IT’S TIME FOR A BOLD, DEFINITIVE STATEMENT

The most important parameter of all Lab tests

Reverse T3 is the most important parameter of all Lab tests, because it relates to stress of whatever origin, especially stress from severe, life threatening or chronic diseases. This is particularly true today, since in our current era, stress is ubiquitous across our civilization.

The value of serum rT3 rises in response to the increased secretion of Cortisol, which follows stress-induced ACTH secretion by the Hypothamus: Cortisol blocks Deiodinase1, which converts T4 to T3 and up-regulates Deiodinase3, which converts T4 to reverse T3.

Thus elevated rT3 accompanies psycho-social or marital stress, physical or chemical insult, infective, toxic or surgical damage, severe wounds, starvation, obesity, cardiovascular events, autoimmune disease – even “burnout“: basically, any aberration from normal function triggers ACTH release from the hypothalamus, with increased Cortisol, reduced T3 and increased rT3, production.

REVERSE T3 IS GARBAGE – VERY IMPORTANT GARBAGE

Reverse T3 is not a metabolite. It is metabolically inactive, non functional “garbage“ and as such, it is viewed as unimportant and is ignored by mainstream medicine: thus it is the least well-understood of all biochemical “markers”.

Ignorance regarding rT3 has led to institutional edicts against testing for it: MDs who order it are regarded as “quacks” and in some jurisdictions (Ontario, for example), are threatened with penalties of one sort or another. Ontario’s Ministry of Health has gone so far as to construct a website, entitled “CHOOSING WISELY”, to warn doctors NOT TO ORDER THYROID TESTS ROUTINELY and in particular, NEVER TO ORDER REVERSE T3!

This ignorance is reflected in the current assessment of rT3’s “normal value”, which is commonly stated as “less than 25 Nanograms/Decilitre”: in reality, any value greater than 13 Ng/DL indicates rT3 overproduction and even values of less than 13, if associated with reduced serum Free T3, can indicate metabolic dysfunction….
For detail regarding this, please see the T3/rT 3 ratio table, in my post entitled ‘Hypothyroidism diagnosis: T3/rT3 ratio” ).

Why is a “Garbage” compound, destined for excretion or destruction, valuable?

Here is the truth of the matter: rT3 is valuable as a parameter because it indicates the degree to which the normal processing of T4 into T3 has been subverted by stress-related Cortisol excess.

The calculation is as follows – T3 and rT3 are assessed, the T3 value (rendered in Picomoles/Litre) is converted to Ng/DL and is divided by the rT3 value: a result of >20 is normal, while <20 indicates suppression of the normal T4-to-T3 process and aberrant conversion of T4, to rT3.

Diagnostic interpretation of the T3. / RT 3. ratio

Once aware of the distorted metabolism, the clinician understands that the patient is functioning under the influence of the Low T3 Syndrome, which is easily corrected with oral T3: without the T3/rT3 ratio, LT3S is not confirmed.

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CHAT GPT

Today, I asked Chat GPT, “In how many diseases is Low T3 implicated, or associated? ” -Here is what it said (lightly paraphrased, for brevity and clarity):

Direct Answer: Low T3, often called Low T3 Syndrome or Euthyroid Sick Syndrome, is associated with dozens of diseases and critical illnesses. It appears across multiple systems—cardiac, metabolic, infectious, autoimmune, and neurological—because it reflects impaired conversion of T4 to T3 during stress or illness.

Key Disease Associations:

1. Cardiovascular Diseases

• Acute myocardial infarction (heart attack) – Low T3 predicts higher mortality

• Heart failure – Low T3 is associated with worse outcomes and poor recovery

• Arrhythmias and ischemic heart disease – Low T3 may be implicated.

