Thyroid dangers in reality? -- EVERYONE VOTES

[biggeek]

I have my own glucose tester. And it doesn't measure in ng/dl. It measures blood glucose in mg/dl...so I'll assume that's a typo on your part.

T3 causes insulin resistance directly? Ok...that's a new one. No. T3 actually increases Beta-adrenergic function, i.e. the beta adrenoreceptors, Beta 1,2,3. These in turn release FFA's from the WAT's to be burned for fuel for bodily functions, instead of burning the existing blood glucose for fuel. Therefore blood glucose levels increase. This is you hyperglycaemia/insulin resistance...and is exactly what happens when you use GH as well. Solution. Use R-ALA to overcome it. Simple and effective. Your "problems" all have solutions if you apply yourself to the problem at hand.

Diabetes? Type I impossible. Obviously. Type II? I have seen ZERO literature to that effect. Hypothetically, if you where obese it could happen.

The only thing I agree with is the bone mineral de-calcificacion loss. But guess what? AAS increase bone mineral deposition. So, there goes that problem as well.

You guys are way too alarmist. I find it amusing that people find T3 very dangerous, and insulin a walk-in-the-park. Vice-versa if you ask me.
I wouldn't touch insulin with a 50 foot pole.

The cardiac/BP problem is the ony real concern I agree with. And only in those people who are genetically predisposed to high BP, or those who are taking an entire shelf of AAS, or lastly, have some type of cardiac defect. Arrythmia for example.

High BP can be counter-acted by 10g L-Taurine/day VERY effectively. Just ask around, and you'll see. I have seen dystolic drops of 20 points when on AAS due to L-Taurine. 120/80 120 = Dystolic 80 = systolic.

Obviously, if you have an existing cardiac problem, T3 is just not for you. that is a given.

Man.. who are you and where did you come from?? ha ha.. these are some of the best threads i've read in a while.. i knew a little about a lot of what you said, but i didn't know the relationships between a lot of it.. but anyway.. hope you hang around more often.. help us answer some serious questions..

have a good holiday..

 

[gjohnson5]

no, you got it wrong, graves disease, is one of many thyroid disorders that can be un-diagnosed or un-noticed. if you have this and you take to much t3 you will defintly fk yourself.

Well My understanding is that graves disease is an autoimmune disorder. The immune system attacking the thyroid causes it to spit out more hormones. The mayoclinic agrees with my understanding http://www.mayoclinic.com/invoke.cfm?id=DS00181
Hence you immune system causes the thyroid malfunction. The question is how do taking sythetic T3 cause an autoimmune disorder?

 

[gjohnson5]

OK so wer are saying the same thing, but I did not say that kids grow due to T3.
Doesn't T3 decline with age as well. So children would have faster metabolism due to high t3 but yet still grow due to GH and other hormones correct?

 

[poantrex]

I have my own glucose tester. And it doesn't measure in ng/dl. It measures blood glucose in mg/dl...so I'll assume that's a typo on your part.

T3 causes insulin resistance directly? Ok...that's a new one. No. T3 actually increases Beta-adrenergic function, i.e. the beta adrenoreceptors, Beta 1,2,3. These in turn release FFA's from the WAT's to be burned for fuel for bodily functions, instead of burning the existing blood glucose for fuel. Therefore blood glucose levels increase. This is you hyperglycaemia/insulin resistance...and is exactly what happens when you use GH as well. Solution. Use R-ALA to overcome it. Simple and effective. Your "problems" all have solutions if you apply yourself to the problem at hand.

Diabetes? Type I impossible. Obviously. Type II? I have seen ZERO literature to that effect. Hypothetically, if you where obese it could happen.

The only thing I agree with is the bone mineral de-calcificacion loss. But guess what? AAS increase bone mineral deposition. So, there goes that problem as well.

You guys are way too alarmist. I find it amusing that people find T3 very dangerous, and insulin a walk-in-the-park. Vice-versa if you ask me.
I wouldn't touch insulin with a 50 foot pole.

The cardiac/BP problem is the ony real concern I agree with. And only in those people who are genetically predisposed to high BP, or those who are taking an entire shelf of AAS, or lastly, have some type of cardiac defect. Arrythmia for example.

