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Males with hypothyroidism - how are you feeling?
I am a young male recently diagnosed with hypothyroidism (Hashimoto's disease). I have been on Synthroid for a little over a month. Most symptoms are slowly disappearing. I would like to hear other experiences and share mine as well.
This is a very old thread and I doubt lech even monitors the Forum any longer. I have been collecting names of member recommended doctors for about the last 4 years. I just sent PM with 3 candidates for you to consider. To access, just click on your name and go to your personal page, then click on messages.
It should be 65 mg of Nature-Throid, of course, not 62, in my earlier note.
The manufacturer of this drug has conversion tables stating the equivalency between 1/2 grain of Nature-Throid and 50mcg of levothyroxine. I wonder why it did not seem to apply to me, that is why my TSH jumped.
The manufacturer of this drug has conversion tables stating the equivalency between 1/2 grain of Nature-Throid and 50mcg of levothyroxine. I wonder why it did not seem to apply to me, that is why my TSH jumped.
Sorry to hear your doctor will not return your calls. I am sure gimel helped you to find a new specialist. I used his recommendation (Dr Kenneth Gross in Seattle) and I am happy. Dr Gross is a kind of specialist who will both listen to you and insist that you follow what he thinks is the best approach. This is optimal. You do not want a thyroid doctor who will do what you tell them. The sense that we know more than our doctors is deceptive: we obsess about our disease -- perhaps for a good reason given how diffuse and debilitating thyroid symptoms are -- while they study it.
Update on my situation: I had been on T4 alone for half a year or so, with little positive results and some odd side effects (e.g excessive thirst); persuaded my GP to substitute each 50 mcg of levothyroxine with 32.5 mg (1/2 grain) of Nature-Throid (Yes, My GP is that kind of a doctor who does what he is told) while I was waiting for my appointment with a specialist. At the end of this approach I was on 25 mcg of synthetic levothyroxine and 62 mg of Nature-Throid. My TSH jumped to 4.5 (test was done after 5 weeks on this combo).
Dr Gross gave me a choice of either adding more Nature-Throid, or going on a T3/T4 combo. I left the decision to him and I am on 75 mcg of levothyroxine + 10 mcg of Cytomel. It has been only a week since I started this and finally my metabolic rate went up quite a bit and my brain fog lifted somewhat (I do a crude thyroid function test -- daily temp/puls monitoring).
I am still not out of the woods but there is a glimmer of hope.
Update on my situation: I had been on T4 alone for half a year or so, with little positive results and some odd side effects (e.g excessive thirst); persuaded my GP to substitute each 50 mcg of levothyroxine with 32.5 mg (1/2 grain) of Nature-Throid (Yes, My GP is that kind of a doctor who does what he is told) while I was waiting for my appointment with a specialist. At the end of this approach I was on 25 mcg of synthetic levothyroxine and 62 mg of Nature-Throid. My TSH jumped to 4.5 (test was done after 5 weeks on this combo).
Dr Gross gave me a choice of either adding more Nature-Throid, or going on a T3/T4 combo. I left the decision to him and I am on 75 mcg of levothyroxine + 10 mcg of Cytomel. It has been only a week since I started this and finally my metabolic rate went up quite a bit and my brain fog lifted somewhat (I do a crude thyroid function test -- daily temp/puls monitoring).
I am still not out of the woods but there is a glimmer of hope.
No worries. The reason I started this was so people like you guys would contribute. West Chester is close to me and I am very interested in checking out that doc.
Sorry we hijacked your thread. Glad you found something useful in our discussions. Knowing how difficult it can be to locate a good thyroid doctor, I started compiling a list quite a while ago and have gotten from members, names of doctors that they would recommend based on personal experience. I have one from the Westchester, Pa. area and another in Cherry Hill, NJ. If these are of interest to you will be glad to send info by PM.
Gimel and lech I appreciate your opinions on this topic and I am still trying to learn more. Every Endocrinologist I have visited with so far knows less than I do about hypothyroidism and I was diagnosed not even a year ago. I have a strong feeling this is due to the conventional thinking that Synthroid (or whatever laboratory produced substance) is the cure for this condition. I am a STRONG believer in natural cures and eating food as close to the natural state as possible. My way of thinking has brought me to look into natural (or animal derived) thyroid supplements. The doctors I have visited would not even comment on this subject and the pharmacist I pay $25 a month to for Synthroid had no knowledge on the subject.
