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Do different compounds use different recepters. Would a more androgenic steriod, say test use the same recepters than an anabolic. e.g. Deca. Is this one of the reasons why those who are on for a long period of time cycle different compounds? Or am I wrong and all anabolic/androgenic compounds use the same pathways?
Good question... here is what I have learned...
Basically, steroids were created to modify testosterone (the body's most potent naturally occuring androgenic-anabolic steroid). To make compounds that had a lower androgenic function and higher ananbolic, in the medical field this is shown on the Therapeutic Index for Anabolic Steroids. To date though, no perfect steroid has been made that is purely anabolic, so they are all referred to as androgenic-anabolic steroids (AAS).
The androgenic function promotes male characteristics. The anabolic portion promotes metabolism and building. How an androgenic-anabolic steroid binds to different AR's determines it's anabolic-androgenic ratio... but receptors are on or off. There are no androgenic recepetors for different compounds however some compounds have a higher affinity for binding with different AR's. One may bind well to muscle cell receptors while another binds better to brain cell recepetors.
For example, testosterone binds well to the cytoplasm of the muscle cells that triggers greater protein synthesis - when combined with high protein intake and resistance trianing results in enhanced muscle building. Testosterone also binds to osteoblasts which stimulates bone mineral density, ... and so on...
To give you an example of the Theraputic Index for AAS, here are a few ratings using testosterone as 1 (the base):
Testosterone: 1
Nandrolone Decanoate: 11-12
Primo: 7-16 (the higher number probably closer to the injectable enanthate version)
Winstrol: 5-20 (again... different forms and ways to administer Stanozolol)
Anavar: 13
Dianabol: 2-7
Not your scientific answer but yes. You change up to hit different receptors. The idea behind "changing up" is that the individual steroid cannot lead to a saturation of the receptors as is the case if one or two steroids is taken over the entire period. This leads not only to good overall results but also to a continuous effect. Also, some compounds ( most commonly ) winny can only be run for a short time say 6 weeks due to the stress on the liver.
One reason for this is that people who have more receptors to turn on will run larger amounts of AAS. A lean 220 pound bodybuilder would use more total androgens than a lean 190lbs BB. So... if this larger fella were to combine nandrolone (a 19-Nor modified testosterone) with testosterone he would get the benefits of both the heavy androgen that has it's beneifits (to include a heavy affinity to binding to receptors that trigger libido increases - in both men and women BTW :D ) with added building power of the safer, and less androgenic (fewer potential sides for BPH, MPB, and so on...) Nandrolone.Quote:
Originally posted by Tank21
Is this one of the reasons why those who are on for a long period of time cycle different compounds?
Basically stacking is used to hit different recepetors in the body with the goal to use larger amounts of AAS to produce the most muscle/performance increases with the fewest risks... or side effects.
Warrior as usual, this is a great answer.
Bump, some good info in this tread.
Pain
good info warrior. bump.
Nice ya hit that one nicely for me. Understand the difference between the two (androgen vs. anabolic) and their respective effects on both protein synthesis and the sorts. So am i right in assuming that if the recepters for test were saturated, and results have failed then you can do two possible things:
1) Increase that specific compounds dosage
or
2) Administer a second compound that would work via a second pathway. e.g Deca.
The reason i am writing this is becuase as some of you know or will find out, prolong use of a compound or compounds in a stack will yeild less results as the time period increases. I am investigating why this is. In addition to recepters and their saturation or availablity, i have heard that these gains may stall as one becomes farther and farther from their biological set point. For example, we are all not genetically engineered to carry 260lbs of muscle or any wieght for that matter and our body resists this weight gain. This i believe is evident by bodybuilders having less success each cycle in comparison to their first. Thanks guys.
I had posted a previous question about injection amounts. Would it be better to slowly increase your dosage in a cycle then running a flat amount for the cycle?
