posted May 21, 2000 07:44 PM            

To minimize side effects in women we first need to understand what causes them. Obviously too much stimulation of our androgen receptors is the main culprit, but why are some AAS better (safer) than others, and why are injectables considered safer than orals (Anavar the exception)?

The current best hypothesis about the masculinizing side effects of AAS is the 'threshold' concept. This theory states that the androgenic effects of AAS only occur when a certain (undefined) minimum number of receptors are stimulated at one time. This would mean that it's not the total dose of AAS that matters, but how much of the AAS is bound to receptors at one time.

There are many variables that can affect this. Sex-hormone binding globulin (shbg) is one very important factor that is often over-looked in females. This protein reversibly binds many hormones and keeps them inactive as long as they are bound. This is the hormone in men that means the difference between 'free testosterone' and 'bound'. Because of the relatively low doses of AAS used by women, individual variations in the level of this hormone can make a huge difference in a women's individual response to AAS. Thus the sound advice to proceed slowly when trying a new drug/dosage regime.

Also important is the half-life of the AAS. Oral winstrol has a very short half-life, which means it gets into your system, peaks rapidly, then gets cleared quickly. This half-life profile is actually not very good for women because it's the large swings (ie high circulating concentrations) that are most likely to cause side effects. Injectable winstrol is slightly better. It releases a little slower than the oral, but because it is water based (no ester side chains) it still can cause large peaks and valleys in the blood levels.

Primo is considered safer for women, but again you need to distinguish between the oral and injectable . The oral Primo also gets 'in and out' relatively quickly, and is therefore a more risky choice. Primo Depot, on the other hand, has an enanthate side chain and is suspended in oil. This makes the primo more soluble in fat and effectively slows it's release over a 10-14 day period.

Deca-Durobolin is another oil-based injectable which has a half-life even longer than Primo injections. We all know how the extreme fat solubility of this compound has caused grief for many a drug-tested athlete long after they've ceased to use it. Though in reality it's effective life is only around 3-4 weeks, tops.

Sustanon is a mixed ester of testosterone which is a favorite among male athletes. This is an interesting mix of quick and slow release esters. It's beauty is in it's delivery of a quick hit but also longer lasting effects (up to 4 weeks).

So what does this all mean for us women? In an ideal world, we would take AAS under the supervision of a doctor who would monitor our blood levels and give us just enough to keep them below the 'threshold' saturation at all times. In reality, even a good doctor wouldn't know exactly what this threshold is, and in the US they certainly are not going to oblige us.

So first of all, go slowly with AAS. Take the minimum amount that will give you the desired effect, and be prepared to discontinue the instant you notice negative side effects. With esters such as Deca keep in mind that the 50 mg you inject this week will still be releasing around 15mg in your next week, and the 50 mg you inject next week will release around another 15 mg, and so on for up to a month. It may be better to use these longer acting esters in a larger initial dose, tapering down each week until week 3-4. For instance something like 100mg first week, 50 mg second week, and maybe 50 mg every second week after that. Sustanon would ideally be used differently. Because of the quick-acting testosterones in it, it's better not to take too much of this stuff in one go. Take small doses every week for not more than 4-6 weeks. Primo is traditionally injected once per week by women. Maybe this is a matter of convenience (it's Sunday so it's time to inject again), but this drug is probably safer used once every 10 days. If you use it more often than this you should adjust the dose downwards. 50 mg per week is not the same as 50 mg every 10 days!! I know how obvious that sounds but it can make a big difference over a longer cycle.

As for cycle length, we can see from the above info that shorter cycles are safer for women using slow release esters (Deca/Primo/Sustanon). This is to avoid build up of them and the potential side effects associated with the build-up. The quicker acting orals (and winny injectable) can be cycled for longer, but it's better to divide the dose up into as many small ones as possible. For instance, get a pill-cutter and divide your winny into 4-6 doses taken evenly through the day/night.

Combining orals with injectables gets very complicated for women. Most women make better gains by stacking, but run a MUCH greater risk of sides. The safest 'stack' would be Anavar with any of the slow-release injectables. Winny with long-life esters should be treated as a risky combo. You've been warned!

Of course everything I just said does not apply to Anavar. For some reason this quick-acting 17-alkylated oral has very low side effects and toxicity for women. Don't ask me why. Just consider it a gift from the gods if you can get hold of it. The only problem with Anavar is it lacks a good 'kick'. By this I mean that it's lack of androgenic properties makes it good for dieting and modest gains without sides, but doesn't give you the same 'juiced' feeling that you get from other AAS.

