Growth Stack Design Principles

Disclaimer: many of the compounds referred to in this article may be controlled substances depending upon where the reader lives, always be respectful and mindful of local laws as it relates to AAS possession and use…

Arguably one of the most common questions in bodybuilding circles is “what is the best stack design for maximizing muscle growth?”. Of course, there will never be a singular answer to this question largely due to the individual variances that exist within people. With that said, there are still some general guidelines that one can employ when deciding for themselves how to proceed with their growth stack design process. Please note that this article is designed for enhanced males, and exogenous use by females is to be considered out of scope.

I also want to throw out that, when someone decides to take the plunge into the world of exogenous hormones, they should always begin with a growth phase. Often, the greatest response to hormones comes with the very first experience and so it shouldn’t be wasted during a period of dieting in my eyes. For the vast majority of folks, putting on quality lean tissue is light-years more difficult than shedding body fat, which can be done quite easily without the need for exogenous support.

The last things worth mentioning before we dive into the meat of this article are really just some housecleaning items. I want to be very clear that the decision to use exogenous hormones should not be taken lightly and in some instances it will now become a lifelong commitment. My personal views at this time are that cycling, or the use of exogenous hormones for short duration followed by a period of coming off completely, is not the wisest philosophy. Although nothing concrete exists in the literature, I tend to speculate that the hormonal roller-coaster caused with this method has the potential to be much rougher on the endocrine system that my preferred “blast and cruise” methodology. Simply stated, you replace the “coming off” phase mentioned earlier with a sustained TRT phase where you utilize exogenous testosterone much like an actual TRT patient would (although bodybuilders will often use higher doses during the cruise phase). I will likely get into the health implications of these methods in a later article.

I would also be remiss if I didn’t mention that exogenous hormones should not be used as a crutch in replacement of a properly structured lifestyle, including but not limited to diet, training, sleep, stress, etc. If you don’t understand how to build the structure, then you have no business decorating the windows.

With that out of the way, there are two primary growth compounds I recommend for growth anchor purposes; nandrolone and testosterone. Both are fantastic at what they do, heavily studied [1-2], and each has their own pros and cons to be aware of.

It will ultimately come down to the individual to do some self-experimentation to determine what their individual response to each is. For most beginner/intermediates, it stands to reason that testosterone is the safer option considering it is bio-identical to that which is endogenously produced in the body. With that said, it also converts to estrogen at a higher rate than nandrolone, a process known as aromatization. The conversion occurs roughly five times higher in testosterone than it does in nandrolone [4]. For those who tend to be estrogenic, this is certainly something to consider.

For more advanced users, nandrolone tends to be my recommended growth anchor compound. Nandrolone binds to the androgen receptor with a significantly higher affinity as compared to testosterone [5]. As mentioned previously, it also has a lower rate of aromatization which means that higher doses can often be run, leading to greater hypertrophy potential in the long-run. Now, a very important characteristic of nandrolone needs to be mentioned here and this kind of gets off-topic a bit as it dives deeper into how aromatization works. Bear with me though, this is something a lot of folks don’t understand and it becomes vital.

Testosterone converts to estrogen largely via the aromatase enzyme, one of the handful of pathways used by the hormone [6]. When estrogen levels become too high, as compared to androgen levels, within the body side-effects can occur. Getting into all the sides is beyond the scope of this article, but just be aware that these are precisely what should be avoided. For those on testosterone, there are compounds called aromatase inhibitors (AIs) [7] which can bind with this enzyme to suppress the rate at which this conversion occurs (or suicidally bind). AIs will be discussed, in depth, in future articles.

For now, just understand that nandrolone does not use this same pathway to convert to estrogen [8] and so the use of AIs to control the rate of aromatization will largely be pointless. For this reason, those who suffer from estrogenic sides on nandrolone are going to have very limited options. If an individual obtains significant, unwanted, side-effects from nandrolone then testosterone is more than likely going to have to be the desired growth anchor for them.

Having an androgen:estrogen (A:E) ratio in the body’s desired range is critical for both quality of life [9], but also for the body’s hypertrophy machinery operating at full speed. I do not advocate for the use of a consistent and/or proactive AI regimen during periods of growth. Without turning this into an article on AIs (that will come later), know that there are many undesirable effects that come with their sustained use, many of which directly go against building lean tissue. In fact, estrogen itself has many strength and anabolic characteristics [10] that make it a worthwhile hormone to only suppress during times of emergency (e.g. actual sides begin to develop). So, the punchline here is to leave estrogen alone unless actual sides develop.

