t-3 question?

[OllllO]

ok, i have been reading for a few months and have read all of the educational stuff and past threads, but i still have a few questions. so try not to flame.

I plan on a t-3/clen cycle to loss some more wieght. i have been on atkins for a year or so, and work out 4-5 times a week. I am about 5'10" 245lb 26% bf

my question. I want to do about a 6 week cycle. i understand that without some sort of AS, most say that t-3 will not be good, do to the loss of mussle. I want to do it right, but i'm not ready to start injecting just yet(i know, i know) so, would it be that bad to do t-3/clen without AS? or is there another option, like an oral that will be safe enough to take? if so, knowing all my info, what would you take with it? all the replys i can get will be helpfull. tia.

[Unoid]

you're already low on muscle, might as well lose a little more to get down to 10% then worry about putting on muscle

[Angelus]

I wouldnt advice t3 it puts a lot of pression on the hart and at 26% BF you cant have the enought resistance to handle it good

[cutting_king]

I wouldnt advice t3 it puts a lot of pression on the hart and at 26% BF you cant have the enought resistance to handle it good

Some people would argue that the Atkins diet puts more pressure on the heart and other organs than t3 would. Remember T3 isn't a thermogenic or a stimulant like Ephedrine is, therefore shouldn't increase the heart rate too much either.
This isn't to say he is ready for T3, just thought i'd point this out

[OllllO]

bump.

any other opinons, or will it be ok without any AS and i shounld just not worry about it?

[OllllO]

anyone??? come on, 50 views, 2 posts??? i'v seen posts where people ask for a source get to be larger then this in 3 mins........hmm, maybe if i ask for a source, it will call attention and get me a few more opinons..j/k

[WEBB]

do not do t3.

[MAXIMA5]

What was your bf% before you started atkins and how long have you been working out 4-5 times per week?

[WEBB]

no to elaborate a little more, t3 is imo is a very dangerous compound to take. imo i would just do clen for 2 weeks on 2weeks off, and on your 2 weeks off use something like an eca stack. i think you would be more than happy with your results.

[WEBB]

i would not suggest any aas yet, wait till you drop your bf down to at the very least 15% and then we'll look at doing up a cycle for ya, and it will be longer than 6 weeks and it will not just contain orals.

[WEBB]

as for your atkins diet, stop that and get into the diet forum and find a good sound diet to follow that will also help your fat loss, and you'll be lighter in no time.

[MAXIMA5]

Again, have you dropped fat over the last year, or have you been plateauing at 26%.
Like Webb said, I'd kick Atkins to the curb.

[OllllO]

Again, have you dropped fat over the last year, or have you been plateauing at 26%.
Like Webb said, I'd kick Atkins to the curb.

thanks for the replys guys! here you go.

I loss 50 lbs on atkins, got down to 230(not working out regularly, just doing phsical work) i did it for about 7 months, then stoped loosing. i stayed on it for about 2 more months, and then quit it. in the last two years, i was not on it, just watching what i eat, and working out about 5 days a week, 4 days of cardio for 30-40 min. i have been lifting heavy(heavy for me) and in the last 1 1/2 year have gained 15lb. bf% has stayed about the same.

now i need to start lossing some more fat. and i can and have, but it's like i'm stuck at this point. i went back on the atkins two months ago, and continued my work outs, but it is not working this time. i don't eat much, i split up small meals threw the day, but still carry fat. my work out is good imo, and i want to take this just to add to it what i am doing now just so i can cut some fat for the summer and all.

hope this gives you some more info.

also, i'm not asking about doing a steroid cycle, really i would rather not do one now(i'm still making gains without) but i have seen where some people say to NEVER do t-3 without. does this still hold true in my case?

[SPIKE]

as for your atkins diet, stop that and get into the diet forum and find a good sound diet to follow that will also help your fat loss, and you'll be lighter in no time.

Like Webb said, I'd kick Atkins to the curb.

Why dont you guys like Atkins?

[SPIKE]

Why dont you guys like Atkins?

Bizzzzzzzump

[WEBB]

t3 is a thyroid stimulant and imo doesnt have much effect on the heart rate.

now, i would just do what i suggeested earlier, do not do the t3, but go ahead with clen. run it 2 weeks on and 2 weeks off. 4ml everyday first thing in the morning on an empty stomach before you do cardio. watch your diet and check out the die forum for some helpful ideas. now on your 2 weeks off use something called an eca stack, take 2 asprin, 25mg ephedra, and a cup of black coffee, then go to the gym and do your cardio. it is also to be taken on a e,pty stomach first thing in the morning.

Hope this helps, WEBB

[edmen2]

t3 is a thyroid stimulant and imo doesnt have much effect on the heart rate.

now, i would just do what i suggeested earlier, do not do the t3, but go ahead with clen. run it 2 weeks on and 2 weeks off. 4ml everyday first thing in the morning on an empty stomach before you do cardio. watch your diet and check out the die forum for some helpful ideas. now on your 2 weeks off use something called an eca stack, take 2 asprin, 25mg ephedra, and a cup of black coffee, then go to the gym and do your cardio. it is also to be taken on a e,pty stomach first thing in the morning.

Hope this helps, WEBB

50 mg of aspirin on an empty stomach. how do u do this w/o puking up a lung?

[Giants11]

t3 is a thyroid stimulant and imo doesnt have much effect on the heart rate.

now, i would just do what i suggeested earlier, do not do the t3, but go ahead with clen. run it 2 weeks on and 2 weeks off. 4ml everyday first thing in the morning on an empty stomach before you do cardio. watch your diet and check out the die forum for some helpful ideas. now on your 2 weeks off use something called an eca stack, take 2 asprin, 25mg ephedra, and a cup of black coffee, then go to the gym and do your cardio. it is also to be taken on a e,pty stomach first thing in the morning.

Hope this helps, WEBB

T3 is not a Thyroid stimulant. It is a thyroid hormone. It is the actual hormone sythesized in your body. And it does have an effect on heart rate. Very much so. Which is why high doses of t3 are not reccomended.

Here's where I'm confused. You say T3 is dangerous but Clen is ok??

I'm not sure what about t3 is dangerous. At high doses yes it can be bad for your heart and yes it will shut down your thyroid temporarily, however used appropriately I believe it is not dangerous.

On the other hand Clenbuterol, which has been shown to cause Myocyte death (Heart Cell) in rats, would certainly be more dangerous in my book. Granted the studies are all done on rats, it's still a concern.

[Knight1811]

t3 is a thyroid stimulant and imo doesnt have much effect on the heart rate.

now, i would just do what i suggeested earlier, do not do the t3, but go ahead with clen. run it 2 weeks on and 2 weeks off. 4ml everyday first thing in the morning on an empty stomach before you do cardio. watch your diet and check out the die forum for some helpful ideas. now on your 2 weeks off use something called an eca stack, take 2 asprin, 25mg ephedra, and a cup of black coffee, then go to the gym and do your cardio. it is also to be taken on a e,pty stomach first thing in the morning.

Hope this helps, WEBB

If you are telling him to do 2 weeks of clen then 2 off, I'm sure you are referring to the overloading of the Beta receptors. And if that's that case, then he should NOT be using ephederine. Ephederine(ephedra is the herbal form) also triggers the beta receptors, but is NON-selective. Whereas, clenbuterol is a very selective beta receptor drug.

Clen is a selective beta receptor drug whereas ephederine is non selective...but at the end of the day, they both stimulate the beta receptors.

