The Thyroid Handbook

I think this may be a nice addition here.



The Thyroid Handbook
by Cy Willson

Take a minute and look around your house, apartment, and dorm room or prison cell. If you’ve been involved in the iron game long enough, you’ll probably have dozens of informational guides scattered around: books, copies of T-mag, your nutrition and training logs, a worn out VHS tape of Pumping Iron, a pair of lacy panties that are, for some inexplicable reason, stuck to the ceiling… no wait, that’s my apartment. Never mind.

So why not add a handbook about one of your favorite glands to your collection? After all, the ol’ thyroid gland is pretty darned important. In this handbook, I’ll give you a rundown on thyroid function and a few related areas. Why is this so important? Well, the thyroid plays a huge role in your endeavor to get that lean look. If your thyroid levels aren’t optimal, losing fat can be one hell of a challenge. But it goes even further than that because the thyroid hormones play important roles throughout the body.

So, after you finish reading this, print it out with that handy-dandy new text feature our web gurus have provided. Use that good, glossy paper too, you know, the kind you use to print off naked pics. After you’ve it printed out, store it along with your most prized bodybuilding possessions. Here we go!


The Big Picture

Just so you know, the thyroid gland is located just below the larynx. It’s responsible for the release of both T4 (thyroxine) and T3 (triiodothyronine). If your thyroid gland is inactive for one reason or another, your metabolic rate could drop as much as 40% below normal (hypothyroidism). On the other hand, an excess of thyroid hormone can increase your metabolic rate by 60 to 100% above normal (hyperthyroidism).

So how are these thyroid hormones synthesized in the body? Glad you asked. In order to form thyroid hormones, you need two very important raw materials, one being tyrosine and the other being iodide. A large glycoprotein called thyroglobulin contains a lot of the tyrosine within it. It then allows oxidized iodine to enter within the thyroglobulin where iodine binds to some of the tyrosine. This is called the iodination of tyrosine. This process causes the formation of monoiodotyrosine and then forms diodotyrosine. Then the diodotyrosine couples with another diodotyrosine, forming a thyroxine molecule. Just think of it like this, di(2) plus di(2) equals T(4). Clear as mud? Good, let’s move on.

The same thing occurs in the formation of triiodothyronine (T3), except it in this case, one of the monoiodotyrosine molecules couples with one of the diodotyrosine molecules. Essentially, the difference between the two is simply the addition or lack of an iodine molecule. Remember, this occurs within the thyroglobulin molecule. Once this has happened and the T3 and T4 (mostly T4) have been formed, the glycoprotein molecules are stored in the follicles of the thyroid.

So, now what happens? Well, when some type of situation occurs in which you need to increase thyroid hormone levels in the blood, your hypothalamus secretes Thyroid Releasing Hormone(TRH), which in turn causes the pituitary to release Thyroid Stimulating Hormone(TSH). TSH "breaks down" the thyroglobulin in the follicles and causes the release of the hormones into the bloodstream.

When thyroid levels get too high, a negative feedback occurs to both TRH and TSH, thus reducing the amount of thyroid hormone that’s secreted. When thyroid levels are too low, then TRH and TSH increase, thus increasing thyroid hormone levels. This is all part of the hypothalamic-pituitary-thyroid axis.

I should also note that very little T3 is actually secreted, and in fact, most of the active T3 that affects various tissues (liver, kidney, and others) is formed via the deiodination of T4 by an enzyme(deiodinase) in the tissues themselves. In other words, the enzyme rips off an iodine molecule from T4, forming T3. This again occurs with T3 to form diiodothyronine or T2, but we’ll talk more about that later.

In the following sections, I’m going to go over each thyroid hormone and give you some brief facts. I’ll do this quickly, as we have more important things to discuss.


L-thyroxine (T4)

This drug is normally used as a replacement therapy in congenital or acquired hypothyroidism and it’s also used to suppress TSH in cases where a person is suffering from hyperthyroidism. It’s released in a 20/1 ratio in respect to T3. T4 is less potent than T3, metabolically speaking, and has a half life of six to seven days in euthyroid humans. (That’s where a person’s thyroid gland is enlarged but it’s not associated with inflammation or cancer. Also called goiter.) The brand name of T4, when it’s bought from the pharmacy, is Synthroid.


