anabolic penis
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No AAS will not increase the size of your dick,some can increase labido quite significantly,which can help with girth sessions,some can also have the opposite effect leaving you with a limp noodle.
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smileyguy said:
Unless a man is still in puberty it has little to do with growth. Natural Penis ENlargement is a forced method of enlargement through stretching and pressure...if a supplement is used to help increase this then be it. With any method of enlargement test's should be performed and results charted to show the effectiveness of any one supplement.
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Penis Enlargement works from deformation of tissues due to the stresses applied to them. There is no anabolic action taking place in the penis. If you did any research at all, you would know that anabolism only occurs on skeletal or striated muscle, not on smooth muscle tissues. The penis is made up of smooth muscle.smileyguy said:
lol, ok taken, but is it through enlargment of cells or increase in cell quantity?
is this growth the bodys responce to trying to adapt to excess stress?
i dont know much about physiology and was wondering about what type of tissue ligaments are made from? does it differ from the smooth/spongy muscle tissue of the penis?
is this growth the bodys responce to trying to adapt to excess stress?
i dont know much about physiology and was wondering about what type of tissue ligaments are made from? does it differ from the smooth/spongy muscle tissue of the penis?
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It is similar to someone pulling on an earlobe for long periods of time... eventually the tissues will expand and the earlobe will become longer.smileyguy said:
That is exactly it...
Ligaments are made up of connective tissues and are generally very inelastic in that they don't have alot of give when stretched. Their main purpose is to attach or connect bone to bone. It is generally tendons that attach muscle to bones. That said, i don't understand why the suspensory ligament is called a ligament and not a tendon.
Ligaments are very different from the smooth/spongy tissues of the penis.
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I always wondered this one too...sikdogg said:
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It does seem to grow, naturally, by anabolism - but many such things are due to a complex cascade of sterols and diols, their effect on each other, and their effect on receptor sites during critical developmental windows. (not to mention heredity factors).
One grows taller in puberty because of the actions of estrogen on the midbones, even males. That's why girls tend to get taller before boys do, they have more direct estrogen than guys ... guys have to get it mostly by aromitization from testosterone.
Arguably, exogenous estrogen injections at the midbone sites during those windows could effect one's final height .... but if a guy already grown went and tried that he wouldn't get taller ... he'd just start to grow tits.
Things that work at some points in one's development don't necessarily always work, ... and the balance of hormone cascade it takes to effect such changes isn't generally available to a non-laboratory effort.
What sterols -can- do is boost one's recuperative rate - so maybe you could recover faster from Penis Enlargement sessions ... and recovery equals new growth. That sort of thing wouldn't be site-specific, like a dick cream, -- you'd have to dose the entire body by whatever means. Personally I wouldn't perform, recommend, or condone that sort of thing .... legally and systemically it's like playing with fire.
There are some test-boosting products out that work -with- (or at least within) one's natural feedback and downregulation mechanisms .... the two best ones right now seem to be: 6-OXO, and Novedex XT. Even then I'd doubt their ability to make any serious change in one's rate of gains ... but they do make you want to go put it -in- somebody.
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Yes at the onset of puberty estrogen play a large role in development but it is also the cause for the closure of the epiphyseal growth plates which signals the end of puberty. Once this has occurred the growth effect of GH, estrogen, etc cease to exert it's growth effects.
Your theory of increased recovery rate is plausible but based on mine and other bodybuilder's experience with Steroid use. There is no correlation between Penis Enlargement gains and steroids use.
As for 6-OXO and Novedex XT, they are aromatase inhibitors. They both act to suppress the converson of testosterone to estrogen by binding to the aromatase enzyme. They are very good at driving down estrogen levels fairly quickly. Doing this can cause an increase in production of testosterone but can also cause negative effects due to low estrogen like an increase in cholesterol levels and a decrease in libido. Driving estrogen too low can also cause an upgregulation of the aromatase enzyme which will create an environment where estrogen will rebound to very high levels which can put you at risk of estro sides like gyno.
Your theory of increased recovery rate is plausible but based on mine and other bodybuilder's experience with Steroid use. There is no correlation between Penis Enlargement gains and steroids use.
As for 6-OXO and Novedex XT, they are aromatase inhibitors. They both act to suppress the converson of testosterone to estrogen by binding to the aromatase enzyme. They are very good at driving down estrogen levels fairly quickly. Doing this can cause an increase in production of testosterone but can also cause negative effects due to low estrogen like an increase in cholesterol levels and a decrease in libido. Driving estrogen too low can also cause an upgregulation of the aromatase enzyme which will create an environment where estrogen will rebound to very high levels which can put you at risk of estro sides like gyno.
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A higher anabolic equilibrium might help with anabolism? I know it's a stretch, no pun intended, but it's just crazy enough to work.
It might be plausible ... a higher anabolic baseline -is- going to give you higher synthesizing of new tissue. But you also need catabolism to break the stuff down first. Larger gains (in recovery power) could probably be had by supplementation with bruise-healing factors like zinc, rutin, and vitamins C and K.