I'd love to get feedback from you women (and men) on your personal experiences with AAS. Everyone's different and we really have to be our own scientists in this field, 'cause nobody else is going to set-up nice, controlled studies for us to learn from.

------------------
The Mad Scientist

[This message has been edited by MS (edited May 21, 2000).]

posted May 22, 2000 12:17 PM            

If so, then this shifts the focus back to differences in structure between the various AAS. Possible 'threshold' effects are extracellular. Structural differences between AAS analogs could also affect the interactions of the AAS-receptor complex with the binding sites on the various genes.

A few possible structure variations come to mind.

AAS where ring A is saturated between carbons 1 and 4 vs. those that are not (eg. stanolone/DHT vs. test.)

modifications that affect the affinity for receptor either by allowing the molecule to be more planar (eg. 19-nor) or other reasons.

modifications that could affect the affinity for SHGB (halo?)

modifications to alter the reactivity of the carbonyl group at position 3:
(this last group includes practically everything remaining...) Some of these modifications may be more effective than others at reducing the activity of that carbonyl group. The lactone structure of oxandrolone just might happen to be very efficient at damping activities relying on that carbonyl group.

Some processes of virilization may be more dependent upon one of these factors than others. For instance: scalp balding may depend upon a stanolone shape. So both oxandrolone and methenolone contribute to balding even if the other androgenic activities are very well damped with these agents.

posted May 22, 2000 04:25 PM            

Your revised cycle sounds ideal to me. Especially if you were tolerating 100mg primo per week. Dropping the Primo slightly (100mg every 10 days) and increasing the Anavar should be nearly as good with reduced risk of sides.

Artemis, you have hit on the crux of the whole AAS issue. Why don't you all get a fund together, send me $1,000,000 and I'll do the research. I mean for instance, we know that Nandrolone doesn't cause acne or hair-loss (or gyno) becuase it can't convert to DHT or estrogen directly. And we also know it hangs out at androgen receptors a lot longer than T but exactly which change in it's structure is responsible for this??

And Oxandrolone still partitions nutrients into muscle, but at reduced efficiency and much fewer sides compared to T or Nandrolone. WHY?? Seems to me if we could combine the active sites of Nandrolone with Oxandrolone in a slow-release depot injection we could become very wealthy people. And while we're at it, lets make this new super-AAS undetectable in a urine test!! (a good return on your million dollar investment).

And you're correct about the orals. The 17-AA all have very fast clearance times. I think around 8 hour half-life for winny, anavar a bit more complicated (bi-phasic half-life at 35 minutes and 9 hours). DBOL/Halo/Anadrol etc... I don't know, but I'll bet they're in the same ball-park. There's just no mechanism I know of that would stabilise these orals for any length of time. It would be another boon to 'medicine' (ok I really mean us iron-heads) if you could stabilise the orals for longer without shooting the liver to pieces. Sigh. Any investors out there?

posted May 23, 2000 10:19 AM            

I'm going nuts not remembering what that article said cause I was thinking, "OOOO better oral dbol and A50's!!"

Late

posted May 24, 2000 12:22 AM            

Nandrolone also has progestational properties. Which if I remember correctly, can act to upregulate the estrogen receptor?

-still working on a solution to the cholestasis concerns... or a work-around.

posted May 25, 2000 07:00 PM            

Nandrolone does have progestational properties. But it actually DOWN-regulates estrogen receptors (ie is anti-estrogenic). You might have it confused with estrogen, which UP-regulates progesterone receptors. This is why fluid retention is such a problem with Deca and birth control pills. They both effectively increase progesterone activity which is the real culprit. In other words anti-estrogens alleviate bloating in part by blocking an increase in progesterone. Hey, hormones get confusing even on a good day.

posted May 25, 2000 07:17 PM            

Both you two (MS and Artemis) need to be confined to a room. And when you both have figured out the perfect roid for all mankind, could you then 'splane it in NORMAL english to the rest of us pore iron heads <:P

heheheh

Late

Lobo

posted May 26, 2000 01:38 AM            

And a related question: how well does quinbolone work? Anybody know?

And yes: estrogen upregulates it's own receptor plus the progesterone receptor, while progesterone downregulates both.
Nature 254:337-339, 1975. My mistake.