L-triiodothyronine (T3)

This drug is also used to treat hypothyroidism and is even used to determine if someone has hyperthyroidism. It’s said to be three to five times more metabolically potent than T4 and has a half-life of £ 2.5 days. Brand names are usually Cytomel or Cynomel. The usual dosages used to treat hypothyroidism are 5 to 25 mcg daily and gradually increasing the dosage to 60 to 75 mcg daily. Some people need as much as 100 mcg daily — 20 to 25 mcg of T3 is approximately the same as 100 mcg of T4.


Everything You Want to Know about Thyroid Hormones (And I Do Mean Everything!

Thyroid hormones exert their effects upon most organ systems and also play a role in development. They increase oxygen consumption and therefore the Basal Metabolic Rate (BMR). They also increase the metabolism of all macronutrients, carbohydrates, lipids, and protein. T3 increases aerobic mitochondria function or respiration, but another thyroid hormone, T2 may actually be responsible for this action.

So, why would bodybuilders want to use thyroid hormones? Simple, they increase the rate at which lipids are oxidized. Hence, more lipid oxidation and less body fat. Sounds great, huh? The problem? Well, thyroid hormones, more specifically T3, also increase protein oxidation. Still, the body ultimately wants to hold on to muscle tissue so you end up losing fat at a greater ratio than muscle.

This has been demonstrated in lab studies involving healthy human males. In one study, seven healthy men were given a low dose of T3 for 63 days and body composition measurements were taken during this time. At six weeks, there was an average weight loss in about a 3/1 ratio in favor of fat mass. (1) So, in essence, for every three pounds of fat, you’ll lose around one pound of muscle. Not too bad. Of course, these guys weren’t following bodybuilding routines, nor were they trying to hold on to muscle tissue by eating large amounts of proteins.

Another way to attenuate these negative effects on muscle tissue is to use anabolic steroids. One study made a great case for this practice. Ten healthy males were given 50 mcg of T3 per day for 28 days. Six of them received a 200 mg/week injection of Testosterone enanthate while the other four received a placebo. Those that received the Testosterone injection saw no loss of lean body mass.(2)

I guess that if you really want to be a "thyroid expert," you should know what else thyroid hormones do. To name just a few things, they play a role in mood, cognitive function, development and growth as a child, and even your blood profile. They decrease LDL levels and even potentiate the effects of adrenergic hormones on lipolysis.(3,4) T3 has even been shown to cause a five-fold increase in the amount of beta 3-adrenergic receptors in white adipose tissue. (The stuff that covers your muscle.) (5) This increase in beta-3 number means that it can increase the effectiveness of norephedrine and ephedrine.

In order to have hopes of controlling these hormones, you need to know exactly what things can affect them. For instance, growth hormone can increase the conversion of T4 to T3. Beta agonists, like norephedrine and ephedrine, may also increase the conversion of T4 to T3. (6,7) The amount of carbohydrates in your diet can have a profound effect, too. It seems that, depending on the person, anywhere from 50 to 120 grams of carbs are needed in order to prevent the decline in T3 during a carbohydrate-restricted diet. Any lower than that, and T3 plummets substantially.(8,9,10) It’s likely this effect is simply dependent on glucose levels in the blood. (11)

I know some of you may be thinking that if you simply provide more substrates (iodine and tyrosine) then you could possibly increase thyroid hormone levels. Unfortunately, this just isn’t so. While dieting, taking in extra tyrosine could possibly provide some support, but iodine will actually have negative effects even while on a low-carb diet. (12)


Enter 3,5-diiodo-L-thyronine (T2)

This derivative of T3 was once thought to be inactive. In fact, most doctors and pharmacists (no offense to my brothers and sister who are involved in those fields) aren’t up to date on the latest research, so they continue to believe what some textbook from 1972 says. The fact is, T2 is indeed very active in terms of metabolic effects.

