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SlimJim300
New member
Messing with our thyroid is serious business. Hopefully this poll will help us see the truths, dangers and myths of synthetic thyroid hormone usage.
Thyroid dangers in reality? -- EVERYONE VOTES
- Thread starter SlimJim300
- Start date
your thyroid will be supressed after T3 cycle, no matter what. thyroid is like a gland like other glands in the endocrine system it regulates its self throug negative feedback mechanisim. you can still deal with rebounds by using 7-keto, guggle, L-tyrosin. also you should increas you claoric intake slightly because diet supress the thyroid naturaly. Plus using AAS after finishing T3 cycle is a good idea, because your thyroid will be supressed so you wil burn less calorie, so the extra unburnned cals will be good with AAS to back muscle.
HGH man
New member
I see an Endocrine Dr. since 86 because my pituitary has tumor. Part of what he had me on is syntroid. He has me do tests each year to see if it is doing what it is suppose to do,it is.About 5 months ago I decided to have him put me on Armour (T-4 and T-3) and get off Syntroid. According to tests that he put me on to see if Armour did it's thing,it did . I think Armour is better than snytroid,it is all natural .
CLOMIDCLOWN
New member
Yeah, what is the difference (healthwise) of synthetic vs. natural thyroid hormones. I noticed that the mexican version of Armour is natural.
celica
New member
This is a paper that my Dr. gives to his patients with slow thyroid-
Thyroid Dysfunction
At the clinic, we have seen a surprisingly large number of patients, mostly women, who present with an array of symptoms that have gone unaddressed, usually for many years- despite persistent complaining to their doctors. Many of these women have been told that they are crazy or at least have psychological problems and they should seek counsel. This is such a large part of our practice that we feel it warrants a discussion. Almost every day, without fail, someone comes in with complaints consistent with hypothyroidism:
Cold
Constipated
Dry skin
Hair falling out
Swelling and fluid retention
Difficulty in concentrating (brain fog)
Brittle nails
Inability to get fever
Weight gain (or can not get it off)
Coarse skin-especially heels
Yellow palms
Cold feet (the spouses will admit to this!)
These are but a few symptoms.
Hypothyroidism may be the most under-diagnosed condition in this country and may contribute to a world of sluggishness and malady that can easily be remedied with a $5 prescription. The problem is that physicians are not willing to trust their clinical judgement, and would rather place it in the hands of the laboratory technician. It has become commonplace to draw laboratory studies to make determinations on thyroid function. The gold standard has become the thyroid stimulating hormone (TSH). We have had many patients who presented to the Clinic, reporting that the other doctor did not lay a hand on them. He did, however do a lab test and determine that their function was normal and therefore so were they. Remind you that this was the specialist, who was being seen only after actually begging the primary care doctor. Most of these patients leave the specialist's office discouraged and disappointed, afterall, he is the specialist. Please do not be discouraged. The symptoms you are experiencing are real and can be abated. You are not crazy.
The problem with all this is the fact that the lab studies can be normal (and usually are most of the time), while the patient can truly be clinically hypothyroid. At the Clinic the majority (greater than 90%) of the patients with suspected hypothyroidism, who are eventually treated with replacement therapy, have normal lab studies.
Have you all become numbers? Why is it that after so many visits, experts have continued to keep you in the same condition that you have been in for years? Why is it that we have been so jaded by the establishment that we continue to ignore the basic facts that are emphasized (hopefully) in our medical training? That is......examine the patient. It is astounding how many people present to the Clinic claiming that no one laid their hands on them. The sad thing is that it is a hands-on diagnosis, and most of the institutions are teaching a hands-off approach.
The Basics
Hypothyroid = Low Thyroid Function
Hyperthyroid = Excessive Thyroid Function
Obviously, these diagnoses are on opposite sides of the spectrum-one high, and one low. However, while the diagnosis of hyperthyroidism can easily be made by laboratory studies, the diagnosis of hypothyroidism very rarely follows the labs. Why?
Without becoming too technical, the answers lie within the cells of the body. Inside of the cells of the body. From a laboratory stand point, we measure the thyroid function by peripheral blood work. We cannot determine moment by moment activity inside of the cells. This is where the true activity of the thyroid hormone is taking place. Thyroxine (or T4), which is produced in the thyroid gland in the neck, must travel to each and every one of the cells in the body and be converted into Tri-Iodothyronine (T3) inside of the cells of the body. The molecular difference between these two substances is essentially very minuscule (T3 has one less Iodine atom), while the functional difference is what makes this discussion pertinent. T3 is the active hormone. That is, it causes all of the metabolic activity that we discussed previously. T4 does not. It must be converted into T3.
Several things prevent the conversion of T4 to T3:
-Estrogen
-Steroids
-Dieting
-Sugar
-Stress
-Medicines
Why Can't They Fix It?
Perhaps this is just plain oversight. It would seem simple to understand that if you could not convert T4 to T3 then why would you continue to give T4 despite the continuation of symptoms? This is what is going on----if you are lucky enough to get your doctor to give you thyroid replacement medications. Most probably, he/she is giving you Synthroid. Problem? Synthroid is synthetic thyroid (syn/throid), and is composed only of T4. The missing component is T3 and needs to be replaced as well. At the Clinic we use Armour Thyroid. It is a desiccated thyroid hormone from the glands of pigs and cows, which contains all of the components (T4, T3, etc.) and is regulated by the United States Pharmacopoeia (USP). Many physicians will tell you that Armour is not regulated, and this is still quite confusing to us as it bears the USP seal and can be found in the Physician's Desk Reference (PDR). They can say what they want, but many thousands of patients have found great relief in replacement therapy with Armour, and a large percentage of those presented while on Synthroid. If you are on Synthroid and you have any of the symptoms listed at the top of the screen, perhaps you should be asking questions. If you have symptoms and your doctor will not address them, get another doctor.
This is not a monopoly.
Find someone who will listen to you. Do not give up. You are not crazy.
Easy Testing For Hypothyroidism:
Basal Body Temperature-One of the most common complaints from people with hypothyroidism is the fact that they have low temperature. Some patients cannot even generate a temperature when they are seriously ill. You may be or know someone who rarely exceeds 98 or 99 degrees at the height of their flu or pneumonia. This may be confusing for those of you who are going through menopause or peri-menopause, but that is for another discussion. In general, you know who you are (Many of you have been dealing with this since childhood). An easy way to evaluate this is to take your resting body temperatures first thing in the morning.
You will need a thermometer which is to be shaken down at night before retiring, and placed on the bedside table. Immediately upon awakening, without stirring (i.e., no excessive movements), reach for and place the thermometer in your mouth. Record the temperature each morning for 10 days. Many of you will be below 97 degrees. Do not let your doctor dismiss these findings, especially in the face of some of the aforementioned.
Exceptional reading for those interested will be found in a book by the late Dr. Broda Barnes entitled Hypothyroidism: The Unsuspected Illness.
Thyroid Dysfunction
At the clinic, we have seen a surprisingly large number of patients, mostly women, who present with an array of symptoms that have gone unaddressed, usually for many years- despite persistent complaining to their doctors. Many of these women have been told that they are crazy or at least have psychological problems and they should seek counsel. This is such a large part of our practice that we feel it warrants a discussion. Almost every day, without fail, someone comes in with complaints consistent with hypothyroidism:
Cold
Constipated
Dry skin
Hair falling out
Swelling and fluid retention
Difficulty in concentrating (brain fog)
Brittle nails
Inability to get fever
Weight gain (or can not get it off)
Coarse skin-especially heels
Yellow palms
Cold feet (the spouses will admit to this!)
These are but a few symptoms.
Hypothyroidism may be the most under-diagnosed condition in this country and may contribute to a world of sluggishness and malady that can easily be remedied with a $5 prescription. The problem is that physicians are not willing to trust their clinical judgement, and would rather place it in the hands of the laboratory technician. It has become commonplace to draw laboratory studies to make determinations on thyroid function. The gold standard has become the thyroid stimulating hormone (TSH). We have had many patients who presented to the Clinic, reporting that the other doctor did not lay a hand on them. He did, however do a lab test and determine that their function was normal and therefore so were they. Remind you that this was the specialist, who was being seen only after actually begging the primary care doctor. Most of these patients leave the specialist's office discouraged and disappointed, afterall, he is the specialist. Please do not be discouraged. The symptoms you are experiencing are real and can be abated. You are not crazy.
