Cy Willson was once a normal, rosy-cheeked youth who spent his days getting the heifers ready for the county fair. Then, one day, while plowing a neighbor girl in the barn, he was bitten on the ass by a radioactive cow. The bite transformed him, giving him strange powers. Most of them, like being able to sleep standing up, were pretty much useless, but others, like being able to digest pharmaceutical texts at great speed, were pretty handy. Of course, he often read some of these pharmaceutical texts before digesting them.

He became an expert on drugs of all kinds. What's more, after experimentation with some of them, he became more than human. He became a Cy-BORG, ready to answer almost any question about androgens or any other drug, for that matter.

Remember, resistance is futile!

Recharging the Boys

Q: Should a steroid user "load" Clomid? I've heard mixed opinions. What about other anti-estrogen drugs?

A: It really depends on the situation. If you're experiencing symptoms of gynecomastia and need to achieve a high blood concentration of the drug quickly, then yes, you should use large dosages over a short period of time. If you simply wish to restore yourself to a eugonadal state, I don't think it's as important to "load." However, I'd really like people to use the following protocol based on what little info we have concerning the restoration of the HPTA.

Essentially, you need to use 100 mg/day of clomiphene (50 mg, twice daily) for at least 2 months. This protocol is based on both anecdotal evidence as well as a few case reports.

One recent case report involved the reversal of a hypogonadal state in a man who'd previously used nandrolone decanoate, stanozolol, and methenolone for several months. The man complained of common hypogonadal symptoms (i.e., loss of libido, fatigue, depression, etc.) and upon investigation his total and free Testosterone levels were 71 ng/dl and 29 pg/ml respectively. (The reference ranges were 260-1000 ng/dl and 34-194 pg/ml, by the way.)

He was then given 100 mg of clomiphene for 5 days and reevaluated 2 weeks later. He reported an improvement in mood, energy, and libido and his total Testosterone was 828 ng/dl. However, after a follow up 2 months later, his symptoms had returned and his total Testosterone concentration was 301 ng/dl. In other words, he suffered a relapse.

They then gave the man 100 mg per day for 2 months and then reevaluated his blood work. They found his total Testosterone was 705 ng/dl and no relapse occurred in subsequent blood work. A similar case reported restoration of the HPTA using the same dosage of clomiphene over a 5 month period.

Anecdotally, I receive many letters from people explaining that they were feeling great when using clomiphene the first 2-4 weeks after their cycle, but seemed to suffer dramatic drops in terms of body composition, mood, energy levels, etc, thereafter.

My guess is that we've been underestimating the amount of time it takes to recover, even when using compounds like clomiphene. Granted, this probably can't be applied across the board as we have to take in many individual factors including what particular androgens the person was using, dosages, length of time, etc., but extended use of the drug seems to be the way to go. (1-2)

HOT-ROX vs. Clenbuterol and T3 in an Epic Cage Match

Q: I'm sick of all you guys saying how HOT-ROX and other supplements are better than real drugs! Bullshit! Everyone knows that T3 and Clen are the way to go! That's the way it's always been. Either admit it or tell me why clen and T3 suck!

A: My, aren't we testy? Anyhow, it's not that clenbuterol and T3 suck, it's just that the formula contained in HOT-ROX is superior for a few reasons. First, as I've reported previously, the lipolytic effects of a beta-2 agonist are indeed greatly enhanced when in a hyperthyroidal state. However, the problem that remains with clenbuterol and other beta 2 agonists is simply the fact that they bind so avidly to the beta-2 adrenergic receptor that they induce rapid down-regulation of receptor content.

Specifically, with clenbuterol, it's been demonstrated that it begins to cause significant down-regulation of these receptors in 24 hours and can reduce receptor content by as much as 45% in as little as a 12 day period. Essentially, it's a Catch-22 as on one hand, the higher the degree of binding, the greater the lipolytic effects, yet on the other hand, you get a greater down-regulation of beta 2 adrenergic receptor content. Hence the reason why clen is really only effective for 2-3 weeks at a time.

As I've explained previously, ephedrine is superior to beta-2 agonists simply because the rate at which it causes down-regulation of these receptors is much slower and it also has the benefit of an anorectic effect which the more selective beta-2 agonists seem to lack.

Even so, with ephedrine, you do eventually reach the point where down-regulation of these receptors occurs and thus the effectiveness is greatly diminished. One of the reasons why T3 is thought to work so well with beta-2 agonists is simply the fact that it can cause up-regulation of these receptors. However, with T3, you have yet another drawback, that being of course, suppression of endogenous thyroid production. Once you discontinue using T3 you'll be in a hypothyroidal state for at least a month. During that month you'll gain fat at a rapid pace, even if you're consuming the same amount of calories as you were previously. (3-8)

To synopsize, the basic limitations of using Clenbuterol and T3 are the following:

Down-regulation of beta 2 adrenergic receptors

TSH suppression

Lack of anorectic effect

No mood enhancement

With HOT-ROX, though, we're able to increase endogenous thyroid hormone concentrations using the ingredients Sclaremax, A7-E, and 100% pure guggulsterones (as opposed to a standardized extract from Commiphora mukul, which typically only contains 2.5% guggulsterones). Thus, HOT-ROX can be used for long periods of time without any worries of suppression, even when discontinuing use.

