Intracellular Hypothyroidism & Thyroid Hormone

THE TRUTH

THE THYROID GLAND MAKES THYROXINE (T4). and CALCITONIN, which lowers blood calcium.

T4 is the raw material from which TRIIODOTHYRONINE (T3) is made. T4 has no other function.
The thyroid gland produces just 20% of the body’s T3: every cell, including the cells in the pituitary gland, uses T4 to make its own T3.

T3 is the cells’ “accelerator”: it increases the efficiency of all cells.

If the thyroid fails to make enough T4, or if the cells are unable to convert T4 to T3, the T3 level inside the cells goes down and the cell is unable to function efficiently. This is called intracellular hypothyroidism

HOW T4-to-T3 CONVERSION HAPPENS

T4 is a protein molecule with 4 Iodine atoms. It is an inactive “prohormone”.
The body has 3 “de-iodinase” enzymes (D1, D2, & D3), which can remove an Iodine atom from T4.
D1 (in the body) and D2 (in the Pituitary) remove a “Special” Iodine atom, to make T3:
T3 has a particular shape, which fits into “T3 receptors” * in all the cells, including those of the pituitary gland. These T3 receptors are designed to accept T3 molecules: when T3 plugs in, it increases the cells’ efficiency.

Deiodinase 3

D3 exists only in the body: it is not present in the pituitary gland.
It removes a different Iodine atom, producing reverse T3 (rT3), instead of normal T3.
Reverse T3 has a different shape than normal T3, so it doesn’t fit into the T3 receptors and doesn’t have any effect on cellular efficiency.
Usually the cells change 60% of available T4 into T3 and 40% into rT3.

All the cells of the body, except the Pituitary, have D1 and D3.
The Pituitary only has D2, for making T3. It does not have D3, so it can’t make rT3.

CATCH 22: Stress

When a human is subjected to stress, whether from high or low temperature, famine, natural disaster, animal attack, infection, poisoning or psychological strain – any stress, everything in the body reduces efficiency so as to save energy which may be needed for repairs.

This is how it works: UNDER STRESS, cortisol is secreted by the adrenal glands, and ….
A: Cortisol blocks D1, but not D2, so no T3 can be made inside any cell, except the cells of the pituitary gland!
B: Cortisol activates D3 and D3 removes the wrong iodine atom from T4, making “rT3”.
C: D3 also destroys any T3 present in the cell, by taking away 1 of its iodine atoms, to produce “T2”, which is completely inactive.
In this way, T3 is removed from all cells in the body, except inside the pituitary gland.

It doesn’t happen in the Pituitary, because the Pituitary has D2, but not D1 or D3.
Therefore the Pituitary “isn’t in the loop” and doesn’t know what is going on.
It keeps on putting out thyroid stimulating hormone (TSH) in accordance with the level of T4 it gets.
So when a human is stressed, the level of TSH in the blood tells the doctor that the Pituitary has enough T4, but does not indicate what is happening in the body: if the doctor understood the above information and did tests to find out the T3 and rT3 level, the diagnosis would be Made and the intracellular hypothyroidism problem could be solved by prescribing triiodothyronine; but unfortunately to date, doctors are specifically instructed not to test for T3 or reverse T3.

Obviously, this is a disaster: inside the cells, there is little or no functioning T3!
I call this INTRACELLULAR HYPOTHYROIDISM: if it stays bad enough for long enough, it can progress to serious illness, which is different from person-to-person depending on which of their cells and organs are most sensitive to the absence of T3.
As an example, see “Takotsubo cardiomyopathy“, a type of heart failure (“broken heart syndrome”) caused by stress.

Recap: Details made simple

The thyroid gland lies in the neck, wrapped around the larynx (the voice-box).
It secretes all the T4 (about 90 to 100mcg daily) and 20% of the T3, for the body.
Every cell imports T4 to make T3 for itself, applying the T3 to maximise its efficiency.
Remember: the Pituitary uses D #2, but all others use D #1, to convert T4 to T3.