Is there any community or group of thyroid doctors (not Endocrinologists who state they treat hypothyroidism, but know less than I) that recommend natural thyroid supplements? I am located in the Philadelphia area and could reallllllly use a good referral. My current Endocrinologist will not even call me back and this is through PENN medical. What a joke this American system is...
I look forward to hearing more from you guys and finding a doctor that has an open mind. One not just focused on kick backs from the corrupt corporations that we have allowed to infiltrate medical community.
Is there any community or group of thyroid doctors (not Endocrinologists who state they treat hypothyroidism, but know less than I) that recommend natural thyroid supplements? I am located in the Philadelphia area and could reallllllly use a good referral. My current Endocrinologist will not even call me back and this is through PENN medical. What a joke this American system is...
I look forward to hearing more from you guys and finding a doctor that has an open mind. One not just focused on kick backs from the corrupt corporations that we have allowed to infiltrate medical community.
"I think you believe the basic rules of hypothesis testing and criteria of statistical significance have been created to conspire against unsubstantiated hunches."
No, I believe that the study started with the null hypothesis that adding T3 to a patient's meds does nothing for the patient beyond T4 only. Also, if the study reflects the typical thyroid patient population, many will not have T4 to T3 conversion problems. Accordingly the results will not show any statistically significant improvement with T3, so the study concludes that T3 has no additional benefit over T4. Yet, we know there are patients that have conversion problems, and low FT3 levels, that do benefit from T3 in their meds.
So, as you stated, study results are very dependent on the way the study is constructed and conducted. We see this all the time in new studies that dispute older studies (that disputed yet older studies).
As for throwing around individual studies, to support a position, believe me I can always list numerous references, but I usually only use one, that is clear and conclusive. My intent is not to prove my biased opinion but to discover the facts. From the many studies that I go through I try to determine if there is adequate evidence on one side or the other. That is why I had to question the idea that thyroid hormone suppression, as expressed by TSH level, was primarily related to FT3. The link I referenced was very conclusive, based on the high degree of correlation of TSH to FT4, for each of the three patients evaluated. Since the correlation was based on TSH and FT4 test results, and the study concluded that about 90 % of the variation in TSH resulted from FT4 levels,that leaves almost no room for TSH being affected by other variables. However, the regression line for each patient was different. That is why the correlation between TSH and FT4 becomes poor to fair when you try to extend the results to the total patient population. In order to be really useful, the TSH to FT4 correlation would have to be established by regression analysis for each patient. Obviously not practical.
As noted,when you try to determine the correlation between TSH and FT4 and FT3 for the total population, that becomes very muddled. Due to patient-to-patient variation, test variability and other factors, the correlation seems to be only poor to fair at best, in spite of TSH being touted as the gold standard for thyroid testing. I have searched extensively for data that quantified the relationship of TSH and FT3/FT4, that might justify it being primary. The best info I have found came from the following source. In this study TSH correlated slightly better with FT4 than FT3, but I found the best part of the info to be the graphical presentation of data in Fig. 2, showing the effect of FT4 on TSH and the more variable results of FT3 on TSH.
http://www.clinchem.org/cgi/reprint/55/7/1380.pdf
I guess the only reason I got into this discussion was to question the idea that TSH is affected mainly by FT3. I know you stated, "Most users do not come to such fora to get authoritative knowledge but to confirm their internet-based self-diagnosis." I have no idea how extensive that is, but I think our Forum has a lot of experienced and dedicated members who try very hard to be objective and really help other members. As such, I think we all have an obligation to question and resolve issues. By doing so we can hopefully present the best info available to our members.
Best to you.
No, I believe that the study started with the null hypothesis that adding T3 to a patient's meds does nothing for the patient beyond T4 only. Also, if the study reflects the typical thyroid patient population, many will not have T4 to T3 conversion problems. Accordingly the results will not show any statistically significant improvement with T3, so the study concludes that T3 has no additional benefit over T4. Yet, we know there are patients that have conversion problems, and low FT3 levels, that do benefit from T3 in their meds.