The problem with all this is the fact that the lab studies can be normal (and usually are most of the time), while the patient can truly be clinically hypothyroid. At the Clinic the majority (greater than 90%) of the patients with suspected hypothyroidism, who are eventually treated with replacement therapy, have normal lab studies.
Have you all become numbers? Why is it that after so many visits, experts have continued to keep you in the same condition that you have been in for years? Why is it that we have been so jaded by the establishment that we continue to ignore the basic facts that are emphasized (hopefully) in our medical training? That is......examine the patient. It is astounding how many people present to the Clinic claiming that no one laid their hands on them. The sad thing is that it is a hands-on diagnosis, and most of the institutions are teaching a hands-off approach.
The Basics
Hypothyroid = Low Thyroid Function
Hyperthyroid = Excessive Thyroid Function
Obviously, these diagnoses are on opposite sides of the spectrum-one high, and one low. However, while the diagnosis of hyperthyroidism can easily be made by laboratory studies, the diagnosis of hypothyroidism very rarely follows the labs. Why?
Without becoming too technical, the answers lie within the cells of the body. Inside of the cells of the body. From a laboratory stand point, we measure the thyroid function by peripheral blood work. We cannot determine moment by moment activity inside of the cells. This is where the true activity of the thyroid hormone is taking place. Thyroxine (or T4), which is produced in the thyroid gland in the neck, must travel to each and every one of the cells in the body and be converted into Tri-Iodothyronine (T3) inside of the cells of the body. The molecular difference between these two substances is essentially very minuscule (T3 has one less Iodine atom), while the functional difference is what makes this discussion pertinent. T3 is the active hormone. That is, it causes all of the metabolic activity that we discussed previously. T4 does not. It must be converted into T3.
Several things prevent the conversion of T4 to T3:
-Estrogen
-Steroids
-Dieting
-Sugar
-Stress
-Medicines
Why Can't They Fix It?
Perhaps this is just plain oversight. It would seem simple to understand that if you could not convert T4 to T3 then why would you continue to give T4 despite the continuation of symptoms? This is what is going on----if you are lucky enough to get your doctor to give you thyroid replacement medications. Most probably, he/she is giving you Synthroid. Problem? Synthroid is synthetic thyroid (syn/throid), and is composed only of T4. The missing component is T3 and needs to be replaced as well. At the Clinic we use Armour Thyroid. It is a desiccated thyroid hormone from the glands of pigs and cows, which contains all of the components (T4, T3, etc.) and is regulated by the United States Pharmacopoeia (USP). Many physicians will tell you that Armour is not regulated, and this is still quite confusing to us as it bears the USP seal and can be found in the Physician's Desk Reference (PDR). They can say what they want, but many thousands of patients have found great relief in replacement therapy with Armour, and a large percentage of those presented while on Synthroid. If you are on Synthroid and you have any of the symptoms listed at the top of the screen, perhaps you should be asking questions. If you have symptoms and your doctor will not address them, get another doctor.
This is not a monopoly.
Find someone who will listen to you. Do not give up. You are not crazy.
Easy Testing For Hypothyroidism:
Basal Body Temperature-One of the most common complaints from people with hypothyroidism is the fact that they have low temperature. Some patients cannot even generate a temperature when they are seriously ill. You may be or know someone who rarely exceeds 98 or 99 degrees at the height of their flu or pneumonia. This may be confusing for those of you who are going through menopause or peri-menopause, but that is for another discussion. In general, you know who you are (Many of you have been dealing with this since childhood). An easy way to evaluate this is to take your resting body temperatures first thing in the morning.
You will need a thermometer which is to be shaken down at night before retiring, and placed on the bedside table. Immediately upon awakening, without stirring (i.e., no excessive movements), reach for and place the thermometer in your mouth. Record the temperature each morning for 10 days. Many of you will be below 97 degrees. Do not let your doctor dismiss these findings, especially in the face of some of the aforementioned.
Exceptional reading for those interested will be found in a book by the late Dr. Broda Barnes entitled Hypothyroidism: The Unsuspected Illness.
juve
New member
Thyroid dangers are extremely overstated, oversimplified and misleading 
N Engl J Med 1975 Oct 2;293(14):681-4 Recovery of pituitary thyrotropic function after withdrawal of prolonged thyroid-suppression therapy. Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH
In 1951, Greer reported the pattern of recovery of thyroid function after stopping suppressive treatment with thyroid hormone in euthyroid [normal] subjects based on sequential measurements of their thyroidal uptake of radioiodine. He observed that after withdrawal of exogenous thyroid therapy, thyroid function, in terms of radioiodine uptake, returned to normal in most subjects within two weeks. He further observed that thyroid function returned as rapidly in those subjects whose glands had been depressed by several years of thyroid medication as it did in those whose gland had been depressed for only a few days
Patterns off recovery of the hypothalamic-pituitary-thyroid axis in patients taken of chronic thyroid therapy
LG Krugman, JM Hershman, IJ Chopra, GA Levine, E Pekary, DL Geffner and GN Chua Teco
To determine the patterns of recovery of the hypothalamic-pituitary- thyroid axis following long-term thyroid hormone therapy, TRH tests were performed on 8 euthyroid nongoitrous patients, 5 euthyroid goitrous patients, and 5 hypothyroid patients while they were taking full doses of thyroid hormone and 3, 7, 10, 14, 17, 21, 28, 35, 42, 49, and 56 days after stopping it. Serum TSH, T3, and T4 were measured before and at multiple intervals over a 4-h period after giving 500 mug TRH iv. In euthyroid non-goitrous patients, the mean duration of suppressed TSH response to TRH (maximum deltaTSH less than 8 muU/ml) was 12 +/- 4 (SE) days after stopping thyroid hormone and the mean time to recovery of normal TSH response to TRH (maximum deltaTSH greater than 8 muU/ml) was 16 +/- 5 days. None of the euthyroid nongoitrous patients ever hyperresponded to TRH; their average maximal deltaTSH was 24.5 +/- 2.2 muU/ml. Serum T4 fell below normal in 4 euthyroid non- goitrous patients, reaching lowest values at 4 to 28 days. While serum T4 was low, deltaTSH was subnormal. Normal increments of T4 and T3 after TRH occurred at 19 +/- 5 and 22 +/- 6 days, respectively. In the 5 goitrous patients, patterns of recovery of pituitary and thyroid function assessed by the same parameters were much less consistent. In the 5 hypothyroid patients, the mean duration of suppressed basal TSH and suppressed deltaTSH was 13 +/- 3 days; mean time to attain a supranormal basal TSH (greater than 8 muU/ml) was 16 +/- 4 days and to reach a supranormal deltaTSH (greater than 38 muU/ml) after TRH was 29 +/- 8 days. Following prolonged thyroid therapy in euthyroid patients, recovery of normal TSH responsiveness to TRH preceded recovery of the normal T3 and T4 response to TRH by 3 to 6 days. Basal serum TSH may be used to differentiate euthyroid from hypothyroid patients 35 days after withdrawal of thyroid therapy; the response to TRH does not improve this differentiation.
