Why do we need another article on HPTA recovery?

[FUZO]

TweetWhy do we need another article on HPTA recovery?



Recently, I’ve received a number of questions regarding the newest over-the-counter HPTA stimulating compound ATD. It seems some believe that anything that requires a prescription is better; and if ATD works, it must work better by throwing in some HCG, Clomid (Clomephine Citrate) or both.

I’ve met many types of bodybuilders. Some are meticulous and methodical about everything they do, from the way they train to the food they put in their mouths. Others train and eat haphazardly, and when that doesn’t work, they get ten different opinions about the latest drugs to use, and then they try them all. The same goes for HPTA recovery.

I have a friend who’s on the fast track to requiring permanent Hormone Replacement Therapy due to his not understanding proper HPTA recovery. His approach is to combine high doses of at least five different androgens for eight to 12 weeks, and then to take three weeks of continuous HCG for “Post Cycle Recovery.”

Let’s take a look at what’s really happening in his body.

First, his natural testosterone production sucks due to years of androgen abuse. But let’s assume that this is the first time doing this so you see can where he’s going. Depending on the lab you use (and how their tests are calibrated) the “normal” reference range of testosterone can vary. For example, Quest Diagnostics has a reference range of 241 – 827.

We’ll call my friend Joe. Joe starts with a testosterone level of 590, which is pretty decent actually. Joe starts his androgen cycle and by the end of week two his natural testosterone production starts to rapidly decline. Here’s why:

For our example, let’s say that Joe is using only Testosterone Cypionate. Testosterone readily aromatizes (converts) via the aromatase enzyme to estrogen. His circulatory levels of estrogen start to rise over the course of the first two weeks. Some of those estrogen molecules attach to the estrogen receptor sites in his hypothalamus—this is the first negative feedback mechanism that reduces testosterone production.

At the same time, Joe’s testosterone levels are through the roof due to the administration of the Testosterone Cypionate. Joe gets blood work at the end of week two. (Actually Joe rarely gets blood work as it’s too “scientific”—but bear with me.) The lab informs him that his testosterone levels were so high that they couldn’t accurately measure them. The test maxes out at 1600.

The testosterone that Joe has administered looks and acts the same way that natural testosterone does in Joe’s body. That’s because the base testosterone molecule that Joe is injecting is in fact identical to the molecule produced by his testicles. The testosterone molecules floating around in his bloodstream also readily attach to the androgen receptors in his hypothalamus. This is the second negative feedback mechanism that reduces testosterone production.

Now Joe’s hypothalamus figures that since his estrogen levels are high and his androgen levels are also high, he must be producing too much testosterone. Put the brakes on! The hypothalamus produces a hormone called GnRH (Gonadotropin Releasing Hormone) that interacts with the pituitary. This is a key hormone in the cascade of events required for Joe’s body to produce testosterone. Because Joe’s hypothalamus figures that he’s producing too much testosterone, it shuts down GnRH production.

Let’s take a look at Joe’s pituitary gland now. Joe’s pituitary is waiting to be told to produce two hormones, LH (Leutenizing Hormone) and FSH (Follicle Stimulating Hormone). The pituitary knows to make these hormones when it interacts with GnRH. But now Joe’s GnRH production is dramatically reduced because his hypothalamus figured that too much manly stuff is goin’ on.

As a result, LH and FSH production also significantly drop. Finally Joe’s testicles are hanging out (the left one slightly lower), waiting for LH and FSH to show up to tell them to do manly things. But when LH and FSH don’t show up, the “boys” start getting lazy. Not only do they stop producing testosterone, but they can also reduce in size. (I’ll come back to this). Raisin nut syndrome ensues and Joe earns the nickname “Two Scoops.”

Let’s fast forward to week eight. Joe’s LH levels have dropped to near 0. His testosterone levels are still high, however, as he’s just finishing his cycle of testosterone. It will take about two weeks for the majority of his last dose of Testosterone Cypionate to clear his system. Then somebody at the gym told Joe that he should use HCG (Human Chorionic Gonadotropin) for three weeks and then start his next cycle.

