GHK-cu affects 306 genes and their transcriptions

[Seth Walsh]

Coming in the near future

 

[elfmaxx]

I can't afford that shit.

 

[bonesoverblood]

Coming in the near future

Woah what's this?

 

[Seth Walsh]

Woah what's this?

I will be back in like June. Look into Histone Deacetylase enzymes. HDACs modify Histone tails and make them wrap more tightly around the DNA, repressing gene expression. It's very likely that GHK-cu is a broad HDAC inhibitor, and its overwhelming effects aren't just a matter of coincidence. GHK-cu aids in Histone Acetyltransferase enzyme actions. HATs convert the Acetyl group on Histones to Acetyl-COA. Histone Acetylation increases gene expression since it loosens the Histones' grip on the DNA, making expression less repressed and can even turn on gene expression in genes that are turned off due to overly tight Chromatins.



Histones aren't wrapped around the actual DNA strand (The Nucleotides), they're apart of the Chromatin, which is a mass of genetic material that compresses and packages the actual ATCG encoded DNA. The Nucleosome wraps around the Histones. The Histones are the nearest protein to the actual encoded genetic data, and therefore can have the biggest influence on how/whether the data is expressed, and this expression can greatly vary depending on how the DNA is packaged. There will always be a variance in DNA expression after Acetyltransferase modifies the Histone.



Given that Histone Acetyltransferase makes the DNA less compact, the entire makeup of the Chromatin changes; it becomes Euchromatin, which is a lightly packed Chromatin (containing DNA, RNA and other genetic related proteins). Euchromatins are almost always under active transcription, which makes sense since the decompressed Chromatin variant (the Euchromatin) can allow for Transciption Factors to reach the target genes, also allowing for gene expression.



It looks like GHK-cu is an inhibitor of the "Histone Deacetylase" enzyme. Just like how you have Fin and AI's as inhibitors of the 5-alpha-reductase and aromatase enzymes respectively.



This is just the cliff notes version of this because there is so much more.



I know it might be hard to understand at first but here's what's happening pretty much.



Histone Deacetylation removes the Acetyl group from the Histones, this causes the Histones to wrap more tightly around the DNA repressing gene expression, or completely turning it off. The Chromatin becomes too tight and Transcription Factors can't reach their target genes, and if some still could, the chance that gene expression is blocked from the inside out, is also greatly increased. So it's like a double/quadruple whammy.



GHK-cu is likely a HDAC inhibitor, stopping the Histone Deacetylase enzyme from removing the Acetyl group from the Histones.



Once a Histone has its Acetyl group removed, there's no enzyme that for instance, adds another group instead, so the Histone is left alone, and tightens to both the ATCG data and the Nucleosome on the otherside, tightening the whole Chromatin.



When HDAC is inhibited, it keeps it's Acetyl group, which is good because Acetyl groups keep the Chromatin relatively losely compact, meaning most genes will be expressed in a way one would want.



However, Histone Acetyltransferase is an enzyme which looks for Acetyl groups to convert to Acetyl CoA groups on the Histones, loosening the hold on the ATCG and modifying the entire Chromatin as a result, turning it into a Euchromatin, which not only turns genes on that previously weren't, and greatly increasing gene expression of genes that are already "on", but also modifying expression of genes to something completely different since the Euchromatin is packed in such a way that Transcription Factors can bind to genetic data that they never attached to before.

 

[Deleted member 685]

I will be back in like June. Look into Histone Deacetylase enzymes. HDACs modify Histone tails and make them wrap more tightly around the DNA, repressing gene expression. It's very likely that GHK-cu is a broad HDAC inhibitor, and its overwhelming effects aren't just a matter of coincidence. GHK-cu aids in Histone Acetyltransferase enzyme actions. HATs convert the Acetyl group on Histones to Acetyl-COA. Histone Acetylation increases gene expression since it loosens the Histones' grip on the DNA, making expression less repressed and can even turn on gene expression in genes that are turned off due to overly tight Chromatins.



Histones aren't wrapped around the actual DNA strand (The Nucleotides), they're apart of the Chromatin, which is a mass of genetic material that compresses and packages the actual ATCG encoded DNA. The Nucleosome wraps around the Histones. The Histones are the nearest protein to the actual encoded genetic data, and therefore can have the biggest influence on how/whether the data is expressed, and this expression can greatly vary depending on how the DNA is packaged. There will always be a variance in DNA expression after Acetyltransferase modifies the Histone.



Given that Histone Acetyltransferase makes the DNA less compact, the entire makeup of the Chromatin changes; it becomes Euchromatin, which is a lightly packed Chromatin (containing DNA, RNA and other genetic related proteins). Euchromatins are almost always under active transcription, which makes sense since the decompressed Chromatin variant (the Euchromatin) can allow for Transciption Factors to reach the target genes, also allowing for gene expression.



