Win a Free Copy of ANABOLIC PHARMACOLOGY
- 05-22-2009, 09:08 AM
Win a Free Copy of ANABOLIC PHARMACOLOGY
This is your chance to win a free copy of ANABOLIC PHARMACOLOGY. How do you win? Post in this thread the questions that you feel are unanswered or unresolved regarding AAS and other anabolics. I will choose the winner based on what I feel is the best unanswered question (I may choose more than one if I feel the questions warrent it). They do not have to be over-the-top scientific nor do they have to be about AAS -- For example, "Can using insulin to gain muscle result in diabetes?" In fact, they don't even need to be answerable - but plus spare us the absurd.
- 05-22-2009, 09:20 AM
I feel this is a very under discussed topic on the forums. Most aas talk is geared towards just bbing. What should the aas regimen of a speed athlete, such as a sprinter, look like? How do they cycle for so long, what dosage, etc?
- 05-22-2009, 09:28 AM
I wanted to add that subjective questions will not be scored very highly (Questions like "Which AAS is best for bulking") unless they are really unique.
05-22-2009, 10:32 AM
05-22-2009, 11:34 AM
Is there a way to determine what anabolic is best suited for your needs(whatever they might be, BB, Speed, etc) by having blood analized before starting a cycle? Also would you be able to determine what pulsing schedule would work best for you?
05-22-2009, 03:25 PM
Since we know that the Q-ratio is almost completely useless in determining how an androgen affects a person, is there any other way to predict how an androgen will work in vivo. Maybe looking at the actual molecular structure itself and determining it's affinity for binding to the AR (since flatter structures generally tend to bind to the AR better).
05-22-2009, 04:26 PM
I would like your opinion on the idea of recreational androgen use for skeletal expansion seth: In your opinion could an increase in final adult be achieved by treatment with DHT without letrozole. My understanding of such a thing would be that non aramotizing DHT would cause an increase in bone growth while lowered amount of estrogen due to suppression would in term slow down the process of the growth plate closure. I would be very interested to hear your opinion on such an issue. Thankyou in advance for your time.
05-22-2009, 05:21 PM
if someone has to run a delayed post cycle therapy, what is the best way to dose hcg and clomid? and should they be run together or should the clomid be followed after the hcg?
05-22-2009, 05:35 PM
I have never used a pro-hormone because of the health problems associated with them. High Cholesterol, high blood pressure, androgen suppression, hepatoxicity, etc.
However, as time goes on and I learn bits more about phs here and there, I am beginning to question the long-term validity of those risks for some products. Suppression can be countered with good pct, cholesterol with other supps and/or diet, etc.
So, my question is, from a medical standpoint, just how detrimental are Phs (assuming proper on-cycle support and pct) on long-term health? If I were to run a couple of cycles over the next few years, would I be increasing my chances of a heart-attack, stroke, kidney failure, cancer, etc?
I am trying to look at the big picture here and do not want to jeopardize my well-being down the road for a few pound of LBM now.
05-23-2009, 11:38 AM
05-24-2009, 11:11 AM
Seth, I dont know if this will be considered a good question or not, it is subjective, but frankly Ive always wanted to ask you. I actually already have your book and its a great great informational guide. Would have been nice to have an index to look like the compound names fast but I cant complain.
But in your opinion, what are the best say..3 (legal) compounds today and why. It could be any reason, lack of sides compared to results, easy PCT, etc. Not only am I curious myself, but I would love to see your input. I realize thats probably not at all what you were looking for but Id love to see an answer.
My other question is pulsing, is it really worth it or not?
05-24-2009, 03:32 PM
I was wondering about the level of effect of testosterone usage. Would a cycle be more beneficial for a person with lower natural test levels? Would a person with higher natural levels need to use more for the same effect?
There seems to be a lot of broscience in this area, but i've never seen anything with actual research.
05-24-2009, 04:37 PM
Based off of the ability to manipulate the chemistry of steroids, and the ability to predict conversion of one hormone into another what can we expect in the future. I mean can we say every steroid ever is already drawn into a book, or based off of the understanding of anabolic androgenic steroids can we expect new creations in the future. As in a another way to tickle our androgen receptors maybe through advancements from current steroids into a chemical compound that can work like a steroids, but have less or side effects. Also how are synthetic steroids created. What raws are used and what methods are used to actually chemically bond every lil element into place to create a large amount of the end product. All a steroid is is simply many smaller pieces put together into something bigger.