Also 25mgs of ephedra is NOTHING. You will need around 200mg of ephedra just to get around 10-15mgs of ephederine out of it.

Knight1811
ps. Why did you bump a 5 month old post? lol. I fell for it too. DAMN!!! :-)

[OllllO]

what i do not understand is clen and eca stack both work on the same receptors right? so it would make no sense to cycle the two? also 4ml of clen?

[OllllO]

what i do not understand is clen and eca stack both work on the same receptors right? so it would make no sense to cycle the two? also 4ml of clen?

T.T.T.

[SPIKE]

imo i would just do clen for 2 weeks on 2weeks off, and on your 2 weeks off use something like an eca stack. .

clen and eca stack both work on the same receptors right? so it would make no sense to cycle the two?

OllllO you're correct. So doing what Webb first listed wouldnt be the most effective protocol, at least on paper.

[Milky87]

the catabolic effect of T3 on muscle can be minimized by having a HIGH protein diet, for this reason, atkins might actually be good for it.

There is an oral steroid called turinabol, look into it. 40mgs would/should be enough to stop muscle loss

[chipghent]

ok, i have been reading for a few months and have read all of the educational stuff and past threads, but i still have a few questions. so try not to flame.

I plan on a t-3/clen cycle to loss some more wieght. i have been on atkins for a year or so, and work out 4-5 times a week. I am about 5'10" 245lb 26% bf

my question. I want to do about a 6 week cycle. i understand that without some sort of AS, most say that t-3 will not be good, do to the loss of mussle. I want to do it right, but i'm not ready to start injecting just yet(i know, i know) so, would it be that bad to do t-3/clen without AS? or is there another option, like an oral that will be safe enough to take? if so, knowing all my info, what would you take with it? all the replys i can get will be helpfull. tia.

You sound like you are in the same boat I was in about 5 years ago. I was about 270 lbs about 6' tall. I was on the Atkins, I would loose 20 lbs and gain 20 lbs when I went off. Loose 30, gain 30, loose 20, gain 20. I was blessed with a really slow metabolism. I finally got a hold of some clen (still on the atkins). I was taking it and working my ass off. Deit, cardio, weights, etc. I wasn't getting the effects of the clen. Did more research, which I should have done in the first place. Clen works best with carbs in your system. Loose the atkins diet, I'll come back to that in a min. When I started eating health with the program I was on, and taking the clen, I went from 270 lbs to 198 lbs in about 6 months. Put a good bit of muscle on too. Stay away from the T3. Not because it doesnt work, and not to knock you or your efforts, but you need to be very well educated on this substance if you are going to take it. And by the questions you are asking you aren't. Guys that take this, and need this, are at a point that they need all the help they can to loose maybe 2 to 5 lbs of body fat. Pro's in other words. And they know what they are doing. Back to the atkins. The Atkins, and some will go nuts when I say this, slows your metoblism severely. You cant lift as much, you cant run as long and you always feel a little tired while you are on it. If you eat healthy while you are working out, you notice you feel like superman compared to the way you feel while on the atkins. Hence, you are getting a better workout and burning more fat and building more muscle than with the atkins. And building more muscle is what helps keep the fat off. You can NOT build muscle properly without carbs, period. Correct???? And your clen will work better as well.

[MAXIMA5]

Jay,

Re: Atkins.

My parents both tried Atkins, and their weight would rollercoaster. I tried it for a while and lost a few lbs a couple years ago, but my body seems to crash when i trey to wean myself of fof it.

I've had more success with a "caveman" style of diet, which I'm sure you're also aware of.

Processed foods are drastically limited. The only processed food I'll eat is oatmeal and yogurt. Everything else is Meat, Veggies, Fruit, eggs, clean dairy.

I know Atkins may work for some people. If it didn't, the country wouldn't have gone through the Atkins craze a few years ago.
I just think if this thread's author has hit a wall on it, it's time to change it up.

[Butterfly23GrL]

ok, i have been reading for a few months and have read all of the educational stuff and past threads, but i still have a few questions. so try not to flame.

I plan on a t-3/clen cycle to loss some more wieght. i have been on atkins for a year or so, and work out 4-5 times a week. I am about 5'10" 245lb 26% bf

my question. I want to do about a 6 week cycle. i understand that without some sort of AS, most say that t-3 will not be good, do to the loss of mussle. I want to do it right, but i'm not ready to start injecting just yet(i know, i know) so, would it be that bad to do t-3/clen without AS? or is there another option, like an oral that will be safe enough to take? if so, knowing all my info, what would you take with it? all the replys i can get will be helpfull. tia.

So I pretty much wrote a novel here - i do admit that it is lengthy - but I hope it helps at least a little bit

Your diet: The Atkins diet classification -high-protein/low-carbohydrate diet in which you are allowed to virtually eat unlimited amounts of protein and fat w/minimal amounts of carbs. In the absence of a minimal amount of incoming carbs, your body quickly goes into an abnormal metabolic condition known as KETOSIS. This condition happens when there is not enough carbs to metabolize fat completely, and waste products known as ketone bodies begin to accumulate in the blood. This is why people often feel cranky and irritable on high-protein/low-carbohydrate diets - b/c your brain cannot function properly without adequate amounts of carbohydrates.Severe ketosis occurs when you eat too much protein and not enough carbohydrates. In a short time period (about 24 hours), glycogen reserves in your liver are depleted, and without adequate levels of glycogen it is impossible to metabolize fats completely to water and carbon dioxide. This lack of livery glycogen distorts the normal metabolism of fat (again, this is where the liver is forced to produce abnormal ketone bodies). At high enough levels, the ketone bodies can short-circuit your appetite-sensing center in your brain --> thus decreasing hunger! Unfortunately, at these same high ketone levels, your body works like crazy to get rid of these abnormal ketones from your bloodstream by increased urination...(hmm? water weight?). This water loss (up to 3-4 lbs) accounts for MUCH of the initial weight loss in the first week of low-carb/high-protein dieting.

WHY YOUR DIET DOESN'T WORK OVER A LONG PERIOD OF TIME: Even worse - your body starts to adapt to continued ketosis by altering the actions of your fat cells; within 3 to 6 months your fat cells basically become fat magnets! These "fat magnets" are going to be ten more times active in their ability to accumulate fat!!!!! Even though you might be following the same high-protein diet, fat loss slows, and then fat begins to re-accumulate.

WHAT TYPE OF FAT HAVE YOU ACCUMULATED THE MOST? Okay, so simply losing weight is not going to be as important as losing abdominal fat! Men who have a waist circumfrence larger than 40 inches (women > 35 in.) have a greater risk of type 2 diabetes and heart disease (think about this when you consider the T3 since T3 raises your heart rate). A couple of things to remember - abdominal fat contains VISCERAL FAT, which surrounds your organs (liver, intestines, colon, gallbladder, pancrease, etc). Visceral fat is metabolically active. This metabolically active visceral fat is implicated in the development of insulin resistance - which in turn increases the insulin levels in your bloodstream. So....HAVING TOO MUCH VISCERAL FAT INCREASES INSULIN LEVELS --> INCREASED FAT STORAGE! (Think of insulin as the "fat storing" hormone.")

Visit this website and look @ DHA, DHEA, EICOSANOIDS, OMEGA 3 FATTY ACIDS: https://www.zonediet.com/free/articl...tzone&id=015#D


The second type of fat is SUBCUTANEOUS FAT - found mainly on your hips, thighs and extremeties (primarily used for long-term storage).