2. Critical Illness & ICU Conditions

• Sepsis and septic shock

• Trauma and major surgery

• Severe burns

• Multi-organ failure

3. Neurological & Autoimmune Disorders

• Stroke and traumatic brain injury

• Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD)

• Multiple sclerosis and neuromyelitis optica spectrum disorder (NMOSD) – thyroid dysfunction often overlaps

4. Endocrine & Metabolic Disorders, if stressful –

Low T3 may result from the disorders shown, or from an associated condition, in

• Primary hypothyroidism (low T4 and T3)

• Hashimoto’s thyroiditis –

• Iodine deficiency –

• Pituitary or hypothalamic disease (secondary/tertiary hypothyroidism)

• Congenital hypothyroidism (cretinism)

5. Chronic Systemic Diseases

• Chronic kidney disease

• Liver cirrhosis and advanced liver disease

• Diabetes mellitus (especially poorly controlled cases)

• Cancer (advanced stages often show Low T3)

Why So Many?

• Low T3 is not solitary: it is a syndrome that occurs as an adaptive response to illness.

• It reflects reduced conversion of T4 → T3 during stress, inflammation, or nutrient deficiency.

• Because metabolism is fundamental to all organ systems, Low T3 shows up in a wide spectrum of diseases.

⚠️(3) Important Note

• Low T3 is often a marker of disease severity, rather than a cause.

• Its presence usually signals worse prognosis in critical illness, cardiovascular disease, and systemic disorders.

• Treatment strategies remain debated—whether to correct Low T3 directly or treat the underlying illness.

In summary: Low T3 is associated with dozens of diseases across nearly every major organ system.
It is best thought of as a “cross-cutting syndrome” rather than a disease-specific finding.

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I also asked chat GPT about diseases associated with elevated levels of reverse T3: its responses reflected conventional medicine’s bias and ignorance.

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Treatment with T3 reduces mortality

My favorite subject

As my readers will be aware by now, one of my “hobby horses“ – perhaps my favourite subject – is the importance of T3, the active thyroid hormone which is manufactured in the tissues, from T4. Regular readers will be familiar with the Low T3 Syndrome (LT3S) and its deleterious effect on body temperature, muscle/fat balance, bowel function, hair follicle death and sebaceous gland paralysis (dry skin), to name a few areas in which the function of T3 is indispensable.

The active thyroid hormone: T3.

Less obvious and less well known, however is T3’s activity in maintenance and repair of nerves and their myelin sheaths and its activity in maintaining muscle – especially Myocardial muscle – and muscle function.

T3 increases the basal metabolic rate and activates the Brown Fat, which regulates body temperature, maintains serum glucose and cholesterol balance and keeps body weight in check. It stimulates oxygen consumption in the tissues, boosts gastrointestinal motility, promotes skeletal growth and bone maintenance, has an integral effect on the development of the brain and nervous tissue in the developing fetus and is essential to myelination. In the adult, T3 enhances alertness, prevents anxiety, promotes cognition and provides feedback to the pituitary to suppress TSH production. In the tissues, T3 directly influences protein synthesis and enzymatic activity. by binding to nuclear receptors: in brief, T3. is essential to all bodily functions.

Thus I was unsurprised to find, in my pursuit of knowledge via the WWW, a paper which I had somehow, previously missed. entitled “Triiodothyronine (T3), inflammation and mortality risk in patients with acute myocardial infarction”.
Written by Salman Razvi, Avais Jabbar, Arjola Bano, Lorna Ingoe, Peter Care, Shahid Junej, Honey Thomas, Caroline Addison, David Austin, John P Greenwood and Azfar G Zaman, it had been published in the European Thyroid Journal on 10th January, 2020 – its DOI is 10.1530/ETJ-21-0085, PMCID: PMC9142797, PMID: 35007210:

I invite you to access it, read it and file a copy, which you should have available, to support you in discussion with your cardiologist if you ever turn up with a heart attack (you should tell the cardiologist that you would like to check your T3. and reverse T3, so as to derive the T3/rT3 ratio for diagnosis of LT3S, if it is present).

