roxie60
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People are struggling why is this so hard, has this always been a nightmare to figure out what is wrong with folks?
http://nahypothyroidism.org/chaos-in-the-thyroid-drug-world/
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Possible to be hypothyroid but have normal tests?
- Thread starter Ocean
- Start date
People are struggling why is this so hard, has this always been a nightmare to figure out what is wrong with folks?
http://nahypothyroidism.org/chaos-in-the-thyroid-drug-world/
SOC
Senior Member
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- 7,849
Have you mentioned this to your doctor? She may not realize how desperate the situation is. Yeah, I know we tell them we're exhausted, etc, but they seem to be weak in inferring the life effects of our symptoms. Sometimes we have to be very, very direct with them.
Are you seeing an ME/CFS specialist, or is it just your local PCP helping you at this point?
PS I checked my daughter's levothyroxine dosage. The doc actually doubled it to 50 mcg after 2 months, so maybe the 88 mcg isn't as high as I thought.
roxie60
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They have a test at this link if people have some lab results and you have been told you have 'normal' thyroid function. Here was my result
Your Score is:82
It is extremely likely that you have thyroid dysfunction causing your symptoms.
Your symptoms are consistent with thyroid dysfunction and your TSH is greater than 2, which although considered in the 'normal' range by many laboratories and physician but the most well done studies demonstrate that a TSH above 2 is not likely 'normal'. It is recommended that you seek a knowledgeable physician who understands the limitations of the TSH to discuss treatment. (see Diagnosis of hypothyroidism: Are we getting what we want from TSH testing? and reference 106).
roxie60
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Is Synthroid considered a T4 only replacement?
roxie60
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Sadly it appears most doctors only treat based on the TSH. They also assume that just dosing T4 replacement will address other T3 tissue levels. Well that appears to be untrue. Synthroid is a T4 only replacement. I was wondering is anyone taking something that combines T4 and T3, what is it called. It looks like many who are just given Synthroid may still have symptoms even though the TSH (pituitary) number improves.
This is from the same site Ema linked above:
This study demonstrated that the normalization of plasma TSH and T4 levels with T4-only preparations provide adequate tissue T3 levels to only a few tissues, including the pituitary (hence the normal TSH), but almost every other tissue will be deficient. This study demonstrated that it is impossible to achieve normal tissue levels of T3 by giving T4 only preparations unless supra-physiological levels of T4 are given. The authors conclude: “It is evident that neither plasma T4 nor plasma T3 alone permit the prediction of the degree of change in T4 and T3 concentrations in tissues…the current replacement therapy of hypothyroidism [giving T4] should no longer be considered adequate…(119).”
The second study compared the plasma TSH, T4 and T3 levels and 13 different tissue levels of T4 and T3 when T4 or T4/T3 preparations were utilized (120). This study found that a combination of T4/T3 is required to normalize tissue levels of T3. The study found that the pituitary was able to maintain normal levels of T3 despite the rest of the body being hypothyroid on T4 only preparations. Under normal conditions it was shown that the pituitary will have 7 to 60 times the concentration of T3 of other tissues of the body; and when thyroid levels drop, the pituitary was shown to have 40 to 650 times the concentration of T3 of other tissues. Thus, the pituitary is unique in its ability to concentrate T3 in the presence of diminished thyroid levels that are not present in other tissues. Consequently, the pituitary levels of T3 and the subsequent level of TSH are poor measures of tissue hypothyroidism, as almost the entire body can be severely hypothyroid despite having a normal TSH level (120).
These studies add to the large amount of medical literature demonstrating that pituitary thyroid levels are not indicative of other tissues in the body and showing why the TSH level is a poor indicator of a proper thyroid dose. These studies also demonstrate that it is impossible to achieve normal tissue thyroid levels with T4 preparations such as Synthroid and Levoxyl. It is no surprise that the majority of patients on T4 preparations will continue to suffer from symptoms of hypothyroidism despite being told their levels are “normal.” Patients on T4 only preparations should seek out a physician who is well-versed in the medical literature and understands the physiologic limitations and inadequacy of commonly used thyroid preparations.