It looks like GHK-cu is an inhibitor of the "Histone Deacetylase" enzyme. Just like how you have Fin and AI's as inhibitors of the 5-alpha-reductase and aromatase enzymes respectively.



This is just the cliff notes version of this because there is so much more.



I know it might be hard to understand at first but here's what's happening pretty much.



Histone Deacetylation removes the Acetyl group from the Histones, this causes the Histones to wrap more tightly around the DNA repressing gene expression, or completely turning it off. The Chromatin becomes too tight and Transcription Factors can't reach their target genes, and if some still could, the chance that gene expression is blocked from the inside out, is also greatly increased. So it's like a double/quadruple whammy.



GHK-cu is likely a HDAC inhibitor, stopping the Histone Deacetyltransferase enzyme from removing the Acetyl group from the Histones.



Once a Histone has its Acetyl group removed, there's no enzyme that for instance, adds another group instead, so the Histone is left alone, and tightens to both the ATCG data and the Nucleosome on the otherside, tightening the whole Chromatin.



When HDAC is inhibited, it keeps it's Acetyl group, which is good because Acetyl groups keep the Chromatin relatively losely compact, meaning most genes will be expressed in a way one would want.



However, Histone Acetyltransferase is an enzyme which looks for Acetyl groups to convert to Acetyl CoA groups on the Histones, loosening the hold on the ATCG and modifying the entire Chromatin as a result, turning it into a Euchromatin, which not only turns genes on that previously weren't, and greatly increasing gene expression of genes that are already "on", but also modifying expression of genes to something completely different since the Euchromatin is packed in such a way that Transcription Factors can bind to genetic data that it never attached to before.

My nigga what are you talking about?

I will be back in like June. Look into Histone Deacetylase enzymes. HDACs modify Histone tails and make them wrap more tightly around the DNA, repressing gene expression. It's very likely that GHK-cu is a broad HDAC inhibitor, and its overwhelming effects aren't just a matter of coincidence. GHK-cu aids in Histone Acetyltransferase enzyme actions. HATs convert the Acetyl group on Histones to Acetyl-COA. Histone Acetylation increases gene expression since it loosens the Histones' grip on the DNA, making expression less repressed and can even turn on gene expression in genes that are turned off due to overly tight Chromatins.



Histones aren't wrapped around the actual DNA strand (The Nucleotides), they're apart of the Chromatin, which is a mass of genetic material that compresses and packages the actual ATCG encoded DNA. The Nucleosome wraps around the Histones. The Histones are the nearest protein to the actual encoded genetic data, and therefore can have the biggest influence on how/whether the data is expressed, and this expression can greatly vary depending on how the DNA is packaged. There will always be a variance in DNA expression after Acetyltransferase modifies the Histone.



Given that Histone Acetyltransferase makes the DNA less compact, the entire makeup of the Chromatin changes; it becomes Euchromatin, which is a lightly packed Chromatin (containing DNA, RNA and other genetic related proteins). Euchromatins are almost always under active transcription, which makes sense since the decompressed Chromatin variant (the Euchromatin) can allow for Transciption Factors to reach the target genes, also allowing for gene expression.



It looks like GHK-cu is an inhibitor of the "Histone Deacetylase" enzyme. Just like how you have Fin and AI's as inhibitors of the 5-alpha-reductase and aromatase enzymes respectively.



This is just the cliff notes version of this because there is so much more.



I know it might be hard to understand at first but here's what's happening pretty much.



Histone Deacetylation removes the Acetyl group from the Histones, this causes the Histones to wrap more tightly around the DNA repressing gene expression, or completely turning it off. The Chromatin becomes too tight and Transcription Factors can't reach their target genes, and if some still could, the chance that gene expression is blocked from the inside out, is also greatly increased. So it's like a double/quadruple whammy.



GHK-cu is likely a HDAC inhibitor, stopping the Histone Deacetylase enzyme from removing the Acetyl group from the Histones.



Once a Histone has its Acetyl group removed, there's no enzyme that for instance, adds another group instead, so the Histone is left alone, and tightens to both the ATCG data and the Nucleosome on the otherside, tightening the whole Chromatin.



When HDAC is inhibited, it keeps it's Acetyl group, which is good because Acetyl groups keep the Chromatin relatively losely compact, meaning most genes will be expressed in a way one would want.



However, Histone Acetyltransferase is an enzyme which looks for Acetyl groups to convert to Acetyl CoA groups on the Histones, loosening the hold on the ATCG and modifying the entire Chromatin as a result, turning it into a Euchromatin, which not only turns genes on that previously weren't, and greatly increasing gene expression of genes that are already "on", but also modifying expression of genes to something completely different since the Euchromatin is packed in such a way that Transcription Factors can bind to genetic data that they never attached to before.

Oh shit it's @x30001

@Lifeisgood72

 

[lasthope]

please tldr i am to low iq to understand

will it help me regrow my hair or not?

 

[Mayorga]

I think we need to do a cellular biology/biochemistry 101 crash course so that looksmaxxers can have some basic understanding of such mechanisms.