N Engl J Med 1975 Oct 2;293(14):681-4 Recovery of pituitary thyrotropic function after withdrawal of prolonged thyroid-suppression therapy. Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH
In 1951, Greer reported the pattern of recovery of thyroid function after stopping suppressive treatment with thyroid hormone in euthyroid [normal] subjects based on sequential measurements of their thyroidal uptake of radioiodine. He observed that after withdrawal of exogenous thyroid therapy, thyroid function, in terms of radioiodine uptake, returned to normal in most subjects within two weeks. He further observed that thyroid function returned as rapidly in those subjects whose glands had been depressed by several years of thyroid medication as it did in those whose gland had been depressed for only a few days
Patterns off recovery of the hypothalamic-pituitary-thyroid axis in patients taken of chronic thyroid therapy
LG Krugman, JM Hershman, IJ Chopra, GA Levine, E Pekary, DL Geffner and GN Chua Teco
To determine the patterns of recovery of the hypothalamic-pituitary- thyroid axis following long-term thyroid hormone therapy, TRH tests were performed on 8 euthyroid nongoitrous patients, 5 euthyroid goitrous patients, and 5 hypothyroid patients while they were taking full doses of thyroid hormone and 3, 7, 10, 14, 17, 21, 28, 35, 42, 49, and 56 days after stopping it. Serum TSH, T3, and T4 were measured before and at multiple intervals over a 4-h period after giving 500 mug TRH iv. In euthyroid non-goitrous patients, the mean duration of suppressed TSH response to TRH (maximum deltaTSH less than 8 muU/ml) was 12 +/- 4 (SE) days after stopping thyroid hormone and the mean time to recovery of normal TSH response to TRH (maximum deltaTSH greater than 8 muU/ml) was 16 +/- 5 days. None of the euthyroid nongoitrous patients ever hyperresponded to TRH; their average maximal deltaTSH was 24.5 +/- 2.2 muU/ml. Serum T4 fell below normal in 4 euthyroid non- goitrous patients, reaching lowest values at 4 to 28 days. While serum T4 was low, deltaTSH was subnormal. Normal increments of T4 and T3 after TRH occurred at 19 +/- 5 and 22 +/- 6 days, respectively. In the 5 goitrous patients, patterns of recovery of pituitary and thyroid function assessed by the same parameters were much less consistent. In the 5 hypothyroid patients, the mean duration of suppressed basal TSH and suppressed deltaTSH was 13 +/- 3 days; mean time to attain a supranormal basal TSH (greater than 8 muU/ml) was 16 +/- 4 days and to reach a supranormal deltaTSH (greater than 38 muU/ml) after TRH was 29 +/- 8 days. Following prolonged thyroid therapy in euthyroid patients, recovery of normal TSH responsiveness to TRH preceded recovery of the normal T3 and T4 response to TRH by 3 to 6 days. Basal serum TSH may be used to differentiate euthyroid from hypothyroid patients 35 days after withdrawal of thyroid therapy; the response to TRH does not improve this differentiation.
i don't know either. its the same thing with killing a man's own testosterone production capabaility. many are so bothered with bringing their own production up after a cycle, but why? its obviously low otherwise there would have been no reason to inject testosterone in the first time? now whats the benefit of having low test levels again? i would take t4/t3 if i had lower than normal thryoid levels immediately and would never stop. its another story with HGH which is very expensive but thyroid hormones and testosterone are dirt cheap. maybe people are scared by "for the rest of your life"? but i have to eat, drink and train for the rest of my life also, and that does not scare me at all. so why bother?brunette said:
Taking thyroid medication is not so simple as to take 1 pill a day. Dosage requirements will change frequently depending on the degree that natural production is supressed, and you will have to get bloodtests monthly or bi-monthly to check your status. I know my mother has to take thyroid medication and she has had 3 dosage changes in the past 6 months just to keep her in the normal range. Due to the short attenuation of cytomel in the human body, taking it 2 times a day on an empty stomach is required...which can be a pain in the ass.
Also, thyroid medication causes hyperglycemia. Its really better to avoid messing with the thyroid if at all possible.
Also, thyroid medication causes hyperglycemia. Its really better to avoid messing with the thyroid if at all possible.
HGH man
New member
Poantrex, is your mother heavy? I know a couple of folks that exceed the limits of the scale and they too have to get tested every month. My niece is one that is like that. She has been on syntroid since 98 and had her doseage increased 8 times now. Because she is overweight. Eventually she will get on diabetes medicine. Try to tell her and she will just said ,Shut up. End of story.
Well I've used T3 3 or 4 times now, between 25-75mcg/day. Never exceeded that dosage for long, and never for more than 4 weeks total. Never noticed any rebound or fat gain afterwards or any muscle loss while on. However, I could never really tell much in the benefit area either. I'll just stick with gear for now, maybe if I get to 220lbs I'll need some T3 along with mega-gear to grow, but not yet.
gjohnson5
New member
I took cytomel for the first time today and I have to say , it felt good not to have to go to sleep right after work or getting tired just walking around the mall. BTW I am about 20% bodyfat. Hopefully after a 6week cycle I should be alot leaner and not be in need of full dosages of T3.
As far as the blood sugar levels go , I think glucorrel-r should be a good complement to rising blood sugar levels along with an increased protein (1.5g per lean muscle mass) and increased fats via nuts in the diet should give muscle gains.
Poantrex , after doing my research here and elsewhere , you seem anti t3. Are you the 1 person who votes "my thyroid is fucked for life"?
As far as the blood sugar levels go , I think glucorrel-r should be a good complement to rising blood sugar levels along with an increased protein (1.5g per lean muscle mass) and increased fats via nuts in the diet should give muscle gains.
Poantrex , after doing my research here and elsewhere , you seem anti t3. Are you the 1 person who votes "my thyroid is fucked for life"?
U
Ulcasterdropout
Guest
bump
S
satchboogie
Guest
my t3 cycles are 2-3 weeks long at peak at 50mcg per day.. down to 25mcg and out.
never a problem.
never a problem.
gjohnson5
New member
satchboogie said:
Hey Satch , why do you use T3 instead of clen , or cutting AAS that won't cause a permanent failure? Since you're pretty lean, I would think T3 would be counter productive to you.
As far as the permanent failure , you can live without a thyroid. I have a relative who's had thier removed and has lived the last 55 years without any problems.
shortstack
Banned
ive been through this b4. thyroid in most part is ok if you do it properly with bloodwork. but, if your irrisponsible it can fuck you up bad. dont take thyroid with first checking your bloodwork before. there are a million un-dioagnosed thyroid conditions in the U.S and if you have one of them and take t3 you could set yourself up for an unwelcome future.
jpl26
New member
SlimJim300 said:
The only problem with using T3 is catabolism and ramping down. As T3 works through proteolytic pathways, you need to use an AAS, and consume enough protein.
It's fairly easy:
1. T3 = increases the burning of fats, carbs and protein
2. Without AAS, your body loses protein(muscle), because it can't synthesize enough protein to off-set the increase in protein degradation produced by the T3.
3. With AAS added to the mix, your body is now in an enhanced state. It can synthesize far more protein then normal.(This is what AAS do. Increase protein synthesis above and beyond normal). This off-sets T3's catabolic effects. and in some cases(Like Fina for example), you can actually gain a bit of muscle if you dial your diet just right.
4. And the BONUS. T3 increases FAT burning as well. So, if you eat enough protein (1.5g/lb of BW), take a moderate dose of AAS(This is dependent on how much T3 you take), you will lose fat, and remain with all your muscle intact.
5. I also have to say that once supressed, YOU ARE SUPPRESSED. Doesn't matter if you're on 150mcg/day or 50mcg/day, your TSH levels are going to be below normal...Normal being (0.8-5.5), through experience they will probably be around 0.1 or 0.2. But there is no need to panic, you CANNOT BURN YOUR THYROID OUT. I'll explain.
6. People with muscular disorders, who's muscles grow out of control (No, this is not good, it can cause great pain because the nerves get compressed. I don't remember the exact name of the disorder, but I'll look it up later.), take around 400mcg of T3 in order to control the muscle growth. As I said before T3 is proteolytic and eats muscle, so that is how they control it. However, the point is, after cessation (And they use this dosage for years on end.), their thyroid recovers in 8-12 weeks. So, burning your thyroid out is IMO just not possible.
7. Ramping down. if you don't ramp down, you're going to end up your T3 cycle suppressed, and with low TSH. It'll take the thyroid roughly 8 weeks to get back up to normal. This is not fun..lethargy, fat deposition, the works.
So, please ramp down. It's fairly easy and it saves you the trouble of 8 weeks of low T3 levels, which aren't fun at all. Take approximately 4 weeks to ramp down from 50mcg to 12.5mcg, ramping down 12.5mcg/week. if you want to go the extra mile, and have a very good pill cutter, you can go down to 6.25mcg for another week....but breaking those tiny T3 pills (25mcg) into 4 squares is almost next to impossible...they tend to just shatter. But if you can do it, by all means, give it a shot.
