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Human Growth Hormone for neurogenesis & brain health

human growth hormone hgh neurogenesis brain health

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#61 MetaphasicSystems

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Posted 01 January 2016 - 07:19 AM

^ 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?


Most successful and intelligent people are healthier than the rest of the population and habitually do aerobic and anaerobic exercise.

So, maybe there is a correlation between exercise and intelligence, we just don't identify as bodybuilders.

#62 playground

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Posted 03 January 2016 - 04:38 AM

 

^ 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?


Most successful and intelligent people are healthier than the rest of the population and habitually do aerobic and anaerobic exercise.

So, maybe there is a correlation between exercise and intelligence, we just don't identify as bodybuilders.

 

 

You're right, there's a strong relationship between exercise and cognition.

Unfortunately, i'm on the wrong computer to give you lots and lots of references to this.

 

But here are some key ones: 

1.  Influence of Exercise on Cognitive Abilities

http://www.ncbi.nlm....les/PMC3951958/
 

2. Exercise, Brain & Cognition Across the Lifespan

http://www.ncbi.nlm....les/PMC3220305/

 

The gist is... exercise causes growth factors to be secreted: eg. growth hormone & testosterone/estrogen etc.

These in turn cause the release of neurosteroids... and these directly affect cognitive functioning.

Exercise builds muscles *and* brains.

 

There's also the detox effect of exercise.  Basically, the increased blood circulation and blood pressure

causes changes in the liver and kidneys which result in the excretion of toxins following exercise.

The longer you stay sedentary and inactive... the more your body accumulates toxins. 

Exercise is a powerful detox mechanism.

 

I remember reading one paper that suggested that rather than spend 30 to 60 minutes

playing Sudoku or doing crosswords, you could use that time more effectively (from a brain health perspective)

if you went for a long walk or medium run.  (Sorry, no reference for that, but perhaps you can google for it)

 

be happy

 

playground


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#63 LongLife

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Posted 24 February 2016 - 11:33 PM

 

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

 

WHAT ABOUT TELOMERES? IF THE CELLS GROW, INCREASE IN SIZE, ALTHOUGH VERY SMALL INCREMENT, DOES THIS HAVE A PLAY ON TELOMERE LENGTH?


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#64 LongLife

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Posted 24 February 2016 - 11:36 PM

 
WHAT ABOUT TELOMERES? IF THE CELLS GROW, INCREASE IN SIZE, ALTHOUGH VERY SMALL INCREMENT, DOES THIS HAVE A PLAY ON TELOMERE LENGTH? HUMMM?

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#65 LongLife

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Posted 24 February 2016 - 11:53 PM

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.

 



#66 LongLife

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Posted 25 February 2016 - 12:16 AM

RESVERATROL_GUY; I live in Northern Peru and went gold prospecting in the San Francisco gorge separating Peru from Ecuador (Cajamarca/Amazona provinces) and yes the dwarf population is rather malnourished, very poor economically and receive near zero assistance. They likely all have "O" blood type too. Their genome would be is cancer resistant. I would like to have a genome sequencing done on one person there, like 23andMe. They (23andMe) recently doubled their fee and when I contacted them I was informed that they are not doing Latin American populations, on and on, their market is G10 countries (not verbatim). 

 

Why do some things do somethings and others don't OR why do somethings do things to some people and not others? I find it contrary to scientific evidence and protocol that we do NOT see research data including the subjects blood type and weight. After all, we are all looking at what something is doing. Therefore doesn't appear that something is missing in the results of most of the scientific published studies? Blood type "A" was OBSERVED during the 1940's to be prone to cancers (now known to be included AB blood types). Body weight is so important for drug/substance dosing but I don't find that data published on research (ie, PubMed).

 

When examining or contemplating issues of hormones and other factors, I think a correlation can be determined rather quickly if these two data points were consistently published. If there are any relationships then answers may be found to why there occurs discrepancies or variables yet determined as to why some things work with some people and not on others. Hummm?



#67 playground

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Posted 28 February 2016 - 09:18 AM

I  want to update this thread with the recent updates elsewhere.

 

See this thread:

http://www.longecity...neuritogenesis/

 

particularly the posts on IGF-2.

 

The argument made there is essentially this.

 

Human Growth Hormone (HGH) is secreted in the greatest quantities prior to birth and immediately after birth.