High BP can be counter-acted by 10g L-Taurine/day VERY effectively. Just ask around, and you'll see. I have seen dystolic drops of 20 points when on AAS due to L-Taurine. 120/80 120 = Dystolic 80 = systolic.

Obviously, if you have an existing cardiac problem, T3 is just not for you. that is a given.

Oh, I see...we should use r-ALA to overcome Thyroid hormone hyperglyecmia. Exogenous thyroid hormones stay in the body for several days, while r-ALA has a half life of around 10-15 minutes. So I guess everyone should be popping a couple pills every 15 minutes.

And maybe you haven't hard, but prolonged hyperglycemia leads to insulin resistance. Prolonged insulin resistance will become Type 2 diabetes. So one leads to the other, obviously. I don't even know why you even mentioned type 1 Diabetes, you just stated the obvious there

As far as bone loss, there are people reporting muscle loss regardless of the
amount of androgens they're using. And these are people using high doses of multiple compounds. So based on that, its not far fethced to assume that bone loss is also happening. There are obviously no studies of anyone using thyroid hormones and steroids in conjunction, so you can't state conclusively that androgens can totally offset bone loss. I'm inclined to say with the dosages guys around here use, probably not.

You know what? I'm done arguing about this. You think you can run thyroid hormones with no repercussions...then whatever. I've seen otherwise in many people who had the same attitude before using it, with a different attitude after having bloodtests done upon stopping T3 use.

 

[gjohnson5]

Why is that a bad idea? This medical report seems to indicate r-ala (just 600mg once a day) can help drop blood sugar and reduce sympoms in diabetic patients. http://www.heranswer.com/rala_neuropathy.asp The idea is to take r-ala throughout the day, not once a day. Then the half life of the drug becomes totally irrelevant.

OK , I'm tired of playing doctor and reading medical stuff from people who ain't doctors. Can we have an pragmatic conversation?

 

[poantrex]

Why is that a bad idea? This medical report seems to indicate r-ala (just 600mg once a day) can help drop blood sugar and reduce sympoms in diabetic patients. http://www.heranswer.com/rala_neuropathy.asp The idea is to take r-ala throughout the day, not once a day. Then the half life of the drug becomes totally irrelevant.

OK , I'm tired of playing doctor and reading medical stuff from people who ain't doctors. Can we have an pragmatic conversation?

Do you know what half life is? It gives you a good idea of how long it takes for a drug to be fully metabolized - in the case of r-ALA that time is absurdly short. It is good to cover cheat meals and what not, but it does not lower blood sugar long enough to be an effective means to prevent prolonged hyperglycemia.

r-ALA won't change H1AC or fasting blood glucose levels - which are both better measures of type 2 diabetes risk. It simply lowers postprandial blood glucose levels due to its very short half life. That means r-ALA is good for those dieting and wanting to lose some pounds, but its absurd to suggest that someone with severe insulin resistance or type 2 diabetes could benefit greatly from it. Doctors use actos, avandia, glucophage, or exogenous insulin for that purpose.

I don't see why you want to debate this anyway, you've already made your mind up and you'll have to live with any repercussions you may have. Just do me a favor and get a bloodtest to see where your TSH is 2 months after you stop using it (cytomel), then we can talk.

 

[gjohnson5]

Do you know what half life is? It gives you a good idea of how long it takes for a drug to be fully metabolized - in the case of r-ALA that time is absurdly short. It is good to cover cheat meals and what not, but it does not lower blood sugar long enough to be an effective means to prevent prolonged hyperglycemia.

r-ALA won't change H1AC or fasting blood glucose levels - which are both better measures of type 2 diabetes risk. It simply lowers postprandial blood glucose levels due to its very short half life. That means r-ALA is good for those dieting and wanting to lose some pounds, but its absurd to suggest that someone with severe insulin resistance or type 2 diabetes could benefit greatly from it. Doctors use actos, avandia, glucophage, or exogenous insulin for that purpose.

I don't see why you want to debate this anyway, you've already made your mind up and you'll have to live with any repercussions you may have. Just do me a favor and get a bloodtest to see where your TSH is 2 months after you stop using it (cytomel), then we can talk.

I'm always open to good information.
1. Yes if your fasting (which I have no reason to fast) then there's an issue. But where is the link between fasting glucose level and cycling sythetic T3. If someone takes sythetic t3 what does that have to do with a healthy person fasting glucose levels . nothing
2. type 2 diabetes. Has anyone ever gotten type 2 diabetes from take a cycle of sythetic T3??

