- This topic is empty.
-
Posts
-
I know she needs treatment, but just felt like posting. Of course her Dr. won’t do anything about it because her TSH is “in range”. I think he is negligent in not giving her a tria to see if her cognitive function improves.
Free T4 .9 (.9 – 1.8)
T3 75 (60-180)
TSH 1.75Writing such a physician is “negligent” is libelous. Such a physician would have the right to sue you and would probably win.
Every physician has their own limit to how far they will go before the risk to their patient becomes too great. The limit is often determined by the physician’s knowledge and their experience. Within the boundaries created by knowledge and experience, each physician has to decide what they are willing to do, what risks to take.
With a primary goal of maintaining safety, risk management becomes very important. Any intervention comes with risks, even if the intervention is indicated. For example, every antidepressant treatment comes with the risk of the patient’s death by suicide even if treatment is suppose to reduce the risk for suicide. Antipsychotics can have some risk of sudden death by cardiac arrhythmia. I have to face that risk every time I prescribe an antipsychotic to a patient.
If the physician sees that the risks are too great, then it is better to do nothing. That is simply smart, non-negligent medicine.
I asked a colleague years ago, why he is so conservative about thyroid treatment. He, after all, is an endocrinologist, is a member of the Endocrine Society, has written his own books about hormone replacement therapy. He said it was because he was afraid and that endocrinologists in general are afraid. As an example, he once gave a young man 9 mcg of T3 and the man developed congestive heart failure. When you get spooked like that, I can see why you become very very careful.
Since he did not know about the nutrition necessary to avoid adverse effects from thyroid hormone, he was further was hampered in maintaining safety when giving thyroid hormone. Physicians in medical school are not taught much about nutrition or its interactions with physical systems. But then, neither are nutritionists since this would require a deep understanding of physiology and medicine. When examining the endocrine, other medical and nutrition textbooks, that discussion is not even going to be there to any significant depth. This requires integration of multiple fields with both breadth and depth. In a world of specialists, this is difficult to do.
Additionally, when giving thyroid hormone, one also has to consider immune system function, gastrointestinal function, adrenal function, etc. Problems in these can make thyroid hormone intolerable and increase the risk of adverse effects – including arrhythmias and heart failure. It may appear simple, but it actually is not when one looks below the surface, in order to help insure the patient’s safety.
If one disagrees with one’s physician, then one can simply find another physician for consultation or primary evaluation and treatment.
ok poor choice of words but Im so frustrated. I havent mentioned any names so legally I think Im ok LOL.
But those labs along with symptoms, just seems like a trial dose of Thyroid replacement seems in order
as far as nutrional support goes, what is your recommendation?
IF tests reveal low
HC (well not nutrition, but supportive)
Vitamin C
Iron
Vitamin A
Iodine
Selenium
Multivitaminothers?
How to heal digestive issues, probiotic?
@wondering 3289 wrote:
ok poor choice of words but Im so frustrated. I havent mentioned any names so legally I think Im ok LOL.
But those labs along with symptoms, just seems like a trial dose of Thyroid replacement seems in order
O.K. I agree. It was a poor choice of words.
If I did not know the person and just have labs, then I would suspect thyroid hormone signaling is not working well if one or more of the following is present in an adult:
Total T4 < 8.0 ug/dL
Total T3 < 100 ng/dL (this varies)
Free T3 < 340 pg/dL
Free T4 < 1.2 ng/dL
TSH > 2.0 uIU/mL (this varies depending on the presence of metabolic problems. Also, if the goal of treatment is optimization, then this criteria is tightened so that a TSH > 1.0 would be suspect for suboptimal thyroid signaling).Whether or not to add thyroid hormone depends on several factors.
This is where obtaining the necessary information via history, physical exam, and other lab tests is important.