Ways you can find out if you have too much visceral fat: get a blood test to measure your fasting insulin level or a blood test to measure your fasting llipid levels (gives you ratio of triglycerides/HDL). If your insulin level results are greater than 15uU/ml - YOU HAVE TOO MUCH VISCERAL FAT or if your TG/HDL ratio is greater than 4.

Carbohydrates: your body's main source of energy - you need them so your pancrease can release insulin. Insulin is important because it attaches to carbs and stores them in the muscles or as fat; grabs on to amino acids (the building blocks of proteins) & stores them in the muscle cell so they can be used for recovery & repair. Carbs are divided into 2 categories (this is what you really need to watch if you're trying to lose fat and gain mass):

-Complex carbs: provide sustained or "timed released" energy (2 types:
Fibrous & Starchy). Where most of your carb intake should originate

-Simple carbs: provide immediate energy. Fruits are its primary source
(but try to limit b/c they contain fructose - easily stored as fat).
Best when consumed 20-30 min. after a workout (PWO), when your body needs to re;lenish its glycogen levels immediately. This is going
to help reduce the recuperation time as well as aid in lean muscle tissue production.

Protein: Every tissue in your body consists of protein; you need it to build muscle tissue. It helps increase your metabolism by 20% every time you eat food containing it, and it time-releases carbs in the form of GLUCOSE so that you will have energy throughout the day. You probably should eat 1-1.5 g of protein/lb of lean body mass. Make sure that your protein consumption isn't too much b/c any extra protein that isn't converted into glucose and used for energy or excreted will provide excess calories. **its unlikely for protein itself to be stored as fat, but if you consistently consume more calories than you need you eventually will have an increase in fat**

Fats: All of the cells in your body contain some fat. They are responsible for lubricating your joints. Hormones are made from fat - so if you get rid of all fat from your diet, your hormonal production will drop resulting in interrupted chemical reactions. Because your TESTOSTERONE production would be halted, the production of lean muscle mass would also stop! At this point, your body is going to start accumulating more body fat than usual in order to keep functioning. There are 3 types of fats:

- Saturated: Commonly found in animal products, vegetable fats (that are altered by hydrogenation (found in palm oil, coconut oil, kernel oil, non-dariy creamers)

-Polyunsaturated fats: they don't affect cholesterol levels - corn oils, cottonseed oil, safflower oil, soybean oil, sunflower oil

-Monounsaturate fats: raise your levels of good cholesterol. Usually high in essential fatty acids and contain some beneficial antioxidant properties. Come from fish oils, virgin olive oil, flaxseed oil, safflower oil and natural peanut butter. GOOD FATS should total 20% of your caloric intake - less than 20% will reduce your hormonal production (think reduction in testosterone). But more than 20% leads to fat accumulation.

Water: To find out how much water your body needs per day, multiply your LBM by 0.66 -> LBM x 0.66 = oz water/day body needs to fxn. properly

So if you're wanting to lose fat you should try maintaining a balance of protein-carb-fat meals (think 1-2-3) 15 grams of fat (monounsaturated), 30 grams protein, 45 grams carbohydrates (protein to carb ratio of 0.7). To figure out this balance you could do:

Take # of grams of protein you plan to consume (per meal) and divide it by 2 to = # of fat grams needed in one meal.
Then take the number of fat grams and add to the number of protein grams to get the # of carbohydrate grams for that meal.
Example below:

30g protein/2 = 15 g of fat
30 g protein + 15 g fat = 45 g carbs

If you want to take this diet approach, I would suggest looking at the Zone diet. It's really simple and actually Dr. Barry Sears (creator of the zone diet) works with NFL players, olympic gold medalist winners and university swim teams. A couple of books you could look at: A Week in the Zone and The Omega Rx Zone and The Anti-Inflammation Zone. You are basically going to be depending on the Glycemic Index and the Glycemic Load - but he makes the diet VERY very simple and EASY to follow.

Now if you want to follow an equal balance of protein to carb type diet, you could do this (reference: *The Body Sculpting Bible For Men - The Way to Physical Perfection by James Villepigue and Hugo Rivera. This diet consists of 40% carbs, 40% protein and 20% fat.
****I really suggest this book if if you already know everything there is to know about weightlifting/exercising/nutrition - it will answer/go over everything for you (nutrition, how to perform an exercise correctly, correct types of food to eat based on your goals, how fast to lift weights, when to lift weights, which exercises to do together, etc. - WOMEN: they also have one for women that I highly recommend as well)


FORMULAS:
- Total Carbs/day = (Total cal/day x 0.40)/4
- Total Protein/day = (Total cal/day x 0.40)/4
- Total Fat/day = (Total cal/day x 0.20)/9
*Divide ea. sum by the number of meals you plan on eating/day*

You need to figure out your Lean Body Mass (LBM) - total weight minus your fat weight. This is going to be useful for deciding calories per day macronutrient amounts/day. Caloric requirements for most men fluctuate roughly b/w 2000 & 2500 cal/day. If you eat the same amt. of calories every day, your body is going to become used to that amount and stop losing fat. So you should probably alternate b/w 2000 & 2500 calories (consume 2000 cal for 2 weeks/following 2 weeks consume 2500). Eat small frequent meals (2-3 hr intervals) to spike your metabolism, maintain a consistent blood sugar level that will allow you to utilize nutrients better, keep more of a stable energy level, and have fewer cravings throughout the day.

What you must apply to every meal/snack: avoid meals that don't have a proper balance of nutrients. Ea. macronutrient has to be present so the body can absorb and use them effeciently. Basically, if you eat a meal that is only carbs, your energy level is going to crash in about 30 min. and your body sill store any carbs not used as fat. Now on the opposite side, if you eat only protein, your body will lack the energy needed from carbs and you will not be able to convert the protein into lean muscle tissue. You're body has a really hard time absorbing proteins in the absence of carbs cz scarce amounts of insulin are available in ea. muscle cell. Also, ratios of ea. macronutrient have to be correct in order to produce the results you want.

NOW ONTO THE NEXT SUBJECT...

WEBSITES TO VISIT:
How Hormones change their target cells:http://arbl.cvmbs.colostate.edu/hboo...on/change.html
Hormones with Cell Surface Receptors: http://arbl.cvmbs.colostate.edu/hboo...n/surface.html
Hormones with Intracellular Receptors: http://arbl.cvmbs.colostate.edu/hboo...intracell.html
“Mechanism of Action and Physiological Effects of Thyroid Hormones: Receptors for thyroid hormones are intracellular DNA-binding proteins that function as hormone-responsive transcription factors, very similar conceptually to the receptors for steroid hormones. Receptors for steroid and thyroid hormones are located inside target cells, in the cytoplasm or nucleus, and function as ligand-dependent transcription factors. That is to say, the hormone-receptor complex binds to promoter regions of responsive genes and stimulate or sometimes inhibit transcription from those genes. Thus, the mechanism of action of these hormones is to modulate gene expression in target cells. By selectively affecting transcription from a battery of genes, the concentration of those respective proteins are altered, which clearly can change the phenotype of the cell.” (Reference: http://arbl.cvmbs.colostate.edu/hboo...id/physio.html)


When it comes to your thyroid, there is a functional process that it goes through known as a feedback loop. The thyroid’s feedback loop isn’t really complex. Basically, the thyroid secretes a hormone when it is signaled by the pituitary gland. The signal is the TSH (thyroid stimulating hormone) & increasing TSH levels tell the thyroid gland to release more hormone. **Thyroid gland sets the rate of metabolism (the rate @ which body uses energy)


How is TSH secretion controlled? Its controlled through the release of TRH (Thyrotropin Releasing Hormone) à this is produced by the hypothalamus. Why is THR released? It is released b/c it is based on circulating thyroid hormone levels in the bloodstream (sensed by the hypothalamus)

So this is where adding more thyroid hormones comes into play…you need to always remember that with most hormones, levels of one can affect the level of another. For example – TRH has a key role in thyroid hormone level and it is also linked to the growth hormone (GH), adrenaline and insulin secretion (remember that diet, exercise and proper amount of sleep also regulate insulin and growth hormone production). When you have an excess amount of thyroid hormones in your system, you get a condition called Hyperthyroidism (a.k.a. thyrotoxicosis) b/c either by overproduction by the thyroid gland or the pituitary gland is releasing excessive TSH.

