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Thre are a troubling theory about thyroid metabolism. Many physician like Dr Wilson, Ray Peat, Dr Lowe explain the bad effect of replacement T4. In fact, many patients have a high RT3 with syntroid or levothyrox.
From Ray Peat
The serum’s high ratio of T4 to T3 is a pitifully poor argument to justify the use of thyroxine instead of a product that resembles the proportion of these substances secreted by a healthy thyroid gland, or maintained inside cells. About 30 years ago, when many people still thought of thyroxine as “the thryoid hormone,” someone was making the argument that “the thyroid hormone” must work exclusively as an activator of genes, since most of the organ slices he tested didn’t increase their oxygen consumption when it was added. In fact, the addition of thyroxine to brain slices suppressed their respiration by 6% during the experiment. Since most T3 is produced from T4 in the liver, not in the brain, I think that experiment had great significance, despite the ignorant interpretation of the author. An excess of thyroxine, in a tissue that doesn’t convert it rapidly to T3, has an antithyroid action. (See Goumaz, et al, 1987.) This happens in many women who are given thyroxine; as their dose is increased, their symptoms get worse.from Wilson
http://wilsonstemperaturesyndrome.com/eManual/Chapters/05WhyNotT4.cfm
Impaired T4 to T3 conversion can lead from T3 preponderance to T4/RT3 preponderance. T4/RT3 preponderance can:
1. Perpetuate decreased T3 production and,
2. Competitively inhibit what T3 is produced.The enzyme 5′-deiodinase converts T4 to T3. It also converts RT3 to T2 (T2 is considered an inactive metabolite). Thus, T4 and RT3 compete for the attention of the same deiodinating enzyme.
It is likely that Wilson’s Temperature Syndrome is perpetuated by this deiodinating enzyme being preoccupied with RT3 at the expense of T4 conversion to T3 (with less T4 being converted to T3 and more therefore being converted to RT3).
This backlog situation leads to what I call T4/RT3 preponderance, as opposed to T3 preponderance.
T4/RT3 preponderance can be problematic in two ways. First, it perpetuates decreased T3 production. Second, it can compete with what T3 is produced, at the level of the nuclear membrane receptor.
Remember, T4 is 4 times less potent, and 3 times longer-acting than T3. So even though it stimulates the thyroid hormone receptor, it does it so much more weakly than T3, that if it occupies the receptor instead of T3, it results in decreased stimulation of the cell.
With T4/RT3 preponderance the thyroid system can get bogged down so that there is insufficient T3 stimulation of the cells.
Note: This all happens outside the blood stream on a cellular level and can’t be measured (p36). It is not necessarily reflected in the blood tests.
THIS AN INTERESTANT POST COME FROM ANOTHER FORUM ABOUT RT3
know of people who HAVE done T3 only protocol to clear RT3….. my wife included.
Some gradually go back to Armour after the protocol and do fine. Others stay on T3 only because the issues they suspect caused/contributed to the RT3 in the first place have not been or cant be resolved. In my wifes case Mercury from her Amalgams interferes with T4==>T3. She was too ill until recently to even consider removing them. Now that she is doing better we will look at whether we can do something about them.
My wife was on “T3 only” for 4 months until RT3 suddenly cleared & minor Hyperthyroid symptoms appeared. She was one of those prepared to take temps 4 times a day, and monitor BP & HR, journal symptoms meds doses etc. She got to 150mcg T3 (Tertroxin) stopped for several days when Hyper symptoms appeared & restarted on 80mcg daily (multidosed). Testing of RT3 near the end of that 4 months showed RT3 was now undetectable.
She remains on that 80mcg dose & has been for a couple of months now. She is doing MUCH better since doing this protocol & losing weight as well. She had been on Aussie “Armour” (Thyroid Extract USP) for almost 2 years prior to this. Adrenals, Sex Hormones, Nutrition, Vit & Mineral levels etc had all been optimised prior to T3 protocol with NO resolution of RT3 problem.
There are in fact many doing this protocol & achieving success in the main. They are NOT doing Wilsons meaning they are NOT cycling the T3. Rather they are doing similar to what the Aussie pharmacist suggested. In fact my wife printed that info out & showed her Doc to consider if Armour wasnt successful. They also find SRT3 & even compounded T3 does not work as well as commercial T3 like Tertroxin & Cytomel.
@Jean 1196 wrote:
THIS AN INTERESTANT POST COME FROM ANOTHER FORUM ABOUT RT3
know of people who HAVE done T3 only protocol to clear RT3….. my wife included.
Some gradually go back to Armour after the protocol and do fine. Others stay on T3 only because the issues they suspect caused/contributed to the RT3 in the first place have not been or cant be resolved. In my wifes case Mercury from her Amalgams interferes with T4==>T3. She was too ill until recently to even consider removing them. Now that she is doing better we will look at whether we can do something about them.
My wife was on “T3 only” for 4 months until RT3 suddenly cleared & minor Hyperthyroid symptoms appeared. She was one of those prepared to take temps 4 times a day, and monitor BP & HR, journal symptoms meds doses etc. She got to 150mcg T3 (Tertroxin) stopped for several days when Hyper symptoms appeared & restarted on 80mcg daily (multidosed). Testing of RT3 near the end of that 4 months showed RT3 was now undetectable.
