How to use clenbuterol

Question: Whenever I use clenbuterol, it works great for about two weeks. After that, I can use ten tabs a day and my temperature will hardly rise. What can I do about this?

Clenbuterol is a beta-2 agonist. It attaches to the same receptor as your natural adrenaline and noradrenaline do. It has a very high bonding capacity to the adrenergic receptor. Whenever a drug fits well onto a cell receptor , the receptor becomes resistant to that drug. For example, the thermogenic effect of ephedrine seems to have a longer duration (though it’s not as potent ) for two reasons: 1) ephedrine doesn’t have a high receptor affinity, and 2) ephedrine is not beta-2 specific.

You might have heard about the newly discovered beta-3 receptors. The receptor is primarily a thermogenic messenger, and over half the thermogenic effect from ephedrine is from beta-3 stimulation. Although the thermogenic message is not as intense as the beta-2 message, beta-3 receptors are very resistant to down-regulation. Clenbuterol, however, has very little beta-3 stimulation.

Until some new synthetic beta-3 agonist is commercially available, the beta agonist of choice is still clenbuterol (although the stronger cimaterol is available as a research chemical in the U.S.). The rapid receptor sensitivity attenuation happens to all users, and the various dosage schemes (i.e., two days on, two days off) just aren’t successful.

This attenuation and the lowering of above-normal body temperature are governed by two different mechanisms. I’ve written about one of them before: the shunting of T4 thyroid away from the active T3 form into the ineffective reverse-T3. Most of the thyroid in the body is the inactive T4 type. The active thyroid that actually fits onto thyroid receptors is a reduced T4, and reduced T4 occurs when one of the iodine atoms is cleaved off the molecule by a specific enzyme (deiodinase). Since we have no way of stopping the T4 from being transformed into ineffective reverse-T3 instead of

he active T3, and there’s no such thing as injectable deiodinase (which would prevent the reduction), the best approach is to supplement the missing T3 with Cytomel, a synthetic T3.

The trouble is, it’s likely a daily amount of Cytomel higher than 25 mcg would eventually stop the production of natural thyroid stimulating hormone (TSH), and the up-regulation will take about 8 weeks. Then, when you go off Cytomel, your body’s still laggin’ ihe down-regulation of the beta-2 receptor. The receptor actually is still in the cell but not in its usual place. The receptor must be at the outside of the cell surface to be available to the beta agonist. There is research showing that the antihistamine ketotifen (trade name Zaditen by Sandoz) in large dosages will up-regulate ox. It sells for 65.10 francs (about $12.25). Because of its appetite-stimulating and muscle-building properties, Zaditen is sold through some of the American AIDS buying clubs. The average price for it in America is $40 a box. The dose needed for the up-regulation of the beta-2 receptors is about 10 capsules (10 mg)–assuming you’ve been using 3 clenbuterol tablets (60 mcg) each day. Sigma Chemicals, the company that has all the bodybuilding goodies that we like but can’t buy (including steroids), does sell ketotifen (the fumarate version is water soluble) in raw bulk form. Keep in mind that even when used with clenbuterol, which both reduces appetite and is more of a stimulant than caffeine, Zaditen will still cause sleepiness and hunger. Those aren’t nice effects, especially if you’re dieting.

Your final solution to sustain clenbuterol’s action is to use both Cytomel (25 mcg) and Zaditen (10 mg) each day after using clenbuterol by itself for 2 weeks . You’ll need only 60 mcg of clenbuterol for a very pronounced thermogenic effect, hypothetically speaking, of course.

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