Thanks to Dominic for posting his comprehensive and fascinating overview of the use of T3 in chronic fatigue syndrome (ME/CFS) and fibromyalgia (FM) Please note that Health Rising does not provide medical advice or recommend treatments and Dominic is not a doctor. Please be aware, as well, that no studies have assessed the efficacy of T3 treatments in these diseases. Because long term thyroid treatments in the absence of overt thyroid abnormalities can cause the thyroid to shut down using thyroid medications in that context is controversial.
- Practitioners and pure T3 treatments
- Dr John Lowe (USA): Supra-physiologic dosages of pure T3 to overcome “thyroid hormone resistance”
- Dr Gordon Skinner (UK): Treating post-viral CFS with thyroid hormones
- Dr E. Denis Wilson (USA): T3 therapy protocol to “reset” impaired T4 to T3 conversion in patients stuck in “conservation mode”
- Dr Kent Holtorf (USA): Breaking a cycle of immune, hormone and mitochondrial dysfunction in CFS and Fibromyalgia
- Dr Barry Durrant Peatfield (UK): Treating a “down-regulated” metabolic status
- Dr Sarah Myhill (UK): Kick-starting CFS/ME recovery with T3
- Dr Jacob Teitelbaum (USA): Treating inadequate T4 to T3 conversion and thyroid hormone receptor resistance
- Paul Robinson (UK): Recovery from CFS with the circadian T3 Method
- Self-treating patients: Successes and frustrations
- Table: CFS/ME Practitioners and key features of their T3 treatment
- Websites – Practitioners
- Websites – Patient advocates
In my search for what could make my wife feel better, I kept coming across stories of patients’ recovery from CFS/ME and FMS involving treatment with pure T3 (i.e. liothyronine, the synthetic form of triiodothyronine). These include stories on Health Rising by Edith Bouvier Dan Burns (x2) and Joy.
In this article, I aim to provide a succinct overview of the approaches and success stories of some CFS/ME and FMS practitioners with supplementation of pure T3 specifically, documenting each practitioner’s approach. But first I will provide background on the T3 hormone, and context to explain why treatments with T3 are so contentious.
T3 is the “active” thyroid hormone, which stimulates activity in almost every cell in the body, apparently by binding to nuclear membrane receptors that control gene expression. Crucially, T3 serves to regulate the body’s metabolic rate by increasing aerobic mitochondrial function. Dr Myhill writes that if the body were a car, then the mitochondria are the “engine” and the thyroid gland is the “accelerator pedal”.
Moreover, researchers are now increasingly discovering T3’s complex role in immune responses (e.g. Jara et al. 2017).
It is important to know that while some of the body’s T3 is produced by the thyroid gland, 80% of circulating T3 is the product of “peripheral” (i.e. localized) conversion of the “less active” T4 hormone (which is produced by the thyroid gland) into T3 by deiodinase enzymes in the cells themselves (especially in the kidney and liver).
However, the story gets a bit more complicated because there are in fact three types of deiodinase enzymes that convert T4: D1 is responsible for conversion of T4 into T3 in most cells of the body, except for in the brain and the pituitary where D2 does the job (De Groot, 2015). D3 converts T4 into an inactive “reverse T3” (RT3) which (sometimes disturbingly) competes with T3 for space on the above-mentioned cells’ nuclear membrane thyroid receptors (note: D3 also converts T3 into T2; the role of this thyroid hormone is still being researched).
Critically, under certain conditions (such as inflammation, fasting or stress), D1 is downregulated and D3 is upregulated, resulting in less T3 and more RT3 at the cellular level. This can result in hypothyroid symptoms – even if the thyroid gland itself is functioning normally (Holtorf, 2014a).
Finally, in order to understand T3 treatment, it is important to realize that thyroid hormones don’t just diffuse into cells but must be actively transported into them, and that the transport of T4 requires much more energy than the transport of T3 (Holtorf, 2014b).
In sum, T3 affects almost every physiological process in the body, and its function depends on the successful conversion of T4 into T3 by enzymes, the transport of thyroid hormones into cells, and the uptake of the hormone by nuclear membrane receptors.
Synthetically produced T3 (i.e. “liothyronine”) is generally sold under the name Cytomel in the USA (Tetroxin in Australia and Timorel in Turkey), and is used to treat hypothyroidism and myxedema coma (i.e. severe hypothyroidism). Supplemented T3 is much better absorbed through the gut than the T4 alternative (95% compared to 50% to 75%) and the “time to peak therapeutic effect” is much faster for T3 than for T4 (48 to 72 hours compared to 3 to 4 weeks).
Drugs.com explains that T3 may be preferred over T4, “when a rapid effect or rapidly reversible effect is desired, or when gastrointestinal absorption processes or peripheral conversion of T4 to T3 is impaired.” Regulating T3 dosage is more difficult, however, because of its potency, and “rapid onset of action may also produce adverse cardiac effects as a result of abrupt changes in metabolic demands” (Drugs.com). To mediate these effects somewhat, compounding pharmacies can produce “sustained-release” or “time-released” T3, which releases the hormone more slowly into the blood.