Everything you've said is basically irrelevant to the issue at hand (taking sythetic T3), but thanks anyway

I'm done now

 

[poantrex]

I'm always open to good information.
1. Yes if your fasting (which I have no reason to fast) then there's an issue. But where is the link between fasting glucose level and cycling sythetic T3. If someone takes sythetic t3 what does that have to do with a healthy person fasting glucose levels . nothing
2. type 2 diabetes. Has anyone ever gotten type 2 diabetes from take a cycle of sythetic T3??

Everything you've said is basically irrelevant to the issue at hand (taking sythetic T3), but thanks anyway

I'm done now

GOOOOD GOD MAN, did that fly right over your head? JESUS CHRIST. Pay attention now:

Fasting blood glucose concentrations are a measure of ones insulin sensitivity - fasting blood glucose is tested to assess ones risk of acquiring diabetes.

see http://www.medterms.com/script/main/art.asp?articlekey=3393

Exogenous Thyroid hormones raise blood glucose for
the duration of time that it is in the body, hence FASTING Blood glucose will be higher.

The effect of thyroid hormones on blood insulin level and metabolic parameters in diabetic rats.

Szkudelski T, Michalski W, Szkudelska K.

Department of Animal Physiology and Biochemistry, University of Agriculture, 60-637 Wolynska 35, Poznan, Poland. [email protected]

The effect of exogenous thyroid hormones on blood insulin and metabolic parameters in diabetic rats was investigated. Three groups of rats were treated with streptozotocin (STZ; 50 mg/kg b.w., intravenously) and one group receiving only saline served as control. Beginning with the third day after STZ treatment, until the last day before decapitation, i.e. for 11 days, two groups of diabetic rats were treated with T3 (50 microg/kg b.w., i.p.) or T4 (250 microg/kg b.w., i.p.). After two weeks, STZ injected rats had lower body weight, hyperglycemia with a simultaneous drop in blood insulin and decrease of T3 and T4 concentrations in comparison to control animals. Liver glycogen content was also reduced, whereas serum lactate, free fatty acids, triglycerides and cholesterol were elevated. Exogenous thyroid hormones given to diabetic rats substantially attenuated hyperglycemia without any significant changes in blood insulin concentration. An additional reduction of body weight gain and depletion in liver glycogen stores were also observed. Thyroid hormones augmented serum lactate and cholesterol and had no beneficial effect on elevated free fatty acids and triglycerides. It can be concluded that in spite of partial restriction of hyperglycemia, thyroid hormones evoked several unfavourable changes strongly limiting their potential use in diabetes.

PMID: 14649872 [PubMed - indexed for MEDLINE]

See also

http://www.kingpharm.com/uploads/pdf_inserts/Cytomel_PI.pdf

All thyroid hormones affect blood sugar levels. (makes them higher) If you buy any brand of cytomel, there is a specific warning about this - this happens not only in diabetics, but EVERYONE that takes exogenous thyroid hormones. I myself have good insulin sensitivity, but when taking cytomel my blood sugar was ALWAYS 15-20mg/dl higher than normal. My fasting blood glucose went from around 70 to over 100.


Having PERSISTANT hyperglycemia will lead to insulin resistance, and if not put in check can lead to type II diabetes.

 

[jpl26]

GOOOOD GOD MAN, did that fly right over your head? JESUS CHRIST. Pay attention now:

Fasting blood glucose concentrations are a measure of ones insulin sensitivity - fasting blood glucose is tested to assess ones risk of acquiring diabetes.

[Quote/]

Again....Flat out wrong. You're regurgitating information you have seen on these boards that is utterly FALSE.

1. Normal BG readings are between 80-120, fasting normally being at about 60mg/dl.

2. He is not running a T3 cycle for life for god's sake, so the hyperglycaemia issue is completely irrelevant.

3. T3 attenuates(leaves your system) completely after 60hrs, but it's half-life is SHORT...only 4 hrs.

4. Now, I'll assume you're a competent bodybuilder, and you eat 4-5 meals/day.

5. The exogeneously ingested T3 will favor FFA burning over glucose burning, therefore glucose levels rise after a meal more than they normally would.

