Human Growth Hormone for neurogenesis & brain health

Hi Normalizing,

Area-1255 is shilling.  He's selling HGH and he's already posted a link to his shop above.

He's also posted a private message to me, with a link to his shop.  "To help a brother out".

He's a salesman. He's going to tell you whatever shit you want to hear, in order to make a sale.

HGH does not make you grow. 

HGH causes the release of IGF-1 in the liver, and IGF-1 makes you grow.

IGF-1 will go everywhere. There's no way to localise IGF-1 in your penis.

IGF-1 will not make your dick bigger.

It will make all of you bigger.

The cheapest sources of HGH are from Chinese sources:

For example:

http://www.gensci-ch...sci/Contact.asp

The cheapest high quality HGH is chinese HGH.

There are  lots of people selling chinese HGH in Europe & America.

They have simply bought it from china, and are reselling to you at a profit.

You can simply buy it from china.

Seriously, don't take HGH to make your dick bigger.

It wont work and you'll be wasting your money.

Edited by playground, 04 October 2015 - 09:18 AM.

Hi Normalizing,

 

Area-1255 is shilling.  He's selling HGH and he's already posted a link to his shop above.

He's also posted a private message to me, with a link to his shop.  "To help a brother out".

He's a salesman. He's going to tell you whatever shit you want to hear, in order to make a sale.

 

HGH does not make you grow. 

HGH causes the release of IGF-1 in the liver, and IGF-1 makes you grow.

 

IGF-1 will go everywhere. There's no way to localise IGF-1 in your penis.

IGF-1 will not make your dick bigger.

It will make all of you bigger.

 

The cheapest sources of HGH are from Chinese sources:

For example:

http://www.gensci-ch...sci/Contact.asp

 

The cheapest high quality HGH is chinese HGH.

There are  lots of people selling chinese HGH in Europe & America.

They have simply bought it from china, and are reselling to you at a profit.

You can simply buy it from china.

 

Seriously, don't take HGH to make your dick bigger.

It wont work and you'll be wasting your money.

This is not to try and dispute your claim, just out of curiosity: why is it that athletes who dope with high amounts of IGF-1 get bloated muscle-wise but don't grow in their bones more than someone on high amounts of testosterone might do (i.e. almost nothing), while people who take very high dosages of HGH do grow bone-wise?

It seems there's another thing responsible for bone growth than just IGF-1.
 

And what you are doing is not shilling? You just linked your own 'personal site' - I wonder how many connections you have with them?  

 

 

HGH does not make you grow. 

HGH causes the release of IGF-1 in the liver, and IGF-1 makes you grow.

 

IGF-1 will go everywhere. There's no way to localise IGF-1 in your penis.

IGF-1 will not make your dick bigger.

It will make all of you bigger.

 

The cheapest sources of HGH are from Chinese sources:

For example:

http://www.gensci-ch...sci/Contact.asp

 

The cheapest high quality HGH is chinese HGH.

There are  lots of people selling chinese HGH in Europe & America.

They have simply bought it from china, and are reselling to you at a profit.

You can simply buy it from china.

 

Seriously, don't take HGH to make your dick bigger.

It wont work and you'll be wasting your money.

These days there are many peptides that cause a release of real HGH. I wonder if they are safer than HGH itself. 

 

ps. in order to generate a HGH-gut one needs to abuse the hormone and use suprafysiological doses. reasonable doses would be the way to go. 

The body self regulates with peptides,  so in that sense they are safer. 
 

 

These days there are many peptides that cause a release of real HGH. I wonder if they are safer than HGH itself. 

 

ps. in order to generate a HGH-gut one needs to abuse the hormone and use suprafysiological doses. reasonable doses would be the way to go. 

 

The body self regulates with peptides,  so in that sense they are safer. 
 

 

IGF-1 mediates most of the benefits of HGH; especially in muscle tissue.

Hi Normalizing,

 

Area-1255 is shilling.  He's selling HGH and he's already posted a link to his shop above.

He's also posted a private message to me, with a link to his shop.  "To help a brother out".

He's a salesman. He's going to tell you whatever shit you want to hear, in order to make a sale.

 

HGH does not make you grow. 

HGH causes the release of IGF-1 in the liver, and IGF-1 makes you grow.

 

IGF-1 will go everywhere. There's no way to localise IGF-1 in your penis.

IGF-1 will not make your dick bigger.

It will make all of you bigger.

 

The cheapest sources of HGH are from Chinese sources:

For example:

http://www.gensci-ch...sci/Contact.asp

 

The cheapest high quality HGH is chinese HGH.

There are  lots of people selling chinese HGH in Europe & America.

They have simply bought it from china, and are reselling to you at a profit.

You can simply buy it from china.

 

Seriously, don't take HGH to make your dick bigger.

It wont work and you'll be wasting your money.

ugh chinese. im sad thats the best we can get.

 

ugh chinese. im sad thats the best we can get.

Look on page one normalizing - I gave a better one then that Chinese garbage..

 

And what you are doing is not shilling? You just linked your own 'personal site' - I wonder how many connections you have with them?  

 

 

HGH does not make you grow. 

HGH causes the release of IGF-1 in the liver, and IGF-1 makes you grow.

 

IGF-1 will go everywhere. There's no way to localise IGF-1 in your penis.

IGF-1 will not make your dick bigger.

It will make all of you bigger.

 

The cheapest sources of HGH are from Chinese sources:

For example:

http://www.gensci-ch...sci/Contact.asp

 

The cheapest high quality HGH is chinese HGH.

There are  lots of people selling chinese HGH in Europe & America.

They have simply bought it from china, and are reselling to you at a profit.

You can simply buy it from china.

 

Seriously, don't take HGH to make your dick bigger.

It wont work and you'll be wasting your money.

 

First,  i don't have a personal site.

