Background information, and a convenient table of values for T3 & rT3, for diagnosing and treating Intracellular Hypothyroidism
Preamble
This is a consideration of the diagnosis of, and therapy for, Intracellular Hypothyroidism (IH), a stress-related condition in which excessive Cortisol secretion blocks Deiodinase 1 (D1), thus preventing conversion of T4 to T3 and promotes T4 conversion to rT3, by upregulating D3.
IH, a.k.a. the Low T3 Syndrome (LT3S), can produce all the symptoms and effects of true Hypothyroidism, up to and including cardiomyopathy and NCDs like MS (those NCDs which are related to true Hypothyroidism). It is therefore a significant entity, although it is not recognised as such, by the “Medical Establishment”
The normal FT3 range in Ontario, was originally quoted as 3.1–6.1 Pm/L1, but according to Ontario’s Ministry of Health, it was changed to 2.8–5.8 pmol/L in 2021.
Logically, this change was unfounded: the roster of candidates for the sample population used to calculate the”new normal” FT3 range must have included people whose FT3 was subnormal , due to unrecognized, asymptomatic IH.
Thus, the official reduction of the lower limit of normal for FT3, to 2.8 Picomoles/Litre constitutes an indictment of the system’s methods of calculating “normal” (for comment and logic re. calculating normal, click the link, “normal”) and results in an increased liability to underdiagnosis of Hypothyroidism.
Reverse T3 (rT3) is not a metabolite
rT3 has no function excepting perhaps to up-regulate Deiodinase 3, thus encouraging degradation of intracellular T3, to T2.
It is ignored by mainstream medicine, on the grounds that it has no metabolic function: the medical establishment does not recognise reverse T3 as the significant “marker” which it is and does not utilise calculation of the FT3/rT3 ratio, in their assessment of patients who complain of Hypothyroid symptoms.
However rT3 is a highly important “marker” of thyroid hormone function, because its level and its comparison with FT3, via the FT3/rT3 ratio, gives an indication of the extent to which T4 is being converted into reverse T3 in our cells and a clear confirmation of that failure to convert T4 into normal T3, which results in “bottoming-out of the serum T3 level and failure to supply those tissues which depend on a T3 supply from the blood.
T3/rT3 ratio
The FT3/rT3 ratio is a sensitive and accurate measure of the degree of IH: it indicates the extent to which T4 is being converted into rT3, instead of normal T3.
The normal range for the T3/rT3 ratio is “greater than 20”.
A ratio of <20 indicate a failure of function of Deiodinase 1.
Non-recognition of IH, by doctors
Between government health agency unawareness of IH and its erroneous “rejigging” of previously proven “normals”, the ministry of health guarantees the mismanagement of thyroid disease.
Is there proof of a higher prevalence of IH, which led to MOH’s error?
Yes: Low body temperature is an indication of individual IH, and as the graph below shows, the worldwide body temperature average has fallen significantly since 1960, as stress levels and NCD prevalence has risen.
It strikes me that the Ministry of Health evidently doesn’t monitor the WHO’s statistics, as one would expect them to: anyone with a correlative brain would notice the body temperature change and would be self-pressured to enquire, “WHY?”.
Background information
There is no “normal” range for rT3
The rT3 range (5–25 ng/DL), as given in the medical literature, is nonsensical: in health, rT3 should not exceed 13 ng/DL (see Cameron Sutherland’s T3/rT3 table).
Logic
(1) If rT3 is 5 ng/DL, the T3/rT3 ratio exceeds 20, even if FT3 is as low as 1.6.
(2) If rT3 is 25 ng/DL, the ratio will be less than 20 unless the serum FT3 is more than 7.6 pmol/Litre (at which level, the patient is hyperthyroid).
(3) A high rT3, and/or low FT3, indicates low production of T3, from T4: T3/rT3 is “skewed” downward.
A Table, for calculation of T3/rT3 ratio, to diagnose IH
This invaluable, time-saving table is copied below, with permission from Cameron Sutherland, PhD:
Legend
– rT3 values are in Nanograms/DeciLitre (Ng/DL),
– T3 is reported in Picomoles/Litre (Pm/L).