 

[Deleted member 3990]

I think we need to do a cellular biology/biochemistry 101 crash course so that looksmaxxers can have some basic understanding of such mechanisms.

Go ahead

My nigga what are you talking about?

He is talking about altering/inhibiting/activating Pathways and other Aspects of Gene activation / disactivation

 

[OOGABOOGA]

Go ahead

He is talking about altering/inhibiting/activating Pathways and other Aspects of Gene activation / disactivation

For what effect? No way I’m reading all that shit sum up the benefits

 

[JustTrynaGrow]

I will be back in like June. Look into Histone Deacetylase enzymes. HDACs modify Histone tails and make them wrap more tightly around the DNA, repressing gene expression. It's very likely that GHK-cu is a broad HDAC inhibitor, and its overwhelming effects aren't just a matter of coincidence. GHK-cu aids in Histone Acetyltransferase enzyme actions. HATs convert the Acetyl group on Histones to Acetyl-COA. Histone Acetylation increases gene expression since it loosens the Histones' grip on the DNA, making expression less repressed and can even turn on gene expression in genes that are turned off due to overly tight Chromatins.



Histones aren't wrapped around the actual DNA strand (The Nucleotides), they're apart of the Chromatin, which is a mass of genetic material that compresses and packages the actual ATCG encoded DNA. The Nucleosome wraps around the Histones. The Histones are the nearest protein to the actual encoded genetic data, and therefore can have the biggest influence on how/whether the data is expressed, and this expression can greatly vary depending on how the DNA is packaged. There will always be a variance in DNA expression after Acetyltransferase modifies the Histone.



Given that Histone Acetyltransferase makes the DNA less compact, the entire makeup of the Chromatin changes; it becomes Euchromatin, which is a lightly packed Chromatin (containing DNA, RNA and other genetic related proteins). Euchromatins are almost always under active transcription, which makes sense since the decompressed Chromatin variant (the Euchromatin) can allow for Transciption Factors to reach the target genes, also allowing for gene expression.



It looks like GHK-cu is an inhibitor of the "Histone Deacetylase" enzyme. Just like how you have Fin and AI's as inhibitors of the 5-alpha-reductase and aromatase enzymes respectively.



This is just the cliff notes version of this because there is so much more.



I know it might be hard to understand at first but here's what's happening pretty much.



Histone Deacetylation removes the Acetyl group from the Histones, this causes the Histones to wrap more tightly around the DNA repressing gene expression, or completely turning it off. The Chromatin becomes too tight and Transcription Factors can't reach their target genes, and if some still could, the chance that gene expression is blocked from the inside out, is also greatly increased. So it's like a double/quadruple whammy.



GHK-cu is likely a HDAC inhibitor, stopping the Histone Deacetylase enzyme from removing the Acetyl group from the Histones.



Once a Histone has its Acetyl group removed, there's no enzyme that for instance, adds another group instead, so the Histone is left alone, and tightens to both the ATCG data and the Nucleosome on the otherside, tightening the whole Chromatin.



When HDAC is inhibited, it keeps it's Acetyl group, which is good because Acetyl groups keep the Chromatin relatively losely compact, meaning most genes will be expressed in a way one would want.



However, Histone Acetyltransferase is an enzyme which looks for Acetyl groups to convert to Acetyl CoA groups on the Histones, loosening the hold on the ATCG and modifying the entire Chromatin as a result, turning it into a Euchromatin, which not only turns genes on that previously weren't, and greatly increasing gene expression of genes that are already "on", but also modifying expression of genes to something completely different since the Euchromatin is packed in such a way that Transcription Factors can bind to genetic data that they never attached to before.

Three main questions.

Is there already a HDAC inhibitor out there? Or is GHK-CU potentially the first of its kind.


Do we know what the actual benifits of increasing gene expression are? Sounds like it would make a huge difference in the body but I'd imagine that in reality it would only have a minor change. the extent to how much HDAC is actually inhibited is also kinda relevant.


What useful purpose does HDAC have? surely there's a benifit to wrapping histone tails more tightly around DNA?



I don't know anything about genes but the thread has definetly interested me

 

[Mayorga]

Is there already a HDAC inhibitor out there?

Yes, many HDIs are known - valproic acid, a substance researched by anti-norwood hobbyists, is one. It is important to mention that there are many (more than 10?) isoforms of the enzyme, so you can't really generalize its effects.

Do we know what the actual benifits of increasing gene expression are?

theoretically and given a very precise mechanism of action, you could do basically whatever you want, kind of akin to gene editing, just a bit further downstream. In reality though, we simply don't have enough knowledge and messing with something that has such broad effects is irresponsible. Its a double-edged sword, really.

What useful purpose does HDAC have?

Its just a mechanism to regulate gene expression first and foremost, but HDACs also play a role in activation/inactivation of proteins by de-acetylating them (a bit of biochem background is useful here).