There is only one AR produced from only one gene in DNA. There are not "different" types of AR's. There are two isoforms, AR-A and is~87 kD, has a normal C-terminus but lacks the N-terminus found in AR-B which is ~110 kD. All androgens act through the X-linked AR. Androgens possess direct (genomic) and indirect (non-genoimc) actions which have been uncovered in most tissues in the body. The indirect actions may be through mediators of secondary transcription factors, regulation of autocrine/paracrine mediators of gene expression, or may influence the secretion of other hormones that mediate androgen effects in distant tissues. In addition it is thought that some of these effects may be the result of plasma protein bound androgen interaction with extracellular receptors (Rommerts 1998). Some of the postulated non-genomic, AR-independent effects of androgens include:
-increases in both liver derived and locally produced IGF-I and IGF-I mRNA (Arnold et al 1996, Mauras et al 1998)
-displacement of glucocorticoids from the glucocorticoid receptor and interference of glucocorticoid binding to glucocorticoid response elements (Hickson et al 1990, Danhaive and Rousseau 1986, Danhaive and Rousseau 1988)
-the release of several autocrine "andromedins" including androgen induced growth factor, schwannoma-derived growth factor, keratinocyte growth factor, and fibroblast growth factor, to name a few (Tanaka et al 1992, Sonoda et al 1992, Yan et al 1992)
-transmembrane influx of extracellular calcium (Koenig et al 1989,
Lieberherr and Grosse 1994, Steinsapir et al 1991)
-activation of extracellular signal-related kinase cascades via binding to a yet unidentified extracellular receptor (Peterziel 1998)
NOTE: Credit for the above due to John Berardi
The differences in androgen action between tissues is now thought to be due to DNA response elements as well as specific co-activators or repressors present in the different tissues.
So all AAS may see to bind the AR and/or exibit non AR mediated effects. So one would need to take into consideration how well the different AAS bind the AR (affinity for the receptor, dissociation times etc.) as well as the pharmacokinetics of these AAS (absorption, distrubition, metabolism, excretion) + the non AR mediated effects of different AAS to account for the difference in effects which are observed.
Well I just booked marked this thread. BUMP
Pain
ichabod is right on as usual. One of the reasons AAS are not used more often in healthcare is the inability to be specific in targeting certain areas without effecting the whole system. Here is one study (I know I just did the post on useless studies) which shows the way SARMs are hopefully going to be developed:
Selective Modulation of Genomic and Nongenomic Androgen Responses by Androgen Receptor Ligands.
Lutz LB, Jamnongjit M, Yang WH, Jahani D, Gill A, Hammes SR.
Department of Internal Medicine, Division of Endocrinology and Metabolism, Department of Pharmacology, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd., Dallas, Texas 75390-8857, USA.
Steroids can induce both transcription-dependent (genomic) and independent (nongenomic) signaling. Here, several classical androgen receptor ligands were tested for their ability to modulate genomic and nongenomic responses, focusing on the role of the oocyte-expressed Xenopus classical androgen receptor (XeAR) in mediating these processes. Cellular fractionation and immunohistochemistry revealed that the XeAR was located throughout oocytes, including within the plasma membrane. RNA interference and oocyte maturation studies suggested that androgen-induced maturation was mediated in part by the XeAR in a transcription-independent fashion, perhaps by altering G protein-mediated signaling. While inducing minimal transcription in oocytes, all AR ligands promoted significant XeAR-mediated transcription in CV1 cells. In contrast, only testosterone and androstenedione potently induced oocyte maturation, while dihydrotestosterone and R1881 actually inhibited testosterone and hCG-induced maturation and signaling. These results suggest that the nature of a steroid-induced signal (genomic vs. nongenomic) may depend on the type of target cell, the receptor location within cells, as well as the ligand itself. The identification of molecules capable of selectively altering genomic vs. nongenomic signaling may be useful in delineating the roles of these pathways in mediating androgen responses, and might lead to the development of novel compounds that specifically modulate these signals in vivo.
The reason you never get a good specific answer on AR receptors is because there still isn't a great knowledge of them and research is trying to catch up. Good thread and I will continue to try add what little bit of knowledge I can and hope others will as well.
im going to bump this because its one of the most informative posts ive read in awhile...the bros at AR have done it again!!!!
BUMP
BUMP~
This is because the anabolic environment that made you grow at 200lbs will not yield the same gains at 220lbs - you simply need a more anabolic environment. Receptors DO NOT downregulate ( Arguments for Downregulation ) - your body is exposed to testosterone everyday of you life. You increase your dose as you increase your size... once you past what you can maintain naturall - now you have to bridge just to sustain.Quote:
Originally posted by Tank21
The reason i am writing this is becuase as some of you know or will find out, prolong use of a compound or compounds in a stack will yeild less results as the time period increases. I am investigating why this is.
Plus - there are NO testosterone recpetors but simply androgen receptors (AR's) that it binds to located throughout your body, in your brain, your skin, your prostate and other sexual organs... and on and on...
