Ken Blanchard's thyroid T3 method | Voyage to Health[/URL]:
KEN BLANCHARD’S MICRO-T3 METHOD
May 31, 2018
“Take some more tea,” the March Hare said to Alice, very earnestly.
“I’ve had nothing yet,” Alice replied in an offended tone, “so I can’t take more.”
“You mean you can’t take less,” said the Hatter: “it’s very easy to take more than nothing.”
– Lewis Carrol “Alice in Wonderland”
I have never met nor corresponded with Ken Blanchard who passed away at the age of 77 in April 2017. From the little I know about him, he was a traditionally educated endocrinologist, with an impressive MIT/Princeton/Cornell educational pedigree and a thriving practice of dedicated patients from which he has only retired shortly before his death. What distinguishes this man from the rest of his colleagues, however, was that he was a very open-minded person who was not afraid to think for himself and question authority. He quickly figured out on his own that normal TSH values did not exclude hypothyroidism. He also realized that there was a connection between hypothyroidism and fibromyalgia, chronic fatigue, PMS, depression, IBS, adult-onset ADHD and other poorly understood conditions of our time. Most importantly, he figured out how to properly dose T3 – which went completely against the grain of what everybody around him was doing.
Dr. Blanchard’s favorite saying was that “when it comes to medicine, the only people who are absolutely certain about anything are medical students, malpractice lawyers, and well compensated expert witnesses”. In 1990 he became interested in adding T3 for his patients who were already on T4 – something that virtually nobody doing back in those days. He quickly found out that most of them felt better initially but then quickly got worse. He described it as “up-down” effect of T3 treatment.
Having done much experimentation, Ken Blanchard arrived at the conclusion that patients who had sufficient amount of T4 in their system, did much better if only tiny amounts of T3 were added to their regimen and if these tiny amounts were compounded in a slow release form. The ratio of T4: T3 he used is 98.5:1.5 which is about 0.375 mcg T3 for every 25 mcg T4. He preferred to use slow release NDT as he found it provided better mental function. The ratio then becomes 2.5 mg SR NDT for every 25 mcg T4 (note that while T3 and T4 are measured in micrograms, NDT is measured in milligrams).
Dr. Blanchard used Levoxyl and Tyrosint as his preferred brands for T4 because they were the purest and free of additives which can trigger allergic reactions. He would usually start patients at low doses of 12.5 mcg (although I believe that patients with dysautonomia and long-term CFS may need to start with even lower doses). He also realized that the timing of thyroid doses was highly individual and required experimentation, and that thyroid levels need to be adjusted based on seasonal and menstrual cycle changes. He also sometimes prescribed T3 as a transdermal gel for those who had GI absorption issues.
By using the above approach, Blanchard was able to restore back to health many patients who have previously failed both on conventional protocol or who have been made much worse by the alternative protocols. Despite that, Blanchard’s method has not gained popularity because it went completely against the currently accepted knowledge.
As out of the box thinker, Blanchard has questioned something that no other physician prescribing T3 has bothered to think about: how did we arrive at the lowest dose of Cytomel pill being 5 mcg? When he began to look into the issue further, it led him to conclude that the reason 5 mcg was the lowest prescribed dose was because Cytomel was originally invented as an alternative to T4 replacement – a trend that never really took off because T3 replacement did not work well compared to T4. These doses were never designed to supplement T4 treatment or to mimic the physiologic production of the thyroid gland. Cytomel, however, found it’s application in the psychiatric profession, where this high dose might have been useful in depression partially by exerting a stimulant-like effect on monoaminergic neurotransmitters.
When Blanchard tried to talk to other endocrinologists about his ideas, they wrote them off as “crazy talk” because in their mind those doses were “homeopathic” and could only work through “placebo effect” – never mind the fact that these are the doses that mimic physiologic thyroid production much better than any other method. It appears that Ken Blanchard never really tried to reach out about his practice to alternative communities or niche groups such as CFS circles, only to his colleagues – which turned out to be an insurmountable task.
I know for a fact that these doses of slow release T3 do work and that it is not a placebo effect. And I believe that it’s a shame that while everyone in those alternative communities has heard about Wilson, virtually anyone to my knowledge has heard about Blanchard, even though I think way more people would benefit and certainly less would be harmed by Blanchard’s method than by Wilson’s method.
(By the way, T3 is not the only hormone we are overdosing patients on. Melatonin is often sold in 5-10 mg doses while physiological doses have been shown to be closer to 0.3 mg (R) – but nobody cares about that either).
Let’s take a more close look at how the thyroid gland works so that you can see for yourself why minimalist approach makes sense.