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,
In a study published in the British Medical Journal, Meir et al also investigated the correlation of TSH and tissue thyroid effect. It was shown that the TSH level had no correlation with tissue thyroid levels and could not be used to determine a proper or optimal thyroid replacement dose. The authors concluded that “TSH is a poor measure for estimating the clinical and metabolic severity of primary overt thyroid failure. … We found no correlations between the different parameters of target tissues and serum TSH.” They stated that signs and symptoms of thyroid effect and not the TSH should be used to determine the proper replacement dose (122).
Alevizaki et al also studied the accuracy of using the TSH to determine the proper thyroid replacement dose in T4 treated individuals. The study found that such a practice of using the TSH, although common, results in the majority of tissues being hypothyroid, except for the pituitary. They conclude, “TSH levels used to monitor substitution, mostly regulated by intracellular T3 in the pituitary, may not be such a good indicator of adequate thyroid hormone action in all tissues (123).”
This is from the same site Ema linked above:
This study demonstrated that the normalization of plasma TSH and T4 levels with T4-only preparations provide adequate tissue T3 levels to only a few tissues, including the pituitary (hence the normal TSH), but almost every other tissue will be deficient. This study demonstrated that it is impossible to achieve normal tissue levels of T3 by giving T4 only preparations unless supra-physiological levels of T4 are given. The authors conclude: “It is evident that neither plasma T4 nor plasma T3 alone permit the prediction of the degree of change in T4 and T3 concentrations in tissues…the current replacement therapy of hypothyroidism [giving T4] should no longer be considered adequate…(119).”
The second study compared the plasma TSH, T4 and T3 levels and 13 different tissue levels of T4 and T3 when T4 or T4/T3 preparations were utilized (120). This study found that a combination of T4/T3 is required to normalize tissue levels of T3. The study found that the pituitary was able to maintain normal levels of T3 despite the rest of the body being hypothyroid on T4 only preparations. Under normal conditions it was shown that the pituitary will have 7 to 60 times the concentration of T3 of other tissues of the body; and when thyroid levels drop, the pituitary was shown to have 40 to 650 times the concentration of T3 of other tissues. Thus, the pituitary is unique in its ability to concentrate T3 in the presence of diminished thyroid levels that are not present in other tissues. Consequently, the pituitary levels of T3 and the subsequent level of TSH are poor measures of tissue hypothyroidism, as almost the entire body can be severely hypothyroid despite having a normal TSH level (120).
These studies add to the large amount of medical literature demonstrating that pituitary thyroid levels are not indicative of other tissues in the body and showing why the TSH level is a poor indicator of a proper thyroid dose. These studies also demonstrate that it is impossible to achieve normal tissue thyroid levels with T4 preparations such as Synthroid and Levoxyl. It is no surprise that the majority of patients on T4 preparations will continue to suffer from symptoms of hypothyroidism despite being told their levels are “normal.” Patients on T4 only preparations should seek out a physician who is well-versed in the medical literature and understands the physiologic limitations and inadequacy of commonly used thyroid preparations.
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)
In a study published in the British Medical Journal, Meir et al also investigated the correlation of TSH and tissue thyroid effect. It was shown that the TSH level had no correlation with tissue thyroid levels and could not be used to determine a proper or optimal thyroid replacement dose. The authors concluded that “TSH is a poor measure for estimating the clinical and metabolic severity of primary overt thyroid failure. … We found no correlations between the different parameters of target tissues and serum TSH.” They stated that signs and symptoms of thyroid effect and not the TSH should be used to determine the proper replacement dose (122).
Alevizaki et al also studied the accuracy of using the TSH to determine the proper thyroid replacement dose in T4 treated individuals. The study found that such a practice of using the TSH, although common, results in the majority of tissues being hypothyroid, except for the pituitary. They conclude, “TSH levels used to monitor substitution, mostly regulated by intracellular T3 in the pituitary, may not be such a good indicator of adequate thyroid hormone action in all tissues (123).”
Symptomatic
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Yes, Synthroid is only T4.
Rand56
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