If you were to oversaturate you recepetors with a single androgenic-anabolic steroid like testosterone propinate at 1500 miligrams per week, your done... you are saturated for your lean weight... anything further would take you to the risky side... the bad side of the risk to benefit ratio where you start binding to receptors that are not what you were looking for (increased blood pressure, stimulation/aggression, oily skin, benign prostate enlargement... yada, yada...). But instead of running 1 gram per week of Test Propinate, results would be better with say... stacking 700mg of Test Propinate with 300mg of Nandrolone Propinate... nearly the same AAS burden on your system.. but you add more anabolic functions from the Nandrolone and cut down on the highly androgenic terstosterone, for less side effects... to include the above as well as it aromatizing to estrogen. Ya dig?Quote:
Originally posted by Tank21
So am i right in assuming that if the recepters for test were saturated, and results have failed then you can do two possible things:
1) Increase that specific compounds dosage
or
2) Administer a second compound that would work via a second pathway. e.g Deca.
Where's Mmaximus? :unsure: He'd really like this conversation... :D and I'd like to hear more input from others too... good thread.
wow.. good ass thread...BUMP
as I was wondering before because of saturation. Would this be why some cycle slowly increase dosages?
Exogenous hormones will shut down your endogenous levels. Whether you were taking 25mg per day of tesosterone propinate - or 100mg... either way your body shuts down. So why slowly raise the dose? Unless you are affraid of a possible allergin or aniphilactic shock from the meds and want to slowly introduce it.Quote:
Originally posted by Trying2Gain
as I was wondering before because of saturation. Would this be why some cycle slowly increase dosages?
Pyramid cycling is no longer mainstream. You start with the maintenance dose or you frontload longer esters to build up blood levels before the first half life - within the first week. And then you don't pyramid down... you'd only be delaying restoration of natural androgen levels. Rather than Pyramiding down you take an anti-e with LH boosting ability like Clomid or other follow up meds.
Rather than slowly increase during a cycle, slowly increase over multiple cycles. One cycle you may try testosterone enanthate at 500mg per week with good results and no known side effects. It then would seem you still have some unoccupied receptors (and especially since you are bigger now than before the first cycle - well... you should be) so you could try 600-700mg next time. This is one reason I do think new users should use short esters - if it is too much the androgen clears out of the system within days - not weeks... but the prospective user would have to be able to administer ED or EOD shots... a pin next to the toothbrush in the morning. :D
thanks
This really is the bottomline. So much info is learned on this - a lot of the info from only 10 years ago has been dramatically thrown out.Quote:
Originally posted by Rickson
The reason you never get a good specific answer on AR receptors is because there still isn't a great knowledge of them and research is trying to catch up. Good thread and I will continue to try add what little bit of knowledge I can and hope others will as well.
The thing is... AAS use for athletes is not mainstream... most research on AAS is for certain wasting diseases like advanced HIV. Look up some abstracts... you would be hard pressed to find one that associates AAS use with athletes - they are based on aging patients or those with diseases that cause the body to breakdown. What we do know on the use of these substances as performances enhancers is from medical professionals who have researched this area with private studies and such... and it really just boils down to keeping up with their research and relating it to what is known about androgen recepetors and training adaption and improvement.
Also - much like anything you take time to learn more about, absorbing many different view points from respectable sources helps you move on and develop some of your own conclusions.
This deserves another bump
bump...indespensible knowledge contained herein that every member should read.
came in at the end, I still haven't read all the posts yet, but heres what I can spit out.
debate is how we find the answers here... half wrong half right, partial info not compete, but another bro may have the other half, ya know...
I am currently researching the different paths to muscle hypertrophy...
One point that has already been said is we still dont have a true understanding of our AR's.
There is info arguing contradicting statements in some reading I've done.
The first thing to know is saturation is hard to come by. To truly saturate your receptors you would have to do it in one lump sum, as the next day approaches your body will find ways to convert, use or distribute to 2nd and 3rd receptor types.
Hidden receptors that are more like carriers or you can say temporary storage areas like with in capillary beds...
I believe over long periods your body can develop a tolerance for a certain amount of hormone...
Ex is a yearlong cycler and then a once a year cycler...
Say the year long bro admins in a fashion like so: low doses (maintenance level) 13 weeks the ups the dose into a higher dose range (growth period) 13weeks, then back to low and then high again.
Always keeping a higher than natural t balance.
The other guy.