Second, gensci-china.com are the manufacturers you idiot.
Third, no, i'm not shilling.

Fourth, you *are* shilling. 

You have PM'd me with a link to your HGH shop. 

You have posted that link to this thread.

Fifth, people *need* to be warned that you're a shill and that

your opinions and views are corrupted by self-interest.

You were clearly encouraging that guy to believe that HGH would make his dick bigger. You *****.

 

ugh chinese. im sad thats the best we can get.

Look on page one normalizing - I gave a better one then that Chinese garbage..

 

Area-1255, you're **** shill. 

This thread is not a marketing opportunity.

Area-1255, you're no longer welcome on this thread.

 

 

 

ugh chinese. im sad thats the best we can get.

Look on page one normalizing - I gave a better one then that Chinese garbage..

 

 

Area-1255, you're **** shill. 

This thread is not a marketing opportunity.

Area-1255, you're no longer welcome on this thread.

 

And clearly your double posting and ridiculous ad hominems are reflecting your 'self-interests'...I'm sorry, did I intimidate you little guy? 

 

Your self interest and lies, revolt me.  

You're taking advantage of the ignorance and trust of others... ultimately, you're a scammer.

You're not welcome here.  Just  go.

 

I am still looking for an answer to whether IGF-1 causes bone growth or not, if anyone knows.

Those who abuse IGF-1 in high amounts don't grow bone-wise, as I've said. Some even shrink, which is known as palumboism - after Dave Palumbo.

Those who abuse growth hormone DO grow, as seen with Rich Piana (who legs, feet, hands and skull grew a bit, whereas Denis Cyplenkov grew extremely much (becoming thicker, not taller) on GH abuse (he reportedly took up to 15iu for long periods of time).

gamesguru, calling in late to work so he can catch up on last night's storm of posts

this is all i could find, not sure it's 100% relevant or answers your question

High insulin-like growth factor 1 (IGF-1) and insulin concentrations trigger apoptosis in the mouse blastocyst via down-regulation of the IGF-1 receptor.
Women with polycystic ovary syndrome have significantly higher rates of pregnancy loss, as well as elevated insulin and IGF-1 levels. In this study, preimplantation embryos exposed to high concentrations of IGF-1 or insulin undergo extensive apoptosis of the ICM nuclei. Lack of BAX expression, the caspase inhibitor, zVAD, or the ceramide synthase inhibitor, fumonisin B1, prevents this event, suggesting involvement of programmed cell death effector pathways. In other systems, the IGF-1 concentration regulates IGF-1R expression and thus high concentrations lead to down-regulation of the receptor. Here, data show a decrease in IGF-1 receptor protein expression, both by confocal immunofluorescent microscopy and by Western analysis upon exposure to 130 nM IGF-1. Insulin-stimulated glucose uptake, an event regulated via the IGF-1 receptor, is decreased upon exposure to excess IGF-1, suggesting decreased function of the receptor. The data also show that, by blocking receptor signal transduction or by decreasing receptor expression, the apoptotic event can be recreated, thus strongly suggesting that the mechanism of high IGF-1 induced apoptosis is decreased downstream IGF-1 receptor signaling. This embryotoxic insult by high IGF-1 levels may be responsible for the high incidence of pregnancy loss seen in women with polycystic ovary syndrome.

 

IGF-1 regulation of key signaling pathways in bone
Insulin-like growth factor 1 (IGF-1) is an unique peptide that functions in an endocrine/paracrine and autocrine manner in most tissues. Although it was postulated initially that liver-derived IGF-1 was the major source of IGF-1 (that is, the somatomedin hypothesis), it is also produced in a wide variety of tissues and can function in numerous ways as both a proliferative and differentiative factor. One such tissue is bone and all cell lineages in the skeleton have been shown to not only require IGF-1 for normal development and function but also to respond to IGF-1 via the IGF-1 receptor. Ligand-receptor activation leads to several distinct downstream signaling cascades, which have significant implications for cell survival, protein synthesis and energy utilization. The novel role of IGF-1 in regulating metabolic demands of the bone remodeling unit is currently under investigation. More studies are likely to shed new light on various aspects of skeletal physiology and potentially may lead to new therapeutics.

 

gamesguru, calling in late to work so he can catch up on last night's storm of posts

this is all i could find, not sure it's 100% relevant or answers your question

 

I wasn't looking for studies (should've made myself more clear) - I've already seen plenty of them.

Rather, I am looking for an explanation for why GH does cause bone maturation (growth) but IGF-1 doesn't, or at least it takes much more IGF-1 (supra-supra-supraphysiological) than GH to achieve any bone growth at all (as I said, test. could produce as much bone growth as IGF-1 injections can - and test is practically useless for adult bone growth).

Perhaps the problem here is that IGF-1 works at the injection site and IGF-1 is injected (mostly, at least) into a muscle, but you cannot inject it into a bone (or can you?)?

Take this example: If I took a huge amount of 100-200mg of DHEA a day, from studies this would lead to significantly heightened IGF-1, as it would if I took several IUs of growth hormone, but could I ever grow from DHEA? It seems hard to believe, doesn't it?

Sorry I post so many studies... in the past I received so many "needs references" ratings that this influenced my style (i hope for the better).

Those studies were to explain skeletal/bone atrophy, literally a shrinking frame, in IGF-1 abusers. 

Prolonged use leads to downregulated IGF-1 receptors, which would be expected to increase apoptosis [of blastocysts: stem cells involved in bone turnover] "off cycle".

You also said IGF-1 is size localized?  Yet here is one study indicating effects of circulating/serum concentrations:

Circulating levels of IGF-1 directly regulate bone growth and density

I don't think GH and IGF-1 share affinity for the same receptors.  The GH/IGF axis just means GH levels regulate the production and secretion of IGF, similar to how LH/FSH levels regulate T & E.  It's like asking, why doesn't hCG get you jacked?  It boosts Test afterall, yes, but only modestly... not to supraphysiologic doses such as can be achieved via Test injections.