The protective effect of T3. on myocardial function

Here is an unexpurgated copy of the first paragraph of Razvi et al’s paper:

“There may be several possible explanations for the protective effect of T3 observed in AMI patients. Thyroid hormones, particularly T3, have considerable modulatory effects on myocardial tissue. In animal studies, T3 has been shown to be safe and cardioprotective in a post-infarct situation, resulting in preservation of ventricular function and arrhythmia reduction. Alterations in T3 levels affect mitochondrial function and have been linked with ischemia-reperfusion injury. In patients with heart failure and those undergoing surgical revascularization, T3 therapy has been shown to improve left ventricular function.”

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Are psychedelics the answer, or are we a missing something?

Preamble

The majority of my posts to “aging and your hormones” are expressions of opinion, based on my wide experience in Urology, General Practice and Hormone Restoration Therapy; but I receive “Infomail” from a number of sources, of which Medscape, the popular medical information website, is prime.
I scan incoming articles briefly, selecting those which seem important (either as information, or as new ideas) or misleading in some way, due to missing information, sloppy organization of research information or frank ignorance of metabolic/hormonal basic science.

I’ve been doing this for 3 years, adding one or two, or sometimes more, articles to my list daily. Therefore as you might imagine, I have a considerable backlog of potential sources for posts: I review the list periodically, jettison the less important pieces and select a few, for comment. Needless to say, many of the saved references are out-of-date, but nevertheless, some are interesting enough to warrant inclusion in my blog.

MANAGING MAJOR DEPRESSION, with PSYCHEDELICS

This one, “Psychedelics and Major Depressive Disorder: A Lot of Promise and a Lot of Questions”, presented in podcast format and uploaded on September 14, 2022, interested me because at that time, I had little information on the subject.

My research efforts however soon led to Johns Hopkins Medicine’s exhaustive note on the subject, which includes a “timeline” report on the progress of psychedelic therapy, beginning in the year 2000! …
I could not compete with their excellent website, so I gave up on the idea of posting, regarding psychedelic therapy for depression is a standalone title: if my readers are interested, access to Johns Hopkins’ report is at https://www.hopkinsmedicine.org/psychiatry/research/psychedelics-research

The format of psychedelic therapy

The format of psychedelic therapy may interest some readers, so I will describe it, briefly: “Psychedelics “, like Psilocybin (from magic mushrooms), LSD, Dimethyltryptamine and Mescaline are known to act on intra-neuronal serotonin 2A (5-HT2A) receptors, producing a wide range of psychological effects (5-HT2A also exist external to nerve cell capsules; but their function is not affected by psychedelics),

Psychedelics induce a 6-to-8-hour state of altered consciousness (essentially, altered perception), which may begin immediately, or after some delay. Visual or auditory hallucinations may occur, with alterations in the sense of self and the perception of the environment, which may be mild, stimulating or powerful enough to be rated as a “mystical experience,” in which a sense of separateness from the environment as well as from other people, manifests.

The therapist therefore prepares the patient via 1–3 sessions, in which the therapists educate the individual about their clinical condition, the underlying “psychomechanisms” and the experience expected following ingestion of Psilocybin, MDMA, LSD or some other psychedelic, such as Ayahuasca. Thus, the therapist ensures that the treatment is suited to the person and that a therapeutic alliance with the patient has been achieved.

Once that hurdle has been crossed, the patient is well prepared for a psychedelic experience and a dosing session is arranged. It begins in the morning, in a comfortable and soothing, “living room style” environment, so that the subject is relaxed, calm, at peace and best prepared to navigate an altered state of consciousness without anxiety. Following the session, if necessary, the patient can stay overnight, with a night monitor.
However some individuals are released to the care of a close family member or friend, returning the next day for “debriefing” and a discussion of the experience with their therapists.

