There has been scientific proof that the cells close down admittance of T3 and T4 when the cells have reached their maximum capacity, and especially if the patient is taking a thyroid preparation from an artificial thyroid preparation of T4 only. This occurs because certain people can not convert T4 into T3, and this can leave an excess of both T3 and T4 in the bloodstream. Then the T3 and T4 may look OK in blood studies, or even high, but we are seeing what is in the bloodstream and not what is actually in the cells — and the doctors will believe in error that the person has enough, or is too high.
Yet, two things present themselves for deliberation: First, Â the cells, become resistant to admit the T3 and or T4 if they are in excess. This can occur from an increase in the T4 only medication, due to a patient complaining of continuing hypothyroid symptoms, when they can not convert T4 into T3. Then there is a surplus of T4 in the bloodstream and the cells shut down access to whatever T3 is there in order to keep from getting overwhelmed. And the Reverse T3 may also appear high, because the cells are actually not getting enough T3.
Resistance can occur from an intensive or prolonged inflammatory illness, then the T4 and TSH may appear normal, and, as above, the Reverse T3 may appear high, while the cells are not allowing access to T3.
Secondly, When taking an RX of Thyroid Hormone Replacement from porcine or another animal, the ratio of T3 to T4 is not what we have in our human bodies. In fact the T3 is way too high, and thus the cell membrane, doing its work, shuts down admittance of more of this hormone, becoming resistant– and the Free T3 can be seen as high, or even very high, influencing of course the levels of T4 and TSH, even when the person’s complaints are exceeding fatigue, hair loss, and other hypothyroidism symptoms. This is very confusing not only to the patients, but to their health practitioners.
Taking an RX of only T4, such as Synthroid or Levothyroxine, often has not corrected the symptoms of hypothyroidism effectively for these reasons. Thus, taking a compounded Thyroid medication, (not from a ‘natural’ animal source), in the ratio that is normal for humans may often be the best answer, that ratio being approx. 14:1 up to 19:1 — until and unless we can compound the animal thyroid gland in the ratio needed for humans. In Europe the standard ration is 17:1.
Let me know what you all think and hear your questions after you review this. For those who are wanting details Here is an Excerpt from the longer article, with the link below
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TSH and serum T4 levels fail to correlate with intracellular thyroid levels. Additionally, the free T3 will also tend to be less accurate with reduced cellular energy. This artificial elevation of T3 due to be reduced uptake into the cell is generally offset by a reduced T4 to T3 conversion due to reduced uptake and T4 and subsequent conversion to T3, making T3 a more accurate marker than the TSH or T4 with physiologic stress. Also, the transporter for reverse T3 (rT3) is similar to T4 in that it is energy dependent and has the same kinetics as the T4 transporter (6,41,45,62,66,67). This property (among others) makes it the most useful indicator of diminished transport of T4 into the cell (45). Thus, a high reverse T3 demonstrates that there is either an inhibition of reverse T3 uptake into the cell and/or there is increased T4 to reverse T3 formation. These always occur together in a wide range of physiologic conditions and both cause reduced intracellular T4 and T3 levels and cellular hypothyroidism. Thus, reverse T3 is an excellent marker for reduced cellular T4 and T3 levels not detected by TSH or serum T4 and T3 levels. Because increased rT3 is a marker for reduced uptake of T4 and reduced T4 to T3 conversion, any increase (high or high normal) in rT3 is not only an indicator of tissue hypothyroidism but also that T4 only replacement would not be considered optimal in such cases and would be expected to have inadequate or sub-optimal results. A high reverse T3 can be associated with hyperthyroidism as the body tries to reduce cellular thyroid levels, but this can be differentiated by symptoms and by utilizing the free T3/reverse T3 ratio, which is proving to be the best physiologic marker of intracellular thyroid levels (see Diagnosis of low thyroid due to stress & illness Graph). The dramatic reduction of T4 cellular uptake with a wide variety of conditions (T3 being less affected) also explains why T4 preparations are often associated with poor clinical response and continued residual symptoms that the unknowing physician assumes is not due to low thyroid, because serum levels look “good†if the physician does not understand the potential effects of reduced thyroid hormone transport. As stated by Hennemann G et al in Endocrine Reviews: “Even a small decrease in cellular ATP concentration results in a major reduction in the transport of T4 (and rT3) but only slightly affects T3 uptake (5).†This makes it inappropriate to use T4-only preparations if treating any condition associated with the following: reduced mitochondrial function or ATP production, which includes insulin resistance, diabetes and obesity 68,69,70,71,106); chronic and acute dieting (4,51,66,72,112,113,114,115,116,117,118); diabetes (69,73,74,75,76); depression (73,77,78,79); anxiety (73,80); bipolar depression (73,77,81,82); neurodegenerative diseases (73,83,84,85,86,87); aging (73,74,88-100); chronic fatigue syndrome (73,101,102); fibromyalgia (73,103,104); migraines (73); chronic infections (73); physiologic stress and anxiety (73,79); cardiovascular disease (73,99,104,105,108) and inflammation and chronic illness (73,109,110,111); Likewise, high cholesterol, fatty acids or triglyceride levels also selectively inhibit T4 transport into the cell as opposed to T3 (57,58,60,72,106,107,114), making T4-only preparations physiologically inappropriate for individuals with high cholesterol or triglycerides or who are chronic dieters, which dramatically increases serum free fatty acids (72). It is not surprising that T3 has been shown to be superior in such patient populations. Fraser et al investigated the correlation between tissue thyroid activity and serum blood tests (TSH, free T4 and T3) and published their results in the British Medical Journal. The study authors concluded that “The serum concentration of thyroid stimulation hormone is unsatisfactory as the thyrotrophs in the anterior pituitary are more sensitive to changes in the concentration of thyroxin in the circulation than other tissues, which rely more on triiodothyronine (T3). They found a suppressed or undetectable TSH was not an indication or a reliable marker of over replacement or hyperthyroidism. They state, It is clear that serum thyroid hormone and thyroid stimulating hormone concentrations cannot be used with any degree of confidence to classify patients as receiving satisfactory, insufficient, or excessive amounts of thyroxine replacement The poor diagnostic sensitivity and high false positive rates associated with such measurements render them virtually useless in clinical practice…Further adjustments to the dose should be made according to the patient’s clinical response. (121)
http://nahypothyroidism.org/thyroid-hormone-transport/
http://www.quackwatch.org/01QuackeryRelatedTopics/armour.html