It'd be difficult to argue that for both sides...
For a ham-handed amateur approach, there would likely be an inverse relation since the exogenous hormones interupt the natural cascades. One might well see higher recovery rates per above, but smaller nutz to go along with it - and then subsequently lower HPTA action when the boosting cycle had ended. - Meaning lower natural anabolism resultant from the previous boost cycle.
Having said that, there are people around who are absolute artists with test and insulin and IGF-1 who can do things we mere mortals would consider majic. But an artform it is, and cost thousands of dollars using subtrates probably obtained by illegal means. (BTW, I'm lifetime drug-free.) Given enough knowledge, who's to say what "can't" be done - such as gene therapy re-expressing the pubescent developmental action, but my advice in the hormone realm is to stay away. The body is made to notice obvious changes like that and it acts to 'fix' them by changing other stuff.
Which is how the aromatse inhibitors work successfully, backwards sortof to actual steroids, by making the body do the work, with concomitant re-equilibrium of the involved cascades.
First off, both products have postive action for chole-sterol. - Which can be off the scale and still be OK as long as it's not decayed from free-radicalization, showing a larger systemic problem. The density lowers due to rancidity and you get agglutination at cracks in the arterial linings, the cracks due to chronic scurvy. The body sends phages out to deal with this and they end up stuck as well -- forming the fibrin-foam plaques .. none of which happens without the free-radicalization and vitamin C / copper deficiency. Anyway ... in the absence of adequate nutrition, "lower" is considered better and the aromatase inhibitors show a reduction in cholesterol on the order of 12%, and a 17% reduction in gross triglycerides.
Secondly I guess is the use of the broadbrush term 'estrogen'. These reactive electrophile AI (aromatase inhibitor - don't want to have to spell that all day ) products more particularly act against the action of estradiol cytochromes at various estrogen receptor sites. Changes in gross estradiol levels themselves are functionally insignificant. As for estrogens, there are 11 main types of estrogen and the AI's are only suicide inhibitors for 6 or 7 of the forms, variously. The remainder, key ones for sterol and mental functions, are left unmolested - and the effected ones are part of the upregulation effect, re-ordering at the low range of normal. Which is lower, but still considered normal, suppressing effected estrogen concentrations to levels that are not high enough to suppress resultant upregulation in gonadotropin action.
The most important regulator of testosterone production in males is estrogen - produced by the conversion of various androgens, testosterone mainly, to estrogens in the body and brain. Estrogen levels signal the hypothalamus to shut down production of gonadotropin releasing hormone, which makes the pituitary stop producing luteinizing hormone, which turns off the signal that tells the testicles to produce testosterone. So, - estrogen levels suppress testosterone levels. Any rise in serum testosterone, normally, aromatizes into more estrogen - causing an inhibitory effect on the hypothalamus (hpt axis), resulting in a shutdown of testicular testosterone production.
AI's work within the hypothalamic pituitary testicular axis to effect, and increase, production of follicle stimulating hormone and lutenizing hormone. -- Which not only increases serum (free, available) testosterone - by creating it, but spermatogenesis as well, increasing fertility and fattening up one's nutz as well. Actual larger nutz ... not smaller ones like you'd see with historical steroid use.
There is a possibility of estrogen rebound at the end of the cycle, but only if one ends the cycle suddenly. (And even then a rebound would be short-lived, too short to grow any tits, since there would be no ongoing cause for it after cessation of the cycle.) The typical use is to go for two bottles, and when the second bottle starts running out, cut the dosage in half across the last week or so. No rebound effect. These AI products raise the entire cascade, like a rising tide raising a ship, so although reordered at a higher level during the cycle, everything is still within range of normal effect ratios. Cutting the dose at the end of the cycle lets everything come back down nice and smooth with no rebound (crash) effect like steroid-related gynomastia.
As for negative effects on libido, .... the testosterone levels are reordering at an average of 188% higher for albumins, 226% higher for serum (for 6-OXO).
Novedex XT is widely quoted at "over 400%". Their actual company figures are 145% and 300% after the first week, 240% and 528% after 4 weeks.
Neither of which is what you'd really consider a libido lowering situation.
Comment ... they're probably going to cause Federal action at those levels. I'd be surprised if this stuff is still available by 2008.
Which is all illuminating regarding the action of current aromitase inhibitors but kindof off topic ...
If you're older than 16 or 17, probably not.
Conceivably, boosting with AI's could aid recovery by raising general synthesis, but I'll quote myself from earlier ... "I'd doubt their ability to make any serious change in one's rate of gains". For Penis Enlargement that is. Working out is another matter, -- but for Penis Enlargement you'd get way farther by just relying on good proven technique on a regular routine.
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Good post...
I had a long winded reply to your post yesterday but was unable to post it due to some technical troubles with the site so i lost it all. I don't recall everything i wrote so here's the short version...
As far a ATD products like Novedex XT goes... they were once touted and the end-all-be-all for raising test levels until it was found that actual test levels didn't rise nearly as was claimed. If i recall correctly, the high testosterone tests levels were attributed to the test not being able to differentiate between actual testosterone and ATD metabolites. I'll try to dig up where i read that...
