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08-29-2004, 07:20 PM #1
Why ppl say not to use GH before 30?
I am just wondering why some people may say not to use GH at 22. I havent grown in a while (height wise). Are there any health risks?
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08-29-2004, 08:04 PM #2Anabolic Member
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bones in the face and jaw still grow into your late 20's if you are a man. Therfore, extra GH may cause them overgrowth. For wome, i dunno.
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08-29-2004, 08:28 PM #3
all bones are still growing when you are 20. that is the purpose of taking growth hormone . i am 19 and am going on a 8 month cycle at 4iu ed!
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08-29-2004, 09:21 PM #4Anabolic Member
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best to take advantage of your high level of gh while you're young. When growth plates arent fused yet, there can be a host of problems due to taking gh too young, like metioned earlier about the abnormal bone growth.
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08-29-2004, 09:24 PM #5Anabolic Member
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Originally Posted by angelxterminator
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08-29-2004, 09:25 PM #6
is that the only reasons?
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08-29-2004, 09:31 PM #7Anabolic Member
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im sure there is more, but there is nothing more freakish looking than enlarged facial bones. Not worth the risk in my opinion.
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08-30-2004, 06:15 AM #8
umm actually the condition you refer to is acromegaly, and it is nearly impossible to obtain such a condition at a younger age due to the fact that your growth plates are NOT fused yet. That condition would be more common in more aged people deciding to take growth hormone . Also the dosages needed for such a condition are very high.
When your growth plates are still open gh will promote chrodocyte proliferation, aka growth, as well as its fat burning and other effects. As long as the growth plates are still open, there is not much risk of acromegaly or other conditions. Read and know what your talking about before you misinform somebody!
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08-30-2004, 06:19 AM #9Originally Posted by aXe
Also nolvadex and clomid are SERMS aka synthetic estrogens, and would be one of the bigger factors in causing stunted growth in a youth on AAS!
BTW
i do not recommend in any way that any youth should use AAS or anything else, i'm just giving you my personal knowledge, as i know it to be correct. The decision to take AAS is a risk that must be taken by that person only, and i think nobody should influence them either way, just give them the facts!
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08-30-2004, 07:54 AM #10
Moush, see my PM!
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08-30-2004, 09:23 AM #11
uh oh buylongterm is bashing my ideas in PM to avoid a flame war....
j/k bro...i just think many people read a few posts and know everything about GH. If used properly at a young age it can be to large benefits.
Did i also mention that while i'm on this cycle i will be getting bi-monthly x-rays to check my g. plates, and will be getting complete bloodwork?
aka. thyroid panel, igf-1 levels, etc. etc.
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08-30-2004, 09:37 AM #12Anabolic Member
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unless you are taking it because you are short (under the supervision of a dr.), there is no "proper" way to take it at as young of an age as you. Where are you coming up with this "proper" way seeing as there are no long term studies done? here is a quote from one of your posts on the 19th.:
[B]originally posted by angelxterminator
"ok i know all the bad hype about teens and hgh, i'm only 19 and not even considering it. i have 1 cycle under my belt, and i'm about to do my second. i know i'm probably too young to be doign this, but i've put my bod through worse, so oh well...."
Why the sudden change in mind?
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08-30-2004, 09:44 AM #13Originally Posted by angelxterminator
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08-30-2004, 09:59 AM #14
the sudden change came after i read about 45 clinical trials of GH induced lateral growth on boys of short stature between the ages of 12-24 years old. Many of them having various disorders ranging from turners syndrome, ISS, GHD, and others. Also many of them were HEALTHY young men who were not happy with their growth rate. All of these boys were compared to a control group in each and every study!
Based on what you just said, aka there have been no long term studies, how would you recommend gh to a 30 year old? Most of the studies have been performed on the patients GH was designed to help, YOUNG people with UNCLOSED growth plates to aid in LONGITUDINAL BONE GROWTH. Its the 30 year olds that the drug was NOT designed for, but everybody just realized what benefits it could reap as your natural GH production begins to lower, which is around 25-30!
The administration of GH at a younger age will be more beneficial, as it will not be replacing GH that is no longer naturally produced, but you are introducing supraphysiological levels to induce rapid growth not normally attainable! That is also the purpose of steroids , but for different goals!
That is what changed my mind. That and a clinical endocrinologist agreed with my approach based on my weight and height, and the results of my epi-x-rays!!!
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08-30-2004, 10:04 AM #15Originally Posted by buylongterm
also the one thing that could be sketchy about doing GH at a borderline age is some of your growth plates could close prematurely, and with high GH levels that could lead to disproportionate growth. So therefore that would lead me to believe there is sort of an age range where gh is not suitable, aka 21-25, as it is borderline! I would do it younger or older than this, depending on what goals you were trying to achieve!
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08-30-2004, 10:06 AM #16Originally Posted by buylongterm
aka do you think i'm stupid for attempting this, etc.?
dont be afraid to hurt my feelings, its not going to sway my judgement on this cycle, your opinion just seems well respected on this board, so i would like to hear it!