Cycles for 13weeks (moderate dosages) then off for 26 weeks then back on
Lets say they are both very good a nutrition, for arguments sake...
Who is going the keep a consistent effort towards muscular hypertrophy?
Who’s going to be worried about some catabolic effect happening no matter how good the diet is.
Ok maybe my point was made kinda half ass
I don’t believe your AR's are ever truly saturated or worn. I also believe that the affinity of different hormones is to the individual... I take 200mg of enanthate and grow, on the other hand the small guy need 400 or 600mg for 11 weeks.
Too many factors.
The more protein held by your frame will need its weight in nutritional value to sustain its area... the more lean mass you put on the more nutrients are required...
However, I once believe the larger you get the higher the androgen dose needed to be... I am just on the cusp of disagreeing... any level higher that your natural T production will yield growth. Tolerance is where to battle is waged. Your AR's in your muscles don’t just stay stagnate if one if damaged or becomes worn another site becomes available…. Kinda like adipose tissue as an estrogen receptor. EX. Your body will adapt to the amount of androgen you supply… the higher the amount the more AR sites will have to accommodate… once the dose is lowered growth doesn’t stop, it may slow down and once again adapted to a lower intake of androgen but growth will never be hindered unless the nutrients are not available.
Factors are tolerance and affinity of the type androgen
And of course the nutritional value/amount to the amount/muscle hypertrophy that occurs during the admin of known androgens
I have some data that can back up my statements but it’s not complete. Funny thing is, some of the posts made on this thread could all be combined to back some of my statements.
Well I disagree with you MMaximus. I think your receptors are actually saturated on very low doses however receptor turnover is constant. I think the different pathways by which hormones influence hypertrophy outside of receptor action is what you are really speaking of especially in testosterones case. You are also discussing constant upregulation with the introduction of more androgens. There may be some upregulation but I don't think it just continues. Interesting thoughts and would love to see some of the research that backs up your ideas. Maybe between all of us we can figure it out.
I didn't explain properly, it wasn't the amount of androgen I was speaking... I meant in order to saturate you would be needed to dose your self in a constant effort because of the bodies natural checks and balances.... whether 200mg or 1000mg 100% saturation could not be done unless the effort were there...
The up regulation is only particular to the more dynamic receptors. the less dynamic are the lower less of an affinity type... what I’m getting at is… there is a tolerance level even for the more dynamic target cells... but having the golden three.... high blood levels of the hormone, the receptors, and the affinity of that receptor the target cells will form more receptor to the rising blood level of the specific hormone... once the dosage is lowered the receptors that have formed will be bound into receptor-chaperonin complexes basically dormant but not permanently inactive. Once the hormone is back at high doses then the receptor will become unbound again... so by lowering and raising the hormone level you will consistently produce or sustain those numerous receptor sites.
Down-reg would happen if the subject did not lower his dose in an individualistic time pattern....
That’s still kinda general the other situation that is occurring is by lowering the androgen stack you can effectively target specific receptor affinity.
Meaning high amount of everything all at once will ensure some type of down-reg.
but using a few self tested androgen (receptor mapping) and cycling them one at a time or in couple but making sure to have some type of low dose period if coupled or sustain a low dose but continue to switch androgens so to effect the more affinitive specific receptors per androgen.
This would also yield a greater growth effect.
Adaptation can also occur whether at low doses or high doses...
But truth be told with out proper estrogen levels and nutrients etc. steroid hormones binding to their associated DNA will not function properly...
I'm not sure if this makes sense all spewed out. What I need is a scanner to properly translate my regurgitated info...
I'm going in circles I think...
Rickson I’ll hit you back once I get some sleep, I’m not sure I can convey anything properly right now...
Warrior made a comment about ratings that I have a theory on also...
mmaximus25 - I agree with you that any dose above the users endogenous androgen production will yield results. What I meant was this... as the user adds more lean weight adding more androgens will keep giving what would be satisfying results and occupy the new recepetors located in the added lean weight from previous cycles.
A person will certainly keep growing off 500 mg of Test Enanthate per week as their only cycles... but as they progress 500mg per week will be less and less noticable and dynamic and with their new size can add more total androgens with less undesirable effects because of the more available recepetors for AAS to produce it's anabolic properties.
Warrior, your getting leaner, it that a new avatarQuote:
Originally posted by Warrior
mmaximus25 - I agree with you that any dose above the users endogenous androgen production will yield results. What I meant was this... as the user adds more lean weight adding more androgens will keep giving what would be satisfying results and occupy the new recepetors located in the added lean weight from previous cycles.