Its a very interesting topic, no doubt, but also one that we currently lack practical knowledge in.

 

[Deleted member 656]

Yes, many HDIs are known - valproic acid, a substance researched by anti-norwood hobbyists, is one. It is important to mention that there are many (more than 10?) isoforms of the enzyme, so you can't really generalize its effects.



theoretically and given a very precise mechanism of action, you could do basically whatever you want, kind of akin to gene editing, just a bit further downstream. In reality though, we simply don't have enough knowledge and messing with something that has such broad effects is irresponsible. Its a double-edged sword, really.



Its just a mechanism to regulate gene expression first and foremost, but HDACs also play a role in activation/inactivation of proteins by de-acetylating them (a bit of biochem background is useful here).


Its a very interesting topic, no doubt, but also one that we currently lack practical knowledge in.

Would it be wise to steer away from using GHK-Cu until we know more about this?

 

[Seth Walsh]

Would it be wise to steer away from using GHK-Cu until we know more about this?

Not at all. I wrote a massive PM to Mayorga then accidentally closed the page on my phone....



HDAC and HAT inhibition can make new memories transcribe into long term memory, overshadowing old memories that you ruminate on. The BDNF can access data easier in a Euchromatin, and write new memories into long term memory.

The PHD guy on the reddit AMA literally said GHK-cu is a HDAC and HAT inhibitor. The repairing of nerves and damaged DNA isn't a coincidence. HDAC inhibitors also work on non epigenetic proteins, like VEGF which helps create new blood vessels. HAT is bad, I made a lot of mistakes in my first post. You always want Acetyl groups on your histones. HAT changes the Euchromatin into a Heterochromatin, which is very tight. So that's bad too. EGCG is a HDAC and HAT inhibitor. I'll be dosing it every few hours everyday for the next few months.

Very busy with college and work now. So I can't let myself stay on here too much because it's a distraction.

My PM to Mayorga was incredibly detailed and I nearly lost my shit when I accidentally closed the tab on my phone.

The 2 reddit threads and the 2 threads on longecity explain all this 100x better than I ever could.

And yes. In a few months I'll experiment with Vorinostat. Vorinostat, CBT, exposure therapy and some GABA meds could literally save people's lives.

Also, look into Bromodomains.

Not trying to make a dramatic exit from the forum or anything but I have lots of exams atm so I can only come online when I'm on the train or something like that.

Not at all. I wrote a massive PM to Mayorga then accidentally closed the page on my phone....



HDAC and HAT inhibition can make new memories transcribe into long term memory, overshadowing old memories that you ruminate on. The BDNF can access data easier in a Euchromatin, and write new memories into long term memory.

The PHD guy on the reddit AMA literally said GHK-cu is a HDAC and HAT inhibitor. The repairing of nerves and damaged DNA isn't a coincidence. HDAC inhibitors also work on non epigenetic proteins, like VEGF which helps create new blood vessels. HAT is bad, I made a lot of mistakes in my first post. You always want Acetyl groups on your histones. HAT changes the Euchromatin into a Heterochromatin, which is very tight. So that's bad too. EGCG is a HDAC and HAT inhibitor. I'll be dosing it every few hours everyday for the next few months.

Very busy with college and work now. So I can't let myself stay on here too much because it's a distraction.

My PM to Mayorga was incredibly detailed and I nearly lost my shit when I accidentally closed the tab on my phone.

The 2 reddit threads and the 2 threads on longecity explain all this 100x better than I ever could.

And yes. In a few months I'll experiment with Vorinostat. Vorinostat, CBT, exposure therapy and some GABA meds could literally save people's lives.

Also, look into Bromodomains.

Not trying to make a dramatic exit from the forum or anything but I have lots of exams atm so I can only come online when I'm on the train or something like that.

This shit can literally help people forget about the "blackpill".

I used to joke about GHK-cu helping with everything. It's proven to prevent HDAC on VEGF. I can only assume it does the same for the epigenetic proteins (histones). PAN HDAC inhibitors aren't completely good because HDAC1 is kind of important.

I'm interested in the HDAC 2,3,4,6 inhibition and it's effect on memory consolidation by allowing BDNF to bind to TCF and target the genes responsible for parts of memory and cognition.

I'm not joking, I will take 200mg EGCG every 4 hours for the next months and then possibly experiment with Vorinostat.

Yes, many HDIs are known - valproic acid, a substance researched by anti-norwood hobbyists, is one. It is important to mention that there are many (more than 10?) isoforms of the enzyme, so you can't really generalize its effects.



theoretically and given a very precise mechanism of action, you could do basically whatever you want, kind of akin to gene editing, just a bit further downstream. In reality though, we simply don't have enough knowledge and messing with something that has such broad effects is irresponsible. Its a double-edged sword, really.



Its just a mechanism to regulate gene expression first and foremost, but HDACs also play a role in activation/inactivation of proteins by de-acetylating them (a bit of biochem background is useful here).


