Intracellular Hypothyroidism & Thyroid Hormone

THE TRUTH

THE THYROID GLAND MAKES THYROXINE (T4). and CALCITONIN, which lowers blood calcium.
It also makes perhaps 10 – 20% of the supply of T3.

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 in the body, including the cells in the brain and the pituitary gland, makes its own T3, from T4.
T3 is the cells’ “accelerator”: it increases the efficiency of all cells.
just as with DHEA, testosterone, estrogen, progesterone, Allopregnanolone and melatonin, there is a progressive reduction of T4 production by the thyroid gland, as we age.

HOW T4-to-T3 CONVERSION HAPPENS

T4 is a protein molecule with 4 Iodine atoms. It is raw material (“prohormone”), for T3.
We have 3 “de-iodinase” enzymes (D1, D2, D3), which remove an Iodine atom from T4.
All the cells in the body and brain, except the pituitary, make T3 by removing the correct iodine atom from T4, using D1 (the cells in the body and brain do not have D2).
The cells in the pituitary gland don’t have D1: they use D2, to change T4 to T3.

T3 has a particular shape, which fits into “T3 receptors” * in all the cells, including those of the pituitary gland.
T3 receptors accept T3 molecules:
When T3 plugs in, it increases the cells’ efficiency: without T3, they can’t work properly.

Deiodinase 3

D3 exists only in the body (including the brain): the pituitary gland. It does not have it.
It removes a different Iodine atom, producing reverse T3 (rT3), instead of normal T3.
Reverse T3 doesn’t fit into the T3 receptors and has no effect on cellular efficiency.

CATCH 22: Stress

When a human is subjected to stress – any stress, whether from high or low temperature, famine, natural disaster, animal attack, infection, poisoning or psychological strain, every cell 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 one of its iodine atoms, to produce “T2”, which is completely inactive.
Thus cortisol removes T3 from all cells except the Pituitary, and all cells “hibernate”.

This doesn’t happen in the Pituitary, because the Pituitary does not have D1 or D3.
The Pituitary uses its D2 to make its T3 and puts out thyroid stimulating hormone (TSH) as usual, according to the amount of T4 it gets from the thyroid.
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 did tests to find out the T3 and rT3 level, the situation would be obvious. However up to now, doctors are specifically taught not to test for T3 or reverse T3.

Obviously, blocking T3 is a disaster: inside the cells, there is little or no functioning T3!
I call this stress-produced condition 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”) which happens to genetically predisposed people, when they are emotionally, or physically, stressed.
In particular, see a case report of cardiomyopathy, in my blog.
The incidence of talk Takotsubo Cardiomyopathy is between 2 and 10 cases per 100,000 hospital admissions.

* Also called “low T3 syndrome”, “functional hypothyroidism”and “nonthyroidal illness”.

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: Pituitary cells use 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 essential for the unborn baby’s brain development and the fetus does not begin to make its own T3 until the 14th week of pregnancy.
The baby’s brain connections are made between the 8th and the 14th week of pregnancy and If the mother is stressed enough to have intracellular hypothyroidism while the “wiring” is being done, subtle deficiencies in brain growth may occur.
This can 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.
blockade of D1 and the promotion of D3 resulted in intracellular hypothyroidism.
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 don’t have enough T3 to keep going.
(4) What does reverse T3 do?
A: Not much: we used to think that rT3 could hitch itself to the receptors and block the entry of T3, but really, all it does is to encourage the actions of D3.
However, rT3 is a perfect “marker” (a blood test signal) for intracellular hypothyroidism.
(5) What are the symptoms of intracellular (“functional”) hypothyroidism?
A: The unfortunate human feels tired, confused, anxious and depressed.
Any “low thyroid” symptoms (see list below) can present themselves – for example:
The skeletal muscles don’t work properly and can be painful.
Some people get muscle cramps.
Some get “Hoffman’s syndrome”, or “stiff person syndrome”.
There is constipation: the “tight” bowel muscles can’t relax to let the stool go through.
There is cognitive loss, fuzzy thinking and confusion, due to 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, there may be dry and itchy skin, the voice gets hoarse, the legs and eyelids 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 starts.
(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 done is TSH and that is normal because the Pituitary is “happy”.
So the Doctor can’t “read” the situation and doesn’t recognise the problem.
Doctors are also told by the medical “system”, specifically, not to prescribe T3
(7) So what does the doctor do to help the patient?
A: The MD may notice depression or confusion, high cholesterol, high blood pressure due to stress and early diabetes, or swollen legs, etc.
So the sufferer gets a pill for each symptom.
(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, such as those above, 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.
It is often confused with chronic fatigue syndrome (CFS).
However, the most appropriate term, in my opinion, is Intracellular Hypothyroidism.

Diagnosis:
In Intracellular hypothyroidism, testing shows 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 if a reduction of the T3/rT3 ratio, to less than 20.0, is found.
Since some people are able to cover-up, or ignore, their low-thyroid symptoms, the incidental finding of intracellular hypothyroidism sometimes shows up even though the patient’s complaints are not typical.

Incidence:
Intracellular hypothyroidism is part of the pattern in all life-threatening illnesses.
It is found in the vast majority of chronic debilitating conditions, in prolonged depression and in morbid obesity, anorexia nervosa and starvation.
It may be the result of the illness, or the cause of it.
It is associated with heart failure, Long Covid, PTSD, Chronic Fatigue Syndrome, ME, Fibromyalgia, MS, infertility with recurrent abortion, major depression, schizophrenia and any condition severe enough for admission to an ICU, including surgical complications.