The use of pure T3 as part of treatments of CFS/ME and FMS is a very contentious topic for three reasons:
Firstly, the role of “low thyroid hormone function” – i.e. cells not getting enough T3 – as an essential mechanism in CFS/ME and FMS is not widely accepted by the medical community. Indeed, only a fraction of practitioners assert that low thyroid hormone function at the cellular level plays a key role in understanding CFS/ME and FMS.
They point to the parallels between symptoms of hypothyroidism and CFS/ME and FMS, including: low basal body temperature, fatigue, muscle aches, weakness, slow reflex relaxation phase, etc. (e.g. Lowe and Yellin, 2008). A recent study that found evidence of “severely depressed tissue T3 levels” in CFS patients provides further weight to their argument (Ruiz-Núñez B, et al., 2018).
Secondly, there is also disagreement within the medical community regarding the treatment of patients with thyroid hormones when their TSH, T4 and T3 blood levels are in the “normal” range. Dr Broda Barnes, Dr Jacques Hertoghe and many others who have followed in their footsteps have had success bringing patients with hypothyroid symptoms – but normal thyroid blood levels – back to good health using thyroid hormone supplementation.
Mainstream endocrinological associations, however, maintain that standard thyroid lab tests are sufficient to assess whether a patient would benefit from thyroid therapy, and that patients with normal thyroid blood levels should not be treated with thyroid hormones irrespective of their clinical symptoms.
The many experiences of patients to the contrary has spurred the creation of patient-led advocacy groups / websites includingThyroid Patient Advocacy (UK), Thyroid UK, Stop the Thyroid Madness, Hypothyroid Mom, The Invisible Hypothyroidism, Mary Shomon and ThyroidChange as well as the publication of many books by patients and doctors alike, including the terrific titles “The Great Thyroid Scandal and How to Survive It (2002),” “Tears Behind closed doors: Failure to diagnose a thyroid condition (2002),” “What your Doctor May not tell you about Hypothyroidism (2004),” “Living Well with Hypothyroidism: What Your Doctor Doesn’t Tell You… That You Need to Know (2005)” “Why Do I Still Have Thyroid Symptoms? when My Lab Tests Are Normal (2010),” and “Stop the Thyroid Madness: A Patient Revolution Against Decades of Inferior Treatment (2011),” “Be your own Thyroid Advocate: When you’re sick and tired of being sick and tired (2018).
Finally, there is also disagreement amongst doctors on the relative effectiveness of thyroid medicines that contain T3 – such as natural (desiccated) thyroid (i.e. from pig extract), synthetic mixes of T4/T3, and pure T3 – compared to the now standard pure synthetic T4 (i.e. Levothyroxine). Indeed, the American Thyroid Association and similar endocrinological associations in other countries maintain that T4 is the best choice for treating hypothyroidism, although many doctors have found that their patients respond better to treatments which contain T3.
As further described in the next section, the fact that some patients may have difficulty converting T4 into T3, that supplemented T4 may be converted into RT3 instead of T3, and that the transport of T4 into the cells requires more energy than the transport of T3 – may explain why therapies that contain T3 have often succeeded when T4-only therapies have failed to improve symptoms. The patient advocacy groups and books cited above also denounce the continued insistence on the use of T4 by the medical establishment, counter to practitioners’ experience.
In sum: given these three ongoing disagreements, treatments for CFS/ME and FMS with pure T3 and despite (most often) normal thyroid lab results are therefore particularly controversial.
Yet still some practitioners prescribe pure T3 to treat CFS/ME and FMS – despite the sometimes great risks they may incur for providing a non-standard treatment (including sanctioning by authorities). The approaches of some of these practitioners are described in the next section.
Note: For the purpose of this overview, I have picked out elements in the approaches of the various practitioners which relate to treatment with pure T3; however, their full approaches are wider in scope and more complex. Some of these practitioners (but not all) advise that T3 should be trialed only if treatments containing T4 or natural thyroid prove ineffective.
Moreover, most advise that pure T3 should be trialed only when other complementary treatments are in place, including adrenal support (e.g. in the form of hydrocortisone or adrenal extracts), and when a certain nutrient status is achieved (particularly in respect to iron and vitamin B12 levels). Finally, practitioners also advise that treatments should, of course, be performed under the supervision of knowledgeable physicians.
In his starkly worded short article entitled “Fibromyalgia – A Medical Mystery Solved” (2007) the late Dr John Lowe unequivocally writes: “the main underlying cause of fibromyalgia […] is too little thyroid hormone regulation of patients’ bodies.” He explains that “resistance” of patients’ cells to thyroid hormone means that these cells “need higher than ‘normal’ amounts of thyroid hormone to maintain normal metabolism.” He and Jackie Yellin explain this further in their technical article: Inadequate Thyroid Hormone Regulation as the Main Mechanism of Fibromyalgia: A Review of the Evidence (2008). Moreover, they describe the mechanisms at work and clinical trials in their gigantic book (1,260 pages!) entitled The Metabolic Treatment of Fibromyalgia (2000). According to Dr Lowe, resistance to T3 can have a number of causes, including mutations in the T3 receptors and T4 to T3 conversion problems.