This is also the same pattern of neurogenesis.

 

HGH is converted to IGF-1 to promote growth in adults.

HGH is converted to IGF-2 to promote growth in infants.

Neurogenesis is off the scale in infancy.

Neurogenesis is marginal in adulthood.

 

The best candidate for a HGH related neurogenesis agent is IGF-2.

 

Here are some articles considering IGF-2 in the context of neurogenesis.

 

IGF2 ameliorates amyloidosis, increases cholinergic marker expression and raises BMP9 and neurotrophin levels in the hippocampus of the APPswePS1dE9 Alzheimer's disease model mice.

Abstract

The development of an effective therapy for Alzheimer's disease (AD) is a major challenge to biomedical sciences. Because much of early AD pathophysiology includes hippocampal abnormalities, a viable treatment strategy might be to use trophic factors that support hippocampal integrity and function. IGF2 is an attractive candidate as it acts in the hippocampus to enhance memory consolidation, stimulate adult neurogenesis and upregulate cholinergic marker expression and acetylcholine (ACh) release. We performed a seven-day intracerebroventricular infusion of IGF2 in transgenic APPswe.PS1dE9 AD model mice that express green fluorescent protein in cholinergic neurons (APP.PS1/CHGFP) and in wild type WT/CHGFP littermates at 6 months of age representing early AD-like disease. IGF2 reduced the number of hippocampal Aβ40- and Aβ42-positive amyloid plaques in APP.PS1/CHGFP mice. Moreover, IGF2 increased hippocampal protein levels of the ACh-synthesizing enzyme, choline acetyltransferase in both WT/CHGFP and APP.PS1/CHGFP mice. The latter effect was likely mediated by increased protein expression of the cholinergic differentiating factor, BMP9, observed in IGF2-treated mice as compared to controls. IGF2 also increased the protein levels of hippocampal NGF, BDNF, NT3 and IGF1 and of doublecortin, a marker of neurogenesis. These data show that IGF2 administration is effective in reversing and preventing several pathophysiologic processes associated with AD and suggest that IGF2 may constitute a therapeutic target for AD.

 

 

Emerging evidence of insulin-like growth factor 2 as a memory enhancer: a unique animal model of cognitive dysfunction with impaired adult neurogenesis.

Abstract

In the current aging society, cognitive dysfunction is one of the most serious issues that should be urgently resolved. It also affects a wide range of age groups harboring neurological and psychiatric disorders, such as Alzheimer's disease and schizophrenia. Although the molecular mechanism of memory impairment still remains to be determined, neuronal loss and dysfunction has been revealed to mainly attribute to its pathology. The discovery of neural stem cells in the adult brain that are proliferating and able to generate functional neurons has given rise to the idea that neuronal loss could be rescued by manipulating endogenous neural progenitor and stem cells. To this end, we must characterize them in detail and their developmental programming must be better understood. A growing body of evidence has indicated that insulin-like peptides are involved in learning and memory and maintenance of neural progenitor and stem cells, and clinical trials of insulin as a memory enhancer have begun. In contrast to the expectation of insulin and IGF1, the roles of IGF2 in cognitive ability have been poorly understood. However, recent evidence demonstrated in rodents suggests that IGF2 may play a pivotal role in adult neurogenesis and cognitive function. Here, we would like to review the rapidly growing world of IGF2 in cognitive neuroscience and introduce the evidence that its deficit is indeed involved in the impairment of the hippocampal neurogenesis and cognitive dysfunction in the model mouse of 22q11.2 deletion syndrome, which deletes Dgcr8, a critical gene for microRNA processing.

 

 

So..  progress on this, finally.

 

 


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#68 littlePawn

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Posted 17 December 2016 - 01:48 PM

Has there been any discussion of this study? Seems HGH may decrease longevity -

 

Althoughadvanced age or symptoms of aging are not among approved indications for growth hormone (GH) therapy, recombinant human GH (rhGH) and various GH-related products are aggressively promoted as anti-aging therapies. Well-controlled studies of the effects of rhGH treatment in endocrinologically normal elderly subjects report some improvements in body composition and a number of undesirable side effects in sharp contrast to major benefits of GH therapy in patients with GH deficiency. Controversies surrounding the potential utility of GH in treatment of a geriatric patient are fueled by increasing evidence linking GH and cancer and by remarkably increased lifespan of GH-resistant and GH-deficient mice. Conservation of cellular signaling mechanisms that influence aging in organisms ranging from worms to mammals suggests that at least some of the results obtained in mutant mice are applicable to the human. We suggest that the normal, physiological functions of GH in promoting growth, sexual maturation and fecundity involve significant costs in terms of aging and life expectancy. Natural decline in GH levels during aging likely contributes to concomitant alterations in body composition and vigor but also may be offering important protection from cancer and other age-associated diseases.