Its a very interesting topic, no doubt, but also one that we currently lack practical knowledge in.

Damn sorry didn't see your post. Deacetylation of histones almost certainly guarantees less gene expression. But your right, HAT can modulate genes and we don't know which ones!

My focus is on the anti fear/memory/anxiety properties from inhibiting HDAC2.

This /u/chemicalbiology dude said 3 years ago that he was working on creating a selective HDACi.

GHK-cu repairs damaged DNA, nerves, inhibits HDAC on VEGF and is presumed to be a HDAC for Acetyl groups on the Histones too. If EGCG, a natural anti-oxidant works on Histones, why wouldn't GHK. Everything seems to tie in. /u/chemicalbiology also said GHK-cu is a HDACi, but no studies confirm that for sure. GHK-cu also is extremely anti-inflammatory, works for hair regrowth, skin health etc. There's anecdotes on longecity from people who took 1mg/kg of Vorinostat daily, and they claimed it made new memories consolidate over old memories.

I have a theory, probably a silly theory, that people are nostalgic and view their early childhood in such an amazing way since their memories could transcribe into long-term memories most easily. Obviously that's not the only reason though

GHK-cu in the body declines with age. *possibly* our ability to consolidate newer memories does too, and therefore we begin to think our recent life isn't as good as "the good old days". But ofc I know that's only a theoretical factor, and completely hypothetical.

A lot can be linked together with all this though. I know nothing more about this than @Mayorga or anyone who can read and interpret what's on the internet.

Those threads from /u/chemicalbiology and one from "musicman" in Nov 2016, and a guy called "tree" from 2014 on longecity are very intriguing though. Bromodomains are something I need to look at too, since cb mentioned that in one of those threads.

Not at all. I wrote a massive PM to Mayorga then accidentally closed the page on my phone....



HDAC and HAT inhibition can make new memories transcribe into long term memory, overshadowing old memories that you ruminate on. The BDNF can access data easier in a Euchromatin, and write new memories into long term memory.

The PHD guy on the reddit AMA literally said GHK-cu is a HDAC and HAT inhibitor. The repairing of nerves and damaged DNA isn't a coincidence. HDAC inhibitors also work on non epigenetic proteins, like VEGF which helps create new blood vessels. HAT is bad, I made a lot of mistakes in my first post. You always want Acetyl groups on your histones. HAT changes the Euchromatin into a Heterochromatin, which is very tight. So that's bad too. EGCG is a HDAC and HAT inhibitor. I'll be dosing it every few hours everyday for the next few months.

Very busy with college and work now. So I can't let myself stay on here too much because it's a distraction.

My PM to Mayorga was incredibly detailed and I nearly lost my shit when I accidentally closed the tab on my phone.

The 2 reddit threads and the 2 threads on longecity explain all this 100x better than I ever could.

And yes. In a few months I'll experiment with Vorinostat. Vorinostat, CBT, exposure therapy and some GABA meds could literally save people's lives.

Also, look into Bromodomains.

Not trying to make a dramatic exit from the forum or anything but I have lots of exams atm so I can only come online when I'm on the train or something like that.

This shit can literally help people forget about the "blackpill".

I used to joke about GHK-cu helping with everything. It's proven to prevent HDAC on VEGF. I can only assume it does the same for the epigenetic proteins (histones). PAN HDAC inhibitors aren't completely good because HDAC1 is kind of important.

I'm interested in the HDAC 2,3,4,6 inhibition and it's effect on memory consolidation by allowing BDNF to bind to TCF and target the genes responsible for parts of memory and cognition.

I'm not joking, I will take 200mg EGCG every 4 hours for the next months and then possibly experiment with Vorinostat.

Damn sorry didn't see your post. Deacetylation of histones almost certainly guarantees less gene expression. But your right, HAT can modulate genes and we don't know which ones!

My focus is on the anti fear/memory/anxiety properties from inhibiting HDAC2.

This /u/chemicalbiology dude said 3 years ago that he was working on creating a selective HDACi.

GHK-cu repairs damaged DNA, nerves, inhibits HDAC on VEGF and is presumed to be a HDAC for Acetyl groups on the Histones too. If EGCG, a natural anti-oxidant works on Histones, why wouldn't GHK. Everything seems to tie in. /u/chemicalbiology also said GHK-cu is a HDACi, but no studies confirm that for sure. GHK-cu also is extremely anti-inflammatory, works for hair regrowth, skin health etc. There's anecdotes on longecity from people who took 1mg/kg of Vorinostat daily, and they claimed it made new memories consolidate over old memories.

I have a theory, probably a silly theory, that people are nostalgic and view their early childhood in such an amazing way since their memories could transcribe into long-term memories most easily. Obviously that's not the only reason though

GHK-cu in the body declines with age. *possibly* our ability to consolidate newer memories does too, and therefore we begin to think our recent life isn't as good as "the good old days". But ofc I know that's only a theoretical factor, and completely hypothetical.