8. Once ramped down.....there will be a brief 1-2 week period where T3 levels, and TSH levels will be slightly sub-normal. Here is where supplements come in. The three best are:
1. Acetyl-l-Tyrosine ( For thyroid hormone production and alertness)
2. Green Tea...to maintain a thermogenic state that does not favor fat deposition due to slightly lowered T3 levels. And is not an adrenergic drug (Non-stimulative), therfore has no effect on the thyroid. About 900mg ECGC's/day is good enough. You can go higher if you wish, but some people have reported slight anxiety at higher doses.
4. And the most important: 7-oxo-DHEA..I prefer the liquid form to the pill/powder form because of better absorption, but in pill form 300mg/day.
7-oxo-DHEA btw increases the levels of T3 and T4 ENDOGENEOUSLY, which is obviously a huge boost during those 2 weeks.
And after those 2 weeks....your T3, T4, and TSH levels should be right on spec.
With the current crop of new supplements which have much better absorption than the old crop, a T3 cycle is really not as dangerous as you think. You just need the right supplements and a good plan of attack.
shortstack
Banned
jpl26 said:
if you think the only risks of taking thyroid are catabolism and ramping down, you have alot to learn
Agreed! There are far too many people that think they can run this shit without repercussions! And most of these people don't get bloodtests to see where they stand after doing the shit. I can almost guarantee most people will have a higher TSH baseline after doing a high dosed cycle of T3, whether they ramp up and down slowly or not. And you won't feel signifigant side effects of having a higher TSH, either.
Thats a problem, and the other problem is that most docs will find their thyroid in the "normal" range and declare that their thyroid is fine...Uhm, normal healthy range for TSH is between 1 -2, 3 and above is the range where most of those 60 and older fall! Definitely not ideal. I've seen a lot of posts from people that have haad their bloodwork done after doing cytomel, and their TSH was above 3....which is not good, at all.
Thats a problem, and the other problem is that most docs will find their thyroid in the "normal" range and declare that their thyroid is fine...Uhm, normal healthy range for TSH is between 1 -2, 3 and above is the range where most of those 60 and older fall! Definitely not ideal. I've seen a lot of posts from people that have haad their bloodwork done after doing cytomel, and their TSH was above 3....which is not good, at all.
I am seeing the general mind set of people on this forum to push the limits - on every thing.
If you are pushing limits on anabolics, then let your other systems run normally and adjust to it, and balance any negative effects.
I know human physiology better than 90% of doctors.
Push limits only on one thing at a time.
It is fool hardy to think that you know everything. When studying human body, the more you know, the more you realise how little you know.
Even great minds can be fooled - think about all those medicines that are withdrawn. We were hearing great things about Vioox, Celebrex and medicines in this category since 15 years, and people had great expectations. Look what happened.
Treat your body with more respect.
If you are pushing limits on anabolics, then let your other systems run normally and adjust to it, and balance any negative effects.
I know human physiology better than 90% of doctors.
Push limits only on one thing at a time.
It is fool hardy to think that you know everything. When studying human body, the more you know, the more you realise how little you know.
Even great minds can be fooled - think about all those medicines that are withdrawn. We were hearing great things about Vioox, Celebrex and medicines in this category since 15 years, and people had great expectations. Look what happened.
Treat your body with more respect.
gjohnson5
New member
jpl26 said:
Don't you think you 1 and 2 are a far fetched. The automatic presence of T3 causes someone to go catabolic?? That would mean that we are all catabolic due to thyroid's natural production. Children grow and get bigger magically without any AAS or increased diet even though children have raging hormones. Definitly some generalizations in those 2 items.
We need need to take into account
1. The person's natural T3 count
2. The dosage they are taking
3. The person's diet
From my understanding of the subject (which is limitied I will say)
1. amino acids
2. glutamine peptides
3. insulin / IGF-1 / GH
4. http://www.nutriline.org/methoxy.htm
I didn't know methoxy increased protein synthesis but the link seems to say that it does. But there are other chemicals that increase protein sythesis besides AAS , this is for sure.
I have read alot about this T3 / catabolism issue and want to learn more in terms of dosages of T3 and results.
shortstack
Banned
gjohnson5 said:
honestly, i had a big disscusiion about this, it was either on here or anabolicreview, and i really dont want to get into it again... do a search
jpl26
New member
shortstack said:
Actually, not really. And there is no need to patronize.
The small little post was meant as a general guideline for a healthy adult.
I can go into cardiac problems associated with T3 if you want, or bone loss associated with T3, but those are cases where the person WAS NOT in a healthy state to begin with.
But, by all means......educate me.
shortstack
Banned
jpl26 said:Actually, not really. And there is no need to patronize.
The small little post was meant as a general guideline for a healthy adult.
I can go into cardiac problems associated with T3 if you want, or bone loss associated with T3, but those are cases where the person WAS NOT in a healthy state to begin with.
But, by all means......educate me.
why do people always want the easy way to answers. just do some reaserch buddy.
your statment is very un-educated.... first of all, a healthy person,can still have a thyroid disorder or disease, this beng why there are ove a MILLION un-diagnosed cases in the US. so basically if someone where to be un-educated and have say.....graves disease (a disease were you have to much thyroid) and say to themselves oh well im pretty healthy im gonna take some t3. you know what could happen...... actually alot of things, maybe and most likeley a "thyroid storm" in which it has a fatality rating of around close to 100%. but no you have all the answers so go ahead buddy, take your thyroid cause you think your healthy, but do me a favor, dont imply that to people that they can take t3 if they think there healthy.
jpl26 said:Actually, not really. And there is no need to patronize.
The small little post was meant as a general guideline for a healthy adult.
I can go into cardiac problems associated with T3 if you want, or bone loss associated with T3, but those are cases where the person WAS NOT in a healthy state to begin with.
But, by all means......educate me.
What? You're absolutely wrong about thyroid hormones not causing weaker bones. Its a WELL documented side effect of thyroxine and triiodothyronine.
In addition, thyroid hormones cause massive hyperglycemia (my glucose is always 20ng/dl higher when taking them) and can cause cardiac problems and high BP in some people.
Bone loss and hyperglycemia concern me the most....hyperglycemia produces a HOST of unwanted effects which can lead to (among other things) insulin resistance and diabetes.
shortstack
Banned
gjohnson5 said:
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.
jpl26
New member
shortstack said:
When you make too much thyroid = hyperthyroidism. Easily countered with beta-blockers such as propanolol, which is what people who have abnormal(high) thyroid production normally take.
And if you're going to try to prove something, at least use some science. Not your opinions, which are baseless.
And Graves Disease? Never ceases to make me wonder how people always single out cases that are so specific to be completely nonsensical to the gist of the thread. Graves disease has a completely different mode of action.
A brief little explanation:
1. Thyroid disease in anormal person? Sure....if you have ZERO iodine in y
your diet. And don't get any from supplements.
Do you even know how the thyroid works?
Only 20% of the circulating T3 in your blood plasma is from endogeneous production. The rest(80%) comes, from the conversion of T4 to T3 via the de-iodinase enzyme(iodine based). This enzyme basically cleaves of an iodine molecule from T4 to make it into T3.
So, if you don't take iodine in any shape or form T4 to T3 conversion is reduced, and you end up with less T3 circulating in your blood plasma.
2. ESS Syndrome. Very common in athletes. Their natural T4 to T3 conversion does not happen efficiently. The problem (due to a whole host of factors), is that the T4 gets converted to rT3 (reverse T3). rT3 is the optical isomer of T3, and is metabolically inactive, therefore, your plasma T3 levels will be low again.
3. Graves disease is not a problem with the thyroid itself. It's a problem with the persons TSH, which is very high. Therefore, it indirectly stimulates the production of too many thyroid hormones. So again, your statement has no basis.
You're welcome to try to debate this with me, but don't ever tell me I haven't done my research...because that is ridiculous.
And lol@thyroid storm...sure, if you took 600mcg in one go.