There's lots of studies linking GH with bone growth/density/composition/metabolism/turnover.  So my guess is, it's all about the supraphysiologic dose.

Edited by gamesguru, 06 October 2015 - 03:14 PM.

"...supraphysiologic dose..."

That pretty much sums it up IMO.  

As for bodybuilders, they are notoriously unreliable when in comes to the amounts of drugs they use.  I'd wager on super-supraphysiologic doses.

Edited by Junk Master, 06 October 2015 - 07:30 PM.

@Gamesguru

Isn't your example the complete opposite, for GH does produce growth, while IGF-1 supplementation doesn't even in bodybuilders who abuse it extremely much (see Dave Palumbo)?

If IGF-1 were to produce the effects, and GH increases IGF-1 which is obviously true, shouldn't IGF-1 supplementation produce bone growth superior to GH? But it never seems to even in those abusing it to the extreme.

Those who have the pituitary tumor who do grow even far into the adulthood (and eventually die of it if not treated) never have "growth-hormone-gut" problems and don't have large muscles in general, and may even have unusually much fat stored on their chest (see Khali the great's manboobs), yet those who inject IGF-1 into the stomach muscle in sufficient amounts experience great muscle growth which results in the obvious "GH gut," and they're much more capable of exercising, and so on and so forth, yet they don't grow.

I ask all of these things because I want to try to supplement with the actual thing that causes bone maturation from GH. If IGF-1 was it, I would take it (or take an precursor like DHEA) but I am 99% certain that no matter how much I abuse IGF-1 or any non-GH precursors, I won't achieve bone maturation (again, as bodybuilders don't seem to ever do).

Also, GH seems to exert an effect on deepening the voice on par with that of DHT (or maybe even superior to DHT) that IGF-1 doesn't seem to produce whatsoever.

Clearly, as you suggest, GH has affinity for receptors that IGF-1 doesn't. I wonder what those receptors are and what safer alternative than GH there is.

maybe part of the reason Robert Wadlows don't grow around the waist is because of not having a huge caloric/protein surplus??  put the question another way, why aren't bodybuilders 9ft tall?

probably you&area are right tho, IGF/test may also play a pivotal role.

I have dyslexia, but I think I said it straightly.  GH will cause a secretion of IGF-1, but not vice versa.  So GH is likely the bad boy/granddaddy/culprit.

there's something fishy/complicated here, but I'm not sure precisely where to begin the investigation...

Akt/protein kinase B promotes organ growth in transgenic mice.
One of the least-understood areas in biology is the determination of the size of animals and their organs. In Drosophila, components of the insulin receptor phosphoinositide 3-kinase (PI3K) pathway determine body, organ, and cell size. Several biochemical studies have suggested that Akt/protein kinase B is one of the important downstream targets of PI3K. To examine the role of Akt in the regulation of organ size in mammals, we have generated and characterized transgenic mice expressing constitutively active Akt (caAkt) or kinase-deficient Akt (kdAkt) specifically in the heart. The heart weight of caAkt transgenic mice was increased 2.0-fold compared with that of nontransgenic mice. The increase in heart size was associated with a comparable increase in myocyte cell size in caAkt mice. The kdAkt mutant protein attenuated the constitutively active PI3K-induced overgrowth of the heart, and the caAkt mutant protein circumvented cardiac growth retardation induced by a kinase-deficient PI3K mutant protein. Rapamycin attenuated caAkt-induced overgrowth of the heart, suggesting that the mammalian target of rapamycin (mTOR) or effectors of mTOR mediated caAkt-induced heart growth. In conclusion, Akt is sufficient to induce a marked increase in heart size and is likely to be one of the effectors of the PI3K pathway in mediating heart growth.

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So after having read this thread, it occurred to me that there might be a way to get only what we non-body-builders want, which is increased brain volume. I wonder if -- don't try this at home! -- cervical or lumbar spine injections of HGH would accomplish that without the muscle effects. (It's not that we men don't want bigger muscles. It's that we don't want to push the IGF1 cancer accelerator harder than we have to in order to sustain brain function.)

If this worked, then skull volume would eventually become a limiting factor; disregarding that could result in death. Perhaps draining off some cerebrospinal fluid would permit maximum growth. (Yes, this is all dangerous fringe science. I'm just pointing out that it might in theory work.)

But first there's a key question: does HGH actually cause neurogenesis, or does it increase brain volume merely by making all the neurons bigger? I wonder about this because body builders aren't generally known for their intelligence. But perhaps all the muscular strain is causing damage to their cerebrovasculature, thereby hiding the neurogenesis that would otherwise benefit them.

Or better yet, has anyone tried this on a rat?

^ interesting how bodybuilders and athletes arent known for their intelligence yet there are more articles on excercise and NGF, BDNF, neurogenesis in general than any other compound or anything else natural there is, that it puzzles me why arent they?

So after having read this thread, it occurred to me that there might be a way to get only what we non-body-builders want, which is increased brain volume. I wonder if -- don't try this at home! -- cervical or lumbar spine injections of HGH would accomplish that without the muscle effects. (It's not that we men don't want bigger muscles. It's that we don't want to push the IGF1 cancer accelerator harder than we have to in order to sustain brain function.)

 

If this worked, then skull volume would eventually become a limiting factor; disregarding that could result in death. Perhaps draining off some cerebrospinal fluid would permit maximum growth. (Yes, this is all dangerous fringe science. I'm just pointing out that it might in theory work.)

 

But first there's a key question: does HGH actually cause neurogenesis, or does it increase brain volume merely by making all the neurons bigger? I wonder about this because body builders aren't generally known for their intelligence. But perhaps all the muscular strain is causing damage to their cerebrovasculature, thereby hiding the neurogenesis that would otherwise benefit them.