A lot can be linked together with all this though. I know nothing more about this than @Mayorga or anyone who can read and interpret what's on the internet.

Those threads from /u/chemicalbiology and one from "musicman" in Nov 2016, and a guy called "tree" from 2014 on longecity are very intriguing though. Bromodomains are something I need to look at too, since cb mentioned that in one of those threads.

That's not all. Desensitization to drugs, killing addictive traits/tendencies have been reported too. People believe it's because the body always wants homeostasis, and with genetic data easily accessible by TCFs and anything bound to them, the body can achieve that homeostasis by upregulating the receptors that the drugs fry. Because in reality, our body doesn't know that it's person is taking drugs and frying various receptors, but it can adapt and upregulate them, probably much more easily if the genetic data isn't locked away in a heterochromatin.

 

[Deleted member 3990]

Not at all. I wrote a massive PM to Mayorga then accidentally closed the page on my phone....



HDAC and HAT inhibition can make new memories transcribe into long term memory, overshadowing old memories that you ruminate on. The BDNF can access data easier in a Euchromatin, and write new memories into long term memory.

The PHD guy on the reddit AMA literally said GHK-cu is a HDAC and HAT inhibitor. The repairing of nerves and damaged DNA isn't a coincidence. HDAC inhibitors also work on non epigenetic proteins, like VEGF which helps create new blood vessels. HAT is bad, I made a lot of mistakes in my first post. You always want Acetyl groups on your histones. HAT changes the Euchromatin into a Heterochromatin, which is very tight. So that's bad too. EGCG is a HDAC and HAT inhibitor. I'll be dosing it every few hours everyday for the next few months.

Very busy with college and work now. So I can't let myself stay on here too much because it's a distraction.

My PM to Mayorga was incredibly detailed and I nearly lost my shit when I accidentally closed the tab on my phone.

The 2 reddit threads and the 2 threads on longecity explain all this 100x better than I ever could.

And yes. In a few months I'll experiment with Vorinostat. Vorinostat, CBT, exposure therapy and some GABA meds could literally save people's lives.

Also, look into Bromodomains.

Not trying to make a dramatic exit from the forum or anything but I have lots of exams atm so I can only come online when I'm on the train or something like that.

This shit can literally help people forget about the "blackpill".

I used to joke about GHK-cu helping with everything. It's proven to prevent HDAC on VEGF. I can only assume it does the same for the epigenetic proteins (histones). PAN HDAC inhibitors aren't completely good because HDAC1 is kind of important.

I'm interested in the HDAC 2,3,4,6 inhibition and it's effect on memory consolidation by allowing BDNF to bind to TCF and target the genes responsible for parts of memory and cognition.

I'm not joking, I will take 200mg EGCG every 4 hours for the next months and then possibly experiment with Vorinostat.

Damn sorry didn't see your post. Deacetylation of histones almost certainly guarantees less gene expression. But your right, HAT can modulate genes and we don't know which ones!

My focus is on the anti fear/memory/anxiety properties from inhibiting HDAC2.

This /u/chemicalbiology dude said 3 years ago that he was working on creating a selective HDACi.

GHK-cu repairs damaged DNA, nerves, inhibits HDAC on VEGF and is presumed to be a HDAC for Acetyl groups on the Histones too. If EGCG, a natural anti-oxidant works on Histones, why wouldn't GHK. Everything seems to tie in. /u/chemicalbiology also said GHK-cu is a HDACi, but no studies confirm that for sure. GHK-cu also is extremely anti-inflammatory, works for hair regrowth, skin health etc. There's anecdotes on longecity from people who took 1mg/kg of Vorinostat daily, and they claimed it made new memories consolidate over old memories.

I have a theory, probably a silly theory, that people are nostalgic and view their early childhood in such an amazing way since their memories could transcribe into long-term memories most easily. Obviously that's not the only reason though

GHK-cu in the body declines with age. *possibly* our ability to consolidate newer memories does too, and therefore we begin to think our recent life isn't as good as "the good old days". But ofc I know that's only a theoretical factor, and completely hypothetical.

A lot can be linked together with all this though. I know nothing more about this than @Mayorga or anyone who can read and interpret what's on the internet.

Those threads from /u/chemicalbiology and one from "musicman" in Nov 2016, and a guy called "tree" from 2014 on longecity are very intriguing though. Bromodomains are something I need to look at too, since cb mentioned that in one of those threads.

That's not all. Desensitization to drugs, killing addictive traits/tendencies have been reported too. People believe it's because the body always wants homeostasis, and with genetic data easily accessible by TCFs and anything bound to them, the body can achieve that homeostasis by upregulating the receptors that the drugs fry. Because in reality, our body doesn't know that it's person is taking drugs and frying various receptors, but it can adapt and upregulate them, probably much more easily if the genetic data isn't locked away in a heterochromatin.

you overdosed on @Ritalincel again

 

[PenileFacialSurgery]

NIGGA WTF DOES ANY OF THIS MEAN AND HOW IS IT USEFUL

 

[Mayorga]

NIGGA WTF DOES ANY OF THIS MEAN AND HOW IS IT USEFUL

If you were to put this info into a tower made of blocks of concepts with the most basic ones at the bottom, where exactly does the tower fall apart?