How do I know? Well, check this out. It’s been shown to increase hepatic oxygen consumption by about 30%. The authors of the study discovered that out of T4 and T3, only T2 was active in stimulating rapid hepatic oxygen consumption. They concluded that it acts rapidly and directly through activation of the mitochondria.(13)

In another study, T3 and T2 were compared in terms of Resting Metabolism (RM) and on the oxidative capacity of tissues that are metabolically active (liver, muscle tissue, brown adipose tissue or BAT, and heart). What they found was that T2 had a dose-dependent effect which increased RM and oxidative capacity. They found the greatest response to T2 was in liver and in BAT, which is exactly what you’d want, if fighting fat was a main concern. The effects again occurred rapidly and independent of protein synthesis. They stated that their results suggested isomers like T2 could be direct mediators of thyroid hormone regulation on energy metabolism.(14,15)

Yet another study also found increased hepatic oxidative capacity and thought that it was due to a direct action upon the mitochondria by T2.(16) Other studies had similar findings.(17,1 And yet another study showed the same thing: increased oxidative capacity and energy expenditure, causing them to deduce that T2 and T3 displayed similar effects.(19) T2 was also shown to have a similar effect to that of T3 on lipid metabolism with T2 actually doing a little better in some tissue.(20)

Okay, so it works in animals you say. What about humans? Although there isn’t a huge amount of research in humans, some does exist. By the way, everyone, here’s an inside tip about product development in the supplement industry. If you want to come up with something new and effective, chances are there isn’t a limitless amount of research on the compound. If there were, some drug company would have put it on the market already!

Anyhow, in one study, using human mono-nuclear blood cells, they found that T2 increased the rate of respiration significantly. (21) So, the efficacy appears to have been established. Can it significantly inhibit TSH like T3 and T4? Well, the studies are somewhat conflicting, but one thing seems to be prevalent amongst them all. That is, TSH inhibition isn’t nearly as severe with T2 as it is with T3.

One study showed that T2 is 13% less inhibitory on TSH levels, as compared to T3. (22) In yet another study, T3 and T2 suppressed TSH to similar levels; however, it took 15 mcg/100g body weight per day of T3 to accomplish this, while it took a whopping 200 mcg/100g body weight per day of T2 to accomplish the same thing. This means it took about 13 times more T2 to exert the same effect on TSH as T3. (23)

One last study. When researchers administered 100 ug/Kg of T3 and 800-1600 ug/Kg of T2 the following occurred: T3 rapidly decreased serum TSH levels within minimal levels after 24 hours. Seventy-two hours after application, TSH levels were still significantly lower than control levels. As far as the T2, TSH levels were transiently reduced and reached their lowest point at 24 hours and increased afterwards. Basal levels were reached 72 hours after an application.

What they found after analyzing the data was that there seemed to be a trend for a dose-dependent (meaning, the higher the dosage, the more TSH was inhibited) suppression of TSH by T2 which did not reach statistical significance. That means it didn’t do it to a significant degree with the dosages used.

Furthermore, it appears as though it took 100 times more T2 than T3 to finally exert the same amount of TSH inhibition. Even using 400 times more T2 than T3, it appears that T3 only allows TSH to be inhibited to just a slight degree less than T2.(24)


One Last Thing

I’ve recently been asked this same question by at least a dozen people. Since using T3 can cause a state of hyperthyroidism that will increase muscle catabolism (amongst other things), will T2 do the same? My answer is that it’s possible it could, to some small degree. It would probably take large doses, taken for prohibitively long times, and even then the amount would be much, much less than you might encounter while using T3.

Still, to be safe, I think you should be using something to offset the possibility, however remote, of muscle catabolism. Obviously, continue exercising (duh!. Secondly, eat the "prescribed" amount of protein, which is 1.5 grams per pound (or at least 1 gram per pound) of bodyweight.

And, if your dad is a renegade pharmacist or doctor, you could even use some sort of anabolic concurrently. I don’t care which. Anything. Testosterone, trenbolone, boldenone, stanozolol, or if you want to go the legal route, Nandrosol, Androsol, Methoxy-7, or Tribex-500.

I’ve tried to present some of the evidence to you as best as possible. Again, I think you should make your own decision. Will I use it? Yep. I’m going to give it a go and compare its effects to that of T3 myself. I’m 100% sure it’ll work, but I’m going to have my TSH monitored and I’m going to compare the two using similar dosing regimens.