So, as you stated, study results are very dependent on the way the study is constructed and conducted. We see this all the time in new studies that dispute older studies (that disputed yet older studies).
As for throwing around individual studies, to support a position, believe me I can always list numerous references, but I usually only use one, that is clear and conclusive. My intent is not to prove my biased opinion but to discover the facts. From the many studies that I go through I try to determine if there is adequate evidence on one side or the other. That is why I had to question the idea that thyroid hormone suppression, as expressed by TSH level, was primarily related to FT3. The link I referenced was very conclusive, based on the high degree of correlation of TSH to FT4, for each of the three patients evaluated. Since the correlation was based on TSH and FT4 test results, and the study concluded that about 90 % of the variation in TSH resulted from FT4 levels,that leaves almost no room for TSH being affected by other variables. However, the regression line for each patient was different. That is why the correlation between TSH and FT4 becomes poor to fair when you try to extend the results to the total patient population. In order to be really useful, the TSH to FT4 correlation would have to be established by regression analysis for each patient. Obviously not practical.
As noted,when you try to determine the correlation between TSH and FT4 and FT3 for the total population, that becomes very muddled. Due to patient-to-patient variation, test variability and other factors, the correlation seems to be only poor to fair at best, in spite of TSH being touted as the gold standard for thyroid testing. I have searched extensively for data that quantified the relationship of TSH and FT3/FT4, that might justify it being primary. The best info I have found came from the following source. In this study TSH correlated slightly better with FT4 than FT3, but I found the best part of the info to be the graphical presentation of data in Fig. 2, showing the effect of FT4 on TSH and the more variable results of FT3 on TSH.
http://www.clinchem.org/cgi/reprint/55/7/1380.pdf
I guess the only reason I got into this discussion was to question the idea that TSH is affected mainly by FT3. I know you stated, "Most users do not come to such fora to get authoritative knowledge but to confirm their internet-based self-diagnosis." I have no idea how extensive that is, but I think our Forum has a lot of experienced and dedicated members who try very hard to be objective and really help other members. As such, I think we all have an obligation to question and resolve issues. By doing so we can hopefully present the best info available to our members.
Best to you.
"they typically do not find any statistically significant difference, so they accept the null hypothesis, which just happens to be that there is no difference".
I think you believe the basic rules of hypothesis testing and criteria of statistical significance have been created to conspire against unsubstantiated hunches.
This is exactly what you are saying.
"If you follow the money, you begin to believe that many of these studies and the professional organizations that promote T4 only, get a lot of funding from the large pharmaceutical companies that, of course, produce T4 meds."
Forest Labs, the maker of Armour is also a for-profit organization. They also make popular antidepressants, diabetes drugs and what not. Do you think studies and organizations they fund get suppressed by Merck?
I think you believe the basic rules of hypothesis testing and criteria of statistical significance have been created to conspire against unsubstantiated hunches.
This is exactly what you are saying.
"If you follow the money, you begin to believe that many of these studies and the professional organizations that promote T4 only, get a lot of funding from the large pharmaceutical companies that, of course, produce T4 meds."
Forest Labs, the maker of Armour is also a for-profit organization. They also make popular antidepressants, diabetes drugs and what not. Do you think studies and organizations they fund get suppressed by Merck?
Yes, studies such as the one you mentioned in 2004 will prove whatever the null hypothesis is, because they typically do not find any statistically significant difference, so they accept the null hypothesis, which just happens to be that there is no difference. Of course these studies probably did include very many patients that have problems converting T4 to T3.
So that conclusion about the benefit of T3 overlooks the problems that many patients have when they are not converting T4 to T3 adequately and their FT3 level is too low. How can they say that these patients wold not benefit from T3 in their med? If you follow the money, you begin to believe that many of these studies and the professional organizations that promote T4 only, get a lot of funding from the large pharmaceutical companies that, of course, produce T4 meds. Here is a recent article citing a study that says that adding T3 is beneficial for many patients.
http://thyroid.about.com/b/2010/05/17/t3-superior-t4-levothyroxine-hypothyroidism-thyroid.htm
Anyway, we're only preaching to the choir.