HCG is very similar in structure to LH and in fact, testicles don’t seem to notice much of a difference. Joe starts to administer HCG every day and his testicles start producing testosterone as a result. After a couple of weeks, Joe’s testicular size starts to return to normal and he thinks that everything is OK.Let’s take a closer look. The HCG directly stimulates the testicles to produce testosterone. Joe’s androgen levels drop slightly over the next few weeks as the Testosterone Cypionate clears his system. However, because of the HCG, they stay in the high-normal range. The HCG also up-regulates Joe’s aromatase activity which increases the conversion of some of that testosterone to estrogen. Joe’s estrogen levels are already elevated from his cycle, so the additional aromatase activity is certainly not welcome. Let’s hope “Two Scoops” doesn’t need a sports bra.

While his testicles are producing testosterone, his hypothalamus still thinks that Joe has too much testosterone as a result of the elevated estrogen levels and still relatively-high androgen levels. Now his pituitary is also getting bored. Three weeks later, Joe discontinues the HCG and gets a blood test. (Yeah right, Joe thinks blood tests are for nerds).

The HCG is fast acting and has cleared his system. His estrogen levels are still quite elevated thanks to the extra aromatase activity, but his testosterone levels are now below 100. As a result Joe can’t get an erection to save his life and is taking Viagra daily to keep up with his girlfriend. Figuring that this is no way to live, he starts his next cycle of testosterone without giving thought to the fact that despite the HCG, he never recovered his HPTA and a few years down the road he’ll be staring into the mirror wondering why he can’t have kids.

Now let’s say that Joe actually listened to us science geek types and took an alternative approach.

This time Joe still takes Testosterone Cypionate. He also takes ATD every night starting at week one. In our tests we used four capsules of Ultra H.O.T. by ALRI. I like ALRI’s ATD analogue because it seems to be the most effective with the fewest peripheral side effects. However, there are other manufacturers out there with respectable ATD products.

As I’ve explained in the past, ATD works via two mechanisms.

First it acts as an aromatase inhibitor dramatically lowering estrogen levels. Joe’s estrogen levels now only experience a modest increase despite taking 700 milligrams of testosterone per week.

Second, ATD occupies the androgen receptors in the hypothalamus in a way that makes that receptor site inactive. It doesn’t do this in muscle tissue though, which turns out to be a good thing! The high androgen levels from his testosterone administration combined with the receptor blocking behavior of ATD causes Joe’s hypothalamus to believe that his testosterone levels are only somewhat elevated.

Let’s fast forward again to week eight. This time Joe’s testosterone levels are again high (slightly higher from last time). Interestingly his LH levels have only dropped by about 30 percent.

Over the next three weeks, Joe only takes ATD nightly. No HCG or other pharmaceuticals. The day after Joe’s last dose of ATD he gets blood work. Joe likes blood work now because he cares about what he’s doing to his body and realizes that an intelligent approach will allow him continued progress while staying healthy.

Joe’s blood work comes back. His total testosterone is actually slightly above the normal range. So is his LH. During the last three weeks, Joe has been stimulating his entire HPTA, not just a single gland. (I should mention that his girlfriend is quite happy too.) Joe can continue taking ATD over the next few weeks and his testosterone will likely continue to rise until it reaches somewhere between 800 and 1200.

But Joe doesn’t get it. He doesn’t understand how completely amazing it is that an over-the-counter supplement not only totally out-performed prescription pharmaceuticals, but also out-performed nature. He tells me that he wants to add some HCG and maybe Clomid. I groan.

I explain to Joe that adding HCG will only shortchange the whole process that makes ATD so effective. If you’re directly stimulating your testicles with an exogenous hormone your pituitary has little need to produce LH or FSH. If testicles are producing lots of testosterone because of the HCG, your hypothalamus won’t be producing much GnRH.

What about Clomid? Clomid works by blocking estrogen receptors in the hypothalamus and in theory wouldn’t interfere with the action of ATD. But let me say this—within two to three weeks Joe was able to maintain above normal testosterone production. Weeks later he was well above normal. Why do you feel the need to add Clomid?

I’ve seen the lab tests. ATD is quite simply the most superior HPTA stimulating compound now known. No need to add HCG, Clomid, Arimidex, Nolvadex or ground-up bull testicles.

Of course in real life, Joe never listened to me. He’s switched to Cialis now. The Viagra was making him see blue.

[Slightly Enhanced]

TweetYo fuzz, where is the source

[FUZO]

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