– Therefore, to calculate the T3/rT3 ratio, we convert T3 values into Ng/DL
(Pm/L÷0.0154=Ng/DL). Then divide T3 (Ng/DL), by rT3 (Ng/DL): normal is <20.
In this table, rT3, written in blue, occupies the yellow row.
T3 (Pm/L) is in the blue column.
T3 (Ng/DL) is in the yellow column.
T3/rT3 results lie at the intersection of the “T3” and “rT3” values.
The pink area shows Abnormal values, and The white, Normal values, of T3/rT3 .
T3/rT3 values, targets for T3 & rT3, and dose of S-R T3
The normal range for the T3/rT3 ratio is “greater than 20”: the optimal range is “greater than 24’“.
Assessment by T3 & rT3 values:
If rT3 is 20–24, a normal T3/rT3 ratio is unattainable unless T3 is in the hyperthyroid range.
For example, if rT3 is 25, free T3 needs to be 7.7 pmol/litre (REALLY hyperthyroid), to maintain a normal T3/rT3 ratio.
Therapeutic Targets:
Arbitrarily, if we assume that the normal FT3 range is 3.1–6.1 picomoles/litre, we can ensure Euthyroidism by titrating the dose of S-R T3, to produce a serum T3 of 4.1–5.5 Pm/L and rT3 of 7–13Ng /DL: here’s the logic:
If T3 is 3.1 Pm/L, T3/rT3 will be > 20 if rT3 is less than 11 Ng/DL.
If T3 is 4.1, T3/rT3 will be > 20 if the rT3 is less than 14.
If T3 is 4.5, T3/rT3 will be > 20 if rT3 is less than 15
If T3 Is 6.1, and rT3 is less than 20, T3/rT3 will be normal.
Guideline for prescribing Sustained-Release T3:
(1) If rT3 is less than 13, and FT3 is greater than 4.0, no Rx is necessary: we can assume that T4 is being converted to T3 in the normal fashion:
(2) T3/rT3 of greater than 24 guarantees effective T4–T3 conversion: again, no prescription, or no change, is necessary.
(3) T3/rT3 of less than 20 diagnoses Low T3 Syndrome (Intracellular Hypothyroidism-IH): SR T3 should be prescribed, or increased if already prescribed.
(4) When T3/rT3 is 20-24, the “thyroid balance” is suspect: fluctuations in the patient’s stress level may result in “cycling”, between normal thyroid balance and intracellular hypothyroidism, with “mood swings” and intermittent hypothyroid symptoms. If symptomatic, the patient should be treated. If not, the test result should be validated by repeating the FT3 and rT3 tests; but rT3 is not reported immediately, so it is better to assume that an SR T3 dose increase is needed.
Observed facts
(1) Re. lowering reverse T3 levels: Based on my experience of more than 200 cases, raising the FT3 to greater than 5.0 pmol/litre, with sustained-release T3 capsules (SR-T3), resulted in serum rT3 levels in the range of 7–10 ng/Decilitre.
This confirmed normalization of T4-to-rT3 conversion and resolution of IH.
(2) Re. Laboratory-diagnosed hyperthyroidism: Occasionally, among my 200 patients, prescribing S-R T3 caused FT3 levels of 6.2-8.0. In most of these few cases, the subjective side effects were hyper-acute vision, with enhanced reds and greens, along with a feeling of being “high” and exceptionally healthy.
Only 3 people experienced “antsiness” and/or an elevated pulse rate and in these 3 cases, lowering the S-R T3 dose resulted in an immediate, uneventful reduction of FT3 to less than 6.2 and cessation of the hyperthyroid symptoms.
(3) In no case did hypothyroid symptoms persist, when FT3 exceeded 5.5.
A reasonable protocol for treating IH with Sustained-Release Triiodothyronine
The desirable target for FT3, during treatment with S-R Triiodothyronine (S-R T3), is 4.4 – 5.5 Pm/L. The target for rT3 is “less than 13” Ng/DL.
These targets proved easily achievable, via weekly estimation of FT3 and titration of the S-R T3 dose:
I began the prescription with10 µg per day and increased the dose weekly in 5 µg (per day) increments, until the FT3 was greater than 4.4.