6. The solution is so simple it's just nonsensical to me you haven't grasped it yet.

The right optical isomer of ALA (R-ALA) at a dosage of 200mg/meal, will reduce the enhanced prost-pandial gucose response caused by the T3, by increasing the activity of the Glut-4's in your muscle and fat cells. Depending on the GI of your meal, your glucose response curve could be practically anyhting.

BUT, There is a slight delay in the release of insulin from the Beta cells in the Islet of langerhans in the Pancreas, when glucose is detected in the bloodstream.

You can take advantage of this delay with R-ALA. How? simply take your R-ALA 10 mins before a meal, so that it has time to translocate the intra-cellular glut-4's to the outside of the cell and join the rest of the extra-cellular glut-4's. Increasing their number anywhere from 30-50%.

Then, when you eat, and glucose levels rise because of the T3, insulin release is reduced because the R-ALA has had time to suck in glucose from the bloodstream into the cells, therefore reducing Blood glucose to normal, and then, the insulogenic surge that would have been higher with T3, is now lowered back to normal, or even below normal by the R-ALA. As glucose levels and insulin levels are normally dependent on one another.

Before answering any question, you really need to evaluate whether you have all the facts of the equation.

And btw, the half-life of R-ALA is not 10-15 min. It's 25-30min. You forget that R-ALA is both fat an water soluble (A phospholipid), and can both enter the cell (Fat soluble) and excrete glucose via water soluble means.

 

[shortstack]

GOOOOD GOD MAN, did that fly right over your head? JESUS CHRIST. Pay attention now:

Fasting blood glucose concentrations are a measure of ones insulin sensitivity - fasting blood glucose is tested to assess ones risk of acquiring diabetes.

[Quote/]

Again....Flat out wrong. You're regurgitating information you have seen on these boards that is utterly FALSE.

1. Normal BG readings are between 80-120, fasting normally being at about 60mg/dl.

2. He is not running a T3 cycle for life for god's sake, so the hyperglycaemia issue is completely irrelevant.

3. T3 attenuates(leaves your system) completely after 60hrs, but it's half-life is SHORT...only 4 hrs.

4. Now, I'll assume you're a competent bodybuilder, and you eat 4-5 meals/day.

5. The exogeneously ingested T3 will favor FFA burning over glucose burning, therefore glucose levels rise after a meal more than they normally would.

6. The solution is so simple it's just nonsensical to me you haven't grasped it yet.

The right optical isomer of ALA (R-ALA) at a dosage of 200mg/meal, will reduce the enhanced prost-pandial gucose response caused by the T3, by increasing the activity of the Glut-4's in your muscle and fat cells. Depending on the GI of your meal, your glucose response curve could be practically anyhting.

BUT, There is a slight delay in the release of insulin from the Beta cells in the Islet of langerhans in the Pancreas, when glucose is detected in the bloodstream.

You can take advantage of this delay with R-ALA. How? simply take your R-ALA 10 mins before a meal, so that it has time to translocate the intra-cellular glut-4's to the outside of the cell and join the rest of the extra-cellular glut-4's. Increasing their number anywhere from 30-50%.

Then, when you eat, and glucose levels rise because of the T3, insulin release is reduced because the R-ALA has had time to suck in glucose from the bloodstream into the cells, therefore reducing Blood glucose to normal, and then, the insulogenic surge that would have been higher with T3, is now lowered back to normal, or even below normal by the R-ALA. As glucose levels and insulin levels are normally dependent on one another.

Before answering any question, you really need to evaluate whether you have all the facts of the equation.

And btw, the half-life of R-ALA is not 10-15 min. It's 25-30min. You forget that R-ALA is both fat an water soluble (A phospholipid), and can both enter the cell (Fat soluble) and excrete glucose via water soluble means.

yes you have had some useful information, but alot of it is BS, as you say. i have family members with such and such thyroid situations, including graves which yes its an auto immune disease. for you to think you can fix a thyroid storm so easily is the most rediculas thing you have said through all your bs. i guess that why they put some people under strick isolation when in risk of thyroid storm huh??? you have done reaserch, but you need to do more, if you have an altered thyroid like graves disease, it may not take you as much as 150mcg to have a thyroid storm, which is very fatal, i dont give a fuck what you say.