With A7-E, we're also able to directly increase levels of enzymes that shuttle substrate and electrons through the mitochondria, as well as increase proton leak across the mitochondrial inner membrane, thereby increasing UCP (Uncoupling Proteins). In general, this means that we're essentially speeding up the metabolism. Also, as an added benefit, A7-E may have anti-glucocorticoid activity. (9-11)

Additionally, the ingredient Sclaremax allows us to activate adenylate cyclase without having to bind and consequently down-regulate beta-2 adrenergic receptor mRNA. In other words, it's a post-receptor agent, which bypasses that first step. Once again, this allows us to use HOT-ROX for prolonged periods without having to worry about a decrease in efficacy.

In case you like hard science, activating adenylate cyclase increases cyclic AMP. As cyclic AMP accumulates in that particular cell — adipose, or fatty cells, for this current discussion — the likelihood that it will bind to protein kinase A increases, and once it binds, protein kinase A then becomes activated. Once it's activated, it then phosphorylates and therefore activates HSL (Hormone Sensitive Lipase), the rate-limiting enzyme necessary for stored triglycerides to be "broken down" and utilized for energy. So, in other words, if you get a compound which increases intracellular cyclic AMP concentrations, you'll get a profound increase in lipolysis (12-13)

I know this is dragging on mightily, but let me get back to thyroid hormone for minute. We have to consider that TSH (Thyroid Stimulating Hormone) activates adenylate cyclase in the membrane of thyroid cells, which in turn elevates cyclic AMP and eventually leads to thyroid hormones being released. So, Sclaremax essentially mimics or acts like TSH, which will further increase endogenous thyroid hormone production. It may also enhance the cyclic AMP response to TSH in thyroid cells as well. (14-17)

Additionally, Sclaremax, like beta 2 agonists, can also be expected to help preserve lean body mass (muscle) while increasing lipolysis. A bonus however, when compared to ephedrine and even more selective beta-2 agonists like Clenbuterol, is that it of course doesn't interact with beta-1 adrenergic receptors and thus doesn't result in excessive stimulation of cardiac tissue. That also means no increase in blood pressure.

Not only that, but since it exhibits a vasodilatory effect, a decrease in blood pressure is expected. Some other benefits would be its' possible antithrombotic effect, thus giving yet another substitute for the use of potentially dangerous substances like aspirin. It may also have antidepressant effects. Last, as an added bonus, since luteinizing hormone exerts its effects on Leydig cells of the testicles (stimulating production of Testosterone) via cyclic AMP, one can expect an increased level of Testosterone with the use of this compound as well. (18-24)

Now, as I explained earlier, these various compounds were chosen not only because of their potent effects individually, but because of their ability to potentiate one another. For instance, it's been shown that lipolysis (activated via an adenylate cyclase activator like Sclaremax) was enhanced by 60% in adipocytes (isolated from human abdominal subcutaneous adipose tissue) taken from subjects with excess thyroid hormone levels. Obvsiously, from this data, we can see how using Sclaremax in the presence of enhanced thyroid hormone levels can lead to a significantly greater increase in lipolysis. (25)

And to top it all off, the product also conatins 5-HTP and acetyl-L-tyrosine, both of which can decrease appetite and improve mood.

Now, what was the question?

Eat the Meat

Q: I've heard a lot of old-school bodybuilders say that you just can't get big without eating plenty of red meat. Is there something to this besides the fact that meat has a lot of protein?

A: You have to eat meat because of the trace amount of androgens and other growth-promoting agents found in the average steak.

I'm kidding of course. If there were one reason why beef would be beneficial, it would simply be due to it's slow rate of digestion caused by the solidity of the protein as well as the fat content, allowing for a slower and steadier release of amino acids in to the bloodstream.

This is also why casein is such a great protein, as I first reported a few years ago. But do I think chicken, fish, or other meats ultimately work well, too? Of course. If you fed one group of bodybuilders nothing but red meat and the other nothing but chicken for a year, you probably wouldn't see any difference between the two groups (assuming all other factors were equal).

What's the dope on Olmifon, Mofo?

Q: Do have any info on adrafinil (brand name, Olmifon)? This is sort of a new smart drug that promises alertness without stimulation. I think European countries use it for treating narcolepsy.

A: Olmifon (adrafinil) is classified as a central-nervous-system stimulant and alpha(1)-adrenergic agonist, being chemically related to modafinil. Modafinil is used in the US to treat narcolepsy. Adrafinil is given orally to mentally impaired elderly people in doses of 600-1200 mg daily in order to improve cognitive function. Since there's little data on Adrafinil, we're forced to use data derived from studies using modafinil as a guide for use.

The "promotion of alertness without stimulation" stems from data indicating that these compounds lack peripheral sympathomimetic effects that are normally observed with amphetamines and related compounds. When modafinil was administered to elderly subjects in placebo-controlled performance studies, they found an improvement in vigilance, enhanced concentration, cognitive function, and mood.

It's also been shown (in healthy subjects, young and old who were deprived of sleep) to reduce subjective feelings of sleepiness and improve memory and efficiency of search tasks. The dosages used to accomplish these effects were anywhere from 200-600 mg/daily. However, the commonly employed doses consist of 200-300 mg/day (usually taken in the morning).

For those who want more info on modafinil, it's half life is around 7-15 hours. Possible side effects include headache, nausea, hypersalivation, nervousness, anxiety, insomnia, euphoria, and to a lesser extent, increased blood pressure and tachycardia.

Because it may cause psychoactive and euphoric effects, along with alterations in mood and perception, it's been classified as a Schedule IV drug.

An anorectic effect is also reported with these alpha(1)-adrenergic agonists. Interestingly enough, some data has recently surfaced indicating that ephedrine's interaction with alpha(1)-adrenergic receptors may be responsible for its anorectic effect as well. This may also be the cause for the feeling of euphoria. (26-31)

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