So that conclusion about the benefit of T3 overlooks the problems that many patients have when they are not converting T4 to T3 adequately and their FT3 level is too low. How can they say that these patients wold not benefit from T3 in their med? If you follow the money, you begin to believe that many of these studies and the professional organizations that promote T4 only, get a lot of funding from the large pharmaceutical companies that, of course, produce T4 meds. Here is a recent article citing a study that says that adding T3 is beneficial for many patients.
http://thyroid.about.com/b/2010/05/17/t3-superior-t4-levothyroxine-hypothyroidism-thyroid.htm
Anyway, we're only preaching to the choir.
I know, I am only teasing. But you must admit that throwing around individual studies, typically from some patient's "advocacy" site is pure loonacy.
I particularly detest the ritual of citing the Lithuanian study published in February 11, 1999 issue of the New England Journal of Medicine, where it shows that adding t3 to treatment with t4 helps mood and cognition. There are many other, more recent studies showing otherwise. Why would anyone with even rudimentary sanity and decency cite just one source to lay and often desperate audiences, and omit other studies, leading to opposite conclusions and different treatment recommendations?
For example: 2004 study: Clin Endocrinol (Oxf). 2004 Jun;60(6):750-7; Ann Intern Med. 2005 Mar 15;142(6):412-24. The later concludes: "Physiologic combinations of L-thyroxine plus liothyronine do not offer any objective advantage over l-thyroxine alone, yet patients prefer combination treatment."
I particularly detest the ritual of citing the Lithuanian study published in February 11, 1999 issue of the New England Journal of Medicine, where it shows that adding t3 to treatment with t4 helps mood and cognition. There are many other, more recent studies showing otherwise. Why would anyone with even rudimentary sanity and decency cite just one source to lay and often desperate audiences, and omit other studies, leading to opposite conclusions and different treatment recommendations?
For example: 2004 study: Clin Endocrinol (Oxf). 2004 Jun;60(6):750-7; Ann Intern Med. 2005 Mar 15;142(6):412-24. The later concludes: "Physiologic combinations of L-thyroxine plus liothyronine do not offer any objective advantage over l-thyroxine alone, yet patients prefer combination treatment."
Only reason I engage in discussions like we have had is not to promote my opinion, but to test what I think to be true. My opinions are almost always based on info I have gathered over time. Whenever someone has a differing view, there is usually something to be learned by discussing the issue. And I always enjoy our discussions. Best to you.
I think we reached the point where both of us should defer judgment to medically trained professionals.
I believe, and this is only a cursory observation, not a deep analysis, which would be way outside my expertise, that the article you cited (http://www.thyroidmanager.org/Chapter6/Ch-6-9.htm) shows pearson's correlations between levothyroxine administration and TSH levels, without controlling for the effect of patient's ability to produce T3. What you need for the sake of this dispute (and I am not sure why are we even engaging in it), is a partial correlation showing [i]pure[/i] a pure effect of T4 on TSH, controlling for patient's capacity to convert T4 into T3, their own endogenous T3 supply and for a host of other factors, such as the initial thyroid status.
I suppose it is statistically feasible to separate the effect of T4 and T3 but there might be some ethical impediments to gathering data using human subjects or human pituitary tissue. This is why it has been done on rats.
This only goes to show you that many accept only the data they like and understand and which speak to their preconceived notions. This is why internet fora are an inherently poor source of medical advice.
Look at the " Is anyone on Armour?" thread where some users demand deleting postings that do not confirm the view on Armour's efficacy. Most users do not come to such fora to get authoritative knowledge but to confirm their internet-based self-diagnosis.
I believe, and this is only a cursory observation, not a deep analysis, which would be way outside my expertise, that the article you cited (http://www.thyroidmanager.org/Chapter6/Ch-6-9.htm) shows pearson's correlations between levothyroxine administration and TSH levels, without controlling for the effect of patient's ability to produce T3. What you need for the sake of this dispute (and I am not sure why are we even engaging in it), is a partial correlation showing [i]pure[/i] a pure effect of T4 on TSH, controlling for patient's capacity to convert T4 into T3, their own endogenous T3 supply and for a host of other factors, such as the initial thyroid status.