100% of the metabolic efficiency of all cells is due to T3.
T3 helps to regulate body temperature, body weight, glucose and cholesterol and everything else from hair and fingernail growth to mood and “well-being”: it controls every cell in the body and brain.

T3 is, particularly, essential for the unborn baby’s brain development and if the mother is stressed enough to have intracellular hypothyroidism, subtle changes in brain growth may lead to cognitive and physical deficits in the newborn: autism spectrum, schizophrenia, dyslexia, ADD, obesity and gender dysphoria are all related to maternal hypothyroidism.

THIS IS WHAT THE DEIODINASES DO – the graphic below shows the process clearly: it was copied from “Cardiomyocyte-specific inactivation of thyroid hormone in pathologic ventricular hypertrophy: an adaptative response or part of the problem?”, by Christine J. Pol, Alice Muller, and Warner S. Simonides, in journal “Heart Fail Review, Nov 24, 2008).

Enzymatic metabolism of thyroxine: the enzymes – D1 & 2 make T3 from T4. 
D3 makes rT3 from T4 and T2 from T3
D1 (in the Body) and D2 (in the Pituitary) make T3 from T4. D3 makes reverse T3 from T4 and T2 from T3, BUT NOT IN THE PITUITARY, where no D3 exists.

FAQ:

(1) What is Deiodinase #3 USED FOR?
A: In either physical or psychological high-stress conditions, D3 SHUTS THE WHOLE BODY DOWN, SAVING ENERGY WHEN LIFE IS THREATENED.
(2) Under stress, does the pituitary gland shut down too?
A: In the Pituitary, D2 makes T3 and no rT3 is produced: the pituitary is unaffected and the output of TSH continues, as usual.
(3) WHY DOES THE BODY LOSE EFFICIENCY ?
A: With T3 formation stopped and available T3 converted to T2, the cells just don’t have enough T3 to keep going.
(4) What does reverse T3 do?
A: We used to think that rT3 could hitch itself to the receptors and block the entry of T3, but all it does is to encourage the actions of D3. However, a high rT3 is an excellent “marker” (a blood test signal) for intracellular hypothyroidism
(5) What are the symptoms of functional hypothyroidism?
A: The unfortunate human feels tired to the point of exhaustion, anxious and depressed. The skeletal muscles don’t work properly and can be painful.
There is constipation, because the bowel muscles are hampered too.
There is cognitive loss because of reduced brain function.
In some organs (varying from individual to individual), “subtotal” stoppage of function can occur (for example, heart muscle paralysis in Takotsubo Cardiomyopathy).
If the problem persists the fingernails get brittle, the hair (e.g. eyebrows) starts to fall out, the voice gets hoarse, the legs swell from retained water, there is a feeling of being cold because the brown fat stops burning glucose, the cholesterol may rise, the body weight goes up and diabetes may start.
(6) If the problem is from insufficient T3, why doesn’t the doctor Prescribe T3?
A: The doctor tests “everything” except T3, T4 and rT3: the only thyroid test is TSH and that stays normal because the Pituitary is “happy”.
So the Doctor can’t “read” the situation and doesn’t recognise the problem.
(7) So what does the doctor do to help the patients symptoms?
A: The MD may notice depression or confusion, high cholesterol, high blood pressure due to stress and early diabetes due to high cortisol and low T3, so the sufferer gets a pill for each of those.
(8) What’s the end result of intracellular hypothyroidism?
A: If the Stressful conditions come to an end, a “remission” may occur. If the situation becomes chronic, serious disease may ensue.
See “INTRACELLULAR HYPOTHYROIDISM“, below.

INTRACELLULAR HYPOTHYROIDISM

Stress-related T3 deficiency, previously termed “Reverse T3 dominance”, is called “Functional Hypothyroidism” by the Metabolic Medicine community. It is also called “Subclinical Hypothyroidism”, “Euthyroid Sick Syndrome” and “Nonthyroidal Illness Syndrome”, by mainstream medicine.
However, the most appropriate term is intracellular hypothyroidism.