Based on his team’s clinical trials (see e.g. Lowe et al., 1996), patients who had failed to recover from FMS with other treatments – including T4 and natural thyroid – and had normal thyroid hormone blood levels prior to treatment, recovered with “supra-physiologic” dosages of pure T3 (i.e. higher than physiologic dosages). His patients generally recovered from FMS with a range of 100 to 150 mcg of pure T3 per day. He argues that the fact that these patients are not overstimulated at these high dosages is further evidence that they have a form of thyroid hormone resistance.
The book he wrote with Dr. Gina Honeyman-Lowe, Your Guide to Metabolic Health (2003), describes when T3 should be trialed, how to go about it, and complementary supplements and methods to monitor progress. Many patients start on a “full replacement dose” of pure T3 (i.e. the amount a normal thyroid gland would produce per day: 20 – 30 mcg), but the starting dose depends on the patient’s health status, severity of symptoms, and other factors. Dr Lowe generally prescribed a single daily dose of pure T3 to be increased gradually by 12.5 – 25 mcg at 1 – 2 week intervals, and then more modest increases of 6.25 mcg as the patient appears to approach the “therapeutic window” (Lowe, 2008) – i.e. “a dose at which the patient has no symptoms of overstimulation, and hypothyroid-like symptoms improve or disappear altogether.”
Their methods are also described in the e-b; ook by Hugh Hamilton: Impaired Sensitivity to Thyroid Hormone (Thyroid Hormone Resistance): A Cause of Heart Disease, Cancer, Autoimmune Conditions, Women’s Health Issues, Strokes, Fibromyalgia, Depression and Other Issues (2016).
Dr John Lowe died in 2012; the many patients he helped expressed their gratitude and shared stories of recovery on Stop The Thyroid Madness and other forums.
The late Dr GRB Skinner was a virologist who authored nearly one hundred journal publications on herpes and other viruses. CFS/ME patients kept getting referred to him by their General Practitioners because of the belief that CFS/ME was initiated and maintained by a chronic virus infection. His insight was that the reason patients don’t recover from an infection is not because the infection becomes chronic, but because the patient becomes hypothyroid as a result of the infection. Dr Sarah Myhill credits Dr. Skinner with pioneering thyroid treatment for post-viral CFS/ME patients.
In his book Diagnosis and Management of Hypothyroidism (2003) Dr Skinner writes that viral infection, food poisoning, childbirth, physical trauma, etc. can be “precipitating causes” for hypothyroidism. He strongly believed that diagnosis of hypothyroidism should be made on clinical grounds (i.e. the patient’s history and physical symptoms) because “a ‘normal’ laboratory test doesn’t say a disease isn’t present.”
Indeed, according to Dr Skinner, the “simple-minded reliance on laboratory tests” – combined with the great diversity of clinical manifestations of hypothyroidism – has unfortunately led to a vast under-diagnosis of the illness. With reference to doctors’ manuals from an era prior to the use of thyroid blood tests (and using his warm Scottish humor), Dr Skinner spends a long chapter of his book describing the clinical features of hypothyroidism – which include lack of whole body stamina, being bed bound, loss of muscle power in arms and legs, inability to chew, cognitive difficulties, “intolerance to all things great and small,” carpal tunnel syndrome, intestinal fermentation (relating to muscle weakness of the intestinal tract), food intolerances, local tenderness in muscles, intolerance to light and other sensory disturbances, etc.
Notably, he debunks the myths that a patient who has lost, rather than gained, weight, or has diarrhea (rather than constipation) or feels hot (rather than cold), cannot be hypothyroid; in fact, that person may very well be hypothyroid.
In terms of treatment, he writes that the type of thyroid “replacement preparation, the dosage and rate of increase of a dosage for a given patient” is “almost an art form.” He used many forms of thyroid hormone, including pure T3. He writes that most patients do better on natural thyroid than T4, and that “the provision of T3 alone does not always do the job” (perhaps because the T2 in natural thyroid plays some as yet unknown important function).
Patients also responded better to thyroid hormone when taking high doses of B-12 vitamin. He found that in most cases, thyroid hormone cured low function of the adrenal glands, but sometimes he accompanied his thyroid treatments with adrenal support to allow the adrenal glands to meet the demand of improved thyroid functions (often 2.5 – 5 mg of prednisolone).
Skinner writes that non-responses to thyroid treatment often occur when prescribed thyroid hormone dosages are too low due to a “preconceived notion of a correct or safe dosage.” He surmised that initial side effects from thyroid treatment, such as palpitations, arose because thyroid receptors may have “atrophied” and the supplemented thyroid hormone gets “backed-up.” This is remedied by reducing the medication for a while and perhaps lowering the rate of increase. He wrote that it may take 1 or 2 years for patients to become well. Amazingly, he describes an international athlete whom he diagnosed with hypothyroidism and hypoadrenalism, who later self-increased his dosage of pure T3 to 400 mcg per day. He calls this self-medication “an ill-advised procedure at these levels,” but points out that “something is happening” that merits further research.
I wish Dr Skinner had entitled his book “Diagnosis and Management of post-viral CFS/ME” – I believe that would have been a more fitting title, and the book would have gotten more attention by the CFS/ME community. The UK General Medical Council opened several hearings against Dr Skinner for his stance on prescribing thyroid hormones. After his death in 2013, many of the patients whom he had helped get their lives back described their recoveries and expressed their thankfulness on healthunlocked.com (UK) and other forums.