I suppose it is statistically feasible to separate the effect of T4 and T3 but there might be some ethical impediments to gathering data using human subjects or human pituitary tissue. This is why it has been done on rats.
This only goes to show you that many accept only the data they like and understand and which speak to their preconceived notions. This is why internet fora are an inherently poor source of medical advice.
Look at the " Is anyone on Armour?" thread where some users demand deleting postings that do not confirm the view on Armour's efficacy. Most users do not come to such fora to get authoritative knowledge but to confirm their internet-based self-diagnosis.
Alright. So, I don't know very much about rats. And I can't make much from the 33 year old study, since there didn't seem to be any statistical evidence, just a conclusion based on the difference in average result with two different ratios of T4:T3. On the other hand I gave you a study that showed statistically valid data (more recent than 1978, I might add LOL) that was done on three humans, that concluded that for an individual, over 88% of the variability in their TSH level was accounted for by their FT4I. So it is your choice -- old rat data, or more recent human data. LOL
Please double check the reference range shown for the last FT4 data. You may have omitted a digit, because most of the range data I see for FT4 is more like 10.2-19.2 p mol/L. At any rate, a FT3 level like current test result is frequently inadequate to relieve hypo symptoms. So that would mean an increase in meds, either more T4, or if your FT4 level indicates inadequate conversion of T4 to T3, then you might also need to supplement with T3 med.
Please double check the reference range shown for the last FT4 data. You may have omitted a digit, because most of the range data I see for FT4 is more like 10.2-19.2 p mol/L. At any rate, a FT3 level like current test result is frequently inadequate to relieve hypo symptoms. So that would mean an increase in meds, either more T4, or if your FT4 level indicates inadequate conversion of T4 to T3, then you might also need to supplement with T3 med.
It's all about rats, from the cold war era at that, but I think the basic relationships between T3 and T4 (still) hold form humans:
"The relative potency of T3:T4:rT3 appeared to be approximately 100:12:1 when estimated from the lowest doses that caused significant inhibition of TRH-induced release of TSH, and approximately 100:6:0.5 when estimated from the doses that caused 50% inhibition of TSH release."
Source: Comparison of inhibitory effects of 3,5,3'-triiodothyronine (T3), thyroxine (T4), 3,3,',5'-triiodothyronine (rT3), and 3,3'-diiodothyronine (T2) on thyrotropin-releasing hormone-induced release of thyrotropin in the rat in vitro.
Chopra IJ, Carlson HE, Solomon DH
Endocrinology. 1978 Aug;103(2):393-402
Not only T3 is decisive but also it becomes more so at higher doses of exogenous supply of the thyroid hormones in question (each administered separately so T4 impact might be even lower, given the T3 "contamination" that results from peripheral tissue conversion of T4 into T3).
Two weeks after diagnosis (September 2010):
FT3: 3.08 (1.71-3.71) pg/ml
FT4: 1.13 (0.70 - 1.48) ng/dl
anti-TG: 4.19 (0-4.11)
TRAb: 1.96 (0-1.8).
anti-TPO: 1.13 (0.0-5.61).
6 weeks after diagnosis (after 4 weeks on Synthroid (Euthyrox) 50 mcg):
FT3: 2.94 (1.8-4.2), pg/ml
FT4: 8.7 (1.5-22.7) pmol/L
Prior to diagnosis, my TSH fluctuated from 0.027 to 6.93 (0.27-4.20)
"The relative potency of T3:T4:rT3 appeared to be approximately 100:12:1 when estimated from the lowest doses that caused significant inhibition of TRH-induced release of TSH, and approximately 100:6:0.5 when estimated from the doses that caused 50% inhibition of TSH release."
Source: Comparison of inhibitory effects of 3,5,3'-triiodothyronine (T3), thyroxine (T4), 3,3,',5'-triiodothyronine (rT3), and 3,3'-diiodothyronine (T2) on thyrotropin-releasing hormone-induced release of thyrotropin in the rat in vitro.
Chopra IJ, Carlson HE, Solomon DH
Endocrinology. 1978 Aug;103(2):393-402
Not only T3 is decisive but also it becomes more so at higher doses of exogenous supply of the thyroid hormones in question (each administered separately so T4 impact might be even lower, given the T3 "contamination" that results from peripheral tissue conversion of T4 into T3).