Intracellular hypothyroidism is characterised by reduction of serum T3 from the individual’s usual level, down to the low end of the “normal” T3 range, along with an elevated reverse T3 *, resulting in reduction of the T3/rT3 ratio.
TSH and T4 levels are normal, unless the patient also has true hypothyroidism.
The diagnosis is made when a reduction of the T3/rT3 ratio, to less than 20.0, is found on testing, in a person who has hypothyroid symptoms.

Intracellular hypothyroidism is part of the pattern in all life-threatening illnesses, in the vast majority of chronic debilitating conditions and in prolonged depression.
It may be the result of the illness, or the cause.
It is associated with heart failure, PTSD, Chronic Fatigue Syndrome, ME, Fibromyalgia, MS, infertility with recurrent abortion, major depression, schizophrenia and any condition severe enough for admission to an ICU.

Intracellular Hypothyroidism is pervasive and is very easily missed by the doctor,therefore a “thyroid profile”, including TSH, T4, T3 and rT3 should be included in every “checkup” test series and should be ordered in the prediagnostic “workup” whenever a patient presents with a new complaint.
Upon receipt of the test results, the doctor should calculate the T3/rT3 ratio** and if it is less than 20, the patient’s T3/rT3 ratio should be restored to >20 (>23 is better), by prescription of slow-release triiodothyronine, in addition to appropriate therapy for whatever disease is diagnosed.

* Please go to my blog on “NORMAL” and scroll down to the section re. the Thyroid.
** See below: /media/drive_D/A User/Documents/A WORK AIDS/Cameron Sutherland’ s T3 – rT3 Worksheet

CALCULATING THYROID TEST RESULTS

In the bloodstream, a “binding protein” captures a lot of the T3, holding it as a backup supply.
That portion of total T3 is inactive, so WE DON’T CHECK TOTAL T3. We check the “FREE”, UNBOUND T3.
References to “T3” in this website always mean “Free T3” (FT3).

Calculating the FT3/rT3 ratio is simple in principle, but mystifying for those who aren’t mathematically inclined.
To obtain the ratio, we must express both free T3 and rT3 in the same scale.
So we divide the FT3 value by 0.0154; for example
FT3 = 4.0 Pm/L /0.0154 = 259.74 Ng/DL.

We then divide the FT3 (Ng/DL) value by the rT3: for example, if T3 is 259.74 and rT3 is 15, the ratio is 259.74/15, = 17.3.
A T3/rT3 ratio of > 20 is normal and>24 is excellent.
A ratio of < 20 indicates preferential conversion of T4 to rT3, instead of T3, which is severe enough to cause the signs and symptoms of intracellular hypothyroidism (IH).

CAVEAT !
IH is easily and safely corrected by taking Triiodothyronine
(T3), but:
(1) T3 is best taken fasting, close to 4AM, to fit our diurnal rhythm.
(2) Triiodothyronine should be supplied in a slow-release capsule, not a rapid-release tablet such as “Cytomel”, because quick-release tablets dump their T3 into the intestine soon after they are swallowed, causing a “spike” of T3 in the serum.
This spike can cause “hyperthyroid” side-effects in the morning.
Further, the half-life of T3 is 2 hours, so after spiking from the rapid-release pills, the serum T3 falls quickly, causing hypothyroid symptoms in the afternoon.
(4) If T4, including the T4 in desiccated thyroid, is prescribed for IH, most of it is converted into rT3. The higher rT3 encourages even more T3-to-T2 conversion by type 3 deiodinase, with further reduction of T3 availability, so the patient’s condition gets worse.
(5) rT3 also slows down absorption of T4 into the cells, so the T4 level in the blood may rise.

THE EASY WAY TO CHECK T3/rT3 BALANCE:
A table renders T3/rT3 calculation quick and easy: you need only read the number at the intersection of the (horizontal) T3 row and the (vertical) rT3 column.
Please see a link to Cameron Sutherland’s “worksheet”, below.