Dr E. Denis Wilson (USA): T3 therapy protocol to “reset” impaired T4 to T3 conversion in patients stuck in “conservation mode”
Dr E. Denis Wilson writes that under conditions of severe stress, metabolism can slow down as a coping mechanism. Some patients get stuck in this “conservation mode”, even after the stress has passed, resulting in “debilitating symptoms” that will sound very familiar to CFS/ME and FMS patients. According to Dr Wilson, this “conservation mode” is characterized by low body temperature; he gave it the name “Wilson’s Temperature Syndrome”. He points to parallels in the symptoms of this condition with CFS and FMS, and writes on his website that patients diagnosed with CFS have “responded dramatically well to proper T3 therapy” and “many patients with Fibromyalgia have been completely cured” with his protocol.
Dr Wilson’s explanation for the mechanism at work is that during stress, the enzyme responsible for converting T4 into T3 (i.e. D1 enzyme) is inhibited. Instead, T4 is converted into Reverse T3 (RT3) which is inactive and blocks nuclear membrane thyroid receptors. The increased level of RT3 then further inhibits the conversion of T4 to T3, because the RT3 competes with T4 for the D1 enzyme (note: D1 can also convert RT4 into the inactive T2) causing the body to get stuck in a “vicious cycle of T4 to T3 conversion impairment.” Dr Wilson writes that “clearing out the RT3 from the tissues can serve to reset the system so that it can function normally again.”
To clear out RT3 from the tissues, Dr Wilson uses cycles of T3 supplementation which serve to halt the production of T4 by the thyroid gland (and without T4 no additional RT3 can be produced). Unlike Dr Lowe, Dr Holtorf, Dr Skinner and others, Dr Wilson generally only provides temporary T3 supplementation in order to reset “patients’ thyroid hormone pathways” and avoid later setbacks (which he suggests may be related to nuclear membrane receptors becoming desensitized with too much T3 supplementation). He likens the approach to cranking the starter cord on a lawn-mower.
The basic treatment Wilson provides (effective, he asserts, for 80% of the patients) is a starting dosage of 7.5 mcg “sustained release” T3 every 12 hours (i.e. 15 mcg per day on day 1) increased by an additional 7.5 mcg twice per day every day (i.e. after 10 days, the patient is taking 75 mcg every 12 hours; so 150 mcg per day). After just a few days on the highest dosage (max 90 mcg every 12 hours; so 180 mcg per day), the patient is weaned off T3 by subtracting 7.5 mcg off each dose every 2 or 3 days. The basic cycle, therefore, lasts about 1 month.
Patients monitor their pulse and look for palpitations (and are prescribed a little T4 to steady pulse and palpitations if needed). Wilson also provides adrenal support such as hydrocortisone or herbal supplements. After each cycle, patients measure their body temperature for a few days to determine if it is steady.
Cycles are repeated, and the maximum dosage is adjusted as needed so that the body’s system of T4 to T3 conversion re-establishes itself and the patient feels well again. Unfortunately, the longer the patient has been sick, the more difficult it is to get the natural system to establish itself again. His cycling protocol makes for fascinating reading, and is described in detail in the free e-books on his website. A journal paper from 2006 describes a successful application of the protocol with 11 CFS patients (Friedman, 2006).
The American Thyroid Association released a critical statement in 2005 aiming to debunk Wilson’s protocol (ATA website), but significantly, doesn’t challenge the “reset” mechanism behind his approach. Until recently, you could search the database of doctors that apply the protocol on Dr Wilson’s website, but it has been removed to protect their privacy.
Dr Kent Holtorf (USA): Breaking a cycle of immune, hormone and mitochondrial dysfunction in CFS and Fibromyalgia
A major insight I gained from Dr Kent Holtorf’s articles is the link between inflammation and T3 regulation. As partially described in the first section, inflammations and other forms of stress lower T3 tissue levels by three main mechanisms:
- by reducing transportation of thyroid hormone into cells (Holtorf, 2014b),
- by downregulating the enzymes responsible for conversion of T4 to T3 (i.e. D1), and,
- by upregulating the enzymes responsible for conversion of T4 to RT3 (i.e. D3) (Holtorf, 2014a).
The resulting RT3 binds and block the T3 receptors, explaining their “decreased sensitivity” or “increased resistance” to T3. Combined with less T3 production, this leads to slowed metabolism, reduced immune responses, etc. (see also: De Groot, 2015). Critically, Dr Holtorf asserts that supplementation with T4 (including when found as part of natural thyroid) can exacerbate the problem because the T4 will be further converted into more RT3 which will block receptor sites.
Going a step beyond Dr Holtorf’s own writing, it was extremely interesting to me to learn that patients can, in fact, get stuck in a “vicious cycle” in which low thyroid function worsens oxidative stress, and the resulting inflammation in turn further depresses thyroid function at the cellular level (Mancini et al., 2016). The “reciprocal modulating relationship” between the thyroid hormones and the immune response is also further described in recent research, including: Devito et al. 2011; Jara et al. 2017 and Zhang et al. 2018.