The thyroid gland secretes on average about 6 mcg of T3 per day. So if someone has their thyroid removed they would need somewhere in the vicinity of 6 mcg of supplemental T3 or perhaps slightly more to account for absorption losses). Those of us who have intact thyroid gland would need way less than that. Let’s also remember that thyroid gland releases T3 into the bloodstream in very controlled, tiny doses throughout the day. It never dumps 6 mcg at once. If we assume that 6 mcg is what is being released over 24 hours that would amount to somewhere around 0.25 mcg of T3 per hour. That is the kind of T3 influx that our body was designed to handle. The rest of T3 comes from the intracellular conversion.
That is the physiologic mechanism of how thyroid hormone is produced in the human body. Very small constant levels of active thyroid hormone are secreted into bloodstream. Much larger amounts of inactive hormone are produced – on average about 100 mcg of T4 per day. The half-life of T3 is only about 1 day. The half-life of T4 is 7 days. This allows for a much larger pool of T4 than T3 to accumulate in the body. This storage pool is what the cells draw upon whenever they need to and the cellular enzymes known as deiodinases convert T4 to T3.
However, if all T4 could be converted T3 on the cellular level, then thyroid gland probably would not be secreting those 6 mcg of T3 per day. We have to assume that because nature does it that way, it is important. This very small and steady blood supply carries with it a chemical message to organs. It signals adrenal glands to produce cortisol. It has an effect on ion channels on plasma membranes. It signals the cells to get ready to uptake and convert incoming T4. And it helps to regulate hypothalamic and pituitary control of the secretion.
There is receptor preference for T4 within the nerves system, making the T4 preferred substrate for neural cells. In addition, T4 might serve as a co-transmitter for norepinephrine. Therefore, T4 is not just some inactive hormone. The right balance of T4 to T3 is crucial.
Most of the body’s T3 is generated from T4 at the tissue level and the cells of that tissue get to decide on what they are comfortable with and control the pace of the conversion in order to match their metabolic capabilities and needs.
If one does not have a good peripheral conversion of T4 to T3 at the tissue level then it’s a separate issue which needs to be addressed. It is best addressed by figuring out what is affecting the conversion and adding supplements that help to maximize it rather than dumping mega-doses of T3 into the bloodstream (I will write more about deiodination regulation later). There are likely people out there with a unique genetic make-up, for example, inborn abnormalities of thyroid receptors, that might feel better on T3 alone. However, it is much safer to start with the minimalist approach because once you get on high doses of T3, your biochemistry will change and it will be very hard to revert to using the minimalist approach. On the other hand as the Mad Hatter put it: “it’s very easy to take more than nothing”.
I believed Ken Blanchard’s bookbecause I have personally observed on many occasions that a tiny 1 mcg dose of slow release T3 is able to raise my fT3 to nearly maximum level. When you take even the lowest available dose of Armour, you get a rush influx of T3 and your serum T3 will shoot up transiently to very high levels (those that are found in patients with severe hyperthyroidism, such as Grave’s disease) and will result in TSH suppression. (If you don’t believe me, check your T3 level one hour after taking your dose and see for yourself). Therefore, once you start taking high doses of T3 or NDT you will make yourself more hypothyroid over the long term which will prompt you to take more and more.
In other words, taking typical doses of external T3 is bound to lead to thyroid resistance and further loss of hypothalamic control over metabolism. What happens when you take higher and higher doses? You keep putting your body into hyperthyroid states, triggering cellular adaptations to hyperthyroidism, stressing your adrenal glands, pushing T1AM levels higher than they need to be and adding to already dysfunctional HPA and HPT axis. If you are like me and have a genetic condition that creates vascular sensitivity to high levels of T3 or if you have problems with cholinergic/ noradrenergic receptors which often happens in prolonged untreated CNS hypothyroidism, or if you have bad HPA function or adrenals than you might find you can’t tolerate high T3 levels very well at all.
Compounded slow release capsules of T3 are ok but they are not ideal. What we really need is manufactured slow release Cytomel at doses of 0.1/0.3/0.5/1.0 mcg. Adding these doses would be able to restore the T3 production in hypothyroid patients back to its normal level and at its normal rate of release, without overwhelming cellular defense and suppressing hypothalamic function.
If one can’t get slow release NDT, one can still benefit from taking micro-doses of NDT, such as 1/4 of 1/4 grain or even tiny specks throughout the day which can be dissolved sublingually to derive the right effect from supplemental T4.
To sum it up, when it comes to T3 replacement Blanchard’s protocol is the proverbial tortoise: that we’ve come to associate with the phrase “slow and steady wins the race”.
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