 

Or better yet, has anyone tried this on a rat?

Hi RG,

We know that HGH achieves it's growth effects via IGF-1 (HGH causes the release of IGF-1 in the liver)

So localising the effects of HGH to, for example, the brain, must be done by administering IGF-1 to the brain (somehow)

I wonder if IGF-1 taken nasally could focus the 'growth' effects of IGF-1 on the CNS.

I presume that IGF-1 would trigger the growth (and proliferation?) of nasal nerves.

I *assume* that IGF-1 would be transported into the brain via these nasal nerves in a similar

manner to NGF.  If this is correct... then we might expect that the locally administered IGF-1

is going to either (a) cause a proliferation of neurons (neurogenesis) and/or (b) cause existing

neurons to simply grow (perhaps in length, or numbers of dendrites, or number of associations

to distal neurons.. or perhaps grow in terms of the width of the cell body... or all of the above).

On the down side... perhaps long term use of IGF-1, in the way i suggest, could change the shape of your

face... growing out your nasal and upper dental regions dis-proportionally to the rest of your face.

It would be interesting to see what the effect of 1/20th or even 1/40th of one IU (of IGF-1) would be taken nasally.

This would be a tiny 'whole body' dose... but would be a sizeable 'local' CNS dose.

Of-course, it's always prudent to start research 'adventures' of this kind with the smallest doses...

and work up...reviewing and revising your knowledge as you proceed.  For all we know, this experiment

might produce similar effects to those reported by yourself (RG) for NGF.

best wishes

playground

Edited by playground, 25 December 2015 - 06:30 AM.

I think there is more to consider. I just saw a pot article suggesting to me that the growth of neurons induced by marijuana caused a diffusion of the connectome at the nerve endings? How are we to know if IGF1 was going to do the same? Will it cause random growth? Wouldn't we need something that would somehow target just those connections that would be productive? I don't think exogenous application of hormones or any substance for the purpose of growth will result in exactly the rejuvenation that we're looking for. It might beneficially support some systems with little in the way of immediately noticeable side effects, but the more distant results may become increasingly difficult to correct as technology advances. Think of Krokodil, the Russian drug that makes you rot like a zombie... the zombie rot isn't noticeable at first and it feels good... people don't recognize what it's doing to them until it's done so much damage it isn't worth caring about anymore. The same can probably be said of pot, and what's to say that using IGF1 in this fashion won't lead to the same phenomena, even if it's different than your arms and legs rotting off until you die. Maybe you're brain and identity start to diffuse terminally until your brain just rots...

I think we need to focus on restoring the function of the body and it's various systems and that doing so will result in the brain and other systems returning to youthful functioning. I'm starting to regard this kind of strategy as potentially dangerous.

Then again, in this case, if the IGF1 is being released in the liver, the delivery is naturally diffuse... but the cells receiving it may become senescence resistant or not die when they should and cause further proliferation of more aged cells? That would only lead to a terminal scenario... I suppose those effects could be mitigated by cycling the stuff with some kind of hormesis activity...

Hi YOLF,

Thanks for your post... it's helped me to clarify my own thinking.

my responses are inside your original text in red.

I think there is more to consider. I just saw a pot article suggesting to me that the growth of neurons induced by marijuana caused a diffusion of the connectome at the nerve endings? How are we to know if IGF1 was going to do the same? Will it cause random growth?

 

Perhaps you are implying that marijuana causes random (CNS) growth.

(I haven't seen the paper you're referring too, and you haven't cited it.....

I am aware of the evidence that cannabis slows down the rate at which dementias progress

and that in various parts of Europe and Israel (and perhaps America too), cannabis is on the

menu in some old people's homes where dementia is diagnosed and the patient requests cannabis therapy)

But "Random Growth" ?   How about "Generic Growth" ?  Or better, "A Growth Facilitator" ?

 

What marijuana does or doesn't do is a separate issue, deserving it's own thread.

Perhaps It's just polluting the current issue to bring in marijuana.

 

 

Wouldn't we need something that would somehow target just those connections that would be productive?

 

The rationale for nasal delivery.. is to *try to* target the IGF-1 on nasal nerves in the *hope* they deliver

the IGF-1 signal to deeper CNS regions.... just as happens with NGF.  The alternative might be occular

delivery (as practiced by Rita Levi-Montalchini) .. but more recent research suggests that delivery is more

efficiently achieved via a nasal route.  I'm afraid i don't have the links to hand.  If you're interested, however,

go through the NGF Spray thread... and look for the articles cited by Resveratrol-guy in the last 5 or 6 pages.

 

It wouldn't surprise me to discover that neurogenesis works in a similar fashion to muscle fiber creation.

Body builders take testosterone (and testosterone analogues) to potentiate rapid growth, and then they

go into the gym and exercise to initiate and stimulate the growth process. 

So, in summary,  the formula is: steroids + exercise.

 

I suspect neurogenesis is promoted with a similar formula of:

 

(IGF-1 or NGF) + mental exercise  (brain trainers, reading, learning, etc)

 

 

I don't think exogenous application of hormones or any substance for the purpose of growth will result in exactly the rejuvenation that we're looking for.

 

Define what you mean by "exogenous application".  

Any chemical injected, drunken or eaten ?

 

Define what you mean by "exactly the rejuvenation that we're looking for"  

The effect i'm looking for is neurogenesis. 

Is that what *you* mean ?

 

But... if you don't believe that any hormone or other drug (for the purpose of growth) will result in rejuvenation...

...then... i'm surprised you are moderator on longecity.org.