Two weeks after diagnosis (September 2010):
FT3: 3.08 (1.71-3.71) pg/ml
FT4: 1.13 (0.70 - 1.48) ng/dl
anti-TG: 4.19 (0-4.11)
TRAb: 1.96 (0-1.8).
anti-TPO: 1.13 (0.0-5.61).
6 weeks after diagnosis (after 4 weeks on Synthroid (Euthyrox) 50 mcg):
FT3: 2.94 (1.8-4.2), pg/ml
FT4: 8.7 (1.5-22.7) pmol/L
Prior to diagnosis, my TSH fluctuated from 0.027 to 6.93 (0.27-4.20)
Just a couple of thoughts for you. If the TSH output from your hypothalamus/pituitary is inadequate to normally cause enough thyroid hormone production, then yes, as you increase your meds, the TSH will go down accordingly and require increasing amounts of meds. Of course if your hypo state is due to Hashimoto's Thyroiditis, then the scenario will be the same. You need to gradually increase thyroid meds as natural production goes down. Have you been tested for the thyroid antibodies, TPO ab and TG ab?
You mentioned the suppression of thyroid hormone production as being primarily due to FT3, not FT4. I have to question the validity of that, based on these data. Have a look at Fig. 6-7. It shows that for three individuals given increasing doses of T4 meds, that their TSH responded with a high degree of correlation. Of course if you look at the data you will also see that there is so much variation from one patient to the others that the correlation is very poor. But this suggests to me that TSH correlates mostly with FT4 levels.
http://www.thyroidmanager.org/Chapter6/Ch-6-9.htm
Another thing I wondered about is your FT3 and FT4 levels. I don't recall ever having seen any data on those.
Regarding any effect of higher altitudes, I know the air is thinner at 3000 feet. Thyroid patients often report having a feeling of being breathless. So wouldn't the altitude add to that feeling? Just a thought with no facts to support it.
You mentioned the suppression of thyroid hormone production as being primarily due to FT3, not FT4. I have to question the validity of that, based on these data. Have a look at Fig. 6-7. It shows that for three individuals given increasing doses of T4 meds, that their TSH responded with a high degree of correlation. Of course if you look at the data you will also see that there is so much variation from one patient to the others that the correlation is very poor. But this suggests to me that TSH correlates mostly with FT4 levels.
http://www.thyroidmanager.org/Chapter6/Ch-6-9.htm
Another thing I wondered about is your FT3 and FT4 levels. I don't recall ever having seen any data on those.
Regarding any effect of higher altitudes, I know the air is thinner at 3000 feet. Thyroid patients often report having a feeling of being breathless. So wouldn't the altitude add to that feeling? Just a thought with no facts to support it.
You were certainly right, Gimel, synthetic hormones and orthodox, T4-based approach, which I really had tried to adhere to since last September, is not for me.
I am not out of the woods yet, though.
Has anyone experienced worsening of their hypothyroid symptoms at higher elevations? I get hopelessly disoriented, irritable and slightly short of breath even at 3000 feet. Prior to levothyroxine therapy, I also could not sleep while in the mountains. Whenever I mention this to a doc, they roll their eyes.
I am also dealing with thirst: another unusual synthroid side-effect. Could this be a calcium-balance related (absence of endogenous calcitonin as a result of thyroid suppression therapy)?
I am not out of the woods yet, though.
Has anyone experienced worsening of their hypothyroid symptoms at higher elevations? I get hopelessly disoriented, irritable and slightly short of breath even at 3000 feet. Prior to levothyroxine therapy, I also could not sleep while in the mountains. Whenever I mention this to a doc, they roll their eyes.
I am also dealing with thirst: another unusual synthroid side-effect. Could this be a calcium-balance related (absence of endogenous calcitonin as a result of thyroid suppression therapy)?
Glad to hear that you are making some progress. Happened to think that you might like to see this quote from a letter written by a good thyroid doctor who treats his patients clinically.
