morning hours – an hour or so before awakening.   ACTH is made by your pituitary and stimulates your adrenals to make cortisol. The CT3M method that Paul Robinson supports is based on the premise that you can’t make cortisol in your adrenals if you don’t have the free T3 hormone that your body needs at the right time of day. If you are just taking T4 (traditional Synthroid) you are taking the pro-hormone that your body has to alter by lopping off one iodine and turning it into the active hormone called T3.   The enzyme that does that, de-iodinase, is based on selenium. If you don’t have enough selenium, you might not be able to activate thyroid hormones. For that, and many other reasons, you may end up with insufficient T3 hormone to satisfy your adrenal glands. Particularly, by taking T4 (or Synthroid) at one time of day, your effective T3 in the early morning when you are making ACTH may be too low to be effective. So, it’s actually low T3 at a critical time of day that leads to the low cortisol. (That’s the hypothesis.) Without sufficient T3 at the right time of day, your adrenal glands make no cortisol because they just don’t have enough “umph” to get off the couch and do their job.

What’s the method? Consider taking pure T3 (or natural dessicated thyroid with T3 in it) one and one half hours prior to your wake up time. If that’s 6 am, do it at 4:30.   If it’s 8, do it at 6:30. We want you to have another full 90 minute sleep cycle after that dose. You have to prepare carefully and lay out the dose on your bedside table with a sip of water, not waking up too much. The usual starting dose is at least 5 mcg of T3, maybe 10. The theory is that taking the free T3 at that time will provide the critical metabolic hormone to your adrenals and pituitary just at the point in time when they are producing pulsatile ACTH, and subsequent pulsatile cortisol. They key is that you don’t use sustained release. thyroid If you feel a wee bit better and have more energy upon awakening, that may be attributable to the T3 itself, but also to the fact that your cortisol is responding nicely. Prove it by taking another saliva series and see if your lab confirms your improvement in symptoms.

WWW. What Will Work for Me.   I have so many clients with exhaustion and early morning fatigue for whom our traditional methods of help have been slow or ineffective.   T3 is a touchy hormone.   There are reasonable concerns about too much causing heart rhythm disorders and bone loss so it needs careful supervision and monitoring. But when I hear credible clients say they weaned off their morning cortisol for the first time in years, I’m paying attention. This may be the opening of a door we hadn’t looked behind before. Time to look a little further.


Pop Quiz

  1. You make most of your cortisol in the late afternoon to match your activity level. T or F   False. You make it in the morning, and that matches your activity level. That’s why most of us feel most energy and creativity first thing in the morning.
  2. Cortisol is made in your adrenal glands in response to ACTH secreted by your pituitary, in response to CRH secreted by your hypothalamus. T or FTrue
    1. It doesn’t matter what time of day you take your thyroid hormone. T or F

    That’s what we have typically said

    1. Too much thyroid can cause fatigue too. T or F

    True. Many elderly have fatigue when over the top limit of normal thyroid range.

    1. T3 is needed for your adrenals to make adequate Coritisol – T or F.

    True, maybe. But maybe not as much as this method suggests. A very interesting idea for research.

    Cortisol is made in your adrenal glands in response to ACTH secreted by your pituitary, in response to CRH secreted by your hypothalamus. T or F


Low Free T3 in the “Normal” Range Predicts Death in Elderly Patients

Low Free T3 in the “Normal” Range Predicts Death in Elderly Patients

Reference: JCEM Iglesias Oct 2013 PubMed Abstract Reverse T3 and Mortality

There is lot’s of talk about thyroid and how important it is for your general well-being. It acts as the idle on your engine, generating power for your body to turn into energy and vitality.   Just how important it is?   Well, this study gives us a clue.   404 patients, over age 65 were admitted into the study when they were admitted into the hospital. They didn’t necessarily stay in the hospital but their overall survival was followed for the next 7years. Their TSH, T4 and T3 were measured. (Not reverse T3).   In that time period, 303 of those patients died (80%). Low free T3 on admission was highly predictive of death in the hospital. The lowest quarter of patients with low free T3 lived only 3 months when their free T3 was less than 3.1 pmols. In the US we use picograms and the conversion is to less than 2.1 pgms. That is low, even in the USA, and is just below the normal range.   But folks in the next third were in what we call normal and their mortality was still greater than the folks in the top third. They only lived 13 months compared to 19 months for folks at the top.

About a third of the patients died of heart disease and they too fit the pattern of predictive deaths with low free T3.   In fact, low free T3 appeared to by particularly important for predicting cardiac mortality.

Now, confounding all this is that the same pattern also matched low TSH. Remember, TSH works inversely to T3.   A low TSH would suggest that your body thinks you are getting more than you need of thyroid. TSH is usually high if free T3 is low. If free T3, T4 and TSH are all low, and predictive of mortality, it may mean your whole system is just giving up and shutting down. If free T3 was low, and your natural systems were working, your TSH should be climbing to raise up your T3 and subsequent free T3.   This particular pattern may be identifying those folks whose whole integrated system of checks and balances is going down.

The conundrum could have been explained by measuring the REVERSE T3.   Remember the adage, “Reverse T3 reverses T3”? This study may be a confirmation that reverse T3 is not an inactive metabolite but rather an active blocker of free T3.   We believe that reverse T3 is induced with stress. Being sick and hospitalized is a great way to induce stress.

The best explanation of the “big picture” would be as follows.   The older you are, the less you can deal with stress. Your mechanisms for adjusting to it are less robust than when you are younger. (Surprised?) If you are sick, you want to have energy available for immune function and repair, so it would be helpful to shift fuel from metabolism to immune function. Reverse T3 would help do that. Makes perfect sense when you are doing things like hibernating, or dealing with infections. But it becomes counterproductive when your body is tasked with a new sort of stress like heart attacks. Then, you just spiral down into a gyre of self-reinforcing trouble. You can’t even make TSH to stimulate your thyroid any more. Without that basic hormone to sustain life, you spiral into death.

The authors of this study warn that this does not prove that treatment prolongs life. We just see an interesting association.   But what would you do?

WWW. What will work for me.   I’m really interested in this. I believe the Free T3 should be monitored in all of us and we should aim to keep it in an optimal range. That may be even more important for us as we age.   That optimal range may be a little higher than we thought. The lower half of our “normal range” may still have higher mortality.   Is treating it helpful? The jury is still out on that one.

Archives can be found at

Pop Quiz

  1. Elderly folks with low free T3 have a much higher mortality than those with normal free T3.   T or F

Yup. In a nutshell

  1. Treatment with T3 will reverse that, T or F

Nope. Not proven at all, but intriguing and maybe.

  1. TSH, thyroid stimulating hormone, also can predict mortality. T or F

True – but in contradictory pattern – backwards

  1. Reverse T3 is induced by stress. T or F


  1. Understanding reverse T3 and free T3 might be useful

Seems to be a good argument for that.