I saw a private endo yesterday and he was particularly interested in my pituitary as my cortisol levels were completely the reverse of what they should be. They are very low in the morning and very very high in the evening.
However I as also hoping he would taken notice of the fact that my Reverse T3 was high and my 'T3 : Reverse T3 ratio' was low which indicates that the T4 is mostly turning into Reverse T3 which blocks T3 from getting into cells and doing what it does. Unfortunately he said that he does not deal with reverse T3 because there is not enough evidence (there's loads because I found it). And if thyroid treatment was necessary he would only treat with synthetic T4.
I am very new to this whole thing because although I have always thought there was something wrong with my thyroid /pituitary I was labelled with fibromyalgia and told to stop looking and accept me diagnosis (before which there were not tests btw).
I was wondering if anyone has had experience with a doctor/ endocrinologist (NHS or private) that takes Reverse T3 and 'T3: Reverse T3 ratio' into account and will prescribe synthetic T3 and /or NDT if necessary.
Apologies for the long post and thank you in advance!
Written by
Just-keep-going
To view profiles and participate in discussions please or .
Well, actually, it's been discovered that rT3 does not block T3 receptors, because it has its own receptors. And rT3 is only in the blood for a couple of hours, anyway, before it's converted into T2. And the rT3 ratio is just unscientific mumbo-jumbo, and meaningless.
The rT3 test is one of those tests that tells you if there is a problem, but not what the problem is. It could be any one of a number of things, like high cortisol, low ferritin, etc. But, unless your FT4 is right at the top of the ranges, it's not a conversion problem that can be fixed by adding T3. Nor does it tell you how well you are converting.
If you want to know how well you convert, just compare the FT4 with the FT3 tested at the same time. Do you have a copy of your last blood test results that you can post on here?
Your cortisol problem just sounds like the early stages of adrenal fatigue, rather than a pituitary problem. I could be wrong, but if it were a pituitary problem, the cortisol would be low all day through. But, with adrenal fatigue, the cortisol is low in the morning, when it should be high, because the adrenals are struggling to make enough, and they continue to struggle all day, and only reach their quota in the evening, when it's time to go to bed, and the cortisol should be low. That is a classic adrenal fatigue problem. But your endo doesn't sound knowledgeable enough to be spending money on.
As greygoose says, there's a lot of mumbo jumbo talked about the RT3:T3. This explanation by a manufacturer of one of diagnostic assays for RT3, clarifies why the measures of RT3 & T3 can in fact, rule out hypothyroidism rather than rule it in:
3’,5’-Triiodo-L-thyronine also known as reverse triiodothyronine or reverse T3 (rT3), differs from 3,3’,5’-Triiodo-L-thyronine (T3) in the positions of the iodine atoms in the molecule. The majority of circulatory rT3 is synthesized by peripheral deiodination of thyroxine (T4). The ratio of rT3 to T3 is a valuable biomarker of the metabolism and function of thyroid hormones because the process of 5’ monodeiodination that converts T4 to T3 and rT3 to 3,3’-T2 is inhibited in a number of non-thyroidal conditions such as fasting, anorexia nervosa, malnutrition, diabetes mellitus, stress, severe trauma or infection, hemorrhagic shock, hepatic dysfunction, pulmonary diseases and others. This scenario is known as "Sick euthyroid" syndrome or “Low T3” syndrome. An elevated ratio of rT3 over T3 therefore helps to exclude a diagnosis of hypothyroidism, particularly in critically ill patients.
The concentration of rT3 could also be high in patients on the following medications: amiodarone, dexamethasone, propylthiouracil, ipodate, propranolol, and the anesthetic halothane.
The concentration of rT3 could be low in patients on Dilantin, which decreases rT3 due to its displacement from thyroxine-binding globulin and therefore generates an excessive clearance of rT3.
In my case, I take propanolol 4 times daily, so it impossible to keep it separate from my T4 that I take at night and my T3 that I take at two intervals during the day. As referred to above, propanolol, via a metabolite, interferes in two ways with RT3, including obstructing its expulsion from the body - such that my Endo wants me to ask my Neuro to swap the beta blocker for a different drug for my essential tremor. But if my blood test showed an RT3 level above range there would be no indication in the numbers, that it was possibly due to my propanolol use; and the extreme proponents of the RT3:R3 ratio would be issuing all manner of dire warnings about my thyroid function and associated thyroid hormone supplementation. In fact I'd guarantee that I'd be told "drop T4 and raise T3" when really, "ditch the BB" could be the solution.
Regarding RT3's alleged blocking of T3 receptors, this may help clarify things a little further:
"It is frequently claimed in articles published on the internet, but not in peer-reviewed papers, that rT3 blocks or 'gets in the way of' the nuclear thyroid receptors. The nuclear thyroid receptors are the sites of action where the primary active thyroid hormone, T3, exerts its effects to drive cellular metabolism and maintain body temperature. There is no credible scientific evidence that rT3 enters the nucleus of the cell at all, and the bulk of the scientific literature states clearly that rT3 does not bind to, and has no known transcriptional activity at, the thyroid receptor. It is, however, known to have potent activity in the cytoplasm as an initiator of actin polymerization in astrocytes in the brain. This is mediated in a non-genomic manner by its binding to a very specific thyroid receptor that exists only in the extranuclear compartment. Actin polymerization is important to cell structure and motility, and particularly important to normal brain development.
Any interpretation of the relative levels of T3 and rT3 must take into account all the factors that affect the activity of all three deiodinases. Reactivation of the D3 deiodinase and down-regulation of the D1 deiodinase contribute to both increased rT3 formation and reduced rT3 clearance, while at the same time reducing T3 synthesis from T4, so conditions affecting the expression of D1 and D3 in this way have a profound impact on circulating levels of T3 and rT3 and the T3/rT3 ratio. The T3/rT3 ratio has therefore been found to have some value in assessing prognosis in severely ill or very elderly patients. There is currently no evidence for a clinical basis for the use of this ratio in routine thyroid function assessment.
Some observed elevations in serum rT3 in the presence of exogenous thyroxine treatment are difficult to interpret, and can depend on the assay used. T4 can cross-react in immunoassays for rT3, resulting in a false increase in rT3 when T4 is high; more reliable tests for rT3 are performed using liquid chromatography/tandem mass spectrometry. A study in euthyroid subjects receiving thyroxine suggested that the observed rise in rT3 was a result of increased substrate availability for the peripheral inactivation of T4. And elderly patients may either have an adaptive response to reduce thyroid hyperactivity at the tissue level, or have some type of non-thyroidal illness with consequent reactivation of D3, in both cases resulting in increased T4 inactivation via conversion to rT3; it has therefore been suggested that older patients with hypothyroidism may require lower replacement doses of T4."
Content on HealthUnlocked does not replace the relationship between you and doctors or other healthcare professionals nor the advice you receive from them.
Never delay seeking advice or dialling emergency services because of something that you have read on HealthUnlocked.
is the T4:T3 ratio in NDT wrong?
Is there a T3 to T4 ratio
Reverse t3 and clearing it advice?
Is there a ‘common’ T4:T3 ratio