For example, if Total T4 is between 8.0 to 12.0 (this range is shifted upwards in women who take birth control), then I would hesitate to add more thyroid hormone. The reason is that there is sufficient thyroid hormone to activate and do it signaling job. If the person shows signs and symptoms of hypothyroidism, but adequate T4, then it is not thyroid hormone production that is the problem but what happens to the thyroid hormone after it is released.
For example, under some circumstances, such as infection, more T4 becomes converted to Reverse T3 than usual. This would then lead to a loss of T3 production and symptoms and signs of hypothyroidism. Adding T3 is an option. Some people respond to T3, with subsequent reduction of Reverse T3 production and normalization of thyroid hormone activation. In some people, however, T3 can also increase inflammatory signaling in the immune system, causing the situation to worsen. T3 may then be not tolerable due to occurrence of palpitations. The best solution would be to investigated further to determine why T4 is becoming converted more so to Reverse T3 then treat the cause, such as infection. Once the cause is determined and treated, thyroid activation to T3 can return.
If Free T3 is low but T4 is normal, then additional questions include: are thyroid binding proteins elevated? For example, if a person is taking birth control pills or if the person has excess estrogen production, then estrogen signaling is elevated. This triggers thyroid binding globulin production from the liver. TBG then binds to thyroid hormones, reducing the free levels of thyroid hormone, causing then a relative state of hypothyroidism.
If T3 is low and T4 is sufficient, then conversion of T4 to T3 is suspect. Questions to ask then include: is there sufficient deiodinase enzyme production to do the conversion? Is there sufficient selenium to make these enzymes? Is there sufficent norepinephrine signaling to trigger deiodinase enzyme production? Is there impaired liver function? etc. etc.
If T4, Free T4 and Free T3 are sufficient, yet TSH is elevated, then the questions include: Is there a problem in transporting thyroid hormone past the blood brain barrier so that it can do its work in the brain? Are there nutritional deficiencies (such as with vitamin A, iron, etc.) which are impairing thyroid signaling? Determining the questions to ask as to why thyroid hormone is not working and determining solutions to the problem would be the better answer, not just adding more thyroid hormone.
Etc. Etc. Etc.
Despite having thyroid test results, there is a lot more information that needs to be obtained to determine whether or not one should add thyroid hormone.
If the physician is confident and wants to dive in to do thyroid replacement, in a clinical trial, to see if it is beneficial, then he or she can do so after doing a risk assessment for the intervention.
There is a lot of complexity underneath the surface of what seemingly is a simple treatment.
Often more data is necessary to help determine risk prior to even a clinical trial of thyroid hormone.
Does the presence of Thyroid antibodies affect your opinion of labs above or labs in general?
Why does mainstream medicine look at TSH so much for Thyroid, but directly look at Testosterone vs. LH when testing for Hypogonadism. Are these not analogous?
@DrMariano 3298 wrote:
O.K. I agree. It was a poor choice of words.
If I did not know the person and just have labs, then I would suspect thyroid hormone signaling is not working well if one or more of the following is present in an adult:
Total T4 < 8.0 ug/dL
Total T3 < 100 ng/dL (this varies)
Free T3 < 340 pg/dL
Free T4 < 1.2 ng/dL
TSH > 2.0 uIU/mL (this varies depending on the presence of metabolic problems. Also, if the goal of treatment is optimization, then this criteria is tightened so that a TSH > 1.0 would be suspect for suboptimal thyroid signaling).Whether or not to add thyroid hormone depends on several factors.
This is where obtaining the necessary information via history, physical exam, and other lab tests is important.
For example, if Total T4 is between 8.0 to 12.0 (this range is shifted upwards in women who take birth control), then I would hesitate to add more thyroid hormone. The reason is that there is sufficient thyroid hormone to activate and do it signaling job. If the person shows signs and symptoms of hypothyroidism, but adequate T4, then it is not thyroid hormone production that is the problem but what happens to the thyroid hormone after it is released.