What happens when you have an excess of these hormones: heat intolerance, increased energy, difficulty sleeping, diarrhea, anxiety, etc. One of the most common conditions associated with hyperthyroidism is GRAVES’ DISEASE – auto-immune disease; over-activity of the thyroid gland sometimes called “diffuse toxic goiter”; basic defect in the immune system that causes production of antibodies that stimulate & attack the thyroid gland (attack causes growth of gland and overproduction of thyroid hormone). Another hyperthyroid condition is FACTITIOUS HYPERTHYROIDISM – assoc. w/ingestion of excessive amts. of thyroid hormone ß Basically what you would be doing by taking the T3.

SIGNS AND SYMPTOMS OF HYPERTHYROIDISM: Weight loss, weakness, protruding eyes, insomnia, increased appetite, restlessness, heartbeat sensations, diarrhea, hair loss, frequent bowel movements, increased sweating, heat intolerance, goiter (visibly enlarged thyroid), itching (all over body), nausea, vomiting, skin blushing and/or flushing, clammy skin, fatigue, hand tremors, high blood pressure, irregular heart bet, graves’ disease

Natural way to effect your thyroid: L-Tyrosine (other part of the hormone) is a non-essential amino acid that your body makes from PHENYLALANINE. The L-form is the isomer found in food and that is usually the form our body uses. You can find tyrosine in fish, poultry, bananas, avacados, almonds and some dairy products.

Essential Fatty Acids – Omega 3 is HIGHLY HIGHLY HIGHLY recommended!!!! Just go to www.drsears.com

Okay, so if you increase the intake of these building blocks for your thyroid hormone production, its not going to automatically produce and release more cz your body is too smart for that. You body only makes enough thyroid hormone to fulfill the use & storage demands. Anyways, while you’re dieting – your body is going to slow the release of thyroid hormone to avoid starvation. ß THIS IS WHY A PROPERLY BALANCED DIET PLAN IS NECESSARY/WHY YOU SHOULD EAT EVERY 2-3 HOURS!!!!

Couple of things that degrade thyroid function: raw cabbage, peanuts, soybeans (especially in men), turnips, mustard, cassava root should all be avoided or consumed in small qty – note: if you cook these foods you should be fine. Foods that contain isoflavones (chemicals that act like hormones once they are consumed). Peroxidase (essential in making T3 & T4) is inhibited by isoflavones (data also links isoflavones to goiter and cancer). Fluoride and mercury exposure needs to be minimized (careful with your tuna and other seafood!)

Taking T4: Some medication does influence its effectiveness. Thyroid meds should not be taken with iron or calcium cz these minerals will bind with the thyroid hormone and make it unavailable for your body to use! So with that being said, you need to avoid milk products at least 2 hours before and after taking thyroid meds. Also, fursomide, methadone, lithium, aluminum-containing antacids, colestipol and rifampicin.

Things that increase T4 Levels: aspirin, danazol and propanolol.

Warning: if you end up screwing up your thyroid gland, you’re basically going to have to take medicine for hypothyroidism for the REST OF YOUR LIFE.

Now T3 (Cytomel)
A while back, T3 was prescribed by itself (w/o T4) for obese people, but it caused an increase in heart complications and cardiac stress so people were forced to stop using it for the treatment of obesity.

How T3 Works: works on the cellular level – increases the metabolism of proteins, carbs and fats & increases heart rate/blood flow.

Benefits of T3: sometimes it benefits bodybuilders – only the ones that can afford to be on a higher calorie pre-contest diet since they will burn excess calories due to the increased metabolic rate. SO….if you have a high body fat percentage, taking T3 will be a very bad idea because a high lean body mass vs. fat mass is not established – that muscle that you do already have will be gone! Plus, you have to establish the proper eating habits and lose fat before you use this “icing on the cake.” If you don’t, you have the likelihood of gaining more fat (and yes, it is possible that you can gain fat while taking it and a BIG possibility of gaining all that you lost plus more once you stop the cycle – since proper eating habits/exercise were not previously established)

Okay, so T3 does have it’s benefits,but….Remember – T3 HAS A CATABOLIC TYPE OF EFFECT (you have the potential of losing significant muscle mass) & long-term use can also decrease your bone density. The reason why people urge you to take T3 with a steroid is due to the fact that T3 increases the amount of protein metabolized. T3 itself is actually not catabolic (shocker, I know!) – corticosteroids are catabolic drugs (directly attack muscle tissue) and T3 doesn’t actually do this. Since it’s such a potent calorie burner, it doesn’t discriminate b/w protein, carbs and fat. DNP has protein sparing properties, but T3 doesn’t so its more likely to burn muscle rather than your fat (kind of like starvation diets). Basically – if you want to avoid muscle loss you really should use an anabolic agent.T3 can also give make your muscles look very soft and flat due to extreme glycogen depletion. This happens b/c there is restricted blood flow to that area and glycogen stores have been depleted (usually carb-loading isn’t going to solve this problem). Clenbuterol is and certain steroids are usually used b/c they offset the lack of “pump” and bring more blood into the muscles causing them to possibly “harden up.” If you are considering T3, I strongly suggest that you look at your family history and see if thyroid disease or diabetes run in your family. About 10% of the public is susceptible to thyroid disease.

REBOUNDING: Remember that your body is always trying to preserve itself in order to maintain homeostasis. In order for you body to preserve itself during this increase of thyroid hormones, it will decline in deiodinase when you restrict your body of carbohydrates cz the body thinks it is starving.(Deiodinase - necessary for your body to convert T4 to T3). So when this declines your metabolism slows down and less calories will be expended when you restrict your carb intake. So, if you're following a high-protein/low-carb diet, expect some decrease in the speed of your metabolism. AGAIN - NOT GOOD ESP. IF YOU HAVE A HIGH BODY FAT % TO START OFF WITH. People usually feel sluglish and have minimal energy when they stop a T3 cycle (so this is why it's necessary to ramp up then ramp down at the end of the cycle)


TIME IT TAKES TO REBOUND: if you are susceptible to thyroid disease -expect a longer rebound to get back your normal thyroid function.

[goose]

This article is by the great `Nandi`,he was a truly amazing guy.