I had a long winded reply to your post yesterday but was unable to post it due to some technical troubles with the site so i lost it all. I don't recall everything i wrote so here's the short version...
Is 6-OXO a steroidal AI?? I thought that it wasn't... From all the studies i've read regarding non-steroidal AI's they do in fact cause a negative impact on lipids. No so for steroidal AI's...Asanon said:
When i say estrogen, i mean to say Estradiol (E2). Of all the estrogens, E2 exerts the most effect to us males. If you think E2 level changes are functionally insignificant then you need to talk to hypogonadal men from boards like Meso and H2 as there are many men that suffer from the change in E2 levels while on TRT. But if you're talking about short term use like several weeks at a time then i tend to agree...
I don't doubt an Ai's ability to raise test, i just question 6-OXO's and ATD's ability to do it. Do you have any studies to support the claims for both?? I know that 6-OXO was well marketed by it's creator Pat Arnold and people on some boards take his words as gospel. I've yet to see and studies proviing his claims.
As far a ATD products like Novedex XT goes... they were once touted and the end-all-be-all for raising test levels until it was found that actual test levels didn't rise nearly as was claimed. If i recall correctly, the high testosterone tests levels were attributed to the test not being able to differentiate between actual testosterone and ATD metabolites. I'll try to dig up where i read that...
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They're not... I was just parsing the term. Most people (not saying you) never realize that cholesterol is a sterol, the main proto-steroid for the entire body, despite it being right there in the name, so I spell it like that with the hyphen from time to time. But studies for both products do show reductions in LDLs, and also triglyceride levels generally. Luteinizing hormone turns on the leydig cells to make testosterone, mainly _from_ chole-sterol. The aromatase inhibitors' positive effects on triglycerides and LDLs might stem directly from using so much cholesterol to make new testosterone.
What I meant by "Changes in gross estradiol levels themselves are functionally insignificant" ... is that any AI-related changes in gross estradiol levels are so small as to be insignificant. The AIs don't act against the gross levels specifically but rather act against the receptor function of specific isomers.
For their ability to raise serum testo levels?
The 6-Oxo findings typically quoted were from a univarate anova double-blind repeated measure multi-crossover study of 6 trained males ages 32 to 40 (not a massive sample, they might not even be confidently covering the 4 blood types there, but the results were reported as an average and not a best-of) presented to the american college of nutrition 44th annual meeting in 2003 by human performance specialists inc. of arizona at the request of an illinois firm called functional foods and neutraceuticals. The aim of the study seems to have been to check for effect and toxicity, the testo-boost findings coming from the report but not having been the point.
The XT study seems to have been funded by the patent holder Therachem. I got bored trying to find it, too much 'info' on the web lately, not enough data. Their chief science officer is (or was) Bruce Kneller. I did come across an interesting thread where he and Patrick Arnold go off on each other for 23 pages (starting on pg2)
http://forum.bodybuilding.com/showthread.php?t=286207&page=1&pp=30
.. with some occasional chemistry.
Something of note for the XT is an apparent -direct- action against estradiol itself, stated as being in the range of 50%. That's not functional insignificance, it's slashing by half!! That's radically different than the effect of 6-Oxo. I don't think I could agree with such action unless proven conclusively in 2nd wave studies to be harmless in protracted use. If someone was going to use XT, they might should do it for one bottle and then take a break.
As for libido, I'm going to have to turn south park off for a bit and see if I can remember what I was going to write ....
Hypogonadism, from a previous side-subject, is defined as serum testosterone levels at or below 300 nanograms per deciliter. At those levels, men can cease having sleep-wood .... the definitive indicator of normal function. Performance failure can be due to stress or fatigue or sado-sexually damaged erotic thresholds, but such people still get wood in their sleep. In hypogonadism, even that can go away.
This would seem to point to a direct link between adrogen levels (testo or testo isomers) and sexual function - as measured by serum availability of free testo.
Higher testo levels increase this functionality, in males, for almost all cases. (in women, extra testo for libido can be hit or miss).
The thing that I didn't want to forget was the potential action on dopamine. Rapid lowering of endogenous estrogen (at the specific isomer scale) has been shown to acutely increase dopamine-mediated behavior (but this subsequently reverse, chronically, across -weeks-.) For the aromatase inhibitors, in addition to adrogenic boosts of libido, there might be a mesolimbic-dopaminergic preloading of the arousal threshold (libido) as well, briefly, across the course of an AI cycle. That would depend on which isomers are effected and responsible, respectively, but the mechanism is interesting to consider. So, either the AI doesn't effect that messolimbic trigger - leaving it with its normal function, plus the body with extra testo, .... or the AI effects it strongly, causing a several-week boost in dopamine-mediated arousal, plus the body with extra testo. Either way, the effect, in males, for libido would have to be positive... not like that nose spray they're working on, but still.
ps -- is there any way to make this typing area bigger?? It oughta be like three times bigger than it is.
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