 

 

It might beneficially support some systems with little in the way of immediately noticeable side effects, but the more distant results may become increasingly difficult to correct as technology advances. Think of Krokodil, the Russian drug that makes you rot like a zombie... the zombie rot isn't noticeable at first and it feels good... people don't recognize what it's doing to them until it's done so much damage it isn't worth caring about anymore. The same can probably be said of pot, and what's to say that using IGF1 in this fashion won't lead to the same phenomena, even if it's different than your arms and legs rotting off until you die. Maybe you're brain and identity start to diffuse terminally until your brain just rots...

 

I think a comparison between a notorious recreational drug which causes catastrophic immune system problems,

and a bio-identical hormone, IGF-1, which has been used, and abused,  for decades *safely*....  is ...  unreasonable.

 

Even the most ferocious consumers of HGH... never exhibited 'brain rot' or any other kind of rot...

they grew and grew and grew... with unsightly distended bellies... but that's as bad as it got.

Even deaths amongst body builders are normally attributed to biologically non-identical anabolic steroid abuse

(rather than HGH or IGF-1)

 

I think we need to focus on restoring the function of the body and it's various systems and that doing so will result in the brain and other systems returning to youthful functioning. I'm starting to regard this kind of strategy as potentially dangerous.

 

I suspect you're right that.. a healthy body (in terms of plenty of exercise, good nutrition, freedom from toxins & pathogens)

will support brain health.  That's almost certainly true... but alas... not in all cases.

We have members on this website with

   (a) brain injury due to stroke 

   (b) brain injury due to one or other form of dementia 

   © brain injury due to trauma.

These people need a little help with their neurogenesis... a popularly considered route to this assistance has been via NGF

and various supplements that promote NGF secretion.

 

The starting point of the current thread is noticing the correspondence between the burgeoning mass creation of neurons

during the last few months before birth and the first few years after birth... and the massive output of HGH at those times.

We also have academic papers testifying to the association of HGH and neurogenesis (cited above, see earlier in this thread)

 

 

Then again, in this case, if the IGF1 is being released in the liver, the delivery is naturally diffuse... but the cells receiving it may become senescence resistant or not die when they should and cause further proliferation of more aged cells? That would only lead to a terminal scenario... I suppose those effects could be mitigated by cycling the stuff with some kind of hormesis activity...

 In the case of those suffering brain injury (stroke, dementia, trauma) .. there might be a particular concern to keep

existent neurons alive ... even the old ones.... if at all possible.   But i acknowledge for other tissues in the body

keeping them alive might lead to some tragic results.

I agree with the first sentence of your post when you said:

  "I think there is more to consider."

I want to know much more about neurogenesis in infants.

What's the pathway that leads from HGH to neurogenesis ?

I presume there's a link between IGF-1 and NGF  ... but that's my presumption, perhaps that's not correct.

Perhaps there's another hormone doing the hard work of neurogenesis in infants. 

It would be very useful to know if that was the case.

If anyone can shed any light on these issues... please post :-)

playground

Edited by playground, 26 December 2015 - 05:21 AM.

I'm not really sure how to characterize cannabis induced brain growth. Whatever it is makes people demotivated and that can't be good. But the study... and I didn't bother to keep track of it, it was just something I read to see what conclusion the stoners would come up with next to get the whole world smoking the stuff, ...determined that nerve fibers became frayed form using it and that would have occurred as growth. So maybe that growth would have occurred as a result of undisciplined habits during use? In any case, most often when we're growing, we're growing older. So any old growth just doesn't meet my standards. The rejuvenation I want to see is the kind that gives you full brain function. We lose this and that capacity at various ages and with all of the aging pathologies removed, we should have all the best features of our brains along with all the knowledge we've acquired. Causing growth in a damaged system is creating cells that are adapted to that damaged system unless the growth is also able repair the system.

I suppose those suffering from such maladies could benefit from neurogenesis, I'm just wondering if someone who is healthy would want to cause growth or if it will complicate further recovery as technology advances. I'm not saying IFG1 would cause the same effects as pot, just giving an example where growth could complicate things. 

I like betaNGF because it's a narrowly targetted growth factor, at least in comparison to IGF1. YOLF is right that we need to do everything possible to avoid the growth of senescent, let alone cancerous, cells. Administering IGF1 intranasally will only lead to a slight local bias in effects; most of it will enter the nasal capillaries and circulate everywhere. The same may be true of betaNGF, but its use has never been tied to cancer. At most, I might grow neurons elsewhere, resulting in some level of itching or pain; the clinical trials certainly warn of this possibility.

I don't doubt that IGF1 or HGH can cause neurogenesis. They're both big hammers which should be able to cause growth anywhere. But unfortunately, that's exactly the problem.

My investigation of the dwarf population in Ecuador, who have only tiny levels of IGF1, has led me to the conclusion that IGF1 should be suppressed to nearly zero in adults beyond reproductive age, in order to protect them from cancer. In other words, when you hit 40 or 50, you need to CRISPR yourself into IGF1 shutdown. So at best, if a dementia patient has no other choice, we could hit them hard with IGF1 targetting the brain, then, months later, disable IGF1. Several users have criticized my draconian position on IGF1 and HGH, saying that I'm throwing out the baby with the bath water. After all, how could I argue against modest use for the enhancement of brain and musculature? Of course, I'm not against such enhancements; I'd like to have them myself. The trouble is, how do we know when enough is enough, when we've crossed the line into cancer? Maybe we could all abuse these substances without limitation, then shut them down as soon as cancer shows up. But, at least presently, cancer detection tends to be too late, so could we really react in time? So I'd prefer to gain tissue enhancements through any other means possible, for example myostatin inhibition, than this untrustworthy duo.

By the way, these dwarfs do not lead healthy lifestyles. They show evidence of insulin resistance, no doubt due to unhealthy carbohydrate intake. Some of them smoke. They don't seem to exercise properly. They don't look healthy in photos. And yet, they have basically the lowest cancer rates in the world. For this reason, I think IGF1 is a more critical enabler of cancer than sugar itself. This is astounding, considering that IGF1 neither damages DNA nor mitochondria. But it seems to be critical to metastatis. And without metastatis, almost every tumor is effectively benign.