Introduction


It has been over 100 years since the discovery by Magnus-Levy that thyroid hormones play a central role in energy homeostasis, and 75 years since the hormones were first used for weight loss. Despite this great length of time, the precise mechanisms by which thyroid hormones exert their calorigenic effect are not completely characterized, and still actively debated. Despite numerous clinical studies having shown that the administration of thyroid hormone induces weight loss, it is not currently indicated as a weight loss agent. This is probably due to the number of side effects observed during thyroid hormone use at the relatively high doses used in the majority of obesity treatment studies. These deleterious effects include cardiac problems such as tachycardia and atrial arrhythmias, loss of muscle mass as well as fat, increased bone resorption and muscle weakness. Nevertheless, thyroid hormones, particularly triiodothyronine (T3) are a mainstay in the arsenal of drugs used by bodybuilders for fat loss. The widespread underground use of T3 warrants an understanding of its mechanism of action, as well as a knowledge of how it is most effectively and safely used, with an eye to minimizing side effects.



Thyroid Function and Physiology


Before jumping right into a discussion of the use of thyroid hormone for fat loss, a little review of thyroid function and physiology might be in order. The thyroid gland secretes two hormones of interest to us, thyroxine (T4) and triiodothyronine (T3). T3 is considered the physiologically active hormone, and T4 is converted peripherally into T3 by the action of the enzyme deiodinase. The bulk of the body's T3 (about 80%) comes from this conversion. The secretion of T4 is under the control of Thyroid Stimulating Hormone (TSH) which is produced by the pituitary gland. TSH secretion is in turn controlled through release of Thyrotropin Releasing Hormone which is produced in the hypothalamus. This is analogous to testosterone production, where GnRH from the hypothalamus causes the pituitary to release LH, which in turn stimulates the testes to produce testosterone.

In addition to T3, it has recently been recognized that there exist two additional active metabolites of T3: 3,5 and 3,3' diiodothyronines, which we will collectively call T2. Studies have shown that 3,3'-T2 may be more effective in raising resting metabolic rate when hypothyroid subjects are treated with T3, than when normal (euthyroid) subjects are given T3. Therefore in normal subjects 3,5-T2 may be the principal active metabolite of T3 (1)

Like the hypothalamic-pituitary-gonadal axis, the thyroid gland is under negative feedback control. When T3 levels go up, TSH secretion is suppressed. This is the mechanism whereby exogenous thyroid hormone suppresses natural thyroid hormone production. There is a difference though between the way anabolic steroids suppress natural testosterone production and the way T3 suppresses the thyroid. With steroids, the longer and heavier the cycle is, the longer your natural testosterone is suppressed. This is not the case with exogenous thyroid hormone.

An early study that looked at thyroid function and recovery under the influence of exogenous thyroid hormone was undertaken by Greer (2). He looked at patients who were misdiagnosed as being hypothyroid and put on thyroid hormone replacement for as long as 30 years. When the medication was withdrawn, their thyroids quickly returned to normal.

Here is a remark about Greer's classic paper from a later author:


"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" (3)

These results have been subsequently verified in several studies.(3)(4) So contrary to what has been stated in the bodybuilding literature, there is no evidence that long term thyroid supplementation will somehow damage your thyroid gland. Nevertheless, most bodybuilders will choose to cycle their T3 (or T4 which in most cases works just as well) as part of a cutting strategy, since T3 is catabolic with respect to muscle just as it is with fat. As previously mentioned, long term T3 induced hyperthyroidism is also catabolic to bone as well as muscle.

The proviso about T4 vs T3 for weight loss alluded to above needs some elaboration. There have been a number of studies that have shown that during starvation, or when carbohydrate intake is reduced to approximately 25 to 50 grams per day, levels of deiodinase decline, hindering the conversion of T4 to the physiologically active T3.(5) From an evolutionary standpoint this makes sense: during periods of starvation the body, teleologically speaking, would like to reduce its basal metabolic rate to preserve fat and especially muscle stores. However, a recent study demonstrating the effectiveness and safety of the ketogenic diet for weight loss recorded no change in circulating T3 levels.(6) So this issue not completely settled. Nevertheless, persons contemplating thyroid supplementation during ketogenic dieting might prefer T3 over T4 since the bulk of the research does suggest a decline in the peripheral conversion of T4 to T3 during low carb dieting.

Now that we have reviewed a little about thyroid function, let's consider just how it is that thyroid hormone exerts its fat burning effects.



Increased Oxidative Energy Metabolism


Thyroid hormone has long been recognized as a major regulator of the oxidative metabolism of energy producing substrates (food or stored substrates like fat, muscle, and glycogen) by the mitochondria. The mitochondria are often called the "cell's powerhouses" because this is where foodstuffs are turned into useful energy in the form of ATP. T3 and T2 increase the flux of nutrients into the mitochondria as well as the rate at which they are oxidized, by increasing the activities of the enzymes involved in the oxidative metabolic pathway. The increased rate of oxidation is reflected by an increase in oxygen consumption by the body.

T3 and T2 appear to act by different mechanisms to produce different results. T2 is believed to act on the mitochondria directly, increasing the rate of mitochondrial respiration, with a consequent increase in ATP production. T3 on the other hand acts at the nuclear level, inducing the transcription of genes controlling energy metabolism, primarily the genes for so-called uncoupling proteins, or UCP (see below). The time course of these two actions is quite different. T2 begins to increase mitochondrial respiration and metabolic rate immediately. T3 on the other hand requires a day or longer to increase RMR since the synthesis of new proteins, the UCP, is required (1).

There are a number of putative mechanisms whereby T2 is believed to increase mitochondrial energy production rates, resulting in increased ATP levels. These include an increased influx of Ca++ into the mitochondria, with a resulting increase in mitochondrial dehydrogenases. This in turn would lead to an increase in reduced substrates available for oxidation. An increase in cytochrome oxidase activity has also been observed. This would hasten the reduction of O2, speeding up respiration. These and a number of other proposed mechanisms for the action of T2 are reviewed by Lannie et al.(7)

What is the fate of the extra ATP produced during hyperthyroidism? There are a number of ways by which the increased ATP promotes an increase in metabolic activity, including the following:

Increased Na+/K+ATPase. This is the enzyme responsible for controlling the Na/K pump, which regulates the relative intracellular and extracellular concentrations of these ions, maintaining the normal transmembrane ion gradient. Sestoft(7) has estimated this effect may account for up to to 10% of the increased ATP usage.


Increased Ca++-dependent ATPase. The intracellular concentration of calcium must be kept lower than the extracellular concentration to maintain normal cellular function. ATP is required to pump out excess calcium. It has been estimated that 10% of a cell's energy expenditure is used just to maintain Ca++ homeostasis. (1)


Substrate cycling. Hyperthyroidism induces a futile cycle of lipogenesis/lipolysis in fat cells. The stored triglycerides are broken down into free fatty acids and glycerol, then reformed back into triglycerides again. This is an energy dependent process that utilizes some of the excess ATP produced in the hyperthyroid state (8). Futile cycling has been estimated to use approximately 15% of the excess ATP created during hyperthyroidism (8)


Increased Heart Work. This puts perhaps the greatest single demand on ATP usage, with increased heart rate and force of contraction accounting for up to 30% to 40% of ATP usage in hyperthyroidism (9)



Mitochondrial Uncoupling


As mentioned, the mitochondria are often characterized as the cell's powerhouse. They convert foodstuffs into ATP, which is used to fuel all the body's metabolic processes. Much research suggests that T3, like another much more potent agent DNP, has the ability to uncouple oxidation of substrates from ATP production. T3 is believed to increase the production of so called uncoupling proteins. Uncoupling protein (UCP) is a transporter family that is present in the mitochondrial inner membrane, and as its name suggests, it uncouples respiration from ATP synthesis by dissipating the transmembrane proton gradient as heat. Instead of useful ATP being produced from energy substrates, heat is generated instead. There are conflicting studies about the importance of T3 induced uncoupling. Animal studies have demonstrated an actual increase in ATP production commensurate with increased oxygen consumption as we discussed above. Other studies in humans have shown that in fact uncoupling in skeletal muscle does occur. This would contribute to T3 induced thermogenesis, with a resulting increase in basal metabolic rate.(10)

To make up for the deficit in ATP production (as well as provide fuel for the extra ATP production discussed above) more substrates must be burned for fuel, resulting in fat loss. Unfortunately, along with the fat that is burned, some protein from muscle is also catabolized for energy. This is the downside of T3 use, and the reason many people choose to use an anabolic steroid or prohormone during a T3 cycle to help preserve muscle mass. Studies have shown this to be an effective strategy (11). (Muscle glycogen is also more rapidly depleted, and less efficiently stored during hyperthyroidism. This may account for some of the muscle weakness generally associated with T3 use.)

