Negative Steroid Side Effects
Inhibition of the hypothalamic / pituitary / testicular axis (HPTA)
To understand inhibition of the HTPA (and hence, testosterone production), we must first understand how testosterone is produced and how this production is controlled in the body. Broadly speaking, the hypothalamus in the brain receives a variety of inputs (various hormones), and decides whether or not more sex hormones should be produced. If the inputs are high, for example, high estrogen or high androgen or both, then it decides that little or no sex hormones should now be produced. However, if all inputs are low, then it may decide that more sex hormones should be produced. It seems that the hypothalamus doesn’t respond only to current hormone levels, but also to the past history of hormone levels.
The hypothalamus (a region in the brain), itself does not produce any sex hormones – instead it produces LUTEINISING HORMONE RELEASING HORMONE (LHRH), and GONADOTROPHIN RELEASING HORMONE (GnRH); which then stimulates the pituitary gland into action.
The pituitary uses the amount of LHRH as one of its signals in deciding how much LUTEINISING HORMONE (LH) it should produce. Proper response depends on having sufficient receptors for LHRH. These receptors must be activated for LH to be produced. The pituitary also uses sex hormone levels (both current and the past history), in deciding how much LH to produce. Some aspects of the pituitary’s behavior are peculiar. For example, too much LHRH results in the pituitary downregulating LHRH receptors, with the result that very high LHRH production, which one would think should result in high testosterone production, actually lowers testosterone production. Another oddity is that while high estrogen levels inhibit the pituitary, still some estrogen is required to maintain a high number of LHRH receptors. So both very low and high levels of estrogen can inhibit LH production.
LH produced by the pituitary then stimulates the testicles to produce testosterone. Here, the amount of LH is the main factor, and high levels of sex hormones do not seem to cause inhibition at this level.
Anabolic/Androgenic steroids are derivatives of testosterone, and therefore have strong genitotropic effects (relating to genitals). For this reason, it will not be surprising that side effects happen to the reproductive system from steroid use. Application of anabolic steroids leads to supra-physiological concentrations of testosterone or testosterone derivatives. Because these systems operate on a negative feedback loop, AAS will try to redress the balance by reducing the secretion of many important hormones (as mentioned above), concerned with the optimal functioning of the gonadal systems.
Many bodybuilders and pseudo-experts have come to believe that elevated estrogen levels alone are the sole cause of HPTA inhibition, and believe that by blocking estrogen, they can block inhibition. The simple fact though is that this is not true, as we would see no inhibition from non aromatizing compounds like TRENBOLONES, STANOZOLOL etc, which are in fact some of the worst culprits. Estrogens do have a part to play in inhibition, but they are not the full story.
So what other suspect beside estrogen can cause inhibition? DHT, which cannot aromatize, has been extensively shown to cause inhibition of natural testosterone production, making any DHT derivative (like stanozolol), or compound that converts to DHT (testosterone), big HPTA inhibitors
Progesterone can also cause inhibition, making progesterone based compounds like NANDROLONES and OXYMETHELONE of major concern. Are there any drugs left that do not cause HPTA inhibition? Not really
Because high androgen levels sustained around the clock will cause inhibition, conventional cycles simply cannot avoid inhibition of LH production while on cycle. But there are ways to temper the suppression:
Avoid having high androgen levels around the clock
This can be done, for example, by using oral AAS only in the morning, with the last dose being approximately at midday. Even 100 mg/day of say METHANDROSTENELONE, can be used in this fashion with little inhibition. The problem with this approach is that gains are not very good compared to what is seen when high androgen levels are sustained around the clock. Plus, if you are stacking these orals with injectables, then blood androgens will be elevated constantly anyway.
Use an amount and kind of AAS that is low enough to avoid inhibition
MESTEROLONE ENANTHATE (PRIMOBOLAN DEPOT™) at 200-400 mg/week may achieve this effect. Again, gains will be compromised compared to a more substantial cycle however. Testosterone esters and Nandrolone are substantially inhibitory even at 100 mg/week so using a low dose of these drugs will simply result in both inhibition and poor gains. Where AAS doses are sufficient for good gains, an interesting pattern is seen. For the first two weeks of the cycle, only the hypothalamus is inhibited, and it produces much less LHRH as a result of the high levels of sex hormones it senses. The pituitary is not inhibited at all: in fact, it is actually sensitized, and will respond to LHRH (if any is provided) even more so than normally. After two weeks however, the pituitary also becomes inhibited, and even if LHRH is provided, the pituitary will produce little or no LH. This then is a deeper type of inhibition. After this point, there seems to be no definite further ‘switching point’ where inhibition again becomes deeper and harder to reverse.
Shorter cycles to reduce inhibition
As a general rule, there seems to be little difference between using AAS for 3 weeks vs. 8 weeks: recovery is about the same either way. Between 8 and 12 weeks, it becomes more and more likely that recovery will be a little more difficult and slower, though even at 12 weeks it is common for recovery to not be too problematic, taking only a few weeks. Cycles past 12 weeks seem much more likely to cause substantial problems with recovery. Most cycles with recovery problems are past the 12 week+ mark.
Libido and erection frequency and duration (men only, obviously), are often increased during the early stages of a steroid cycle, as endogenous and exogenous testosterone levels are both at a temporary high. As the weeks pass however, performance levels do tend to suffer as the endogenous androgen level goes subnormal since it is most often only natural testosterone levels which are the main libido ‘drivers’.
Intermittent use of endogenous testosterone stimulating compounds such as HCG, CLOMIPHENE CITRATE, and MESTEROLONE, can go a long way to ensuring a minimization (note: NOT total avoidance) of all the negative side effects that a suppressed HPTA cause during a cycle. These compounds also go a long way toward getting the system back up to full strength in a short space of time post cycle, so avoiding the dreaded ‘crash’. One foreign medical study has shown there is conclusive evidence to suggest that on cessation of AAS use, a ‘RESTITUTIO AD INTEGRUM’ (or complete recovery to the original condition), is always seen with regard to endogenous testosterone levels, testicular size, and sperm production, once steroid activity is finished; something the doctors would definitely prefer you didn’t know.
Please note that this excerpt is only a small sample of the book chapter it is taken from. A great deal more content is available on this and many other topics in the Break the Code book.
Excerpts from Break The Code
© 2015—2016 Asgard Publications Inc.