And near 100% fatality? That number is complete and utter BS. No offense. As I stated before Beta-blockers reduce thyroid hormone production significantly. Run a search for propanolol and it's uses. It's the most common drug in treating thyro-toxicosis in patients with hyperthyroidism.
And btw, as T3 increases your metabolism, it also lowers your total cholesterol. Which again is beneficial.
Gist of my post: T3 has many, many uses in our pharmaceutical arsenal, but just because you don't understand it's mechanisms, doesn't mean you have to have to be afraid of it, and make other people afraid of it.
jpl26
New member
[Quote/]
Don't you think you 1 and 2 are a far fetched. The automatic presence of T3 causes someone to go catabolic?? That would mean that we are all catabolic due to thyroid's natural production.
At homeostasis, when your body is in equlibrium, protein turnover = protein degradation. Your body synthesis protein from the AA's you eat btw.
Children grow and get bigger magically without any AAS or increased diet even though children have raging hormones. Definitly some generalizations in those 2 items.
No generalizations whatsoever. and what makes children grow isn't T3, it's their VERY HIGH levels of GH. If you look at a GH vs time(in years) graph,
GH levels are amazingly high at 1-3 years old, before reaching a maximum at 18-21, and then levelling off steadily downwards as we get older.
A 20 year old has twice the levels of GH as a 40 year old. Put it that way.
We need need to take into account
1. The person's natural T3 count
Not necessary. Once you start a T3 cycle, your endogeneous production of T3 is basically zero. The only reason I can fathom for knowing your natural T3 levels, is to compare them to post-T3 cycle level ones.
2. The dosage they are taking
Agreed. High T3 intake = A need for more androgenic steroids.
Low T3 intake = you can use milder steroids.
3. The person's diet
Can't argue with that one. You got to get your protein intake in the 1.5-2.0g/lb range(of your bodyweight), to off-set the exogeneous T3's catabolic effects, and reap it's fat burning rewards. But again, this is very much dose-dependent.
From my understanding of the subject (which is limitied I will say)
1. amino acids (They don't do much at all)
2. glutamine peptides (I agree.)
3. insulin / IGF-1 / GH (I agree. But very dangerous for beginners..because of the insulin)
4. http://www.nutriline.org/methoxy.htm
I didn't know methoxy increased protein synthesis but the link seems to say that it does. But there are other chemicals that increase protein sythesis besides AAS , this is for sure.
Methoxy-Flavone is a known bad supplement. Never get your information from any type of web source. Get it from peer reviewed journals.
I have read alot about this T3 / catabolism issue and want to learn more in terms of dosages of T3 and results.[/Quote]
Don't you think you 1 and 2 are a far fetched. The automatic presence of T3 causes someone to go catabolic?? That would mean that we are all catabolic due to thyroid's natural production.
At homeostasis, when your body is in equlibrium, protein turnover = protein degradation. Your body synthesis protein from the AA's you eat btw.
Children grow and get bigger magically without any AAS or increased diet even though children have raging hormones. Definitly some generalizations in those 2 items.
No generalizations whatsoever. and what makes children grow isn't T3, it's their VERY HIGH levels of GH. If you look at a GH vs time(in years) graph,
GH levels are amazingly high at 1-3 years old, before reaching a maximum at 18-21, and then levelling off steadily downwards as we get older.
A 20 year old has twice the levels of GH as a 40 year old. Put it that way.
We need need to take into account
1. The person's natural T3 count
Not necessary. Once you start a T3 cycle, your endogeneous production of T3 is basically zero. The only reason I can fathom for knowing your natural T3 levels, is to compare them to post-T3 cycle level ones.
2. The dosage they are taking
Agreed. High T3 intake = A need for more androgenic steroids.
Low T3 intake = you can use milder steroids.
3. The person's diet
Can't argue with that one. You got to get your protein intake in the 1.5-2.0g/lb range(of your bodyweight), to off-set the exogeneous T3's catabolic effects, and reap it's fat burning rewards. But again, this is very much dose-dependent.
From my understanding of the subject (which is limitied I will say)
1. amino acids (They don't do much at all)
2. glutamine peptides (I agree.)
3. insulin / IGF-1 / GH (I agree. But very dangerous for beginners..because of the insulin)
4. http://www.nutriline.org/methoxy.htm
I didn't know methoxy increased protein synthesis but the link seems to say that it does. But there are other chemicals that increase protein sythesis besides AAS , this is for sure.
Methoxy-Flavone is a known bad supplement. Never get your information from any type of web source. Get it from peer reviewed journals.
I have read alot about this T3 / catabolism issue and want to learn more in terms of dosages of T3 and results.[/Quote]
jpl26
New member
poantrex said:
I have no idea where you get your information, but the clinical spectrum for TSH and T3 is:
Normal TSH: (0.4 uIU/ml - 5.5 uI/ml)
Normal T3(total): Between 60 -181 ng/dl
They are both directly related in most cases. Low TSH = Low T3, as the thyroid is not stimulated enough. In cases where you self-administer T3, endogenous T3 and T4 production drops to zero, and your TSH to about 0.1 or 0.2.
How do i now this? I take blood tests. Which most people don't.
After cessation of my T3 cycles, without the 2 week endogeneous T3 cycle booster cycle included, my normal total T3 and TSH are 80ng/dl, and 1.1 uIU/ml respectively.
Knowing how your body works is step 1 to becoming a better bodybuilder/athlete. And if you don't get blood tests done, I don't think you should be using AAS. Blood tests are probably the most overlooked component of any AAS/T3 etc.. cycle.
jpl26
New member
poantrex said:
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.
biggeek
New member
jpl26 said:
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
New member
shortstack said:
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?
jpl26 said:
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
New member
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?
OK , I'm tired of playing doctor and reading medical stuff from people who ain't doctors. Can we have an pragmatic conversation?
gjohnson5 said:
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
New member
poantrex said:
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
gjohnson5 said:
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.
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jpl26
New member
poantrex said: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
Banned
jpl26 said:poantrex said: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.
jpl26 said:poantrex said: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.
Whatever you say fonz.
1. Normal BG readings are between 80-120, fasting normally being at about 60mg/dl.
1. The "normal range" for fasting blood glucose is 65-120. 90 and above are considered insulin resistance. I never said that 80-120 isn't normal, although i would be very leery of the upper end of tthat at fasting.
2. Nobody said he was. But, thats not to say damage can be done during that time frame.
3. Hyperglycemia is prolonged while using any type of thyroid hormone. It generally remains for as long as the drug remains in the body.
4. ...
5. Thats not even the fucking point. The point is, exogenous thyroid hormones cause hyperglyecmia and it is NOT Just after meals like you are trying to say. I have seen this in myself 24 hours after a dose of cytomel - strangely high blood glucose readings.
6. Due to #5, r-ALA will only be helpful for prevening postprandial hyperglycemia. It won't offset prolonged hyperglycemia unless you pop a couple of pills every 15 minutes.
7. The half life of r-ALA. Not that it makes a huge difference, because whether the half life is 15 minutes or 25 minutes, it aint gonna help someone with insulin resistance problems or diabetes. Aside from preventing surges in blood glucose after meals. But, I remember macrophage specifically stating that the half life of r-ALA is around 10 minutes.
8. Its interesting that you don't dispute the issue with bone loss. Hmm.
jpl26
New member
poantrex said:jpl26 said:poantrex said:GOOOOD GOD MAN, did that fly right over your head? JESUS CHRIST. Pay attention now:
[Quote/]
8. Its interesting that you don't dispute the issue with bone loss. Hmm.
I will never understand why people never use some small amount of logic before feeding more fuel to the fire.
Let's see:
T3 ALONE = Bone dcalcification...via mineral loss I never disputed this.
BUT, T3 is meant to be run with AAS. Hope you got this rather simple point.
And guess what? As I stated before, AAS INCREASE mineral bone deposition and off-set any bad effects from ther T3.
Want some proof?
Ok. And this on ELDERLY women, which suffer from osteoporosis, far worse than anything T3 can do to ant BB'er in a short-term 8-week T3 cycle.