→ source (external link)



#69 YOLF

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Posted 17 December 2016 - 01:57 PM

It should be no surprise that growth must occur under good conditions rather than aging conditions. HGH without AGE breakers, genome stability, and other therapies won't yeild much and people need to stop being fed this idea of monotherapies saving the day. It's been said a billion times, there is no silver bullet. HGH is at best for the young, and IGF1/Deer Antler Velvet has been shown to produce increased healthspan and normal lifespans since ancient times. HGH monotherapies and the like will always get hyped b/c you can't get them without someone who can profit from them.


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#70 Omega 3 Snake Oil

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Posted 19 December 2016 - 01:50 AM

I'm waiting on HGH testing results through my naturopath, I may be getting a scrip soon. I have Lyme (and I'm worried, prion disease) and my autonomic nervous system is a mess. If there is some sort of atrophy of my thalamus/similar, does anyone think HGH might help?



#71 YOLF

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Posted 22 December 2016 - 04:08 AM

I'm waiting on HGH testing results through my naturopath, I may be getting a scrip soon. I have Lyme (and I'm worried, prion disease) and my autonomic nervous system is a mess. If there is some sort of atrophy of my thalamus/similar, does anyone think HGH might help?

GNRH creates alot of neurosteroids down stream, but it might castrate you if you use too much. I would use that with the HGH and cycloastragenol to increase replicative capacity. Bad Monkey Botanicals has good stuff in powder. I was thinking about getting a kg of cyclo one of these days, so I could see myself doing it sooner if I get the same rate and don't have to spend as much. Telomere length will help most for atrophy, though getting some suped up adipose derived mesenchymal stem cells could help too. Thiamine HCl, and perhaps substrates for methylation (cyanocobalamin) and methyl donors (MSM? TMG?) could help some. Bacopa and Lions Mane? Don't take Bacopa around people until you know how it will affect you :p



#72 Omega 3 Snake Oil

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Posted 22 December 2016 - 04:23 AM

 

I'm waiting on HGH testing results through my naturopath, I may be getting a scrip soon. I have Lyme (and I'm worried, prion disease) and my autonomic nervous system is a mess. If there is some sort of atrophy of my thalamus/similar, does anyone think HGH might help?

GNRH creates alot of neurosteroids down stream, but it might castrate you if you use too much. I would use that with the HGH and cycloastragenol to increase replicative capacity. Bad Monkey Botanicals has good stuff in powder. I was thinking about getting a kg of cyclo one of these days, so I could see myself doing it sooner if I get the same rate and don't have to spend as much. Telomere length will help most for atrophy, though getting some suped up adipose derived mesenchymal stem cells could help too. Thiamine HCl, and perhaps substrates for methylation (cyanocobalamin) and methyl donors (MSM? TMG?) could help some. Bacopa and Lions Mane? Don't take Bacopa around people until you know how it will affect you :p

 

I don't know what GNRH is, and how it can castrate me?

And cycloastragenol?

mesenchymal stem cells?

Sorry this is all over my head
 



#73 YOLF

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Posted 22 December 2016 - 05:59 AM

GNRH is gonadotropin releasing hormone. It's the master hormone which is responsible for androgens, estrogens, neurosteroids, and more! Overdoses of it are used for chemical castration as the body stops producing its own for 30-60 days. 

 

Cycloastragenol is a telomerase inducer, it's shown to lengthen critically short telomeres and is thought by more well informed people to prevent cancers in most cases. I wouldn't take it if you already had cancer. It's about as expensive as gold from some manufacturers, but doses are effective at 5mg, and you can bargain shop. I get powder and put it in enteric capsules or take it with chitosan and bioperine. Either way I have good results from the more affordable stuff, though approximating dosages accurately for peak benefit and cost efficacy is impossible as there isn't enough data to use for estimates.