Edited by resveratrol_guy, 27 December 2015 - 02:54 PM.

Hi RG,

good post ! 

My reply in red below.

I like betaNGF because it's a narrowly targetted growth factor, at least in comparison to IGF1. YOLF is right that we need to do everything possible to avoid the growth of senescent, let alone cancerous, cells. Administering IGF1 intranasally will only lead to a slight local bias in effects; most of it will enter the nasal capillaries and circulate everywhere. The same may be true of betaNGF, but its use has never been tied to cancer. At most, I might grow neurons elsewhere, resulting in some level of itching or pain; the clinical trials certainly warn of this possibility.

I don't doubt that IGF1 or HGH can cause neurogenesis. They're both big hammers which should be able to cause growth anywhere. But unfortunately, that's exactly the problem.

 

Yes, i agree, it's a big hammer.  It's unselective. 

It makes everything grow, not just those precious neurons.

You're absolutely right about this.

 

But maybe for CNS damage caused by stroke, dementia & trauma that's exactly what you want.

CNS tissue exists in a particular environment.   It's not floating in thin air, it exists in a superstructure lattice of

supporting membranes and fibers.  And aside from this lattice superstructure neurons crucially need a supply

of nutrients and oxygen... this infrastructure needs to be provided either before, or at the same time, that:

 (i)  existing neurons are making new connections and/or

(ii)  new neurons are being created

 

I'm suggesting that IGF-1 has the ability to build the superstructure lattice and provide the infrastructure

to deliver the oxygen and nutrients to new and/or developing neurons.  On that basis, IGF-1 might

be better than beta-NGF, for encouraging neurogenesis (in the case of stroke, dementia & trauma).

 

A brief digression here:

A few years ago there was much interest in the idea of neural stem cells being used in Parkinsonism.

They tried implanting these stem cells in the (estimated) position of the brains of Parkinson sufferers.

I now wonder if those trials would have been so much more successful had those cells been delivered

in an IGF-1 rich medium.  (But this is speculation, of-course)

My investigation of the dwarf population in Ecuador, who have only tiny levels of IGF1, has led me to the conclusion that IGF1 should be suppressed to nearly zero in adults beyond reproductive age, in order to protect them from cancer. In other words, when you hit 40 or 50, you need to CRISPR yourself into IGF1 shutdown. So at best, if a dementia patient has no other choice, we could hit them hard with IGF1 targetting the brain, then, months later, disable IGF1. Several users have criticized my draconian position on IGF1 and HGH, saying that I'm throwing out the baby with the bath water. After all, how could I argue against modest use for the enhancement of brain and musculature? Of course, I'm not against such enhancements; I'd like to have them myself. The trouble is, how do we know when enough is enough, when we've crossed the line into cancer? Maybe we could all abuse these substances without limitation, then shut them down as soon as cancer shows up. But, at least presently, cancer detection tends to be too late, so could we really react in time? So I'd prefer to gain tissue enhancements through any other means possible, for example myostatin inhibition, than this untrustworthy duo.

By the way, these dwarfs do not lead healthy lifestyles. They show evidence of insulin resistance, no doubt due to unhealthy carbohydrate intake. Some of them smoke. They don't seem to exercise properly. They don't look healthy in photos. And yet, they have basically the lowest cancer rates in the world. For this reason, I think IGF1 is a more critical enabler of cancer than sugar itself. This is astounding, considering that IGF1 neither damages DNA nor mitochondria. But it seems to be critical to metastatis. And without metastatis, almost every tumor is effectively benign.

Well.... i know you're aware of this meta-analysis paper:

IGF-1R as an anti-cancer target—trials and tribulations

http://www.ncbi.nlm....les/PMC3845553/

This meta-analysis reviewed the evidence for IGF agonists as

a treatment for various cancers.   Their results were mixed and did not

demonstrate that IGF-1/R antagonists might be protective for non-dwarfs.

There might be multiple effects of the genetic mutation that leads to

Laron's (Dwarfism) disease.  One might be stunted growth another might be

some reduced susceptibility to inflammation, or increased resistance

to the formation of cancerous cells.... perhaps via increased apoptosis.

However, i take your point.  You could easily be on to something with this. 

So you might be right... IGF-1 might, in some way not clearly visible to us

yet, be implicated cancer.   A similar accusation exists for estrogen and testosterone.

But, let's be clear... it's one thing to say that Chem X facilitates cancer.

It's quite another to say that Chem X *causes* cancer.  I suspect, that endogenous

hormones like IGF-1, Testosterone and estrogen are not themselves *causing*

cancer.  But they (arguably) may, or may not, promote the growth of a triggered cancer.

regards

playground

Edited by playground, 27 December 2015 - 08:15 PM.

Dear reader,

This whole argument, supported as it is with scientific and statistical evidence

that Testosterone & DHT causes prostate and other cancers, ... is disinformation.

It's simply wrong... and perhaps it is deliberately wrong.

It turns out there is plenty of evidence to the contrary.

I refer any interested reader to "Ageless: The Naked Truth about Bioidentical Hormones"

By Susan Somers. 

She cites surveys and research that simply contradict the "orthodoxy" by 180 degrees.

The argument is....  When you take bio-identical hormones it boosts your immune system.

Your body is better able to destroy cancer cells at an early stage.  Plus, for that proportion

of cancers caused by pathogens, a heightened immune system is more able to deal with

the pathogen in an appropriate way.

This argument seems to make a lot of intuitive, common-sense, sense.. to me.

This is part of established clinical practice.  For those suffering with a diminished immune

system, or a  severe infection, doctors have the freedom to recommend steroids.  The

steroids work by boosting the immune system.   So clearly, if someone takes HRT (Hormone

Replacement Therapy) it will boost their immune system.