1: J Bone Joint Surg Br. 2002 May;84(4):497-503. Related Articles, Links
Positive effects of anabolic steroids, vitamin D and calcium on muscle mass, bone mineral density and clinical function after a hip fracture. A randomised study of 63 women.
Hedstrom M, Sjoberg K, Brosjo E, Astrom K, Sjoberg H, Dalen N.
Department of Orthopaedics, Karolinska Institute and Danderyd Hospital, Sweden.
A total of 63 women who had an operation for a fracture of the hip was randomly allocated to one year of treatment either with anabolic steroids, vitamin D and calcium (anabolic group) or with calcium only (control group). The thigh muscle volume was measured by quantitative CT. The bone mineral density of the hip, femur and tibia was assessed by quantitative CT and dual-energy x-ray absorptiometry and of the heel by quantitative ultrasound. Quantitative CT showed that the anabolic group did not lose muscle volume during the first 12 months whereas the control group did (p<0.01). There was less bone loss in the proximal tibia in the anabolic group than in the control group. The speed of gait and the Harris hip score were significantly better in the anabolic group after six and 12 months. Anabolic steroids, even in this moderate dose, given in combination with vitamin D and calcium had a beneficial effect on muscle volume, bone mineral density and clinical function in this group of elderly women.
Publication Types:
Clinical Trial
Randomized Controlled Trial
PMID: 12043767 [PubMed - indexed for MEDLINE]
Next time, try to throw something at me that I won't chew up.
Ta-da.
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jpl26
New member
shortstack said:
Look brainiac.....stop trying to back-peddal.
You equated Graves disease with the use of exogeneously administered T3, not knowing it had a completely DIFFERENT mode of action...it's an auto-immune disease.
That by itself, renders any opinion of yours non-existent on the subject.
jpl26
New member
poantrex said: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
The effect of thyroid hormones on blood insulin level and metabolic parameters in diabetic rats.
I think your use of studies says it all. We aren't diabetic rats.
Your argument would have a little bit more credibility if you had used HUMAN diabetic individuals, but you didn't. So that's that.Next time, use the proper studies that are relevant to the discussion at hand.
Fonz, you can browse pubmed and find a study. You're such a braniac...I am impressed. BUT where is the study of simultaneous Cytomel and anabolic steroid use? Eh? That study you posted means nothing.
There is no proof that steroids can offset thyroid hormone bone loss - and in fact, bone loss is still likely because most people are reporting muscle loss with thyroid hormone use. Even with high doses of multiple compounds, like I mentioned earlier. If muscle loss is occuring, bone loss is also likely to occur.
Next time, use the proper studies that are relevant to the discussion at hand.
By the way - if you knew a damn thing about pharmacology, you'd know that rats mimic humans in nearly every way when it comes to drug reactions. I can't think of a single exception to that. Besides which, if you doubt that thyroid hormones cause increased blood sugar, simply look at any insert to prescribed thyroxine or triiodothyronine, in which it explicitly states that blood sugar will be higher during use (for all individuals).
There is no proof that steroids can offset thyroid hormone bone loss - and in fact, bone loss is still likely because most people are reporting muscle loss with thyroid hormone use. Even with high doses of multiple compounds, like I mentioned earlier. If muscle loss is occuring, bone loss is also likely to occur.
Next time, use the proper studies that are relevant to the discussion at hand.
By the way - if you knew a damn thing about pharmacology, you'd know that rats mimic humans in nearly every way when it comes to drug reactions. I can't think of a single exception to that. Besides which, if you doubt that thyroid hormones cause increased blood sugar, simply look at any insert to prescribed thyroxine or triiodothyronine, in which it explicitly states that blood sugar will be higher during use (for all individuals).
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shortstack
Banned
poantrex said:Fonz, you can browse pubmed and find a study. You're such a braniac...I am impressed. BUT where is the study of simultaneous Cytomel and anabolic steroid use? Eh? That study you posted means nothing.
There is no proof that steroids can offset thyroid hormone bone loss - and in fact, bone loss is still likely because most people are reporting muscle loss with thyroid hormone use. Even with high doses of multiple compounds, like I mentioned earlier. If muscle loss is occuring, bone loss is also likely to occur.
Next time, use the proper studies that are relevant to the discussion at hand.
By the way - if you knew a damn thing about pharmacology, you'd know that rats mimic humans in nearly every way when it comes to drug reactions. I can't think of a single exception to that. Besides which, if you doubt that thyroid hormones cause increased blood sugar, simply look at any insert to prescribed thyroxine or triiodothyronine, in which it explicitly states that blood sugar will be higher during use (for all individuals).
oh thats the ab guy, lol.....
nuff said.
jpl26
New member
poantrex said:Fonz, you can browse pubmed and find a study. You're such a braniac...I am impressed. BUT where is the study of simultaneous Cytomel and anabolic steroid use? Eh? That study you posted means nothing.
There is no proof that steroids can offset thyroid hormone bone loss - and in fact, bone loss is still likely because most people are reporting muscle loss with thyroid hormone use. Even with high doses of multiple compounds, like I mentioned earlier. If muscle loss is occuring, bone loss is also likely to occur.
Next time, use the proper studies that are relevant to the discussion at hand.
By the way - if you knew a damn thing about pharmacology, you'd know that rats mimic humans in nearly every way when it comes to drug reactions. I can't think of a single exception to that. Besides which, if you doubt that thyroid hormones cause increased blood sugar, simply look at any insert to prescribed thyroxine or triiodothyronine, in which it explicitly states that blood sugar will be higher during use (for all individuals).
"nearly every way".......
Rats, pigs, mice etc... I deleted about 5,000 studies on my computer on them.
What counts is human studies. Allthough I'll admit they are hard to find, they are really the only completely and totally useful piece of information.
Non-human studies make you extrapolate your answers in a statistical fashion. That leads to errors.
I'd rather not have to go along with those errors.
But Ok, use your rat studies. Whatever floats your boat. It's your opinion.
At least you have one. The other guy, doesn't even know what we're talking about. Which is amusing.
You know, my biggest problem with exogenous thyroid hormone use is that post treatment TSH will likely be higher. It won't always be out of normal range assuming the person in question is eating a hypercaloric diet and exercising, but it is often higher. For example, if one individual has a TSH of 1.5 before doing anything and then a TSH of 3 after stopping cytomel use, is that ideal? (I've seen this happen) No its not ideal, and thats why there are far better means of losing weight in my opinion. Personally morning cardio always makes me feel better and i'm sure as hell its better for my long term health than using a shitload of stimulants and thyroid hormones.
I think a lot of people that get bloodtests done don't even realize this is happening, because they get their bloodtest result and their doctor sees that their TSH is in the "normal range". Normal range is NOT always normal for a healthy person. Its like saying a testosterone level of 300ng/dl is fine because its in the "normal range". There are 80 year old men that produce more than that naturally, and I sure as hell don't want to be at that level for the rest of my life.
I think a lot of people that get bloodtests done don't even realize this is happening, because they get their bloodtest result and their doctor sees that their TSH is in the "normal range". Normal range is NOT always normal for a healthy person. Its like saying a testosterone level of 300ng/dl is fine because its in the "normal range". There are 80 year old men that produce more than that naturally, and I sure as hell don't want to be at that level for the rest of my life.
gjohnson5
New member
poantrex said:
I want you to reread your own words. The highlighted word is PERSISTENT. So if a person does a 2 week to 1 month cycle at 50mcg what proof is there that the person will attain a significant amount of insulin resistance? Basically your trying to make the jump between a cycle of T3 and a chronic problem. You haven't posted any information which would lead me (or other apparantly) to believe that there is a connection between a cycle and a person with legitimate hyperthyroid.
The same is true about your bone loss issue. You study conducted on rats has little signifigance in this context when we are talking about humans.
If you have some information dealing with humans taking synthetic hormone and becoming diabetic , then I will read it with great interest and stop my cycle immediently.
jpl26
New member
Ok, I found a rather interesting study on bodybuilders and T3 levels.
1: J Clin Endocrinol Metab. 1993 Apr;76(4):1069-71. Related Articles, Links
Ingestion of androgenic-anabolic steroids induces mild thyroidal impairment in male body builders.