Cameron Sutherland’s T3/rT3 worksheet
/media/drive_D/A User/Documents/A WORK AIDS/Cameron Sutherland’ s T3 – rT3 Worksheet 24Jan2019 working copy.xlsxDownload .
Open with excel or compatible app.
Column 1 shows FT3 in Pm/L.
Column 2 is FT3 in Ng/DL.
First row shows rT3.
The FT3/rT3 ratio appears at the row/column intersections:
The PINK area = normal range, the WHITE area = Intracellular Hypothyroidism range.

TREATMENT OF INTRACELLULAR HYPOTHYROIDISM

IH is easily and safely treated with slow-release T3, but most doctors do not believe in, accept or even recognise the diagnosis and doctors are specifically and forcefully instructed not to test for T3 or rT3 and not to prescribe T3.
They call the illness “low T3 syndrome” and prescribe T4, expecting reliable conversion to T3.
This is disastrous: the T4 is preferentially metabolised to rT3, making the situation worse.
Most doctors are unfamiliar with Deiodiinase 3 and don’t believe patients who say that they get worse when they take T4: if the patient complains, they prescribe more T4 (Synthroid or Eltroxin).

HOW MUCH T3 does a person need?

Everyone has an individual requirement for T3, so we begin with a low dose and increase it sequentially, using weekly or two-weekly blood tests to determine when the correct dose has been reached.
Most people’s “blood – brain barrier” (BBB) allows T3 to enter the brain and the pituitary easily and when prescribed T3 comes into the pituitary, it reduces TSH production to almost zero, and the thyroid responds by making less T4.
The thyroid is also sensitive to T3 level to some extent and quite often, it reduces T4 output.
So in most cases, on-treatment tests show a higher T3, low-normal T4 and very low TSH.

Interestingly, some people’s BBB blocks entry of T3 and in those cases, since the Pituitary’s T4 supply is down because the thyroid isn’t making enough, the pituitary puts the TSH up, to call for more T4.
When this happens, tests show high TSH, low T4 and upper-normal T3.
This situation is easily solved by adding a little T4 to the prescription or by changing the prescription to desiccated thyroid, which contains 70% T3 and 30% T4.

REMISSION:

Spontaneous remission of functional hypothyroidism may follow stress relief, because preferential activation of Deiodinase #3 ceases when the stress level and Cortisol output return to normal.
However most subjects promptly increase rT3 production and relapse into IH when a stressful situation arises.
The most spectacular example of remission and relapse of an intracellular hypothyroidism-based condition is found in cases of Takotsubo Cardiomyopathy.

ADRENAL FATIGUE”
Chronic stress causes prolonged increase of cortisol output by the adrenal glands.
Cortisol inhibits type 2, 5-deiodinase and promotes D3, reducing conversion of T4 into T3, increasing rT3 production and increasing conversion of T3 into (inactive) T2.
By these mechanisms stress, whether physical, as in terminal illness, catastrophic infection, severe injury, major surgery, burns etc., or psychological, produces Intracellular Hypothyroidism.
After a while under prolonged stress, the adrenals no longer respond with high cortisol production and cortisol tests may show low levels.*
Practitioners unfamiliar with deiodinase metabolism and intracellular hypothyroidism are at a loss to explain the low cortisol levels and the patient’s continuing complaints. They assume that the symptoms are due to low cortisol production, so they call the condition “Adrenal Fatigue”.
Therefore many ill effects caused by Functional Hypothyroidsm are blamed on “Adrenal Fatigue”, a fanciful label which is inappropriate, as far as I am concerned.

* BY WHAT MECHANISM DOES “ADRENAL FATIGUE” COME TO BE ?
We don’t know the mechanism of cortisol output reduction – there is nothing wrong with the adrenal glands.
Certainly, the symptoms of Adrenal Fatigue are indistinguishable from those of IH.
So perhaps the cause is simple: we know that metabolic slowdown due to IH affects the whole body except the Pituitary.
The adrenals are part of the body. So if, as we would expect, the adrenals respond to inadequate intracellular T3 in the same way as all our other cells, a reduction of efficiency and reduced cortisol production is inevitable and unsurprising.
Therefore the failure of cortisol production, referred to as “Adrenal Fatigue”, observed in IH is simply a previously unrecognised manifestation of Intracellular Hypothyroidism an has nothing to do with the abilities of the Adrenal glands.