 

[Deleted member 656]

If you were to put this info into a tower made of blocks of concepts with the most basic ones at the bottom, where exactly does the tower fall apart?

Something tells me he'd have an easier time getting his head around @Seth Walsh's posts then he'd have addressing this.

Not at all. I wrote a massive PM to Mayorga then accidentally closed the page on my phone....



HDAC and HAT inhibition can make new memories transcribe into long term memory, overshadowing old memories that you ruminate on. The BDNF can access data easier in a Euchromatin, and write new memories into long term memory.

The PHD guy on the reddit AMA literally said GHK-cu is a HDAC and HAT inhibitor. The repairing of nerves and damaged DNA isn't a coincidence. HDAC inhibitors also work on non epigenetic proteins, like VEGF which helps create new blood vessels. HAT is bad, I made a lot of mistakes in my first post. You always want Acetyl groups on your histones. HAT changes the Euchromatin into a Heterochromatin, which is very tight. So that's bad too. EGCG is a HDAC and HAT inhibitor. I'll be dosing it every few hours everyday for the next few months.

Very busy with college and work now. So I can't let myself stay on here too much because it's a distraction.

My PM to Mayorga was incredibly detailed and I nearly lost my shit when I accidentally closed the tab on my phone.

The 2 reddit threads and the 2 threads on longecity explain all this 100x better than I ever could.

And yes. In a few months I'll experiment with Vorinostat. Vorinostat, CBT, exposure therapy and some GABA meds could literally save people's lives.

Also, look into Bromodomains.

Not trying to make a dramatic exit from the forum or anything but I have lots of exams atm so I can only come online when I'm on the train or something like that.

This shit can literally help people forget about the "blackpill".

I used to joke about GHK-cu helping with everything. It's proven to prevent HDAC on VEGF. I can only assume it does the same for the epigenetic proteins (histones). PAN HDAC inhibitors aren't completely good because HDAC1 is kind of important.

I'm interested in the HDAC 2,3,4,6 inhibition and it's effect on memory consolidation by allowing BDNF to bind to TCF and target the genes responsible for parts of memory and cognition.

I'm not joking, I will take 200mg EGCG every 4 hours for the next months and then possibly experiment with Vorinostat.

Damn sorry didn't see your post. Deacetylation of histones almost certainly guarantees less gene expression. But your right, HAT can modulate genes and we don't know which ones!

My focus is on the anti fear/memory/anxiety properties from inhibiting HDAC2.

This /u/chemicalbiology dude said 3 years ago that he was working on creating a selective HDACi.

GHK-cu repairs damaged DNA, nerves, inhibits HDAC on VEGF and is presumed to be a HDAC for Acetyl groups on the Histones too. If EGCG, a natural anti-oxidant works on Histones, why wouldn't GHK. Everything seems to tie in. /u/chemicalbiology also said GHK-cu is a HDACi, but no studies confirm that for sure. GHK-cu also is extremely anti-inflammatory, works for hair regrowth, skin health etc. There's anecdotes on longecity from people who took 1mg/kg of Vorinostat daily, and they claimed it made new memories consolidate over old memories.

I have a theory, probably a silly theory, that people are nostalgic and view their early childhood in such an amazing way since their memories could transcribe into long-term memories most easily. Obviously that's not the only reason though

GHK-cu in the body declines with age. *possibly* our ability to consolidate newer memories does too, and therefore we begin to think our recent life isn't as good as "the good old days". But ofc I know that's only a theoretical factor, and completely hypothetical.

A lot can be linked together with all this though. I know nothing more about this than @Mayorga or anyone who can read and interpret what's on the internet.

Those threads from /u/chemicalbiology and one from "musicman" in Nov 2016, and a guy called "tree" from 2014 on longecity are very intriguing though. Bromodomains are something I need to look at too, since cb mentioned that in one of those threads.

That's not all. Desensitization to drugs, killing addictive traits/tendencies have been reported too. People believe it's because the body always wants homeostasis, and with genetic data easily accessible by TCFs and anything bound to them, the body can achieve that homeostasis by upregulating the receptors that the drugs fry. Because in reality, our body doesn't know that it's person is taking drugs and frying various receptors, but it can adapt and upregulate them, probably much more easily if the genetic data isn't locked away in a heterochromatin.

You're saying GHK-Cu could have a significant impact on gene expression but we have no idea which genes, and in spite of that we still ought to be using it?

 

[zeno]

you know science, ive been taking finasteride for 2 months have i permanently fucked myself?