Deyssig R, Weissel M.
Third Medical University Clinic, Vienna, Austria.
Self-administration of very high doses of androgenic anabolic steroids is common use in power athletes because of their favorable effect on performance. Since androgenic steroids decrease serum T4-binding globulin (TBG) concentrations dramatically, we were interested in the effects of this procedure on thyroid function: we performed TRH tests (200 micrograms Relefact, i.v.), with blood withdrawal before and for 180 min after injection, for determination, using RIA kits, of serum concentrations of total and free T4, total T3, TSH, and TBG in 13 young (20-29 yr old) male body builders with clinically normal thyroid glands, who were all in the same state of training. Five of these athletes admitted taking androgenic anabolic steroids at an average total dose of 1.2 g/week for at least 6 weeks before the tests. TBG, total T4, and total T3 were significantly (P < 0.001) decreased, whereas basal TSH and free T4 were not significantly different from the values of the other 8 without androgenic steroids. The maximum TSH increase after TRH administration (mean +/- SE, 16 -/+ 6 vs. 9 -/+ 4 mU/L; P < 0.05) was relatively increased, whereas the T3 response to TRH (0.61 -/+ 0.10 vs. 1.13 -/+ 0.13 nmol/L; P < 0.05) was relatively decreased in the group receiving androgens. The 5 patients taking androgens had significantly greater weight (114 vs. 90 kg; P < 0.01) and higher total cholesterol levels (6.3 -/+ 1.3 vs. 3.8 -/+ 0.3 mmol/L; P < 0.05) together with very low high density lipoprotein cholesterol levels (0.20 -/+ 0.03 vs. 1.03 -/+ 0.10; P < 0.001) than the controls. PRL levels were normal and similar in both groups. We conclude from our results that high dose androgenic anabolic steroid administration leads to a relative impairment (within the normal range) of thyroid function. Whether this is due to a direct thyroid hormone release (or synthesis?)-blocking effect of these steroids needs further investigation.
PMID: 8473383 [PubMed - indexed for MEDLINE]
The study was quite literally buried in Medline.
So AAS impair total T4 and Total T3, but have no effect on TSH and free T4.
It seems as though AAS block the T4-T3 conversion to a certain degree, which would explain the lowered T3 levels, yet normal TSH.
Also, HDL cholesterol went down(naturally...all AAS lower it), and prolactin levels stayed the same.
But take a look at the weight differential between the controls and the AAS group....114Kg vs 90Kg ( Or 256lbs vs 198lbs)...that sure is a lot.
Therefore, IMO adding a 12.5mcg dose of T3 with your AAS cycle is more than likely a good idea, in order to bring T3 levels back up to normal. Lowered T3 levels enduce lethargy btw.
1: J Clin Endocrinol Metab. 1993 Apr;76(4):1069-71. Related Articles, Links
Ingestion of androgenic-anabolic steroids induces mild thyroidal impairment in male body builders.
Deyssig R, Weissel M.
Third Medical University Clinic, Vienna, Austria.
Self-administration of very high doses of androgenic anabolic steroids is common use in power athletes because of their favorable effect on performance. Since androgenic steroids decrease serum T4-binding globulin (TBG) concentrations dramatically, we were interested in the effects of this procedure on thyroid function: we performed TRH tests (200 micrograms Relefact, i.v.), with blood withdrawal before and for 180 min after injection, for determination, using RIA kits, of serum concentrations of total and free T4, total T3, TSH, and TBG in 13 young (20-29 yr old) male body builders with clinically normal thyroid glands, who were all in the same state of training. Five of these athletes admitted taking androgenic anabolic steroids at an average total dose of 1.2 g/week for at least 6 weeks before the tests. TBG, total T4, and total T3 were significantly (P < 0.001) decreased, whereas basal TSH and free T4 were not significantly different from the values of the other 8 without androgenic steroids. The maximum TSH increase after TRH administration (mean +/- SE, 16 -/+ 6 vs. 9 -/+ 4 mU/L; P < 0.05) was relatively increased, whereas the T3 response to TRH (0.61 -/+ 0.10 vs. 1.13 -/+ 0.13 nmol/L; P < 0.05) was relatively decreased in the group receiving androgens. The 5 patients taking androgens had significantly greater weight (114 vs. 90 kg; P < 0.01) and higher total cholesterol levels (6.3 -/+ 1.3 vs. 3.8 -/+ 0.3 mmol/L; P < 0.05) together with very low high density lipoprotein cholesterol levels (0.20 -/+ 0.03 vs. 1.03 -/+ 0.10; P < 0.001) than the controls. PRL levels were normal and similar in both groups. We conclude from our results that high dose androgenic anabolic steroid administration leads to a relative impairment (within the normal range) of thyroid function. Whether this is due to a direct thyroid hormone release (or synthesis?)-blocking effect of these steroids needs further investigation.
PMID: 8473383 [PubMed - indexed for MEDLINE]
The study was quite literally buried in Medline.
So AAS impair total T4 and Total T3, but have no effect on TSH and free T4.
It seems as though AAS block the T4-T3 conversion to a certain degree, which would explain the lowered T3 levels, yet normal TSH.
Also, HDL cholesterol went down(naturally...all AAS lower it), and prolactin levels stayed the same.
But take a look at the weight differential between the controls and the AAS group....114Kg vs 90Kg ( Or 256lbs vs 198lbs)...that sure is a lot.
Therefore, IMO adding a 12.5mcg dose of T3 with your AAS cycle is more than likely a good idea, in order to bring T3 levels back up to normal. Lowered T3 levels enduce lethargy btw.
Fonz, Some AAS will lower total T4 and T3, but T3 And T4 resin uptake will be higher. Free T3 and Free T4 also generally remain the same. Thyroxine binding globulin also will be lower during AAS use. There are studies that have shown this. So most AAS have no signifigant impact on thyroid function, with the exception of oxandrolone which can lower thyroid function.
This is an awesome thread.. jpl26, it say's you're 'banned' and I hope that's a mistake or joke, because you kick ass. Poantrex too, your debate is exactly the kind of thing we need around here. Solid, cutting edge discussion regarding issues that affect all of us.
Keep kicking ass. Let me know what the final conclusion is. Maybe make a post when you guys come to an agreement, because I even had trouble following EVERYTHING that was said, I'm guessing a lot of people are struggling too.
Thanks!
Keep kicking ass. Let me know what the final conclusion is. Maybe make a post when you guys come to an agreement, because I even had trouble following EVERYTHING that was said, I'm guessing a lot of people are struggling too.
Thanks!
gjohnson5
New member
ocisbomb said:
As far as I can see the only real and OBJECTIVE danger is shutdown.
The other 3 issues
1. graves disease
2. bone loss
3. diabetes
are either hyperbole, like the 7 foot englishman tale in the movie Bravehart who had lightning bolts shooting out of his arse, or fiction.
Armandinho C.
New member
When I used T3 and T4, I lost gains... don't liked this......
And i'm never saw peoples who have gains whit T3...
And i'm never saw peoples who have gains whit T3...
gjohnson5 said:
Are you FUCKING stupid?
Look at the fucking prescribing papers that come with american prescribed thyroxine or triiodothyronine sodium! They MENTION in the papers that thyroid meds are KNOWN to cause BONE LOSS/OSTEOPOROSIS, WEAKNING OF BONES, AND HIGHER BLOOD SUGAR. THAT IS AMONG OTHER SIGNIFIGANT SIDE EFFECTS.OBIVOUSLY, FUCKING with exogenous hormones will cause a very high chance that normal hormone balance will not return to the level it was at previously. This is a very real danger that happens all the fucking time, and If you don't believe me ask all the guys in the HRT forum, that are on HRT because of steroid hormone use.
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todoveritas
New member
IMHO there is no such thing as "safe" use of Cytomel (T3) outside a medical setting. There is only "informed use" which minimizes risk. Consider the many other complications besides permanent thyroid suppression. Personally, I think the cardiac risks are the worst. Especially in the competitive setting: The K loss/diuretic use/metabolic probs compounded by clen/ECA stacks make the risk of arrhthymia very real.