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08-30-2004, 10:22 AM #17Originally Posted by angelxterminator
Interesting......is your baseline GH level normal?? What kind of effect on final height does your doc think 4IU will give??
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08-30-2004, 11:23 AM #18Originally Posted by RedBaron
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08-30-2004, 11:27 AM #19Originally Posted by Badgerman
As far as final height that is not really predictable until treatment is started, and body changes are monitored. Everybody reacts differently to gh, aas, etc... and as with anybody else, i could have adverse reactions to this proposed cycle and have to stop immediately. Hopefully that will not be the case, but anything can happen! The best i can do is to minimize any risk factors and hope for the best results possible!
The cycle has not been started yet, but in a month or two after some more research the cycle plan will by finalized and reviewed, and treatment will begin! Once the cycle is started i will begin posting any changes/sides/results i do gain!
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08-30-2004, 01:17 PM #20Anabolic Member
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Originally Posted by angelxterminator
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08-30-2004, 01:26 PM #21Anabolic Member
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p.s. AngleX...it looks like you're in for one EXPENSIVE cycle...but you already knew that.
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08-30-2004, 01:46 PM #22
ohhh yea bro, expensive is not the word.... its in the area of $4,500!!!!
the main factor for that price is the gh, and rIGF-1. igf-1 is some expensive **** for local growth(not LR3)...
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08-30-2004, 01:49 PM #23Originally Posted by aXe
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08-30-2004, 01:49 PM #24
BTW MOUSH< sorry man, didn't mean to hijack your thread!
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08-30-2004, 02:07 PM #25Originally Posted by angelxterminator
What did the doc say are the negative sides you could be facing...... and specifically what would cause you to terminate tx?
Please pm me links too!! Thanx
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08-30-2004, 06:15 PM #26
negative sides are the same as the sides experienced by the older gh using population. The only adverse effects i could see that they wouldn't would be self-induced gigantism, or disproportionate growth, but if either had begun to show, use would be discontinued immediately, minimizing if not eliminating additional side effects!
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09-01-2004, 12:50 AM #27
Bro why so expensive for your source I got a very reliable source and according to what I calculated ... for a 4iu/ED for 8months it would cost $1971.20 for Gentropin and $2016 for Jintropin
Why you paying so expensive?
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09-01-2004, 04:54 AM #28Originally Posted by angelxterminator
$2200 for the growth hormone
$900 for the rIGF-1
$200 for the pgf2a
$120 for 24 amps of testoviron (test e)
$400 for an 8-9 month supply of letrozole
$325 for the anavar (500 pills)
$20 for the clomid
$70 for 8 months of slin
$4235...... i was close with my guess!!!
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09-01-2004, 04:56 AM #29Originally Posted by Angelis
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09-03-2004, 06:29 AM #30Originally Posted by angelxterminator
It is true that pediatrics don't tend to get acromegaly, and it is true that it is more likely in the adult population, but the dosages that have been shown to cause such deformaties is not all that high.
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09-03-2004, 06:39 AM #31Originally Posted by angelxterminator
Both Nolvadex and Clomid are non-steroidal agents. Neither one is a synthetic estrogen.
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09-03-2004, 06:41 AM #32Originally Posted by angelxterminator
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09-03-2004, 06:46 AM #33Originally Posted by aXe
There have actually been several long term studies done on the pediactric group (21 and younger), but no long term studies done on the adult group.
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09-03-2004, 07:16 AM #34Originally Posted by DBarcelo
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09-03-2004, 08:45 PM #35
Clomid is NOT classified as a SERM, at least not medically. It is not a synthetic estrogen, but it does have an estrogenic effect. It also has an anti-estrogenic effect. The estrogenic effect is caused by the initiation of endocrine events, not by any form of synthetic estrogen in it's chemical composition (2-[p-(2-chloro-1,2-diphenylvinyl)phenoxyl]tri-ethylamine citrate). There is also NOTHING to suggest that Clomid plays any role in stunting growth. Clomid does cause an increase in testosterone production in males, but as part of it's anti-estrogenic effect, it competes with estrogen receptor sites (not selective sites, which disqualifies it from being a SERM) and delays the replenishment of intracellular estrogen receptors (which are responsible for aromatizing testosterone into estrogen).
Nolvadex , once again is not any form of synthetic estrogen, (Z)2-[4-(1,2-diphenyl-1-butenyl) phenoxy]-N, N-dimethylethanamine 2-hydroxy-1,2,3-propanetricarboxylate. And Nolvadex is an anti-estrogen. I don't see how an anti-estrogen could possibly be a synthetic estrogen.
Nolvadex is considered to be a SERM (selective estrogen receptor modulator), but that has nothing to do with anything being a synthetic estrogen.
Just because two things compete for a binding site does not mean they are the same thing, or even all that simular, it's just the fact that the one binding site is responsible for more than one thing and may be overpowered by one thing over the other.