Looking at it objectively, however, I think you’ll see which is better. These are exciting times in this industry, aren’t they? Good luck and train hard.


References Cited

1. Lovejoy JC, et al. "A paradigm of experimentally induced mile hyperthyroidism: effects on nitrogen balance, body composition, and energy expenditure in healthy young men." J Clin Endocrinol Metab 1997 Mar;82(3):765-70

2. Zachwieja JJ, et al. "Testosterone administration preserves protein balance but not muscle strength during 28 days of bed rest." J Clin Endocrinol Metab 1999 Jan;84(1):207-12

3. Berne, Robert M, et al. Physiology 4th ed., 1998.

4. Muller MJ, Seitz HJ. "Thyroid hormone action on intermediary metabolism. Part II: Lipid metabolism in hypo- and hyperthyroidism." Klin Wochenschr 1984 Jan 16;62(2):49-55

5. Rubio A, et al. "Thyroid hormone and norepinephrine signaling in brown adipose tissue. II: Differential effects of thyroid hormone on beta 3-adrenergic receptors in brown and white adipose tissue." Endocrinology 1995 Aug;136(8):3277-84

6. Chambers JB, et al. "The effects of propanolol on thyroxine metabolism and triiodothyronines production in man." J Clin Pharmacol 1982; 22: 110-16

7. Wilkins M.R, et al. "Effect of propanolol on thyroid homeostasis of healthy volunteers." Postgrad Med J 1985; 61: 391-4

8. Pasquali R, et al. "Effect of dietary carbohydrates during hypocaloric treatment of obesity on peripheral thyroid hormone metabolism." J Endocrinol Invest 1982 Jan-Feb;5(1):47-52

9. Serog P, et al. "Effects of slimming and composition of diets on VO2 and thyroid hormones in healthy subjects." Am J Clin Nutr 1982 Jan;35(1):24-35

10. Spaulding SW, et al. "Effect of caloric restriction and dietary composition of serum T3 and reverse T3 in man." J Clin Endocrinol Metab 1976 Jan;42(1):197-200

11. Kventy J, et al. "Effect of oral glucose feeding on thyroid hormone action in human mononuclear blood cells." Thyroidology 1990 Aug;2(2):53-7

12. Reinhardt W, et al. "Effect of small doses of iodine on thyroid function during caloric restriction in normal subjects." Horm Res 1993;39(3-4):132-7

13. Horst C, et al. "Rapid stimulation of hepatic oxygen consumption by 3,5-di-iodo-L-thyronine." Biochem J 1989 Aug 1;261(3):945-50

14. Lanni A, et al. "Calorigenic effect of diiodothyronines in the rat." J Physiol 1996 Aug 1;494 (Pt 3):831-7

15. Goglia F, et al. "Action of thyroid hormones at the cellular level: the mitochondrial target." FEBS Lett 1999 Jun 11;452(3):115-20

16. Lanni A, et al. "Effect of 3,3’-diiodothyronine and 3,5-diiodothyronine on rat liver oxidative capacity." Molecular and Cellular Endocrinology. Volume 86, Issue 3. 1992

17. Lanni A, et al. J. Endocrinol. 136:59-64 1993.

18. O’Reilly I, Murphy MP. Acta Endocrinol. 127:542-546 1992.

19. Lanni A, et al. "3,5-Diiodo-L-thyronine and 3,5,3’-triiodo-L-thyronine both improve the cold tolerance of hypothyroid rats, but possibly via different mechanisms." Pflugers Arch 1998 Aug;436(3):407-14

20. Varghese S, Oommen OV. "Thyroid hormones regulate lipid metabolism in a teleost Anabas testudineus (Bloch)." Comp Biochem Physiol B Biochem Mol Biol 1999 Dec;124(4):445-50

21. J. Kvetny. Horm. Metab. Res. 24:322-325, 1992.

22. Moreno M, et al. "Effect of 3,5-Diiodo-L-thyronine on thyroid stimulating hormone and growth hormone serum levels in hypothyroid rats." Life Sciences, Volume 62, No.26, pp. 2369-2377, 1998.