I
i am what i am
Guest
todoveritas said:
Why did you bump up a post over a year old???
Castro_bigdog
New member
T3 sucks dont waste your money on somthing that can fu*k you up.........
MassDestruction
New member
People are funny, take IGF-1, HGH, Tren, Anadrols...but somehow T3 is dangerous..
How very funny.
How very funny.
Actually JPL is very correct with his statement, I have done much research on this topic and have used t3 doses at 150mcg for 4-6 weeks on end, and have done many cycles and always got blood work, not only have I discuessed this issue with 2 doctors I have many articles I will try to find, one is in the New Anabolic Reference Manual and every article stated how practically impossible it is to burn out your thyroid, my doctor said he has had pateints on thyroid meds for 10 years or more and once he takes them off their thyroid function is back to 100% normal after very minimal time. The body is very smart and in all of my reading I have yet to see proof of a thyroid being burnt out ( healthy thyroid) from supplementing with t3,t4 for longer periods of time, 8-12 + weeks. Like I said, I have done countless cycles at very high doses with blood work before and durning and after with NO problems at all.
solidspine
New member
The little bit of T-3 we take does not affect your thyroid,
And I think t=3 is a wasted anyway, diet, cardio, clen and Fina work 1000% better
And I think t=3 is a wasted anyway, diet, cardio, clen and Fina work 1000% better
SlimJim300 said:
there is without a doubt a rebound effect when using t3 and coming off, also if dose is kept low and not used for more then 30 days/time tapering off should help to minimize any rebound.
I personally feel men benefit more then women from t3 useage and women are the ones who are more prone to having thyroid issues then men are
st8grad
New member
brunette said:
Well, nothing. Except for the fact the replacing what is already there and putting the human equation into the process is not ideal. The natural biological process that is regulated by a well functioning thyroid can only be replicated to the best of humans ability.
It's the same as chopping off you leg being no big deal since you can get an artificial one. No big deal right? You can walk, run, jump, etc. Would you risk it though?
Guys who are afraid of T3 should just stick to a ECA stack, but yet ECA have dangers in them as well...
micksnowdog
New member
wow this was a good thread, started in 2004 tho haha. wonder what new evidence supporting both side has come to light of late.
Piper25
New member
I have tried it 3 times with clen and my diet was spot on as I was leaning previously and I was using aas and I got nothing but low BP down to 50/90 and I would always get pins and needles. I thought clen by itself worked better.
I would also get pins and needles lots aswell.
I dont see what the hype is but many love it so i am assuming it differs from user to user.
I would not use it more than 8 weeks...12 tops but thats pusshing and never go over 100mcg's...
Palumbo will assure you that no matter what your body will normalize due to negative feed back loops and you will produce naturally after some point also depending on user, length and biology.
I had much better results from ECA than clen or t3. clen works good for 1 week then nothing even with benadryl.
I would also get pins and needles lots aswell.
I dont see what the hype is but many love it so i am assuming it differs from user to user.
I would not use it more than 8 weeks...12 tops but thats pusshing and never go over 100mcg's...
Palumbo will assure you that no matter what your body will normalize due to negative feed back loops and you will produce naturally after some point also depending on user, length and biology.
I had much better results from ECA than clen or t3. clen works good for 1 week then nothing even with benadryl.
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A
ALIN
Guest
Best used cycled. Short periods,,,taper up,,,then taper down until off.
Long term use MAY cause issues but most have no real problems with sensible use.
Ok so here is a ? for anyone to help me. 6 weeks ago I started having joint pain in my feet 1st then knees wrists....ect My hands became swelled and are painful in the joints. THe doc have not clue what it wrong I ran a cycle test, anenanate (sp?) They tested me for rheumatoid arthritis, lupus, mono, thyroid....1st they thought it was RA but that came back neg, and was put on prednisone-swelling is now gone I still have the hair loss, fatigue, really blood shot eyes. My thyroid came back hyperthyroid really bad. i have to see the endocrinologist and get a thyroid scan. Long story short could this all be caused by those steroids? I have been off for over 4 weeks now but my labs are out of wack. IK havde also run a cycle in the past and never had any problems. Anyone with ideas would be great !
Thanks
Thanks
Tatyana
Elite Mentor
I have read that steroids induce a mild hyperthyroidism while you are on them as it competes with thyroxine (T4) for the binding proteins.
Four weeks off? What were you taking? What was the half life?
Hyperthyroidism is typically caused by an autoimmune disorder, however it can occur if people take T3.
i dont like T3 or clen for that matter
My friend just competed and was taking 200mg T3/day to cut down...fuck that!!
It also took him months to recover and to this day he does 1 hour of cardio a day to sort of stay lean, and his diet is spot on. Im not extremely familiar with the finer points of T3 i do have general knowledge of the compound but although it works I dont think it is something to be used lightly.
My friend just competed and was taking 200mg T3/day to cut down...fuck that!!
It also took him months to recover and to this day he does 1 hour of cardio a day to sort of stay lean, and his diet is spot on. Im not extremely familiar with the finer points of T3 i do have general knowledge of the compound but although it works I dont think it is something to be used lightly.
ArmaniAK47
New member
I used T3 briefly, at a low dose.. 12.5-50mcg for about a week.. tapered up and down..
about the 4th day my heart was doing crazy rhythms and stuff...but nothing terrible.. (my gf just happened to be laying on my chest and heard it..)
the 5th or 6th day all of a sudden, sitting down at a meal out I felt a weird "movement"(?) feeling in my thyroid.. then I immediately had an overwhelming "sense" I was going to die.. like the heart attack symptom "fear of impending doom" ... my face felt hot and I ran to the bathroom and tried to sit and breath and calm down... after about 30-40 minutes I left the bathroom.. noone knew what was wrong with me... I went back and kept taking it a day or two tapering down.. my heart continued odd rhythms..
for about 3 months after my thyroid was high and I had these..."panic attacks" they sucked...
my resting heart rate was over 100, I couldnt work out and couldnt bring myself to eat... I lost all the mass I had worked for for years before...
Then, once I came back to normal.. I got fat for a while.. still not working out, but eating better...
then my levels are fine now, and I am back at it...
The shit worked.. during that week i lost like a belt adjustment in the first few days... but man it fucked me up.. I wont ever use it again..
about the 4th day my heart was doing crazy rhythms and stuff...but nothing terrible.. (my gf just happened to be laying on my chest and heard it..)
the 5th or 6th day all of a sudden, sitting down at a meal out I felt a weird "movement"(?) feeling in my thyroid.. then I immediately had an overwhelming "sense" I was going to die.. like the heart attack symptom "fear of impending doom" ... my face felt hot and I ran to the bathroom and tried to sit and breath and calm down... after about 30-40 minutes I left the bathroom.. noone knew what was wrong with me... I went back and kept taking it a day or two tapering down.. my heart continued odd rhythms..
for about 3 months after my thyroid was high and I had these..."panic attacks" they sucked...
my resting heart rate was over 100, I couldnt work out and couldnt bring myself to eat... I lost all the mass I had worked for for years before...
Then, once I came back to normal.. I got fat for a while.. still not working out, but eating better...
then my levels are fine now, and I am back at it...
The shit worked.. during that week i lost like a belt adjustment in the first few days... but man it fucked me up.. I wont ever use it again..
kiwee
Banned
theres no fuckin way this happened with 6days of t3...what other drugs were you on ???(steroids, gh, prohormones, clen, medications, antibiotics, illegal substances, etc etc etc)
Para_Shoot
New member
Maybe now he needs to go on T3 for life. Plenty of people are on T3 for life, for other reasons than steroids of course, but nonetheless, they are on for life. Why would he struggle with what he thinks is a slow operating thyroid by doing excessive cardio and strict diet for weight managemnt. He should pony up and accecpt the fact he *may* have damaged his tryroid with his T3 use, and now he should goto the doctor and if the values are ay off then have the doctor put him on T3 for life. Problem solved.
BodyND
New member
woah dude pm me please im very interested in hearing about this tumor on you pituitary gland have they removed it or what i just got checked for that becasue i had low TSH and things werent adding up.