"The ultimate criterion for dose adjustment must always be the clinical response. I have prescribed natural dessicated thyroid for your patient (Armour or Nature-Throid). These contain T4 and T3 (40mcg and 9mcg respectively per 60mg). They are more effective than T4 therapy for most patients. Since they provide more T3 than the thyroid gland produces, the well-replaced patient’s free T4 will be around the middle of its range or lower, and the FT3 will be high-“normal” or slightly high before the AM dose."
"The ultimate criterion for dose adjustment must always be the clinical response. I have prescribed natural dessicated thyroid for your patient (Armour or Nature-Throid). These contain T4 and T3 (40mcg and 9mcg respectively per 60mg). They are more effective than T4 therapy for most patients. Since they provide more T3 than the thyroid gland produces, the well-replaced patient’s free T4 will be around the middle of its range or lower, and the FT3 will be high-“normal” or slightly high before the AM dose."
In May my TSH was still over 3, I felt under the weather, changed doctors, my dose of levothyroxine was increased, gradually, to 125 mcg. After six weeks at that dose, my TSH was 1.3, which theoretically should be fine. However, I was disoriented, confused, fatigued -- I believe more than ever -- and experienced a rare side effect of synthroid (levothroid): terrible thirst. I needed to drink about a half a gallon of water during the night night and at least a gallon during the day, all of it with a terrible sense of urgency. I gained 6 pounds, my Achilles tendons, calves and heels ached more than before. I finally asked my doctor to replace 50 mcg of levothyroxine with half a grain (32.5 mcg) of armour (I believe those who argue that the proportion of exogenous t4 to t3 should be 10:1, otherwise, frequent and unnecessary dose increases might be needed as endogenous thyroid production is suppressed in reaction primarily to t3, not to t4). Three days later, I am better and beginning to notice some rudimentary thought processes resuming in my brain. I am worried though that I may need more and more of armour and that I will have to fight for it. Furthermore, as I switch to armour I am going to be interacting with doctors who will do what I want, not what is clinically proven and sound. But so be it, T4 alone is obviously not for me.
I saw a terrible GP but he made one good suggestion: to take medication at bedtime, on empty stomach. There is sound evidence that taken this way, levothyroxine is absorbed better, without altering circadian rhythm. I feel better, sleep better and behave like early stages intelligent life form.
Bolk, Nienke MD; et. al. "Effects of Evening vs Morning Levothyroxine Intake: A Randomized Double-blind Crossover Trial." Archives of Internal Medicine. 2010;170(22):1996-2003, Vol. 170 No. 22, Dec 13/27, 2010, Clinical Endocrinology 66 (1), 43-48, Volume 66, Issue 1, pages 43-48, January 2007.
If anybody knows a good endocrinologist in the Seattle area, please let me know.
Bolk, Nienke MD; et. al. "Effects of Evening vs Morning Levothyroxine Intake: A Randomized Double-blind Crossover Trial." Archives of Internal Medicine. 2010;170(22):1996-2003, Vol. 170 No. 22, Dec 13/27, 2010, Clinical Endocrinology 66 (1), 43-48, Volume 66, Issue 1, pages 43-48, January 2007.
If anybody knows a good endocrinologist in the Seattle area, please let me know.
The most important thing for you is to find a good thyroid doctor that will treat you clinically, by testing and adjusting FT3 and FT4 as necessary to relieve symptoms, without being constrained by resultant TSH levels. If you need confirmation of this, I can provide you plenty of links to good articles and scientific studies. I wish I could say that American doctors are better at diagnosing and treating thyroid problems than elsewhere, but good thyroid doctors are hard to find.
I suggest you check out the doctor tomorrow by asking if he is willing to test and treat you clinically as I describe above. I also suggest that you ask if he is willing to prescribe any thyroid meds other than T4 types. If the answer to either question is no, then you will need to keep looking for a good thyroid doctor. If you find that you need one, perhaps members can provide a recommendation or help locate one for you.
I suggest you check out the doctor tomorrow by asking if he is willing to test and treat you clinically as I describe above. I also suggest that you ask if he is willing to prescribe any thyroid meds other than T4 types. If the answer to either question is no, then you will need to keep looking for a good thyroid doctor. If you find that you need one, perhaps members can provide a recommendation or help locate one for you.
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