Countering T3 induced muscle loss with AAS or prohormones makes sense from a physiological viewpoint as well. Thyroid hormone muscle protein breakdown is mainly mediated via the so-called ubiquitin-proteasome pathway. (12). (There are several independent metabolic pathways of protein breakdown in the body. For instance, another pathway, the lysosomal pathway, is responsible for the accelerated rate of muscle protein breakdown during and after exercise.) Testosterone administration has been shown to decrease ubiquitin-proteasome activity. (13) So AAS specifically target the muscle protein breakdown process stimulated by T3.

What may not be an effective strategy to maintain muscle mass during a T3 cycle is the use of exogenous growth hormone (GH). Studies have shown that when GH and T3 are administered concurrently, the increased nitrogen retention normally associated with GH use is abolished. This has been attributed to the observation that T3 increases levels of insulin like growth factor binding protein, reducing the bioavailability of igf-1 (14). Nevertheless, GH has fat burning properties independent of igf-1, so using GH with T3 would act additively to speed fat burning, but with little if any preservation of lean body mass. So again, if GH is used in conjunction with T3, anabolic steroid/prohormone use would be indicated.



Andregenic Receptor Modulation


Administration of T3 has been shown to upregulate the so-called beta 2 adrenergic receptor in fat tissue. What is the significance of this effect for fat loss? Before fat can be used as fuel, it must be mobilized from the fat cells where it is stored. An enzyme called Hormone Sensitive Lipase (HSL) is the rate-controlling enzyme in lipolysis, or fat mobilization. The body produces two catecholamines, epinephrine and norepinephrine, which bind to the beta 2 receptor and activate HSL. The upregulation of the beta 2 receptor due to T3 results in an increased ability of catecholamines to activate HSL, leading to increased lipolysis.

Bodybuilders often use drugs like clenbuterol, which bind to the beta 2 receptors and activate them in the same way as the body's endogenous catecholamines. The use of clenbuterol along with T3 can produce an additive lipolytic effect: T3 increases the number of receptors, while clenbuterol binds to the receptors activating HSL and increasing lipolysis. Since clenbuterol itself downregulates the beta 2 receptor, most bodybuilders use clenbuterol in a two week on/ two week off cycle, the rationale being that this minimizes downregulation and allows receptor recovery. Another option is to use the antihistamine ketotifen concurrently with the clenbuterol. Studies have shown that ketotifen attenuates the beta 2 receptor downregulation caused by clenbuterol (15). Moreover, research in AIDS patients has shown that ketotifen blocks the production of the proinflammatory and catabolic cytokine TNF-alpha (16). This may be of relevance to bodybuilders since there is evidence showing TNF lowers both testosterone and IGF-1 levels quite significantly (17) (18), while strenuous exercise elevates TNF levels. (19)

Besides increasing beta 2 receptor density in adipose tissue, T3 upregulates this receptor in human skeletal muscle (12). This has some very intriguing if somewhat speculative implications for the combined use of clenbuterol and T3. Animal studies have shown that catecholamines, particularly clenbuterol, inhibit Ca++ dependent skeletal muscle proteolysis (20). Like the lysosomal and ubiquitin-proteasome pathways discussed above, Ca++ regulated proteolysis is yet another way for the body to degrade muscle protein. Again the implications are enticing: Increased beta 2 receptor density from T3 use, coupled with the beta 2 agonist clenbuterol, could slow this pathway of muscle catabolism.

Another adrenergic receptor important to lipolysis is the alpha 2 receptor, which impedes fat mobilization by counteracting the effects of the beta 2 receptor. There are some conflicting studies about the effects of T3 on the alpha 2 receptor, with studies showing either a downregulation (21) or no effect (22). If T3 does in fact downregulate alpha 2 receptors, this would further aid lipolysis.

Studies in rats have shown that inducing hyperthyroidism increases the lipolytic beta 3 receptor density in white adipose tissue by 70% (23). Beta 3 receptors are abundant in human white adipose tissue as well, and if T3 administration has the same effect in humans, this could could contribute significantly to T3 induced fat loss. This might also argue for taking a currently available beta 3 agonist such as octopamine along with T3 and perhaps clenbuterol.



Decreased Phosphodiesterase Expression


In hyperthyroid patients as well as in normal subjects given T3, levels of the enzyme phosphodiesterase are lowered in fat cells (20). When lipolytic hormones like epinephrine (adrenaline) bind to the beta 2 receptor described above, they initiate a signaling cascade mediated by the so called “second messenger” cyclic AMP (cAMP). cAMP in turn acts on other cellular enzymes to initiate and maintain lipolysis. The original signal is terminated when cAMP is degraded by the enzyme phosphodiesterase. Clearly, maintaining elevated cAMP levels, by lowering phosphodiesterase concentrations with T3, will prolong lipolysis.

As an aside, caffeine is thought to exert at least a portion of its lipolytic action by lowering phosphodiesterase in fat cells. Interestingly, Viagra and Cialis are also phosphodiesterase inhibitors but their action seems to be limited to relaxing vascular smooth muscles.



Increased Growth Hormone Secretion


In vitro, animal, and human studies have all demonstrated that T3 administration increases growth hormone production. (24)(25) Since GH is calorigenic aside from any increase in igf-1, elevated GH may contribute to some of the fat burning associated with T3 administration. This effect may obviate the need for the use of expensive recombinant HGH, as mentioned above.



Decreased Insulin Secretion


Insulin is well known as a lipogenic hormone. It promotes fat storage by facilitating the uptake of fatty acids by adipocytes, and reducing lipid oxidation in muscle tissue. Several studies have shown that thyroid hormone is associated with glucose intolerance resulting from decreased glucose stimulated insulin secretion (26).

This defect in insulin secretion is believed to result from an increase in the rate of apoptosis (programmed cell death) of pancreatic beta cells as a direct effect of thyroid hormone excess.(27) This process is reversible, since when thyroid hormone is withdrawn the rate of beta cell replication increases until homeostasis returns. However, there are conflicting studies regarding the effects of T3 on insulin. For example, Dimitriadis et al (28) showed a decrease in glucose stimulated insulin secretion, consistent with (25), but an increase in basal insulin. They also observed increased insulin clearance, with a compensatory increase in basal insulin secretion.