A person will certainly keep growing off 500 mg of Test Enanthate per week as their only cycles... but as they progress 500mg per week will be less and less noticable and dynamic and with their new size can add more total androgens with less undesirable effects because of the more available recepetors for AAS to produce it's anabolic properties.
Yeah... I know where you were coming from bro...
In theory but yet to be proved is the whole reason you see the enormous pro's and non-pro bb'ers... is directly to their effort and contribution of producing more receptor sites in the targeted cell area... possibly not a contribution effort from most but definitely an unknown effort.
sorry, I did leave out the discipline of nutrition, high intensity training to match the types of doses taken, the proper non-negative environment, good genes, skeletal frame, awesome transmittal of steroid to receptor protein along with a good negative feed back system(bad ass endocrine system) and heart(as in will power) ya know.
I also believe that once that type of mass has been built it’s a matter of maintenance with nutrition. To increase mass at that level becomes increasingly harder. That’s why AAS is not the only sup, but insulin and GH are brought into to anabolic mix...
Me personally, I would like to keep a maintenance schedule but plan a higher than maintenance cycle once a year.
No matter what the choice is, its a personal one... and the individual will always have to accept the bottom line that your altering your body and even more so by experimenting... I've accepted this... I also do not plan on procreating... I should have never started with Dan Duchaine's theories...lol
There's a biochemist/physiologist in all of us...right
AAS is a supplement a very powerful one.
I'm sorry I'll stay to the thread topic, I dont mean to mis direct
dude it's 3:55 am here, the ship is going down brother...see ya
this is a great thread..........keep up the excellent work guys.
bump.
peace IFL79
Biggity bump, we got some really good info from some very bright bro's on this tread.
Pain
bump. I actually feel like a winner for once.
LOL...I'm not through yet. Actually I think we are on the same page Maximus to a certain extent I just think it is being over simplified. We are leaving out things like the change in half-life for receptors, how easily receptors are forming dimers, the other influences that hormones have completely outside of receptor actions. I agree that it is likely that there is some initial upregulation of receptors but I am not sure how long that effect last when one introduces large amounts of hormones. I still don't understand why you thank receptors don't get filled. I have never seen anything to support that in anything I have ever read.
Rickson, War...
Yes we are over simplifying things by focusing so intently around target cells... But the most complex arena to dwell into is the checks and balances your endocrine system must go through each day... This discussion would be much easier if a few of you bros were all sitting around in the same room... It’s hard to cover all the ins and outs...
But I sense you’re aware of up-regulation down regulation and adaptation.
So....heres more of my spit... Up regulation can occur in any receptor site not just AR's and what is not being focused on is the effect on the rest of your body when a large amount of hormone is introduced... as a negative feed back system our bodies use hormones as messengers...
What can not accurately be described is the homeostasis of our body's when using high amounts of androgens, although any amount above a natural level would be large.
From the times of Walter Cannon and his homeostasis theory our body's have such great homeostatic controls that you will have successfully effected your entire body through manipulation of even one single hormone.
I'm going to go back to the receptor topic... This info in my head does not come from studies or articles. I have an Anatomy text book and a physiology text book from Elaine N. Marieb... perhaps some here taking a physiology course may be familiar with this information.
There is no clear tolerance or time frame it would take an individuals receptors to down regulate... all receptors are not equal and can be described as dynamic target cells and less dynamic... but when up-regulation does occur as you know the more dynamic target cells for which ever specific hormone will form additional receptor sites. This is not rare as we have many homeostatic imbalance symptoms daily, weekly, all the time; most anomalies are due to a compulsive or erratic hormonal disturbance.
Since we are focusing on steroid hormones and the direct gene activity my statements come from functional properties of the hormones target cells.
Since steroid hormones and thyroid hormones diffuse easily into their target cells, theses two have a prime arena for up regulation, although, half life is the only culprit for dosing a particular hormone.
One may not realize that the vast majority of hormones injected into our bodies are under a cleansing attack almost immediately... different per individual. Yet the majority of the hormone is removed by our kidneys and liver. But keep in mind hormones are so powerful that target organs are affected at low concentrations.
The constant dosing that occurs in AAS users must be done to keep circulating hormones in the blood to keep a particular rate of release and at what ever speed, speed of is inactivation as a constant removal process is ever applying.
This is one reason why saturation can not truly happen, your body is in constant effort to keep in homeostasis...