For example, under some circumstances, such as infection, more T4 becomes converted to Reverse T3 than usual. This would then lead to a loss of T3 production and symptoms and signs of hypothyroidism. Adding T3 is an option. Some people respond to T3, with subsequent reduction of Reverse T3 production and normalization of thyroid hormone activation. In some people, however, T3 can also increase inflammatory signaling in the immune system, causing the situation to worsen. T3 may then be not tolerable due to occurrence of palpitations. The best solution would be to investigated further to determine why T4 is becoming converted more so to Reverse T3 then treat the cause, such as infection. Once the cause is determined and treated, thyroid activation to T3 can return.
If Free T3 is low but T4 is normal, then additional questions include: are thyroid binding proteins elevated? For example, if a person is taking birth control pills or if the person has excess estrogen production, then estrogen signaling is elevated. This triggers thyroid binding globulin production from the liver. TBG then binds to thyroid hormones, reducing the free levels of thyroid hormone, causing then a relative state of hypothyroidism.
If T3 is low and T4 is sufficient, then conversion of T4 to T3 is suspect. Questions to ask then include: is there sufficient deiodinase enzyme production to do the conversion? Is there sufficient selenium to make these enzymes? Is there sufficent norepinephrine signaling to trigger deiodinase enzyme production? Is there impaired liver function? etc. etc.
If T4, Free T4 and Free T3 are sufficient, yet TSH is elevated, then the questions include: Is there a problem in transporting thyroid hormone past the blood brain barrier so that it can do its work in the brain? Are there nutritional deficiencies (such as with vitamin A, iron, etc.) which are impairing thyroid signaling? Determining the questions to ask as to why thyroid hormone is not working and determining solutions to the problem would be the better answer, not just adding more thyroid hormone.
Etc. Etc. Etc.
Despite having thyroid test results, there is a lot more information that needs to be obtained to determine whether or not one should add thyroid hormone.
If the physician is confident and wants to dive in to do thyroid replacement, in a clinical trial, to see if it is beneficial, then he or she can do so after doing a risk assessment for the intervention.
There is a lot of complexity underneath the surface of what seemingly is a simple treatment.
Often more data is necessary to help determine risk prior to even a clinical trial of thyroid hormone.
http://www.bprcem.com/article/S1521-690X(09)00074-8/abstract
Volume 23, Issue 6, Pages 769-780 (December 2009)
Thyroid function is modulated by genetic and environmental causes as well as other illnesses and medications such as gonadal or sex steroids. The latter class of drugs (sex steroids) modulates thyroid function. Gonadal steroids exert their influence on thyroid function primarily by altering the clearance of thyroxine-binding globulin (TBG). While oestrogen administration causes an increase in serum TBG concentration, androgen therapy results in a decrease in this binding protein. These effects of gonadal steroids on TBG clearance and concentration are modulated by the chemical structure of the steroid being used, its dose and the route of administration. Despite the gonadal steroids-induced changes in serum TBG concentrations, subjects with normal thyroid glands maintain clinical and biochemical euthyroidism without changes in their serum free thyroxine (T4) or thyroid-stimulating hormone (TSH) levels. In contrast, the administration of gonadal steroids to patients with thyroid diseases causes significant biochemical and clinical alterations requiring changes in the doses of thyroid medications. Similarly, gonadal steroid therapy might unmask thyroid illness in previously undiagnosed subjects. It would be prudent to assess thyroid function in subjects with thyroid disease 6–8 weeks after gonadal steroid administration or withdrawal.
===============================
Increasing TT
reduces SHBG
reduces TBG
CBG ??????what is does to CBG (cortisol binding globulin)
……
@wondering 3301 wrote:
Does the presence of Thyroid antibodies affect your opinion of labs above or labs in general?
Why does mainstream medicine look at TSH so much for Thyroid, but directly look at Testosterone vs. LH when testing for Hypogonadism. Are these not analogous?
The presence of thyroid antibodies helps one arrive at the diagnosis, e.g. Hashimoto’s Thyroiditis.