The tobacco industry managed to easily subvert the medical/research communities into

producing bullshit research results showing that tobacco was practically harmless... that

most of the cancers were caused by poor diet and lack of exercise, that industrial pollutants

were the likely source of most lung cancers.... and other such bullshit results. Just lies.

Similar story with the toxic poisons administered to cancer patients as 'treatments'.

How about AZT to aids patients?... a known carcinogen!

How about medical authorities recommending water fluoridation ?

How about dental authorities recommending mercury in fillings ?

Clearly, it's all bullshit.

I recommend you reflect on this relatively recent orthodoxy that Testosterone causes cancer.

And also that growth hormone might cause cancer.

it's not adding up.  Both growth hormone and testosterone/estrogen strengthen the immune

system, reduce bodily fat deposits, increase muscle mass and improve cognitive functioning.

I suggest interested readers consult the evidence provided by Susan Somers in "Ageless".

Maybe 'the powers that be' simply *can't* tell the truth.  If everyone went on HRT at retirement,

maybe 70% of retirees would live 10 or 20 years longer.  How much would that cost in pension payments ?

How much revenues would the medical industry lose if older people spent decades of retirement

in flourishing good health ?

playground.

Here are some answers:

Increasing GH has a correlation with increasing prolactin, which will explain why some people develop manboobs.  Just take at look at many GH releasers and many will cause an increase in prolactin except for ipamorelin.

Intelligence has to do more with the connections in the brain then size.  Also unless there is a study that backs this believe up of bodybuilders then it just seem like a negative stereotype oftentimes perpetuate by the media and kept alive by the public.  Let's also remember that bodybuilders are famous for been muscular, so when people go to them is often to see their muscles not their ability to understand Quantum Physics.

Marijuana shrinks parts of the brain such as the amygdala and hyppocampus.  The thing that can cause an increase is HU-210 it has a similar structure to THC but is not THC, and just as important the experiment only lasted 10 days.

Estrogen causes the ability of bones to stop growing which begins during puberty, stopping people from getting taller with GH, This could explain why some bodybuilders didn't got taller if they began after this happen or was already well underway.

If you want to increase your brain size with chemicals then why not NSI-189 & Dihexa.  Perhaps having your GH level at the level of a 20 year old or slithly higher would be good, but going much higher may be an unnecessary risk.

If you're concern of cancer cause by GH then why not take supplements with anti-cancer / anti-tumor effects.

Sources:

http://www.scienceda...51016083817.htm

http://nugs.com/arti...ippocampus.html

 

 

After the ten day study, the THC-like compound increased the rate of brain cell formation in the hippocampus by 40%!  

http://www.scienceda...40415181156.htm

 

 

The size and shape of two brain regions involved in emotion and motivation may differ in young adults who smoke marijuana at least once a week, according to a new study. The findings suggest that recreational marijuana use may lead to previously unidentified brain changes, and highlight the importance of research aimed at understanding the long-term effects of low to moderate marijuana use on the brain.

http://www.scienceda...80602160845.htm

 

 

Long-term, heavy cannabis use may be associated with structural abnormalities in areas of the brain known as the hippocampus and amygdala, according to a new article in the Archives of General Psychiatry.

http://www.scienceda...00222161843.htm

 

"One of the main findings that really struck us was that there was a distributed system here. Several brain regions, and the connections between them, were what was most important to general intelligence," explains Gläscher.

http://www.ncbi.nlm....pubmed/17901908

 

 

Pharmacological management of children with short stature: the role of aromatase inhibitors.

Damiani D1, Damiani D.

Abstract

OBJECTIVE:

To review the use of aromatase inhibitors, a novel treatment strategy for patients with short stature, which aims at delaying bone age advancement. Skeletal maturation is estrogen-dependent even in male children.

SOURCES:

We performed a MEDLINE search of studies published in the last 10 years, including aromatase, short stature, and early puberty as keywords. The most informative articles on indications, dosages, treatment schedules, and side effects of aromatase inhibitors were included in the review.

SUMMARY OF THE FINDINGS:

It has become increasingly clear that bone age advancement depends on the production of estrogen and its effect on the growth plate. In boys, testosterone is converted to estradiol by the cytochrome P450 enzyme aromatase. The use ofaromatase inhibitors has been shown to be effective in prolonging the length of the growth phase in children with idiopathic short stature, constitutional growth delay, delayed puberty, as well as in children with growth hormone deficiency, in which bone age advancement jeopardizes the results of hormonal replacement therapy with growth hormones. As yet, significant adverse effects have not been reported, and results are encouraging in terms of effective increase in height, whenever the indication for the drug is appropriate.

CONCLUSIONS:

Among the pharmacological treatments for short stature, aromatase inhibitors are indicated in cases in which bone age advancement may constitute an obstacle for reaching a final height that is in keeping with the family's target height.

http://www.ncbi.nlm....pubmed/25137428

 

 

Letrozole vs anastrozole for height augmentation in short pubertal males: first year data.

Neely EK1, Kumar RB, Payne SL, Ranadive SA, Suchet DI.

Abstract

CONTEXT:

Aromatase inhibitors are used off-label to treat short stature in peripubertal boys.

OBJECTIVE:

To investigate short- and long-term hormonal and auxologic differences in short pubertal boys treated with letrozole (L) oranastrozole (A).

DESIGN:

PATIENTS are seen for laboratory evaluation and physical examination every 6 months, bone age yearly, DEXA and spine film every 2 years. They will be followed until they reach their final height. This is a preliminary report after 1 year of treatment.

SETTING:

A single academic children's hospital outpatient clinic.