She remains on that 80mcg dose & has been for a couple of months now. She is doing MUCH better since doing this protocol & losing weight as well. She had been on Aussie “Armour” (Thyroid Extract USP) for almost 2 years prior to this. Adrenals, Sex Hormones, Nutrition, Vit & Mineral levels etc had all been optimised prior to T3 protocol with NO resolution of RT3 problem.
There are in fact many doing this protocol & achieving success in the main. They are NOT doing Wilsons meaning they are NOT cycling the T3. Rather they are doing similar to what the Aussie pharmacist suggested. In fact my wife printed that info out & showed her Doc to consider if Armour wasnt successful. They also find SRT3 & even compounded T3 does not work as well as commercial T3 like Tertroxin & Cytomel.
If order to overcome t3 one needs to find the cause of it. People with rt3 when seen in a clinical setting potentially are found through FIA 5000 to be low in many minerals such as zinc, copper, selenium, vitamin D. One can also examine iodine content to find it can also be low. Correcting lifestyles, nutrient imbalances, sleep patterns, past emotional trama, starvation (if present), other hormone imbalances (dhea/cortiso ratio, e2, progesterone, ect), malaborption will help correct this abnormality of time. In general the majority of the problem occurs from a stressful event causing a high cortisol:dhea which over time weakens the adrenals. When I see high rt3 in many causes this is a potential sign of actually low cortisol when the person is of older age. The younger the person the more likely it may be overactive adrenal glands. By addressing the low cortisol levels in many cases this will resolve the rt3 issue over time. Rt3 is not the cause by a symptom of the cause. There has not been strong clinical supporting the evidence about “resetting” the mechanism that causes this. Several people have been on armour and adding more t-3 resolve the issue. The question is what is this imbalancing with t3 doing to other tissues in the body such as the brain function.
This study demonstrates that TSH and T4 levels are poor measures of tissue thyroid levels, TSH and T4 levels should not be relied upon to determine the tissue thyroid levels and that the best estimate of the tissue thyroid effect is the rT3 level and the T3/rT3 ratio
I don’t finf any study who explain that low cortisol is the cause of high rT3, may be you are right, but I don’t find any study…
The Journal of Clinical Endocrinology & Metabolism 2005; 90(12):6403–6409
Thyroid Hormone Concentrations, Disease, Physical Function and Mortality in Elderly Men
Annewieke W. van den Beld, Theo J. Visser, Richard A. Feelders, Diederick E. Grobbee, and Steven W. J. Lamberts Department of Internal Medicine , University Medical Center Utrecht, 3508 GA Utrecht, The Netherlands
This study of 403 men investigated the association between TSH, T4, free T4, T3, TBG and reverse T3 (rT3) and parameters of physical functioning. This study demonstrates that TSH and/or T4 levels are poor indicators of tissue thyroid levels and thus, in a large percentage of patients, cannot be used to determine whether a person is euthyroid (normal thyroid levels) at the tissue level. In fact, T4 levels had a negative correlation with tissue thyroid levels (higher T4 levels were associated
with decreased peripheral conversion of T4, low T3 levels and high rT3). This study demonstrates that rT3 inversely correlates with physical performance scores and that the T3/rT3 ratio is currently the best indicator of tissue levels of thyroid.
This study showed that increased T4 and RT3 levels and decreased T3 levels are associated with hypothyroidism at the tissue level with diminished physicial functioning
and the presence of a catabolic state (breakdown of the body). This study adds to the mounting evidence that giving T4 preparations such as Synthroid and Levoxyl are inadequate for restoring tissue euthyroidism and that a normal TSH cannot be relied upon as as an indication of euthyroidism, as it has a very low sensitivity and specificity for hypothyroidism. This poor sensitivity and specificity is further decreased with the presence of one or more systemic illnesses, including diabetes, heart disease, hypertension, systemic inflammation, asthma, CFS, fibromyalgia,
rheumatoid arthritis, lupus, insulin resistance, obesity, chronic stress and almost any other systemic illness.
Low T3 syndrome, with low T3 and high reverse T3, is almost always missed when using standard thyroid function tests, as the T3 level is often in the low normal range and reverse T3 is the high normal range, again making the T3/rT3 ratio the most useful marker for tissue hypothyroidism and as a marker of diminished cellular
functioning. The authors of this study conclude, “Subjects with low T3 and high reverse T3 had the lowest PPS [PPS is a scoring system that takes into account normal activities of daily living and is a measure of physical and mental functioning]…
Furthermore, subjects with high reverse T3 concentrations had worse physical performance scores and lower grip strength. These high rT3 levels were accompanied by high FT4 levels (within the normal range)…These changes in thyroid hormone concentrations may be explained by a decrease in peripheral thyroid hormone metabolism…
Increasing rT3 levels could then represent a catabolic state, eventually proceeding an overt low T3 syndrome.”
.I feel Hardasnails is on the money with this and I don’t like the use of T3 only to bring down RT3 without first checking the things Hard talked about my RT3 goes up when my Estraddiol E2 goes up I take 4 grams a day of Armour and I am on 30 mgs a day of Cortef “HC”. My RT3 goes up when my Estradiol E2 goes to high. I am on TRT take Testosterone meds to keep my levels up I am Hypopituitary and need to treat this and my Thyroid with my low Cortisol levels. Do to my age 65 and being on TRT I need to take Arimidex to keep my Estadiol down. On my last set of labs my Estradiol was to high and my RT3 came back at 43 high range 11 to 32 ng/dL been keeping my E2 levels down just did labs again last week I will update my post here about my RT3 when my labs come back in about 2 weeks.
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