However, they don’t necessary help determine whether or not to add thyroid hormone.
@JanSz 3304 wrote:
Increasing Total Testosterone
reduces SHBG
reduces TBG
CBG ??????what is does to CBG (cortisol binding globulin)
……
Estrogens increase Cortisol-Binding Globulin, as does Thyroid hormone.
What testosterone does directly is not so clear. Various animal studies show that adding testosterone either raises CBG or reduces CBG depending on the species studied.
However, the studies do not simultaneously determine what happens to the estrogens. Testosterone, after all, is a precursor to estradiol.
Speculating:
if adding testosterone significantly increases estradiol, then CBG may increase.
If adding testosterone does not significantly raise estrogen (which is usually not the case), then CBG may not change, or may decrease if testosterone has a direct effect on liver production of CBG.
@DrMariano 3307 wrote:
The presence of thyroid antibodies helps one arrive at the diagnosis, e.g. Hashimoto’s Thyroiditis.
However, they don’t necessary help determine whether or not to add thyroid hormone.
Hello Dr M,
Does the presence of high ANTI-TPO strongly suggest Hashimoto’s? Can there be other reason’s that these antibodies are high?
This was taken from old labwork of mine (2005).
ANTI-THYROGLOBULIN AB <2.0 (0.0-2.0)
ANTI-TPO ANTIBODY 3.7 (0.0-2.0)
FREE T4 1.3 (0.8-1.8)
T3, FREE 312 (230-420)
TSH, Ultra Sensitive 3.1 (0.40-5.50)My doctor didn’t mention anything about Hashi’s or even that I was hypo after this test. Years later, I feel that it’s catching up to me. Over the last year I feel as if I’m a mess. I can’t concentrate, motivation is gone, always tired / fatigued. It is progressively getting worse.
I don’t have antibody information on any recent labwork however my current labs look like this:
TSH 5.6 (0.450-4.500)
REVERSE T3 328 (90-350)
T3, FREE 3.2 (2.0-4.4)
FREE T4 1.31 (0.82-1.77)Could Hashi’s create problems with thyroid conversion, elevating RT3?
I apologize in advance to the OP as I did not mean to side track his thread.
The presence of anti-thyroglobulin antibodies and anti-thyroid peroxidase antibodies supports the diagnosis of Hashimoto’s Thyroditis.
When to add thyroid hormone depends on how much thyroid hormone one is still producing. When suboptimal thyroid hormone levels are present and the patient is exhibiting signs and symptoms consistent with this, then one could decide to add thyroid hormone, depending on additional considerations.
If the inflammatory response around the thyroid gland as a result of Hashimoto’s Thyroiditis spreads sufficiently to the rest of the immune system, it would be possible for reverse T3 to become elevated.
Additionally, if one has one autoimmune illness, the chances of having several more autoimmune illnesses is greatly increased, increasing the likelihood of generalized inflammatory cytokine signaling between immune system cells and the rest of the body.
@wondering 3290 wrote:
as far as nutrional support goes, what is your recommendation?
IF tests reveal low
HC (well not nutrition, but supportive)
Vitamin C
Iron
Vitamin A
Iodine
Selenium
Multivitaminothers?
How to heal digestive issues, probiotic?
How about the amino acid L-Tyrosine which is the precursor for thyroxine?
“L-Tyrosine
Direct precursor to Thyroxine, Adrenaline and Nor-adrenaline
Essential amino acid in the production of dopamine
Mild stimulatory effect on the central nervous system
Assists in optimizing thyroid hormone levels, increased mood, concentration, and productivityUsed to treat conditions:
Depression or mood disorder
Poor coping ability
Fatigue
Low sex drive
Low metabolism
Drug abuse (when combined with Tryptophan)
Improves endurance under stress
Effective as an appetite suppressant
Suggested dosage for healthy adults ranges from 500 to 1,500 mg per day “
- You must be logged in to reply to this topic.