 

Mesenchymal SCs are SCs which were initially taken (and fractioned off) from your bone marrow, but have now been found in high quantities in adipose (fat) tissue. They show a wide array of therapeutic benefits, though I'm not sure if I've seen a study using them on hypothalamus or thalamus atrophy... They are relatively inexpensive for the wide array of anti aging benefits they provide, and better results are seen using low doses more frequently. Results gained from short term use of high doses of MSCs tend not to be permanent. Users here have sworn by them when nothing else would work for them and they thought they were lost causes.

 

No problem, we're here to spread knowledge and keep people appraised of the best technologies so they don't accept any less and we keep our doctors and researchers working for their money. We hope this leads to a cure for aging, which generates 95% of the healthcare economy. Though we may not be effective in all hospital networks and we don't guarantee you won't get talked down from our standards by indifferent or under informed FDA worshippers. 


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#74 Omega 3 Snake Oil

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Posted 06 January 2017 - 06:38 PM

Just got my 24 hour HGH test back. Results surprised me, I'm actually above the normal range:

4910 pg/24 hours
(range: 1065-4722)

I've more or less lost the ability to reach deep sleep. I manage maybe three hours of very light, poor quality sleep per night, and this has been the case since July.

Any thoughts? I'm about to turn 35, have Lyme disease and (I suspect) something neurodegenerative.



#75 Madman

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Posted 14 January 2017 - 10:35 PM

Try DSIP, Deep sleep inducing peptide, this has dramatically improved the quality of my sleep and the time in deep sleep per night.



#76 Omega 3 Snake Oil

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Posted 14 January 2017 - 10:59 PM

Try DSIP, Deep sleep inducing peptide, this has dramatically improved the quality of my sleep and the time in deep sleep per night.

 

where do you obtain this?



#77 Madman

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Posted 15 January 2017 - 11:34 AM

I order from an online peptide supplier in the UK, I'm not sure if its permitted on this forum for me to give you the actual site name/s here or by PM ? If you google search peptides I'm sure you will find a few sites in your country or USA also.

 

If you choose to use it, the dosage range I personally get success with is 1mg per night, others do well with as low as 100mcg per night right before bed.


Edited by Madman, 15 January 2017 - 12:32 PM.

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#78 VII

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Posted 01 November 2018 - 04:15 AM

I've seen some speculations here about what doses are used in bodybuilding. For what it's worth those elite bodybuilders you're posting pictures of are using at minimum 30 iu's per day. Up to 100 iu's is not uncommon. Much of their prize money is invested in HGH for better rankings and more prize money in their next competition. Typical amateur doses are 4-10 iu's.

 

And the gut is from insulin which adds visceral fat behind the abs.


Edited by VII, 01 November 2018 - 04:18 AM.


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#79 John250

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Posted 01 November 2018 - 04:31 PM

I've seen some speculations here about what doses are used in bodybuilding. For what it's worth those elite bodybuilders you're posting pictures of are using at minimum 30 iu's per day. Up to 100 iu's is not uncommon. Much of their prize money is invested in HGH for better rankings and more prize money in their next competition. Typical amateur doses are 4-10 iu's.

And the gut is from insulin which adds visceral fat behind the abs.

It really depends on the brand of the HGH. Some of the lower level bodybuilders who can’t afford it will use the generics and sure they can use up to 30 iu daily but Pharma grade like Serostim they typically use around 18-20iu daily which is A LOT! In fact HIV patients are prescribed 18iu per day. I use around 1.5-2iu’s when maintaining. Insulin is how they get REALLY huge and they use ALOT of that combined with the HGH. The problem is that alters insulin resistance and many of them can become prediabetic when they stop using it. The gut comes from what you mentioned but also from force feeding. These guys eat 10-15k calories per day from clean food sources which is insane. I worked with a pro along time ago and here is an example of his diet for just one day.

Breakfast: 12 whole eggs, 4cups oatmeal, 8 tbsp peanut butter

Meal2: 100g whey isolate, 150g waxy maize

Meal 3: same as meal 2

Meal4: 16oz ground beef, 12oz angel hair pasta

Meal 5: 12 oz flounder, 6 cups white rice

Meal 6: 14 oz chicken breast. 16oz yam, 4tbsp olive oil

Middle of night: 50g whey protein blended with 4 bananas, 4tbsp peanut butter and 2 cups oats.

Edited by John250, 01 November 2018 - 04:32 PM.






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