NOTES AND DEFINITIONS:
(1) Low T3, from true hypothyroidism or from IH, in women can cause infertility or abortion.
If a pregnancy persists, T3 deficiency during the first trimester may cause maldevelopment of the baby’s brain, causing learning disability, gender dysphoria, ADD/ADHD, Autism, Schizophrenia and other neurocognitive states (? dyslexia, etc).
The foetus begins T4-to-T3 conversion for itself at approximately 12 weeks gestation.
Thereafter, it is independent of the mother’s T4 supply, as long as there is sufficient iodine and selenium in the mother’s blood.

(2) Stress: “Perceived stress” is stress subconsciously perceived by the brain, even if the individual claims to be stress-free.
Reasons for “perceived stress” include psychoshock (including abuse) and PTSD, life-threatening infections, severe injury and surgery. However it can be due to any disturbance of body or mind.
Even dieting, vitamin or mineral deficiencies, toxins or diseases like heart failure can be the cause.
Basically, whatever “stresses you out”, physically or emotionally, can start the problem.
Perceived stress, with or without subjective or objective stress, is present in close to 100% of ICU patients and can be proven by checking theT3/ rT3 ratio.
“Subjective stress”
is consciously “felt” and can be described by the individual.  
“Objective stress”
is stress to, or on, the individual, as observed by others.

(3) Intracellular (“Functional”) hypothyroidism is a condition presenting with recognised, or unrecognised, hypothyroid symptoms and signs in which T3 is reduced and reverse T3 rises. FH can coexist with true hypothyroidism.
IH cannot be diagnosed with a TSH test: it is necessary to calculate the T3/rT3 ratio.
IH must not be treated with T4, because it will be converted into rT3, not T3.

(4) “Desiccated Thyroid” pills are made from dried porcine or bovine thyroids and contains 30% T3 and 70% T4. Human thyroid tissue contains 20% T3 and 80% T4, but the disparity is insignificant.
Bovine & Porcine T3 and T4 are bioidentical with the human hormones.
A person with IH, treated with Dessicated thyroid, is getting a lot of T4 and may get worse symptoms by overproducing rT3 from it (see (3), above).

(5) TSH diagnoses true hypothyroid disease, but cannot be used to diagnose IH.

The TSH value is not related to the body’s satisfaction with intracellular T3, which to date can only be assessed by estimating FT3/rT3.
The TSH test is only relevant to the Pituitary’s satisfaction with its T4 supply.

(6) As thyroid function deteriorates and slows, so does the rest of the body.
Thus no system is exempt from the effects of Hypothyroidism: it can make you fat, cause hair loss (especially the outer 1/3 of the eyebrows) and dry skin. It can make your skin coarse and your voice hoarse.
Hypothyroidism can weaken bowel muscles, which results in constipation.
It can affect the eyes, tear glands (“dry eye”), long nerves (peripheral neuropathy), skeletal muscle (weakness and muscle aches) (6) and heart muscle (7, 8 – below).
It can cause leg swelling, or puffy eyes and face, from fluid retention.
It can cause numbness and tingling of the fingers.
It can cause brittle fingernails.
In the worst cases, atrial fibrillation, heart failure or dilated cardiomyopathy (7,8) may result from intracellular hypothyroidism.
Briefly put, Intracellular Hyothyroidism can cause almost any symptom you can name, because it can affect any organ.

Re. muscles and the heart, see Hoffmann’s syndrome (effect on skeletal muscle) and cardiomyopathy (effect on heart muscle).
Also see:
a case history, entitled “Hypothyroidism-induced reversible dilated cardiomyopathy” (note that this patient recovered when treated with T4, which in my opinion was lucky: she would have done better with T3) and
My own history of Intracellular Hypothyroidism.