As opposed to AIs, androgens can be used strategically for those that tend to be on the higher end of estrogenic activity. Again, it isn’t the overall amounts of estradiol in the system but rather the A:E ratio that largely determines whether one is going to be at risk for sides and/or lower quality of life. DHT derivatives such as drostanolone (masteron), stanozolol (winstrol), and mesterolone (proviron) can be used for this purpose as they do not convert to estrogen themselves and have a high androgenic profile. These compounds also tend to have a high affinity for binding with sex hormone-binding globulin (SHBG) [11] which leaves more free testosterone available to bind to the androgen receptor. Although it is debatable if this is nothing more than a short-term effect, ultimately regulated by the body’s feedbacks, it is still worth mentioning as a possible benefit to those using testosterone as their growth anchor compound.

Oral AAS can be used, but should never be confused for actual anchor compounds. The primary purpose of an oral based AAS should be as an accessory to your growth anchor compound of choice. They can also be used strategically around the workout to increase work capacity and intensity, secondarily leading to greater hypertrophy potential. Both methandrostenolone (dbol) and oxymetholone (anadrol) are great for this purpose. I do not recommend wasting time with other oral AAS variants as they are largely either going to be a waste, highly hepatotoxic, or both. As mentioned above, stanozolol is a bit of a gray area and can be considered an exception if used for the reasons outlined earlier.

Although I am well aware that this may upset folks, I firmly believe that if the need for AIs arises, you are either running too much gear or have designed a stack which your body does not agree with. Instead of continuing to use AIs as part of a band-aid solution, the individual should immediately lower overall AAS doses and/or determine which compound is problematic and then drop it. At the risk of beating this horse to death, AIs are very harsh on our bodies and I also feel strongly that a growth stack should promote as little stress in our body as possible. Abstaining from AIs equals less systemic stress, less systemic stress equals a happier body, and a happier body has the potential to be a more efficient “growth machine”.

These low stress environments are potentially another reason why you can make greater progress using minimalist stack designs when you plan intelligently. I’m a vocal advocate of using a minimum effective dose philosophy, and some stack designs I see floating around the internet are just horrifying. Start small, increase only when necessary, and take a break when the body is giving signs it needs a break.

In a “perfect” world, the individual will simply stick largely to the following compounds for growth purposes:
– Testosterone
– Nandrolone
– Growth Hormone
– Insulin

These are all going to be identical to endogenous hormones in the body so it is likely not a large leap to reason these would provide the most “bang for your buck”. Using things like growth hormone and insulin is not a realistic option for everyone, so that’s why I took time to elaborate above.

REFERENCES

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2. Geusens P. Nandrolone decanoate: pharmacological properties and therapeutic use in osteoporosis. Clin Rheumatol. 1995 Sep;14 Suppl 3:32-9. Review.
3. Velema MS, Kwa BH, de Ronde W. Should androgenic anabolic steroids be considered in the treatment regime of selected chronic obstructive pulmonary disease patients? Curr Opin Pulm Med. 2012 Mar;18(2):118-24.
4. RYAN KJ. Biological aromatization of steroids. J Biol Chem. 1959 Feb;234(2):268-72.
5. Kicman AT. Pharmacology of anabolic steroids. Br J Pharmacol. 2008 Jun;154(3):502-21. Review.
6. Boon WC, Chow JD, Simpson ER. The multiple roles of estrogens and the enzyme aromatase. Prog Brain Res. 2010;181:209-32.
7. De Ronde W, de Jong FH. Aromatase inhibitors in men: effects and therapeutic options. Reproductive Biology and Endocrinology : RB&E. 2011;9:93.
8. Centrella M, McCarthy TL, Chang WZ, Labaree DC, Hochberg RB. Estren (4-estren-3alpha,17beta-diol) is a prohormone that regulates both androgenic and estrogenic transcriptional effects through the androgen receptor. Mol Endocrinol 2004 May;18(5):1120-30. Epub 2004 Feb 5.
9. Bondarenko VO. [The significance of the androgen-estrogen ratios in the clinical picture of sexual disorders in men]. Lik Sprava. 2000 Jan-Feb;(1):44-7. Ukrainian.
10. Lowe DA, Baltgalvis KA, Greising SM. Mechanisms behind Estrogens’ Beneficial Effect on Muscle Strength in Females. Exercise and sport sciences reviews. 2010;38(2):61-67.
11. Sinnecker G, Köhler S. Sex hormone-binding globulin response to the anabolic steroid stanozolol: evidence for its suitability as a biological androgen sensitivity test. J Clin Endocrinol Metab. 1989 Jun;68(6):1195-200.