For example, you can't drink grapefruit juice while taking certain immuno-suppressants, because the grapefruit juice competes with the drug for the same binding site and makes the drug less effective if not useless. The drug and the grapefruit are not simular in any way or made from the same thing, but that binding site has to work on both chemicals.
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09-03-2004, 09:46 PM #36Originally Posted by DBarcelo
Selective Estrogen Receptor Modulator (SERM) Compounds that bind with estrogen receptors and exhibit estrogen action in some tissues and anti-estrogen action in other tissues. The ideal SERM would deliver all the benefits of estrogen without the adverse effects. ex: Clomiphene Citrate (Marketed as Clomid or Serophene). Tamoxifen (Marketed as Nolvadex).
Aromatise Inhibitor (AI) Aromatase inhibitors exhibit a very different mechanism of action than SERM’s. Aromatase inhibitors prevent the conversion of androgens into estrogen in fat, muscle, breast, and brain. ex: Anastrazole (brand name Arimidex ). FEMARA (letrozole tablets).
NOTE: Clomid and Nolvadex are both anti-estrogens belonging to the same group of triphenylethylene compounds. They are structurally related and specifically classified as selective estrogen receptor modulators (SERMs) with mixed agonistic and antagonistic properties. This means that in certain tissues they can block the effects of estrogen, by altering the binding capacity of the receptor, while in others they can act as actual estrogens, activating the receptor. In men, both of these drugs act as anti-estrogens in their capacity to oppose the negative feedback of estrogens on the hypothalamus and stimulate the heightened release of GnRH (Gonadotropin Releasing Hormone). LH output by the pituitary will be increased as a result, which in turn can increase the level of testosterone by the testes.
Although these two are related anti-estrogens, they appear to act very differently at different sites of action. Nolvadex seems to be strongly anti-estrogenic at both the hypothalamus and pituitary, which is in contrast to Clomid, which although a strong anti-estrogen at the hypothalamus, seems to exhibit weak estrogenic activity at the pituitary.
by William Llewellyn
...........Last edited by angelxterminator; 09-03-2004 at 11:09 PM.
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09-03-2004, 11:20 PM #37
AND.... any chemical that has estrogenic acitivty CAN work to slow or prematurely close growth plates!
Clomiphene
Synthetic Estrogen
Oral
Clomid is a very weak, synthetic
estrogen and thus belongs to the group
of sex hormones. In school of medicine
Clomid is normally used to trigger
ovulation. Clomid also has a strong
influence on the
hypothalamohypophysial testicular axis.
It stimulates the hypophysis to release
more gonadotropin so that a faster and
higher release of FSH (Follicle
Stimulating Hormone) and LH
(Luteinizing Hormone) occurs. This
results in an elevated endogenous
testosterone level. Clomid is especially
effective when the body’s own
testosterone production, due to
anabolic /androgenic steroids , is
suppressed. In most cases Clomid can
normalize the testosterone level and
the spermatogenesis within 10-14 days.
For this reason Clomid is primarily
taken after steroids are discontinued.
Even greater results can be acheived by
combining Clomid with HCG .
Paradoxically, although Clomid is a
synthetic estrogen it also works as an
anti-estrogen. The reason is that
Clomid has only a very low estrogenic
effect and thus the stronger estrogens
which, for example, form during the
aromatization of steroids, are blocked
at the receptors.
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09-04-2004, 07:27 PM #38Originally Posted by angelxterminator
A SERM is a selective estrogen receptor modulator, yes. They do compete with estrogen at the receptors. But they do not have to exhibit any estrogenic action (and normally don't) but they can CAUSE an estrogenic action in women. In men, there is no estrogenic action, it is an anti-estrogen only.
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09-04-2004, 07:45 PM #39Originally Posted by angelxterminator
I already provided both chemical structures and you can see that they are NOT structurally related in any way.
As I said before, only one is a SERM, the other isn't. And that's the classification from the PDR.
Anti-estrogens do not act as actual estrogens and SERMs do not act as actual estrogens. Only in women does Clomid cause an increase in estrogen, in men it increases testosterone, but not directly. Estrogen is increased very indirectly. It's not like taking synthetic testosterone. If a woman takes a synthetic testosterone, they have testosterone in their body. If a man takes a synthetic estrogen, they end up with estrogen in their body. Clomid is in no way a synthetic estrogen. I have no idea where you get your information from, but you are mis-informed and you should find a new source of information.
Neither one of them works by opposing any negative feedback of estrogens in the hypothalymus.
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09-04-2004, 07:54 PM #40Originally Posted by angelxterminator
There is a synthetic estrogen on the market and it's given to women and girls as an IV drip. There is no adverse reaction to estrogen treatment related to premature growth plate closure.
Clomid is not listed as a sex hormone, is not considered a sex hormone and can't be confused with a sex hormone.
Clomid is used for non-ovulatory women. I already explained how it works in women to increase estrogen and it works the same way to increase testosterone .
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