So if in fact the hyperthyroid state is associated with lower insulin levels, this could explain a portion of hyperthyroid stimulated lipolysis. The obvious downside here is that insulin is also an anabolic hormone. Basal insulin concentration is thought to limit the action of the ubiquitin-proteasome degradative pathway of muscle protein breakdown (29). Of course supplementing with insulin during T3 use would be counterproductive. However, as mentioned above, anabolic steroids inhibit ubiquitin-proteasome activity, so their use could counter any loss in muscle anabolism resulting from a drop insulin levels.



The Future


As mentioned at the beginning of this article, a major roadblock in the adoption of T3 by the medical community as an antiobesity agent is its deleterious effect on the heart. Recent research has identified two isoforms of the thyroid hormone receptor, TRalpha and TRbeta. The TRalpha-form may preferentially regulate the heart rate, and an experimental agent, GC-1, has been developed that selectively binds the TRbeta receptor, with minimal effects on the heart (30). The distribution and actions of TRalpha and TRbeta throughout the body are not yet well characterized. However should it turn out that TRalpha is specific to the heart, then drugs like GC-1 may turn out to be effective fat burning agents with a much safer profile that T3 or T4.

One alleged “futuristic” agent that is here now is T2, or 3,5-Di-iodo-L-thyronine, the T3 metabolite discussed above. Unfortunately, this product does not live up to its hype. It has been claimed to be as or more effective that T3 for fat burning with minimal suppression of endogenous thyroid production. Regarding the relative effectiveness of T2 as a lipolytic agent, and its effect on TSH, this topic was thoroughly covered in a recent article by Bryan Haycock in Muscle Monthly:




All of my research into this subject has led me to the same conclusion reached by Mr. Haycock. That is, T2 is only slightly less suppressive of TSH than is T3, and only packs a portion of the lipolytic punch of T3, with no ability to increase the expression of the UCPs, which is a major determinant of the action of thyroid hormone.



Summary


We have discussed a number of ways by which T3, and its active metabolite T2 act to increase resting energy expenditure. Also discussed were some drawbacks of T3 use, such as cardiac stress, as well as the potential loss of muscle mass. It is ironic that the latter may be of more concern to many bodybuilders that the other more serious potential impacts on health. Nevertheless, used moderately and for short periods (a couple of months or less) in people with no preexisting cardiovascular disease T3 has a relatively safe medical profile, compared to other lipolytic agents like DNP. Perhaps most importantly we have presented substantial evidence that even the long-term use of supraphysiological levels of T3 does not damage the thyroid gland.


References:

(1) Endocrinology 2002 Feb;143(2):504-10 Are the effects of T3 on resting metabolic rate in euthyroid rats entirely caused by T3 itself? Moreno M, Lombardi A, Beneduce L, Silvestri E, Pinna G, Goglia F, Lanni A.

(2)(Greer,M. N Engl J Med 244:385, 1951)

(3)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.

(4) J Clin Endocrinol Metab 1975 Jul;41(1):70-80 Patterns off recovery of the hypothalamic-pituitary-thyroid axis in patients taken of chronic thyroid therapy. Krugman LG, Hershman JM, Chopra IJ, Levine GA, Pekary E, Geffner DL, Chua Teco GN

(5) Int J Obes 1983;7(2):123-31 The effect of a low-calorie diet alone and in combination with triiodothyronine therapy on weight loss and hypophyseal thyroid function in obesity. Koppeschaar HP, Meinders AE, Schwarz F.

(6) Am J Med 2002 Jul;113(1):30-6 Effect of 6-month adherence to a very low carbohydrate diet program. Westman EC, Yancy WS, Edman JS, Tomlin KF, Perkins CE.

(7) J Endocrinol Invest 2001 Dec;24(11):897-913 Control of energy metabolism by iodothyronines.
Lanni A, Moreno M, Lombardi A, de Lange P, Goglia F

(8) Clin Endocrinol (Oxf) 1980 Nov;13(5):489-506 Metabolic aspects of the calorigenic effect of thyroid hormone in mammals. Sestoft L.

(9)Annu Rev Nutr 1995;15:263-91 Thermogenesis and thyroid function. Freake HC, Oppenheimer JH.

(10) J Clin Invest 2001 Sep;108(5):733-7 Effect of triiodothyronine on mitochondrial energy coupling in human skeletal muscle. Lebon V, Dufour S, Petersen KF, Ren J, Jucker BM, Slezak LA, Cline GW, Rothman DL, Shulman GI.

(11)J Clin Endocrinol Metab 1999 Jan;84(1):207-12 Testosterone administration preserves protein balance but not muscle strength during 28 days of bed rest. Zachwieja JJ, Smith SR, Lovejoy JC, Rood JC, Windhauser MM, Bray GA.

(12) Genome Res 2002 Feb;12(2):281-91 In vivo regulation of human skeletal muscle gene expression by thyroid hormone. Clement K, Viguerie N, Diehn M, Alizadeh A, Barbe P, Thalamas C, Storey JD, Brown PO, Barsh GS, Langin D.

(13) J Clin Endocrinol Metab 2003 Jan;88(1):358-62 Related Articles, Links Differential anabolic effects of testosterone and amino Acid feeding in older men. Ferrando AA, Sheffield-Moore M, Paddon-Jones D, Wolfe RR, Urban RJ.

(14) J Hepatol 1996 Mar;24(3):313-9 Effects of long-term growth hormone (GH) and triiodothyronine (T3) administration on functional hepatic nitrogen clearance in normal man. Wolthers T, Grofte T, Moller N, Vilstrup H, Jorgensen JO.

(15) Cardiovasc Res 1998 Oct;40(1):211-22 Terbutaline-induced desensitization of human cardiac beta 2-adrenoceptor-mediated positive inotropic effects: attenuation by ketotifen. Poller U, Fuchs B, Gorf A, Jakubetz J, Radke J, Ponicke K, Brodde OE.

(16) Eur J Clin Pharmacol 1996;50(3):167-70 Ketotifen in HIV-infected patients: effects on body weight and release of TNF-alpha. Ockenga J, Rohde F, Suttmann U, Herbarth L, Ballmaier M, Schedel I.

(17)Endocrinology 1998 Jun;139(6):2863-8 Tumor necrosis factor-alpha inhibits leydig cell steroidogenesis through a decrease in steroidogenic acute regulatory protein expression. Mauduit C, Gasnier F, Rey C, Chauvin MA, Stocco DM, Louisot P, Benahmed M.

(18) Growth Horm IGF Res 2001 Aug;11(4):250-60 Tissue-specific regulation of IGF-I and IGF-binding proteins in response to TNFalpha. Lang CH, Nystrom GJ, Frost RA.

(19) Exerc Immunol Rev 2001;7:18-31 Exercise and cytokines with particular focus on muscle-derived IL-6. Pedersen BK, Steensberg A, Fischer C, Keller C, Ostrowski K, Schjerling P.

(20) Am J Physiol Endocrinol Metab 2001 Sep;281(3):E449-54 Catecholamines inhibit Ca(2+)-dependent proteolysis in rat skeletal muscle through beta(2)-adrenoceptors and cAMP. Navegantes LC, Resano NM, Migliorini RH, Kettelhut IC

(21) J Clin Endocrinol Metab 2002 Feb;87(2):630-4 Regulation of human adipocyte gene expression by thyroid hormone Viguerie N, Millet L, Avizou S, Vidal H, Larrouy D, Langin D.