At that point, the patient’s hypothyroid symptoms were reassessed, prior to considering a change of dose.
If the symptoms persisted, and/or the serum FT3 was less than 4.4, the dose of S-R T3 was increased by 5 µg.
If FT3 exceeded 6.1 Pm/L, the dose was reduced (again, by 5 µg).
Maintenance dose of sustained-release Triiodothyronine
The SR T3 dose at which the FT3 is between 4.5 and 6.1, with elimination of the patient’s hypothyroid symptoms, is continued. Repeat thyroid profile, excluding reverse T3, is repeated after 2 weeks, so as to confirm a steady level of FT3.
The thyroid profile, including reverse T3, is repeated 4 weeks following the final prescription, so as to ensure that the dose of SR T3 is correct and that the TSH and T4 levels are acceptable.
Occasionally, T3 fails to enter the pituitary and when that happens, the TSH rises and a prescription for T4 is necessary.
Following laboratory proof that the dose is appropriate, tests are repeated every three months, for one year and subsequently, every six months, for surveillance.
CAVEATS
(1) The patient is informed of the possibility of atrial fibrillation (AF) and instructed that tachycardia should be reported to the physician immediately.
AF did not occur in any of my cases.
(2) Sustained-Release T3 (SR T3) is prescribed instead of Cytomel, the reason being that as a rapid-release formulation, Cytomel produces a “spike” of FT3 in the morning, which can cause hyperthyroid symptoms.
(3) Once the symptoms have abated and the dose of S-R T3 has been titrated to acheive a serum FT3 of 4.5 – 6.2, , further dose adjustments can be made “by rule of thumb”, on the basis of serum FT3 values alone and without routinely repeating the rT3: a six-monthly, “checkup” thyroid profile, including rT3, is sufficient.
(4) SR T3 should be taken as close to 4 AM as possible, so as to mimic the diurnal rhythm of T4 production.
(5) The half-life of supplemental T3 is 12-18 hours, so follow-up FT3 tests should be done at noon, or later.
(6) Especially since AF is a possibility, each patient is carefully instructed not to “double-dose” SR T3: the treating physician must calculate the need for any dose increase, on the basis repeat estimation of FT3 and changes in symptomatology, both.
(7) If hyperthyroid symptoms nonetheless ensue, the patient should immediately reduce the SR T3 by 5 µg per day and the thyroid profile should be re-estimated.
(8) If the lower limit of normal for T3 is held to be 2.8, the mainstream MD will miss many more diagnoses than he/she will if it is 3.2.
This valuable, time-saving table is copied below, with permission from Cameron Sutherland, PhD: rT3 values are in Nanograms/DeciLitre (Ng/DL), while T3 is reported in Picomoles/Litre (Pm/L). Therefore, to calculate the T3/rT3 ratio, we first convert T3 values into Ng/DL (Pm/L÷0.0154 = Ng/DL), then divide T3 (Ng/DL), by rT3 (Ng/DL).
The normal value for the ratio is “less than 20”.
The optimal value for the ratio is “more than 23”.
High rT3, and/or Low FT3, indicates low production of T3, from T4.
Calculating T3/rT3
rT3 values are reported in Nanograms/DeciLitre (Ng/DL), while T3 is reported in Picomoles/Litre (Pm/L)
Therefore, to calculate the T3/rT3 ratio, we first convert T3 values into Ng/DL ……(Pm/L÷0.0154 = Ng/DL).
Then we divide T3, in Ng/DL, by rT3 (Ng/DL): The normal is >20, and optimal is >24.
There is no “normal” range for rT3:
The rT3 range (5–25 ng/DL), as given in the medical literature, is nonsensical (see Cameron Sutherland’s T3/rT3 table, below):
(1) If rT3 is 5 ng/DL (very low), the T3/rT3 ratio will exceed 20 even if FT3 is as low as 1.6 pmol/Litre.
(2) An rT3 of 25 ng/DL, yields a ratio of less than 20 unless the serum FT3 exceeds 7.6 pmol/Litre, at which level, the patient would be hyperthyroid.
(3) A high rT3, and/or low FT3, indicates low production of T3, from T4: T3/rT3 is “skewed” downward.
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