GENERAL SYMPTOMS OF HYPOTHYROIDISM:

T3 hormone is the efficiency factor for all body parts and the problems resulting from lowered T3 depend on which part of the individual’s body is most sensitive to lack of T3, so symptoms are many and varied. Virtually any symptom may present, including those from Adrenal slowdown.
Many people with Hypothyroidism, either “true” hypothyroidism from underproduction of T4, or “functional” (intracellular) hypothyroidism, with metabolic loss of T3 within the cells, report sluggishness, anxiety, “brain fog”, cognitive loss and a feeling of low energy, in addition to the classical hypothyroid complaints (see below).

SYMPTOMS, SIGNS, DIAGNOSIS, TREATMENT OF HYPOTHYROIDISM 
SYMPTOMS short list
Fatigue
Low motivation
Depressed mood
Impaired memory
Poor sleep quality
Weight Gain
Depression
anxiety
Reduced sex drive, male or female
Heavy or irregular “periods”
PMS
Infertility
Recurrent abortion
Subtle inconsistency of a baby’s brain development
Chronic yeast infections
Muscle weakness, including Myocardial weakness (see Ref # 6,7,8).
Muscle aches
Joint Pain, stiffness, swelling
Constipation
Difficulty staying warm
Hoarseness
Difficulty breathing
Slower heart rate
Puffy face, Dry skin, Acne
Brittle hair and nails
Calloused heels
Headaches
Premature gray hair  
Brittle fingernails
SIGNS OF HYPOTHYROIDISM
Slow pulse, Irregular pulse, Low BP,
Temperature < 36°C
Dry skin + Dry hair / grey hair
Heel calluses
Hair loss from the head, legs or eyebrows (outer 1/3)
Swelling below lower eyelids
Skin swelling over the shins
Hoarse, “thick” speech,
Dry cough
Slow thinking, confusion
Memory loss,
Untidyness
Home in endemic area
Economic disadvantage
History suggesting FH
High-stress job
High-stress job partner
High-stress life partner
Separation, divorce
(Parents): difficult children
(Children): difficult parents
Childhood abuse of whatever type
Chronic illness, eg.
Celiac Disease or gluten intolerance
Severe illness, with ongoing anxiety
Difficult life circumstances
Poverty
Dependent relatives
Anxious personality disorder
Other psychopathy, schizophrenia and “bipolar disease”
Family history of hypothyroidism
Retirement, social isolation
Alcohol / tobacco / THC /drug habit
TYPES/CAUSES of HYPOTHYROIDISM
1:   Iodine deficiency
2:   Selenium deficiency
3:   Hashimoto’s thyroiditis
4:   Ionising radiation
5:   Therapeutic radiation
6:   Thyroid / Pituitary Surgery
7: Unknown cause
8:   Prescribed medication
9:   Stress (IH)
10: Worse IH with Eltroxin *
11: Hypopituitarism 
TEST RESULTS ASSOCIATED WITH HYPOTHYROIDISM
Elevated blood cholesterol level
Borderline blood sugar/A1C
High TSH, with or without low T4
Low T3, High reverse T3, Low FT3/rT3 ratio, with or without high TSH
“Adrenal Fatigue”
Low DHEA, Testosterone, Oestrogen, Progesterone, Allopregnanolone
Fluid retention, with or without heart failure  
Iodine &/or Selenium deficiency
HEAVY METAL OVERLOAD CAN CAUSE SIMILAR SYMPTOMS: the Urine should be checked for Heavy Metal “burden”
TREATMENT
Eltroxin*, plus iodine and/or selenium, for # 1 – 8.
Compounded, slow-release T3, for # 9, 10 & 11.
Selenium (2 Brazil nuts per day will provide enough).
Iodine (2 drops of Lugol’s iodine per day).
Iron: serum iron (“Ferritin”) should be kept >100.
DHEA, 50mg/day (men) and 25-50mg/day (women) reduces symptoms.
* Eltroxin makes #9 MUCH worse.
CONDITIONS ASSOCIATED WITH Intracellular Hypothroidism
Long-COVID syndrome,
POST-FINASTERIDE syndrome,
CFS/FM, Gulf war syndrome, PTSD (CHILDHOOD or ADULT), Depression,
Lyme Disease,
Goitre,
Menopause, Psychiatric conditions, autism, Type I or II Diabetes, obesity, peripheral neuropathy, Alzheimer’s, Autoimmune diseases (rheum. arthritis, lupus, sarcoidosis, Sjogren’s, etc.),
Fibrillation, heart failure, Takotsubo Cardiomyopathy,
Adrenal Fatigue,
Crohn’s disease, Ulcerative colitis, Diverticulitis,
Heavy-metal overload,
Multiple sclerosis (MS), Hypercholesterolaemia, Heart failure,
Chronic anxiety/depression, Schizophrenia
ALL TYPES OF SEVERE ILLNESS, or admission to an ICU.
MY OWN PROBLEM WITH FUNCTIONAL HYPOTHYROIDISM