Similar to Dr Wilson, Dr Holtorf prefers to use compounded “timed-release T3”, but just once per day. Following in Dr Lowe’s path, Dr Holtorf also advises his patients to build up to supra-physiologic dosages over time (100 mcg or more) based on clinical symptoms and an optimal RT3 to T3 ratio – as measured by blood tests. Dr Kent Holtorf’s approach to treating CFS and FMS further includes enhancing mitochondrial function, balancing other hormones, and treating infections. His approach is also explained by Cort in this article.
More information is available on the website of the National Academy for Hypothyroidism, headed by Dr Holtorf. The Holtorf Medical Group has three locations in the USA offering treatments.
In his excellent book, Your Thyroid and How to Keep It Healthy (2006), Dr Durrant Peatfield explains that in CFS/ME and FMS the “underlying problem is a down-regulation of [a patient’s] metabolic status” that most commonly originates with a viral illness, a major operation or a major life event. In viral cases, he explains, the virus inactivates a key enzyme responsible for producing eicosapentaenoic acid (EPA). Although Dr Durrant Peatfiled doesn’t explain the mechanism, he writes that this inactivation results in tissues unable to “respond properly to thyroid hormones”, in turn affecting adrenal activity.
In sum, many of the presenting symptoms of CFS/ME and FMS are a consequence of “adrenal and thyroid insufficiencies.”
A major insight I gained from Dr Durrant Peatfield’s book was the connection between the thyroid and the adrenals. Indeed, adrenal hormone status impacts T4 to T3 conversion, T3 transport into the cells and also the responsiveness of thyroid hormone receptors in the cells. Unlike Dr Skinner, Dr Durrant Peatfield makes the case that low adrenal function must be dealt with prior to thyroid hormone treatment to avoid overwhelming the body. He writes that “a failure of thyroid [treatment] to restore health may be largely down to adrenal problems.”
A further insight I gained from his book is the posited link between low thyroid function and inflammation via the gut: low thyroid function affects gut motility, leading to gut dysbiosis and fungal/candida overgrowth; this causes leaky gut which results in antigens, pathogens and toxins in the blood. This chain of events results in patients who suffer from inflammatory, auto-immune and allergic diseases.
Regarding treatments for low thyroid function, Dr Durrant Peatfield, like Dr Skinner, generally prefers treatments with natural thyroid, but indicates that “severe cases” may only respond to T3 due to problems in T4 – T3 conversion. He describes starting with 10 mcg of T3 and increasing every 5 days or so by10 mcg based on careful clinical observations (he provides no maximum dosage in his book). With time, he writes, the T4 to T3 conversion problem may subside, and it may be possible to introduce T4 for some patients. He emphasizes the importance of a flexible approach, as long as symptoms are monitored.
He prescribes adrenal glandulars or physiological levels of hydrocortisone ahead of thyroid treatments. Additional elements of his treatment protocol, described in great detail in his book, include balancing other hormones (DHEA, oestrogene and progesterone), eliminating candida, healing the gut, liver detoxification, and improving nutritional status through vitamins, minerals, and EPA (e.g. primrose oils).
Patients are instructed to monitor their progress by taking their waking and evening temperatures. With time as the “whole system revert[s] to normal on treatment” thyroid treatment may become less necessary or unnecessary altogether.
I also think that the title of Dr Durrant Peatfield’s book doesn’t do justice to the wealth of knowledge on metabolic status it contains – and therefore may have largely gone unnoticed by the CFS/ME community. Under pressure from the UK General Medical Council for offering controversial thyroid treatments – and in order to be able to continue to advise patients – Dr Durrant Peatfield voluntarily gave up his medical license in 2001.
Dr Sarah Myhill’s approach to treating CFS/ME is described in her book Diagnosis and Treatment of Chronic Fatigue Syndrome and Myalgic Encephalitis: It’s Mitochondria, Not Hypochondria. 2nd Edition (2018) and her website. She concentrates less on the thyroid hormone than the practitioners already cited above. Instead, she focuses on restoring the function of mitochondria, including by treating sources of inflammation (i.e. infectious, auto-immune and allergic), particularly those originating in the gut. Yet in her chapter on correcting thyroid and adrenal function, she describes that, based on her experience, “some people only feel better using pure T3”, as opposed to T4 or mixes of T4/T3.
She goes on to relate that, in addition to following a strict ketogenic diet, one of her patients required 180 mcg of T3 to “recover completely from her CFS.” Interestingly, this is the only specific example of complete recovery described in her book.
Dr Myhill’s treatment plan for T3 is a starting dose of 10 mcg split into 3 doses over the course of the day, and increased over time. She refers readers to Paul Robinson’s book for further detail on a trial with T3 (see below).
In addition to the treatment of low thyroid function as described above, Dr Myhill offers the interesting hypothesis that there may be a need to “kick-start” the brain out of “safe mode” into “normal function mode.” She cites Dr John Kaiser: “I believe it is reasonable to imagine very sick mitochondria being stuck in a dysfunctional mode similar to a heart muscle that is fibrillating,” and requiring a “kick-start” to get out of this mode.