05-25-2009, 07:26 AM
05-25-2009, 03:23 PM
I have one for you Seth regarding PCT and the 'testosterone taper method'.
It has been discussed quite a great deal on other forums such as t-nation, here's a thread for your convenience (although I'm sure you probably know how it works!)
Test Taper Protocol
This method of coming off AAS slowly, as opposed to the sharp halt in androgens following a cycle, is supposedly better for hpta recovery, minimising losses on cycle and reduces the dosages of other PCT agents (e.g. SERMS) during recovery.
Do you feel this is a viable method for PCT recovery?
...and if so could it (and should it) be advised for other compounds such as PH/DS?
05-25-2009, 03:37 PM
if HGH lasts for 1-2 days, and the CJC-1295 version lasts for a week, is there any way to tweak existing compounds to make them last longer? realistically, if we can increase a GH product to last 4x longer, could we do the same to steroids for bi monthly injections?
myostatin blockers - why isn't this being pursued through all science venues with regards to it slowing down the wasting disease of AIDS?
cancer cells grow faster when introduced to GH. is it possible to stop the spread of cancer via blocking/shutting down internal GH? follow up question : can we do that while making a strain of GH that is doseable, that cancer doesn't recognize?
that's all i got right now, sorry if its subpar.
05-25-2009, 04:09 PM
Wouldn't running Clomid 25mgs ED on cycle be a smart way to help prevent the shutdown of natural test production?
05-25-2009, 06:37 PM
05-25-2009, 07:56 PM
05-25-2009, 08:00 PM
05-25-2009, 08:10 PM
05-25-2009, 08:12 PM
05-25-2009, 08:16 PM
05-25-2009, 08:20 PM
05-25-2009, 08:27 PM
05-25-2009, 08:39 PM
05-25-2009, 08:50 PM
05-25-2009, 09:11 PM
05-25-2009, 09:24 PM
Genetic predisposition is the by far the most significant and non-modifiable risk factor that can be associated with the development of many disease states in the long run. There really is no way to clearly quantify the significance of AAS on the development of a given pathophysiology due to the numerous variables that can also be playing an underlying masking role.
Evolutionary Muse - Inspire to Evolve
05-25-2009, 09:32 PM
05-25-2009, 09:34 PM
05-25-2009, 09:42 PM
Some steroids are produced by genetically engineered bacteria while some are produced through organic synthesis. the starting material depends on what is being produced and what can be obtained cheaply. There are some published synthetic routes out there and some of the more efficient ones could probably be found in the patent literature. I have a bunch of older synthetic routes but they would probably be laughed at by modern synthetic organic chemists.
05-25-2009, 09:45 PM
05-25-2009, 09:47 PM
can you become sterile even with proper pct consisting of just a serm. (thats all alot of people can get their hands or just choose not to use hcg)
05-25-2009, 09:57 PM
Myostatin blockers are being pursued for wasting disorders.
Cancer cells grow faster in response to GH largely due to increases in IGF-1. IGF-1 works through the AKT pathway and the AKT pathway is usually is a major driver of tumor growth. IGF-1 receptor blockers as well as AKT inhibitors are being developed as anti-cancer agents. The question is, will these resulting in global cellular starvation and thus it becomes a race of which will die first, cancerous tissue or normal tissue?
Since the pro-cancerous effects of GH are largel mediated through elevations in IGF-1 you would have to produce a GH that does not elevate IGF-1. This is probably not possible for maintaining the growth-promoting effects of GH but may be possible while retaining the "leaning" effect of GH.
05-25-2009, 09:59 PM
05-25-2009, 10:02 PM
05-25-2009, 10:02 PM
I was going to offer to be your best friend but I guess its not needed.
Im really digging all these questions and the answers given so far.
I would love to see a dumbed down explanation on tapering. Im gonna look around and read up and try to understand but just throwing it out there. Like, since Ive been researching Epi, maybe you could use that. I am pumping you for info, I wont be bashful.
Thanks for doing this regardless.
05-25-2009, 10:05 PM
05-25-2009, 10:08 PM
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