The follow-up schedule is selected ad hoc, to include an interview one year later: generally, well-prepared subjects, given a psychedelic, carefully observed and “debriefed” by well-trained therapists, achieved a therapeutic benefit lasting 3 to 6 months, on average: response rates of 70%-80%, significantly greater than the 50% (or so) rates with conventional therapy, were sometimes observed.

Progress, since 2022

Since 2022, dozens of studies have been done and consensus has been reached: unequivocally, although research into the use of other compounds continues, Psilocybin has proven to be the best of the psychedelics for therapy in major depression and its place in the compendium has been confirmed.

The following milestones are memorable:

· In March 2023, the NIH, offering an explanation of the M.O. of the psychedelics, averred: “Psilocybin and MDMA, particularly, have shown promise as therapies for treatment-resistant depression and PTSD” ……………………….. They encourage (neuronal) plasticity by binding to the intracellular 5-hydroxytryptamine 2A receptor,to boost formation of dendritic spines, via which new inter-neural connections develop.

· In August 2023, JAMA (Vol 330, #9) reported a randomized trial of single-dose Psilocybin in the treatment of Major Depressive Disorder, concluding that “Psilocybin treatment was associated with a clinically significant, sustained reduction in depressive symptoms and functional disability, without serious adverse events). A single 25 mg dose of psilocybin was recommended.

· In February 2024, the Journal “Scientific Reports” stated that “Psilocybin treatment for major depressive disorder (MDD) and TRD has recently been awarded ‘breakthrough therapy’ status by the FDA. With over thirty registered trials (> 2000 patients), psilocybin treatment for depression (sometimes with comorbid anxiety, alcohol use, or other, disorders) is on the forefront of the renewed interest in therapeutic use of psychedelics.”

CURRENT STATUS

AI Overview:

In 2023, in Australia, the Therapeutic Goods Administration (TGA) approved psilocybin for treatment-resistant depression.

On April 8, 2025, the state of New Mexico’s Governor signed the Medical Psilocybin Act into law. This law creates a state-run program allowing patients with qualifying medical conditions to access psilocybin under the care of licensed healthcare providers.

Therapeutic psilocybin is not yet approved in other countries, including the United States and Europe.

My Two Cents (a Caveat):

All this is great; but as usual, none of the many reports which I perused makes mention of the background explanation for major depression.

In particular, there is
– no mention of the hormonal and biochemical status of the Major-Depression patient,
– no mention of efforts to correct aberrations of that status, prior to treatment,
– no thought regarding the possibility of heavy metal, PFAS or other toxicity, which may have contributed to the patient’s mental state,

The individual is diagnosed with “major depression” and listed for a trial of Psychedelic therapy, with
– no question of management for pre-existing PTSD,
– no consideration of menopausal hormone deficiency,
– no investigation for deficiencies of testosterone, progesterone, allopregnanolone, DHEA or Thyroid-3 which develop as we age, or other toxicity and
– no caveats regarding therapy for other medical conditions.

This is not satisfactory.

The patient is diagnosed with “majordepression” by a (presumably) HRT–naïve psychologist or psychiatrist, who has not been trained in metabolic medicine and is relegated, willy-nilly, to a basically risky trial of psychedelic therapy! –
This, without prior examination for and correction of the many pre-existing conditions which can form the foundation of the patient’s aberrant thought processes.

It does not seem to have occurred to “the powers that be” in this particular field, that correction of aberrations of the individual brain’s chemical/hormonal millieu might be the only therapy necessary, to solve the psychological problem with which the person presents, nor that the effects of the psychedelic experience might be enhanced significantly by normalization of the conditions in which the brain cells must function.

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What’s the connection with DHEA?

DISH/Multiple Exostoses

DISH (Diffuse Idiopathic Skeletal Hyperostosis) is a disease of the thoracic spine (the chest section of the backbone), which develops without inflammation, by hardening (calcification) of the ligaments which join the vertebrae together.

The underlying pathology of DISH was initially described by Forestier and Rotes-Querol in 1950, based on specimens and a series of 200 patients, referring to the condition as “senile ankylosing hyperostosis” (a much better name).