In order to affect this “kick-start,” she proposes – as long as all other treatment options are in place – trials of pure T3 (“20 – 60 mcg, possibly more”) or natural thyroid (“1 – 3 grains, possibly more”), or alternatively Ritalin or Provigil. This allusion to “kick-starting” or moving from one metabolic state to another (or from a “vicious” to “virtuous cycle”) echoes the hypothesis of Dr Wilson.
Dr Myhill was also subject to multiple hearings by the UK General Medical Council for prescribing thyroid hormones when blood tests are normal; charges were dropped each time following strong support for her by her patients.
Dr Jacob Teitelbaum (USA): Treating inadequate T4 to T3 conversion and thyroid hormone receptor resistance
Thyroid treatment is arguably not the core of Dr Jacob Teitelbaum’s protocol for treating CFS and FMS, which is based on improving sleep, overcoming hormone deficiencies (including adrenal hormones), treating underlying infections, improving nutrition and “exercise as able” (i.e. SHINE). Yet on his website Vitality 101 with Dr T, he describes hypothalamic dysfunction, Hashimoto’s thyroiditis, as well as “inadequate conversion of T4 to T3” and “receptor resistance” as causes of “underactive thyroid hormone” in CFS and Fibromyalgia.
Dr Teitelbaum usually starts treating patients with a T4/T3 mix. Interestingly, he explicitly writes that he has found Dr Lowe’s approach of high pure T3 dosage “to be helpful in many patients.” Receptor resistance, he writes, “is often resolved in one or two years on the high-dose T3 therapy as the body heals from fibromyalgia and/or chronic fatigue syndrome.”
Paul Robinson describes his recovery from CFS symptoms with pure T3 after being sick for 15 years in his book Recovering with T3: My Journey from Hypothyroidism to Good Health Using the T3 Thyroid Hormone (2011). He was a hypothyroid patient taking T4 medication, but was sleeping 4 to 6 hours during the day and could hardly get up the stairs of his house. Because his thyroid blood lab results were in range, his doctor told him his hypothyroidism was “cured” and he must have CFS/ME. Interestingly, he also had a virulent case of glandular fever (Epstein Barr Virus) many years earlier when he was in his 20s.
He kept researching and found a doctor who would prescribe him T3; he improved greatly at first, but then stagnated. He didn’t feel fully recovered until he discovered that by modulating the timing of his T3 supplementation, he could affect total daily production of cortisol and other adrenal hormones, and cure his “adrenal insufficiencies”. (The hypothalamic-pituitary systems depends on T3 to start production of these hormones. ) He now uses pure T3 without complementary adrenal steroids or extracts, supplementing T3 according to the natural daily production rhythm of T3. Notably, this involves a relatively large T3 dose between 4 and 5 AM.
Robinson dubbed this protocol the “circadian T3 method” (CT3M). This method also works with T4/T3 combinations but does not work well with time-release T3. He also complements his treatment with various supplements and dietary changes. He has taken pure T3 (which he calls “T3-monotheraphy”) for over 20 years.
His own personal dosage is 60 mcg split into 4 doses. He achieved this dosage by going up in small increments of 2.5 – 5 mcg every 3 to 14 days based on observations of the effects.
Dozens of CT3M success stories are posted by patients on Paul Robinson’s website. Note that Dr Sarah Myhill refers her readers to Paul Robinson’s “excellent book” for details on trials with pure T3. I also think if he had entitled his book “Recovering from ME/CFS with T3”, his book would have gotten more attention by the CFS/ME community.
The stories of recovery from CFS and FMS with treatments involving pure T3 (and T3 containing thyroid hormone preparations) are circulating through books, articles and patients’ forums. However, because pure T3 treatments are not recognized as a standard treatment for CFS/ME and FMS in any country, and few doctors provide them, many patients have started self-treating with T3 as is evidenced in the conversation on online forums. (c.f. healthunlocked.com, tpauk.com, www.rt3-adrenals.org, Science for ME, etc.).
Patients provide each other with advice on the form of T3 and other thyroid hormones, timing, starting dosage, rate of increase, complementary hormones and supplements, etc. Reading these forums gives a sense of the patients’ frustrations with the lack of a standard protocol and lack of support from doctors to navigate a treatment that is challenging to get right. Initial progress is also often accompanied by setbacks that patients struggle to understand.
A summary of best-practices from patients’ experiences with pure T3 is available on the website Stop The Thyroid Madness. The website also provides testimonies from patients diagnosed with Fibromyalgia and CFS that have recovered after treatment with natural thyroid or pure T3.
Over the past decades, there have been many positive experiences using pure T3 in treating patients diagnosed with CFS/ME and FMS. Generally, successful treatment dosages of pure T3 are much higher than the thyroid glands produce naturally, suggesting either “thyroid resistance” at the cellular level (due to T3 receptors being blocked by RT3, receptor mutations or other reasons), or T4 to T3 conversion problems.
Most practitioners emphasize starting on a low dosage and increasing incrementally based on how the patient feels. Some practitioners advise patients to wean off T3 or introduce T4 (e.g. as part of natural thyroid) once the body is again able to convert T4 into T3, in order to avoid later setbacks. Several practitioners emphasize the importance of providing adrenal supports in tandem to allow the body to cope with an increase in metabolic rate.