If you think the above list is fanciful, please read my own history of FH in the blog post, ON THE SUBJECT OF FIBROMYALGIA“, for the whole story.

REFERENCES:

(1) Trans Am Clin Climatol, 2013;124:26-35, Cracking the code for thyroid hormone signaling: Antonio C Bianco 1 PMID: 23874007, PMCID: PMC3715916
(2) Endocrinology, 2021 Aug 1;162(8):bqab059. doi: 10.1210/endocr/bqab059.Deiodinases and the Metabolic Code for Thyroid Hormone Action, Samuel C Russo 1 Federico Salas-Lucia 1 Antonio C Bianco 1 PMID: 33720335, PMCID: PMC8237994 (available on 2022-03-15),
DOI: 10.1210/endocr/bqab059
(3) Endocr Rev. 2019 Aug 1; 40(4):1000-1047. doi: 10.1210/er.2018-00275. Paradigms of Dynamic Control of Thyroid Hormone Signaling, Antonio C Bianco 1 Alexandra Dumitrescu 1 Balázs Gereben 2 Miriam O Ribeiro 3 Tatiana L Fonseca 1 Gustavo W Fernandes 1 Barbara M L C Bocco 1 , PMID: 31033998, PMCID: PMC6596318, DOI: 10.1210/er.2018-00275
(5) Clinical Endocrin., Volume81, Issue5, Review, November 2014, Pages 633-641: Defending plasma T3 is a biological priority Sherine M. Abdalla, Antonio C. Bianco: 05 July 2014 https://doi.org/10.1111/cen.12538
(5) https://cbhrt.ca/2021/10/23/thinking-about-normal/
(6) Hoffman’s syndrome – A rare facet of hypothyroid myopathy, Swayamsidha Mangaraj and Ganeswar Sethy, Neurosci Rural Pract. 2014 Oct-Dec; 5(4): 447–448. doi: 10.4103/0976-3147.140025PMCID: PMC4173264PMID: 25288869 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4173264/
(7) Hypothyroidism-induced reversible dilated cardiomyopathy, by P Rastogi, A Dua, S Attri, and H Sharma, J Postgrad Med. 2018 Jul-Sep; 64(3): 177–179. doi: 10.4103/jpgm.JPGM_154_17
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6066629/
(8) Myocardial Induction of Type 3 Deiodinase in Dilated Cardiomyopathy (experimental, Mice), Ari J. Wassner,1Rebecca H. Jugo,1David M. Dorfman,2Robert F. Padera,2Michelle A. Maynard,1Ann M. Zavacki,3Patrick Y. Jay,4 and Stephen A. Huang1 Thyroid. 2017 May 1; 27(5): 732–737. Published online 2017 May 1. doi: 10.1089/thy.2016.0570PMCID: PMC5421592PMID: 28314380 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5421592/
(9) Thyroid Hormone Transport into Cellular Tissue, Journal of Restorative Medicine 3(1):53-68, April 2014, DOI:10.14200/jrm.2014.3.0104, by Kent Holtorf, Holtorf Medical Group (HMG),I can supply further references, on request.

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