Testing:
Intracellular Hypothyroidism is pervasive, but is usually missed by doctors.
It can be “silent”, especially in confident people who have high self-esteem and tend to endure mild symptoms without complaint.
Therefore a “thyroid profile“, including TSH, T4, T3 and rT3 should be included in every “checkup” test series, regardless of the reason for the checkup.

Calculation, from the test results:
T3 is reported in picomoles per litre and rT3 is reported in nanograms per DL.
We divide the T3 result (converted to ng/DL) by the rT3 result: the number thus obtained is the “T3/rT3 ratio” **.
It should be >20, or ideally, >24.
Intracellular hypothyroidism is diagnosed if the ratio is <20.
We rate the severity of intracellular hypothyroid as follows:
7 – 10 = mild, 11 – 15 = moderate and 16 – 20 = mild.
If T3/rT3 is less than 21, treatment should be prescribed, to return the ratio to > 20
(>23 is better), by prescription of slow-release triiodothyronine, in addition to appropriate therapy for whatever other disease is diagnosed.

Treatment protocol:
“Cytomel”, a commercially available rapid-release triiodothyronine (T3) tabletis available, but tends to cause hyperthyroid “spikes” of serum T3 soon after it is taken and T3 “Crash”, with recurrence of hypothyroidism symptoms, in the late afternoon.
Compounded T3, in a slow-release format, is preferred, because it does not produce a T3 spike or crash and the symptom relief persists throughout the day.
The prescription begins at 5 µg of triiodothyronine taken at, or close to, 4 AM.

Blood testing for T3 is done weekly and the prescription is increased by 5 µg per day, until the serum T3 is >5 pmol/L.

When a test result of greater than 5 pmol of T3/L is received, the prescription is continued without increasing the dose.
Both T3 and rT3 are estimated a week later: the prescription is increased by a further 5 µg/day if T3/R. T3 is <20, or continued at the then level, if it is >20.

Follow-up:
T3/rT3 is checked every 3 months for one year: if it is >30, or consistently >20 for the full year, or If the T3 level exceeds 6.4 pmol/L , a smaller dose of triiodothyronine can be tried, “on spec”.
Occasionally, it may prove possible to discontinue T3 treatment. However a relapse to intracellular hypothyroidism is likely, if stress recurs.

* 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, for a backup supply.
That portion of total T3 is inactive, so WE DON’T CHECK TOTAL T3.
We check the “FREE”, UNBOUND T3.
Therefore 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 in Canada, 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).

The easy way to check T3/r T3 balance:
A table renders T3/rT3 calculation quick and easy: you only need to 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”, in MS “Excel”, 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 instructed not to test for T3 or rT3 and not to prescribe T3.
They call IH “low T3 syndrome” and prescribe T4, expecting it to convert to T3.
This is disastrous:
T4 is preferentially metabolised to rT3, making the situation worse because the rT3 helps cortisol to activate D3.
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.

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.
When prescribed T3 raises the pituitary’s T3 level, the gland reduces TSH production to almost zero, and the thyroid responds by making less T4.
So most on-treatment blood tests show a higher T3, low-normal T4 and very low TSH.

Interestingly, some people’s BBB blocks entry of T3 and then, If 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.

Prescribing Desiccated Thyroid
Changing the prescription to desiccated thyroid sounds like an attractive idea, but desiccated thyroid is 70% T4 and 30% T3. So taking it results in the patient getting a large load of T4 along with their T3.
The T4 is immediately converted to reverse T3, which makes calculating T3/rT3 balance difficult.
Having said which, some people with IH do quite well on desiccated thyroid.

REMISSION:

Spontaneous remission of functional hypothyroidism may follow stress relief, because preferential activation of Deiodinase #3 stops 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”
After a while under prolonged stress and IH, the adrenals no longer respond with high cortisol production and cortisol tests may show low levels.*
Practitioners unfamiliar with deiodinase metabolism and IH can’t 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”.
So, 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.
The symptoms of Adrenal Fatigue are indistinguishable from those of IH, so perhaps the cause is simple:
Metabolic slowdown in IH affects the whole body except the Pituitary.
The adrenals are part of the body.
So if 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 not surprising.
Therefore the failure of cortisol production in “Adrenal Fatigue” seen in IH may just be a previously unrecognised manifestation of Intracellular Hypothyroidism and 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, as super-confident people do.
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 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 IH 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 presents with recognised, or unrecognised, hypothyroid symptoms and signs, reduced T3 and High rT3.
IH 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 T4 will be converted into rT3, not T3.

(4) Bovine & Porcine T3 and T4 are bioidentical with the human hormones. “Desiccated Thyroid” pills, made from dried porcine or bovine thyroids, consist of
30% T3 and 70% T4.
Human thyroid tissue contains 20% T3 and 80% T4, but the disparity is insignificant.
So, a person with IH, treated with Dessicated Thyroid, is getting genuine thyroid hormone, but the pills contain a lot of T4 and the patient 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.
TSH is only relevant to the Pituitary’s satisfaction with its T4 supply.
TSH is not related to the body’s satisfaction with intracellular T3.
Intracellular T3 deficiency can only be assessed by estimating FT3/rT3.

(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 (check 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, stiffness and muscle aches) (6) and heart muscle (7, 8).
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: see the list of low thyroid symptoms, below.

(7) Re. muscles and the heart, see Hoffmann’s syndrome and stiff person syndrome (effects on skeletal muscle) and cardiomyopathy (effect on heart muscle).
Also see: a case history, entitled “Hypothyroidism-induced reversible dilated cardiomyopathy” (this patient recovered when treated with T4, which in my opinion was lucky: she would have done better with T3) and see my history
(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 jobAleman all got will be just perfect. Thanks. Okay,
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.
(10) “Stiff person syndrome” – https://my.clevelandclinic.org/health/articles/6076-stiff-person-syndrome

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