I am particularly intrigued by several practitioners’ hypothesis that pure T3 supplementation may serve to “kick-start” metabolic pathways (or break vicious cycles), perhaps related to T4 to T3 conversion, interactions between thyroid hormones and the immune system, mitochondrial function, or the brain. In other words, the “kick-start” model posits that thyroid supplementation could be used to break the body from a homeostasis of illness (i.e. an equilibrium state that is maintained by physiological processes) to a homeostasis of health.
However, along with these apparent commonalities, there are also many variations to the pure T3 treatments promoted by doctors and patients. Crucially, it appears that the treatment is quite sensitive: a variance in the type of T3 (i.e. time-release vs. non time-release), time of day, frequency (i.e. number of times per day), starting dosage, maximum dosage, pace of increase, cycling/weaning, complementary adrenal supports, iron status, vitamin B-12 status, etc. could make all the difference in the success or failure of the treatment.
Finally, it appears that the ideal treatment mode depends on the individual, and some patients do better on combinations of T3 and T4. This makes me wonder if perhaps CFS/ME and FMS patients who have tried T3, but for whom it has not had a positive impact, have simply not taken it according to a mode suitable for them.
In the absence of a standard protocol, patients are discussing these treatment variations in online forums. Whereas a lot of valuable information is shared, it is done in an ad-hoc and unstructured way. Moreover, I believe this information is often not accessed by CFS/ME and FMS patients because it is labeled as treatment for hypothyroidism (which they have been told they don’t have on account of normal laboratory blood results).
A comprehensive and structured place for the collection of experiences with pure T3 (and other thyroid hormone treatments) in the context of the CFS/ME and FMS community would arguably be of immense value for advancing the treatment of patients diagnosed with CFS/ME and FMS.
The Low T3 Series on Health RIsing
- The Atypical Thyroid Issues in Chronic Fatigue Syndrome (ME/CFS), Plus a New Thyroid Subset?
- Pure T3 Thyroid and Stories of Recovery from Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia: An Overview.
- The Relevance of Research on Critical Illnesses for Chronic Fatigue Syndrome ME/CFS: A vicious cycle between cytokines, oxidative stress and thyroid hormones
|Practitioner||Key features of the treatment||Mechanisms addressed|
|Dr John Lowe||– Supra-physiologic dosage (100 – 150 mcg of T3 per day)
– Single dose in the morning
– Pure T3 (not time-release)
– Starting dosage depends on health status, severity of symptoms, etc. Most patients start with “full replacement dose.”
– Pace of increase is 12.5 – 25 mcg of T3 every 1 to 2 weeks. More modest increases (6.25 mcg) as patient appears to approach effective dosage.
– Complementary supplements
|– Cellular “resistance” to T3 (e.g. T3 receptor mutation)
– Problems in conversion of T4 to T3
|Dr Gordon Skinner||– Emphasis on clinical diagnosis (not blood tests)
– Used all thyroid hormone preparations (T4, T3 and natural thyroid)
– However, little detail in his book on pure T3; describes cases of T4 and natural thyroid
– Sometimes provided adrenal support (prednisolone)
|– Post-viral CFS/ME leading to hypothyroidism
– Problems in conversion of T4 to T3
|Dr E. Denis Wilson||– “Wilson T3 Protocol”
– Uses “sustained-release T3”
– Supra-physiologic dosage (up to 90 mcg twice per day; i.e. 180 mcg total per day)
– Most patients start at 7.5 mcg every 12 hours and increase by an additional 7.5 mcg twice per day every day (i.e. after 10 days the patient is taking 75 mcg every 12 hours = 150 mcg per day)
– After reaching the peak dose, patients wean off T3 by subtracting 7.5 mcg at each dose every 2 or 3 days
– Cycle is repeated as necessary until temperature is stable and patients feel well
|– Patients being “stuck” in the conversion of T4 to RT3 following a stressor|
|Dr Kent Holtorf||– Uses time-released T3
– Supra-physiologic dosage (> 100 mcg)
|– Problems in conversion of T4 to T3
– T3 receptors being blocked by RT3
|Dr Barry Durrant Peatfield||– Uses natural thyroid or T3
– Emphasis on adrenal supports for thyroid treatment to work
– Nutritional support and treating the gut
|– T4 to T3 Conversion block
– T3 receptor uptake resistance
– Adrenal insufficiencies
|Dr Sarah Myhill||– Correcting thyroid hormone levels, but no preference for pure T3
– Yet recognizes that some patients only feel well on pure T3 at supra-physiologic dosage (e.g. 180 mcg).
– Always in combination with other treatments
– Starting dosage of 10 mcg split into three doses across the day.