Because steroid hormones are diffused by their target cells in a quick fashion this creates an arena of affinity, tolerance, up regulation, down regulation, and the presence of chaperonin complexes.
The only event that would cause up regulation is high blood levels of said hormones... the affinity of the target cell would cause the forming of new receptors to accommodate the high blood level. The tolerance is unknown and specific to individual. The two ending scenarios are if levels are dropped in a timely fashion the additional receptor sites will have a chaperonin complex response and be protected from proteolysis... Once the hormone is present again the complex dissociates and those additional receptors sites will once again bind to DNA and influence transcription... However if the dosage is not lowered in an individualistic time manner down regulation will occur, not only to prevent the target cells from overreacting but because hormones effect not only the number and affinity of their receptors but also receptors that respond to other hormones.
EX progesterone induces a loss of estrogen receptors in the uterus, antagonizing estrogen's actions. On the other hand, estrogen causes those same cells to produce more progesterone receptors, enhancing their ability to respond to progesterone.
My statements in the above come from Ch 17 of Human Anatomy & Physiology.
(Steroid Hormones and Direct Gene Activation CH17 The Endocrine System p612 of Human Anatomy & Physiology fifth edition.
Elaine N Marieb, R.N.,PhD.)
Yes the body will have multiple homeostatic imbalances due too the high amount of androgens but you must focus from area to area. It is too hard to explain to individuals that are not well versed or of understanding of the body's detailed functions to jump from focus to focus... I think you and Warrior understand this. My only problem is retrieving data from other that text books. Online articles spur my reading but I am coming straight from a physiological stand point. That is another reason why I send questions to different university professors, in hope to get confirmation on text book reading.
Back to the anabolic-androgenic ratio... I was doing some reaing last night and found a good break down for ya... I'll try to type it in here...
Androgenic Functions
Initial growth of the penis (men) and clitoris (female)
Growth and development of the seminal vesicles (men)
Growth and development of the prostate gland (men)
Increased density of body hair
Development pattern of pubic hair
Increased density and distribution of facial hair
Deepening tone of the voice
Increased oil production of the subaceous glands
Increased libido and awakening of sexual interest (both sexes)
Certain "male" personality characteristics
Anabolic Functions
Increased skeletal muscle mass
Increased bone density
Increased hemoglobin concentration
Increased red blood cell mass
Enhancement of the immune system, especially T-lymphocytes
Influence on the distribution and quantity of body fat
Increased nitrogen retention and protein synthesis
Increased visceral organ size
Increased retention of several electrolytes
Increased height during puberty (synegism with growth hormone)
BTW - one of those gray area topics is how androgenic functions aid in the anabolic response. Anyone who has used Trenbolone can say it is a very effective steroid, one which is highly androgenic - more so than testosterone mg per mg...
:wg:
Nice brother, where did you find the Therapeutic Index for AAS... is it medically published?
I can not find any foreign study on receptor affinity and tolerance specific to an AAS. The information I have is from text book but it does not specifically name a synthetic androgen as the hormone. Only a reference to a steroid hormone…
Therefore we may be left with known studied theory... and… self experimentation.
If a foreign study has been made I would wonder if the study had taken place in harsh times such as WW11 on soldiers and prisoners. Possibly even a Russian study in the years following...?
Semper fi to all that fight and die in battle...
Yes, but I got a lot of this info from a book I am currently reading:Quote:
Originally posted by mmaximus25
Nice brother, where did you find the Therapeutic Index for AAS... is it medically published?
http://images.amazon.com/images/P/07...CMZZZZZZZ_.jpg
Really good book. The author is against use of anabolic steroids on athletes without medical supervision - but seems to supports the use with. He states a few times that he pioneered some of todays wisdom that shows AAS does enhance performance and muscle growth in athletes... most medical journals used to say anabolic steroids had no effect other than placebo on athletes. :p He is full of good info... very good read.
And I used to think bodybuilders were dumb! It's gonna take me a few rereads just to get my brain around some of this.
I recently heard that researchers have discovered that long-term cocaine use can actually "fry" the pleasure center (wherever that is) in your brain. In other words, it permanently reset the cells to require the higher dose of serotonin (or whatever it is) just to be normal, with the result that the user was never able to experience pleasure naturally as intently as before heavy long term use. (Which of course explains the reason for addiction.)
Is this what is meant by "down regulating"? And is the consensus then that that sort of permanent impairment is not possible with AS?