(22) Metabolism 1987 Nov;36(11):1031-9 Alpha 2- and beta-adrenergic receptor binding and action in gluteal adipocytes from patients with hypothyroidism and hyperthyroidism. Richelsen B, Sorensen NS

(23) Br J Pharmacol 2000 Feb;129(3):448-56 Regulation of beta 1- and beta 3-adrenergic agonist-stimulated lipolytic response in hyperthyroid and hypothyroid rat white adipocytes. Germack R, Starzec A, Perret GY

(24) Braz J Med Biol Res 1994 May;27(5):1269-72 Role of thyroid hormone in the control of growth hormone gene expression. Volpato CB, Nunes MT.

(25) Am J Physiol 1999 Aug;277(2 Pt 1):E370-9 Related Articles, Links Low-dose T(3) improves the bed rest model of simulated weightlessness in men and women. Lovejoy JC, Smith SR, Zachwieja JJ, Bray GA, Windhauser MM, Wickersham PJ, Veldhuis JD, Tulley R, de la Bretonne JA.

(26) Life Sci 2002 Jul 19;71(9):1059-70 Evidence for a deficient pancreatic beta-cell response in a rat model of hyperthyroidism. Fukuchi M, Shimabukuro M, Shimajiri Y, Oshiro Y, Higa M, Akamine H, Komiya I, Takasu N.

(27) Diabetologia 2002 Jun;45(6):851-5 Thyroxine induces pancreatic beta cell apoptosis in rats.
Jorns A, Tiedge M, Lenzen S.

(28) Am J Physiol 1985 May;248(5 Pt 1):E593-601 Effect of thyroid hormone excess on action, secretion, and metabolism of insulin in humans.= Dimitriadis G, Baker B, Marsh H, Mandarino L, Rizza R, Bergman R, Haymond M, Gerich J

(29) Curr Opin Clin Nutr Metab Care 2000 Jan;3(1):67-71 Effects of insulin on muscle tissue.
Wolfe RR.

(30) J Steroid Biochem Mol Biol 2001 Jan-Mar;76(1-5):31-42 Selective modulation of thyroid hormone receptor action. Baxter JD, Dillmann WH, West BL, Huber R, Furlow JD, Fletterick RJ, Webb P, Apriletti JW, Scanlan TS.


goose.....

[Butterfly23GrL]

after i just spent all that time writing my post!!!

This article is by the great `Nandi`,he was a truly amazing guy.


goose.....

[SPIKE]

This article is by the great `Nandi`,he was a truly amazing guy.

That he was Goose, that he was buddy.

after i just spent all that time writing my post!!!

You're telling me that you write that entire post?

[Milky87]

That post is a little suspect, its far too long to be typed (by a sane person atleast), and the different coloured headings.... I dont know anyone who would be bothered do those. And the links?

I say ctrl+c, ctrl+v all the way

[SPIKE]

That post is a little suspect, its far too long to be typed (by a sane person atleast), and the different coloured headings.... I dont know anyone who would be bothered do those. And the links?

I say ctrl+c, ctrl+v all the way

That's what I was thinking. There's nothing to prove by saying that you wrote that, I'd prefer to have someone say they copied and pasted it from elsewhere then say that. Ah whatever.............

[Butterfly23GrL]

That post is a little suspect, its far too long to be typed (by a sane person atleast), and the different coloured headings.... I dont know anyone who would be bothered do those. And the links?

I say ctrl+c, ctrl+v all the way

Yeah, I actually did type almost that whole thing (pretty damn close - and that's why I sourced my references!), thank you very much!!! Most of that research info involves what I do for a living. Plus, it doesn't take me five minutes to type only a few words... you know, it's just like men - you try to do something nice but it's never appreciated! some of us are able to write intelligent post without using ctrl+c and ctrl+v!!!

[OllllO]

Yeah, I actually did type almost that whole thing (pretty damn close - and that's why I sourced my references!), thank you very much!!! Most of that research info involves what I do for a living. Plus, it doesn't take me five minutes to type only a few words... you know, it's just like men - you try to do something nice but it's never appreciated! some of us are able to write intelligent post without using ctrl+c and ctrl+v!!!

I appreciated it...thank you very much!!!

[Barbell]

Hi All,

Does anyone know whether T3 should be taken on an empty stomach such as first thing in the morning before breakfast and again afternoon before a meal or after food?

I'll be running a T3/Clen combo and i've always taken clen on an empty stomach before breakfast and again in the afternoon.

Also is it advisable to take T3/Clen at the same time of day or different times?

Appreciate your help.

Regards

Barbell

[MAXIMA5]

Hi All,

Does anyone know whether T3 should be taken on an empty stomach such as first thing in the morning before breakfast and again afternoon before a meal or after food?

I'll be running a T3/Clen combo and i've always taken clen on an empty stomach before breakfast and again in the afternoon.

Also is it advisable to take T3/Clen at the same time of day or different times?

Appreciate your help.

Regards

Barbell

It doesn;t really matter. They effect your body differently. I take at least 75% of my T3 dose in the morning, if not all. If I choose to break up the T3 dose, I take the last 25% later in the day.

[AleX-69]

Well I think if you know what you are doing T3 (and T4 even more) is a much healthier option than clen is (at least for me)..

I won't touch clen anymore. Maybe some of you didn't now that clen causes heart cells to die?... Moreover it is not that effective for burning fat. Hell, i even burn more fat using regular ECA...

@goose

nandi R.I.P.

[OneMoreSet]

Yeah, I actually did type almost that whole thing (pretty damn close - and that's why I sourced my references!), thank you very much!!! Most of that research info involves what I do for a living. Plus, it doesn't take me five minutes to type only a few words... you know, it's just like men - you try to do something nice but it's never appreciated! some of us are able to write intelligent post without using ctrl+c and ctrl+v!!!

I appreciate you

[Jay-Ace]

Yeah, I actually did type almost that whole thing (pretty damn close - and that's why I sourced my references!), thank you very much!!! Most of that research info involves what I do for a living. Plus, it doesn't take me five minutes to type only a few words... you know, it's just like men - you try to do something nice but it's never appreciated! some of us are able to write intelligent post without using ctrl+c and ctrl+v!!!

I think the reason why your post was spooked was the length, complexity and overall "look & feel" of it... Especially with the choice of font.

I myself would look at that and be suspicious but a thorough search engine hammering with quotes from your post has thrown up no results so I would be inclined to believe that the post is self-written


Good advice from yourself and magic as usual

T3 is indeed a very powerful hormone, I know from my own Hypothyroidism and my advice to you buddy is to get bloodwork done by ya doc before considering it.... For all you know you could have a thyroid problem that teh doc can prescribe something for!!

[shifty_git]

I think the reason why your post was spooked was the length, complexity and overall "look & feel" of it... Especially with the choice of font.

I myself would look at that and be suspicious but a thorough search engine hammering with quotes from your post has thrown up no results so I would be inclined to believe that the post is self-written


Good advice from yourself and magic as usual

T3 is indeed a very powerful hormone, I know from my own Hypothyroidism and my advice to you buddy is to get bloodwork done by ya doc before considering it.... For all you know you could have a thyroid problem that teh doc can prescribe something for!!

dude, 2 year old thread! lol

[MAXIMA5]

"To be, or not to be, t'is the question."

I wrote that.


Seriously though, Goose, that was a great article.
Made me feel better about using T-3 for short interevals.

Anyone have any opinions about the two different ways to cycle T-3?

There's obviously the taper up, maintain, then taper down.
Then there's the high dose for 5 days, then 2 day taper, then 5 days off and repeat.