– Refers to Paul Robinson’s book for further detail on trial with T3
– In addition: Use T3 to kick-start the brain out of “safe mode” into “normal function” mode (20 – 60 mcg of T3, possibly more)
|– T3 receptors being blocked by RT3
– Brain perceptions of imbalances in the energy equation
|Dr Jacob Teitelbaum||– Usually starts patients on T4/T3 mix
– Has found Dr Lowe’s approach to be helpful in many patients
– 1 or 2 years high dose T3 therapy to treat receptor resistance
|– Problems in conversion of T4 to T3
– T3 receptors resistance
|Paul Robinson||– “Circadian T3 Method” – early morning dosage is key to power-up the adrenals
– T3 or T3/T4 mix
– Not “time-release”
– Increases / decreased in 2.5 – 5 mcg every 3 to 14 days to find optimal dosage. Slowing when close to final T3 dosage
|– Problems in conversion of T4 to T3
– Adrenal insufficiencies
Broda Barnes and Lawrence Galton, 1976. Hypothyroidism: The Unsuspected Illness. (Book)
Kenneth Blanchard, 2012. Functional Approach to Hypothyroidism: Bridging Traditional and Alternative Treatment Approaches for Total Patient Wellness. (Book)
Benoît Claeys, 2015. En finir avec l’hypothyroïdie: Ce que votre médecin ne vous dit et que vous devez savoir (Book)
Leslie J DeGroot, 2015. The Non-Thyroidal Illness Syndrome. Endotext
De Vito, Paolo & Incerpi, Sandra & Pedersen, Jens & Luly, Paolo & B Davis, Faith & J Davis, Paul. (2011). Thyroid Hormones as Modulators of Immune Activities at the Cellular Level. Thyroid: official journal of the American Thyroid Association. 21. 879-90.
Barry Durrant Peatfield, 2006. Your Thyroid and How to Keep It Healthy. (Book)
Friedman M, Miranda-Massari JR, Gonzalez MJ. 2006 Supraphysiological cyclic dosing of sustained release T3 in order to reset low basal body temperature. Puerto Rico Health Science Journal. 25(1):23-9
Hugh Hamilton, 2016. Impaired Sensitivity to Thyroid Hormone (Thyroid Hormone Resistance): A Cause of Heart Disease, Cancer, Autoimmune Conditions, Women’s Health Issues, Strokes, Fibromyalgia, Depression and Other Issues. (Book)
Kent Holtorf, 2014. Peripheral Thyroid Hormone Conversion and Its Impact on TSH and Metabolic Activity. Journal of Restorative Medicine 2014; 3
Kent Holtorf, 2014. Thyroid Hormone Transport into Cellular Tissue. Journal of Restorative Medicine 2014; 3
Jara EL, Muñoz-Durango N, Llanos C, Fardella C, González PA, Bueno SM, Kalergis AM, Riedel CA. 2017. Modulating the function of the immune system by thyroid hormones and thyrotropin. Immunol Lett. 2017 Apr;184:76-83.
John C. Lowe, MA, DC, Richard L. Garrison, MD, Alan J. Reichman, MD, Jackie Yellin, BA, Mervianna Thompson, RN, MSN, APN, Daniel Kaufman, MD, 1997. Effectiveness and safety of T3 (triiodothyronine) therapy for euthyroid fibromyalgia: a double-blind placebo-controlled response-driven crossover study: Clinical Bulletin of Myofascial Therapy, 2(2/3):31-58.
John Lowe, 2000. The Metabolic Treatment of Fibromyalgia. (Book)
John Lowe and Gina Honeyman-Lower, 2003. Your Guide to Metabolic Health. (Book)
John Lowe, 2007. Fibromyalgia – A Medical Mystery Solved. Thyroid UK Website.
John Lowe and Jackie Yellin, 2008. Inadequate Thyroid Hormone Regulation as the Main Mechanism of Fibromyalgia: A Review of the Evidence. Thyroid Science 3(6): R1-14
Sarah Myhill, 2018. Diagnosis and Treatment of Chronic Fatigue Syndrome and Myalgic Encephalitis It’s Mitochondria, Not Hypochondria. , 2nd ed.: (Book)
Antonio Mancini, Chantal Di Segni, Sebastiano Raimondo, Giulio Olivieri, Andrea Silvestrini, Elisabetta Meucci, and Diego Currò, 2016. Thyroid Hormones, Oxidative Stress, and Inflammation. Mediators of Inflammation.
Ruiz-Núñez B, Tarasse R, Vogelaar EF, Janneke Dijck-Brouwer DA, Muskiet FAJ., 2018. Higher Prevalence of “Low T3 Syndrome” in Patients With Chronic Fatigue Syndrome: A Case-Control Study. Frontiers in Endocrinology (Lausanne).
Gordon Skinner, 2003. Diagnosis and Management of Hypothyroidism. (Book)
- Denis Wilson, 1996. Wilson’s Temperature Syndrome: A Reversible Low Temperature Problem. (Book)
Jingping Zhang, Jingjing Huang, Kasimujiang Aximujiang, Chenbo Xu, Abulaiti Ahemaiti, Guixia Wu, Li Zhong & Kurexi Yunusi. 2018. Thyroid Dysfunction, Neurological Disorder and Immunosuppression as the Consequences of Long-term Combined Stress. Scientific Reports volume 8, Article number: 4552
- Vitality 101 with Dr T (Dr Jacob Teitelbaum)
- Recovering with T3 (Paul Robinson).
- Wilsons’ Temperature Syndrome (Dr E. Denis Wilson)
- Dr Sarah Myhill
- The National Academy of Hypothyroidism
- Dr Malcom Kendrick (UK)
- Dr David Borenstein (USA)
- Dr Rind (USA)
- Dr Simone Koch (Germany)