Recent studies have found a significant association between DISH and metabolic disorders, such as diabetes mellitus, hyperinsulinemia, obesity, dyslipidemia, and hyperuricemia/Gout.

The slow deposition of calcium in the ligaments between the vertebrae produces bony bridges which freeze the vertebrae together, preventing movement and producing an unmistakable x-ray image, which Portuguese physicians humorously, but accurately, call “biks de papagai”, because typically, the x-ray picture looks exactly like parrot (papagai) beaks.

Exostoses at muscle attachments, beside heavily-used joints

In DISH, Calcium deposition also occurs in the tissues around other heavily used joints, such as the elbows, knees and Achilles tendons, causing exostoses (bony growths, or “spurs”), at the point of attachment of tendons to bone.

The prevalence of DISH increases with every decade of life beyond 50 years. 15-25% of North Americans over the age of 50 years are affected and males are twice as liable to it, compared with females. However North Americans, on average, do not undertake sufficient heavy exercise to stress the tendons around the knees, ankles and elbows: so in many cases, limb-joint exostoses are absent, or too small to notice.

Since the early-morning back pain and stiffness of the DISH are relieved by stretching and mild exercise, affected men avoid visiting the doctor for as long as they can.
When they do attend the family physicians office, blood tests for inflammation are negative and physical examination discloses nothing, so both patient and physician blame the symptoms on “aging” and x-rays of the thoracic spine, which would show typical, obvious bony bridges between the vertebrae and thus provide a facile and instant diagnosis of DISH, are not ordered …………….. the diagnosis is missed.

Heberden’s Nodes

Heberden’s nodes, named for Dr. William Heberden, are small, paired, pea-sized bony growths that occur on the end (distal) -joints of the fingers. They are said to be due to osteoarthritis, but they often develop in the absence of any other osteoarthritic changes.

About 50% of women and 25% of men develop Heberden’s nodes by the age of 80–85 years and they are sometimes accompanied by “Bouchard’s nodes”, which are similar lumps, appearing on the Proximal (closer to the heart) finger joints.

Both Heberden’s and Bouchard’s nodes tended to be painful and tender when they are developing, but eventually the discomfort settles down. The fingers lose mobility and may “freeze” in a slightly “bent” position, causing reduced dexterity.

There is no effective treatment for Heberden’s and Bouchard’s nodes. Heat, splinting, exercises and physiotherapy have been tried, “NSAID” painkillers and steroids (including injections) have been prescribed; but generally, the nodes continue to develop.

Flexor tendon nodules and Dupuytren’s contracture

Small bumps, called “Notta’s nodules”, or simply “Flexor tendon nodules” sometimes develop on the tendons which pull the fingers into the “fist” position. The lumps are sometimeslocated just below the retention bands which hold the tendons close to the finger joints and when they do, the result is “trigger finger”.
They can also be located in the palm, where they don’t produce any tenderness or disability, but can be easily located on examination of the palm.
If It doesn’t produce a trigger finger, a Flexor tendon nodules is asymptomatic.

Dupuytren’s contracture

In this condition, the tendons stiffen and shorten, becoming tough cords that pull the fingers inward, so that the hand eventually assumes a “claw” position.

Treatment is as difficult (and commonly, as unsuccessful) as it is for Heberden’s nodes: steroid injections usually fail to solve the problem and in some cases, surgery is warranted.

What condition links Heberden’s nodes, Bouchard’s nodes, Palmar tendon nodules and Dupuytren’s contracture ?

I put this question to Chat GPT, which responded, noncommittally and unhelpfully, as follows:
“Heberden’s nodes, Bouchard’s nodes, palmar tendon nodules, and Dupuytren’s contracture are all conditions that cause abnormal growths or thickenings in the hands and fingers. They are all associated with connective tissue abnormalities and tend to develop with age” .…

In other words, chat GPT was unable to Identify a link.

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