PATIENTS:

Boys with age >10 years, bone age ≤ 14 years, clinical and hormonal evidence of central puberty, and either height < fifth percentile or predicted adult height (PAH) more than 10 cm below mid-parental height (MPH).

INTERVENTION:

Letrozole (2.5 mg) or anastrozole (1 mg) was administered orally each day.

MAIN OUTCOME MEASURES:

Hormonal and clinical parameters, growth velocity, and change in bone age and PAH.

RESULTS:

Thirty-nine boys have completed 1 year of treatment. Baseline means were age 14.1 years, PAH 166 cm, and testosterone 198 ng/dL. At 1 year, letrozole resulted in higher LH (L 6.1 ± 2.5 vs A 3.2 ± 1.7 IU/L) and testosterone (1038 ± 348 vs 536 ± 216 ng/dL) with lower estradiol (2.8 ± 2.8 vs 5.6 ± 2.9 pg/mL) and IGF-1 (237 ± 51 vs 331 ± 79 ng/mL). First year growth velocities were identical (7.2 cm/year), but an increase in PAH was greater in the anastrozole group (4.2 ± 3.5 vs 1.4 ± 4.4 cm, p = 0.03) after 1 year.

CONCLUSIONS:

We present first-year data from a direct comparison of anastrozole and letrozole for height augmentation in shortpubertal boys. Letrozole was more potent in hormonal manipulation than anastrozole. First-year growth velocities were comparable, but improvement in PAH was greater in the anastrozole group. It remains to be seen if positive PAH trends will translate to increase in final height in either group.

http://www.news-medi...6/02/38835.aspx

 

 

Long-term, heavy cannabis use may shrink brain's hippocampus and amygdala

I have some additional questions. 

 

1.  What's the half life of HGH ?

 

2.  What's the half life of IGF-1 ?

 

3.  How much IGF-1 is produced from a dose of say 333 mcg of HGH ?

 

4.  Let's say you take some dose of HGH on day 1.

This will initiate whole body growth (via IGF-1).

My question is:

For how long will the trophic effects of this dose persist ?

I day, 1 week, 1 month,  6 months ?

 

5.  The number of brain cells a new born baby has rapidly increases shortly after

being born.  This is the most concentrated period of neurogenesis for humans

(probably other primates too).  Millions, or billions, of new neurons are created

during these early months.  My question is:  Is it HGH that causes that storm

of new brain cell creation ?  If not, which hormone _is_ responsible for this ?

 

1. 25.7min or less

2. 10-20min

3. I haven't found any info.

4. Minutes

5.  NGF & BDNF

Side note, many people in a different forum, which focus on peptides, have come to the conclusion that using GH injections isn't the best option.  Instead they recommend to use something like Ipamorelin(increase the amplitude) and GHRH (forces a release) for increasing GH.

2 reasons been:

They last longer in the body then one injection of GH.

They are less likely to produce desensitization.

Sources:

http://www.evolution...growth-factor-1

 

 

GF-1 variants are split into two groups: IGF-1 LR3 and DES IGF-1 (usually presented as IGF-1 DES). Base IGF-1 has a very short half life (about 10-20 minutes); as a result, it is quickly destroyed by the body. This is why IGF-1 was modified to make the amino acid analog IGF-1 LR3 (Long). The other variant of IGF-1 called DES IGF-1 is a truncated version that is 10X more potent than IGF-1. Both variants are similar to its root but have different actions, allowing them to function in a specific ways.

http://www.ncbi.nlm..../pubmed/1348664

 

 

Half-life of exogenous growth hormone following suppression of endogenous growth hormone secretion with somatostatin in type I (insulin-dependent) diabetes mellitus.

Mullis PE1, Pal BR, Matthews DR, Hindmarsh PC, Phillips PE, Dunger DB.

Abstract

OBJECTIVE:

To estimate the half-life of growth hormone in young adult patients with type I (insulin-dependent) diabetes mellitus following bolus injection and prolonged exposure for the purpose of deconvolution analysis of plasma growth hormone profiles to determine growth hormone secretory rates.

DESIGN:

In the bolus study, an intravenous bolus injection of 100 mU of biosynthetic human growth hormone was given while endogenous growth hormone was suppressed by a continuous infusion of somatostatin under three different glucose clamp conditions: normoglycaemia (5 mmol/l) with normoinsulinaemia (65 pmol/l); hyperglycaemia (12 mmol/l) with normoinsulinaemia; and normoglycaemia with hyperinsulinaemia (360 pmol/l). In the infusion study, the effect of prolonged and repeated growth hormone exposure upon the growth hormone half-life was estimated. Three pulses of 60 minutes growth hormone infusion (6 mU/kg/pulse) two hours apart under euglycaemic somatostatin suppression were applied.

PATIENTS:

Six young adult patients with type I (insulin-dependent) diabetes mellitus were studied in both the bolus and the infusion study.

RESULTS:

Mean GH half-lives by mono-exponential analysis were not significantly different remaining unaltered by the short-term metabolic changes of hyperglycaemia and hyperinsulinaemia. Data were therefore pooled yielding an overall mean GH half-life of 13.6 minutes (range 11.9-19.4). Applying a bi-exponential model mean GH half-lives were 3.1 minutes (range 2.5-5.9) for the rapid phase of distribution of the hormone and 13.8 minutes (range 9.6-16.9) for the decay of GH from the circulation. The GH half-life during the infusions studies did not vary with repeated exposure but was significantly longer (mean half-life of 25.7 minutes; range 19.4-37.1) than during the bolus studies (P less than 0.001).

CONCLUSIONS:

The half-life of exogenous r-hGH is not affected by glucose or insulin concentrations but increases after prolonged GH exposure in young adults with type I (insulin-dependent) diabetes mellitus.

Edited by noot_in_the_sky, 31 December 2015 - 06:21 PM.

Edited by MetaphasicSystems, 01 January 2016 - 07:14 AM.