Is stacking necessary?

ILiftBig

Member
This study has some important finding because it shows that there is a saturation level with anabolic steroids. In other words a point in which more is not better. It also further shows that some steroids compete with others when being stacked and either displace the other ones or actually inhibit their actions.

1: Pharmacol Biochem Behav. 2006 Mar;83(3):410-9. Epub 2006 Apr 17. Links

Stacking anabolic androgenic steroids (AAS) during puberty in rats: a neuroendocrine and behavioral assessment.

Wesson DW, McGinnis MY.
The University of Texas at San Antonio, Department of Biology, 6900 North Loop 1604 West, San Antonio, TX 78249, USA.
Anabolic androgenic steroid (AAS) abuse is increasing in teenagers. We examined the effects of stacked AAS in adolescent male rats. Stacking, in which multiple AAS are taken simultaneously, is commonly employed by humans. Beginning at puberty gonadally intact male rats received testosterone, nandrolone, or stanozolol. Additional groups received stacked AAS: testosterone + stanozolol, nandrolone + stanozolol, or nandrolone + testosterone. Injections continued during tests for sexual behavior, vocalizations, scent marking, partner preference, aggression and fertility. Body and reproductive tissue weights were taken. Sexual and aggressive behaviors were increased by testosterone yet inhibited by stanozolol; nandrolone had no effect. Stacking testosterone with stanozolol prevented the inhibitory effects of stanozolol. Body weight was decreased by testosterone and all stacked AAS. Cell nuclear androgen receptor binding in brain was significantly increased in nandrolone males and decreased in stanozolol males; testosterone males were slightly higher than controls. Androgen receptors in stacked groups were intermediate between individual AAS suggesting that stanozolol competed with other AAS for androgen receptors despite its low affinity. The results indicate that stacking AAS influences the effects of individual AAS on behavioral and endocrine measures, and levels of androgen receptor occupation are not directly correlated with AAS effects on behavior.
PMID: 16603236 [PubMed - indexed for MEDLINE]

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eeenteresting.....

My thoughts: there can be some competition for the AR, but using AAS actually increases the number of androgen receptors, and they don't necessarily ever reach a saturation point- this is more like an attenuative effective- your body trying to maintain homeostasis.....start low dose, finish medium, and take decent-sized breaks with good pct and flawless nutrition and supplementation and you will be golden.

This is why tapering does not work:

Your endogenous cortisol levels rise sharply after about the 4-6th week of a cycle in relation to increased TST levels- and many of the gains seen after the 4th or 5th week have more to do with a competitive anti-catabolic effect than anything else, UNLESS:
1. you substantially increase the dosage (increase by 1/3 or even double it)
2. you inhibit the limiting factor in some other manner (in this case, cortisol)- I probably wouldn't attempt this- it can lead to some other major issues
3. you find a way to manipulate other suppressive factors- ie. SHBG
4. you add in something that delivers some non-AR mediated effects that work in concert with the single compound you are using (ie. stacking)

Think of it in a ratio-based fashion- weeks 1-3 (depending on esterfication, type of compound used, etc.) test levels begin to rise way above baseline, and concommitant cortisol has not begun to increase substantially- so the TST-CRT ratio is positive. This positive ratio decreases with time and as cortisol levels increase, unless the dosage is adjusted upward or cortisol production is blocked (again, do not attempt this). By week 4,5, or 6, the ratio becomes neutral, but you will still incur gains due to the anti-catabolic nature of anabolics and remember cortisol antagonism is not the same as blocking cortisol production, big difference. However, the gains will be in a much slower fashion.

Several Solutions- I suggest these b/c I have seen them work in the real world, and not on rats, lol- single compound solutions:
1. I prefer the KISS approach- and this would apply to injectibles only- start with one compound- and double the dose at week 5- I would have a finite length in mind to the cycle, and have some type of goal in mind, and don't go over 8-9 weeks. This will keep that ratio positive the entire time- but have a good PCT ready, you will need it...
2. Fast-acting oral- double or increase the dose by 1/3 at day 17 until cessation at day 35

Stacking:
1. Start with a single injectible- something aromatizing with type I and II effects- test would be a good fit. Add in stanozolol or mesterolone at week 5 to knock out SHBG
2. Start with an injectible (aromatizing) and an oral (non-aromatizing) to jump start- and on week 5, increase the dose by 1/3 to 1/2
3. reverse 2 and use a non-aromatizing inject, and an aromatizing oral, and on week 5, double the dose
4. Start with solution 2 or 3, and then add in GH, slin, and/or IGF-1 instead of ****ing with the dose

you don't necessarily have to stack AAS or PHs for them to work- it is more of a timing and dosage manipulation to get the most bang for your buck.....
 
Saturation of the AR does occur and at fairly low doses. Even if there is upregulation (which has been debated to death) it would only be relevant in skeletal muscle and would likely only occur in satellite cells and would not significantly expand the pool of receptors.

Even though saturation occurs and different AAS will compete with the AR there are non-AR effects that seem to differ from one molecule to the next. So, like rms80 said, that should be the purpose behind stacking is to take advantage in differences between off-target effects.

I do disagree with rms80 on a few points. The first is that tapering has no benefit. When one discontinues usage abruptly, if cortisol levels have risen either later in the cycle or after discontinuation, then the total absence of any endogenous or exogenous anabolic androgen will allow for the full catabolic effect of elevated cortisol to be exerted without opposition. Although any dose of androgen is suppressive, it is not an on/off switch.

The belief that SHBG is suppressive is one that needs to be updated. Large doses of AAS rapidly exceed the binding capacity of SHBG and many AAS have little to no binding to SHBG anyway. Additionally, albumin binding will compensate for a reduction in SHBG since albumin has a very large binding capacity. Furthermore, SHBG has a protective effect against some of the side effects of AAS.
 
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