 

[Seth Walsh]

you know science, ive been taking finasteride for 2 months have i permanently fucked myself?

I don't know your situation at all. If you think somethings wrong then you can work from there.

 

[zeno]

I don't know your situation at all. If you think somethings wrong then you can work from there.

sex drive/EQ is noticeably worse and i also think my mental state worsened so im anxious about it and i wanna stop, plus my hair didnt stop shedding.. whats the chance i fucked myself for good, ive read horror stories in hackstasis..if u can pm me

 

[Seth Walsh]

Something tells me he'd have an easier time getting his head around @Seth Walsh's posts then he'd have addressing this.

You're saying GHK-Cu could have a significant impact on gene expression but we have no idea which genes, and in spite of that we still ought to be using it?

I don't know exactly how Histone Acetyltransferase modulates certain gene expressions, but preventing deactylation on Histones will just increase expression and reduce repression. The anti-cancer properties come from the increased expression from the p53 gene which is a tumor supressor. We don't really have genes that are inherently/deliberately there to be bad. ie: We don't have genes that need to be silenced, but still existing; we're just not made like that. More than 92% of our Chromatins are Euchromatins anyways. Preventing Acetylation is akin to preventing Methylation on the Cytosine alleles. Both are just something we don't want. It seems HDAC inhibitors can also be HAT and HMT (https://en.wikipedia.org/wiki/Histone_methyltransferase) inhibitors.

I don't know a thing about Histone Methylation specifically but I can assume it's involved in gene silencing just like how Methylation on the Cystosine alleles turns off the gene. Look into the "Horvath Clock", it explains how Methylation on the Cystosine nucleotide is used as a marker of epigenetic aging.

I'd look at Acetylation and Methylation as things that increase/activate, or decrease/deactivate genes and their expression. Although the 2 aren't perfectly reciprocal, it's a good way to get a grasp on things and as to why Histone Deacetylation is pretty much always bad.

Gene expression from damaged DNA wouldn't happpen, as the DNA would be repaired before expression is increased. GHK-cu is doing all of this. Cancer tumor suppression via p53, hair growth, skin health, wound healing, nerve repair, DNA repair, increased blood vessel health through prevention of VEGF deacetylation (which is non-epigenetic).

 

[SurgerySoon]

For the last few days I've been injecting 5-6 mg per day of GHK-Cu. Do you think the dose is too high? Should I go even higher? Also, do you think that's a high-enough dose to obtain noticeable improvements to collagen and skin quality?

 

[Seth Walsh]

For the last few days I've been injecting 5-6 mg per day of GHK-Cu. Do you think the dose is too high? Should I go even higher? Also, do you think that's a high-enough dose to obtain noticeable improvements to collagen and skin quality?

Yes holy shit, do like 0.3mg max

Yes holy shit, do like 0.3mg max

And 0.3mg is enough for all the benefits.

 

[Deleted member 3990]

Do you even check wickr me jfl

Besides, from the things I read I think Copper peptides are far too weak on skin and hair changes, so I also doubt they will do much on transcriptions
Histogen deactylation seems interesting nontheless, will look into (upcoming) drugs which specialize on it

 

[Seth Walsh]

Do you even check wickr me jfl

Besides, from the things I read I think Copper peptides are far too weak on skin and hair changes, so I also doubt they will do much on transcriptions
Histogen deactylation seems interesting nontheless, will look into (upcoming) drugs which specialize on it

I deleted wickr. GHK-cu specifically *might* work so well because of possible epigenetic alterations, not because it's a copper peptide. It's glycl l-histidyl l-lysine and there's stuff online about lysine and arginine residues being important in epigenetic modifications like methylation, acetylation etc.

EGCG is a HDAC, HAT, DNMT and HMT inhibitor and I've been taking it every few hours for the past day and a half. I definitely feel different, in a good way. Feel like I have less fear. Very weird feeling. Feels like I'm on a strong benzo for the first time ever with no desensitization/tolerance.

 

[Deleted member 3990]

I deleted wickr. GHK-cu specifically *might* work so well because of possible epigenetic alterations, not because it's a copper peptide. It's glycl l-histidyl l-lysine and there's stuff online about lysine and arginine residues being important in epigenetic modifications like methylation, acetylation etc.

EGCG is a HDAC and HAT inhibitor and I've been taking it every few hours for the past day and a half. I definitely feel different, in a good way. Feel like I have less fear. Very weird feeling. Feels like I'm on a strong benzo for the first time ever with no desensitization/tolerance.

interesting

so the normal peptides are dwarfes compared to GHK ?

I deleted wickr

How will you ever keep in touch with your old friend then
Doesnt look like you can really avoid me tho, jfl

@Gebirgscel

 

[Seth Walsh]

interesting

so the normal peptides are dwarfes compared to GHK ?

They're incomparable if they can't modify the way DNA is read. Copper peptides are still cool, but I'm coming to realize GHK-cu is many things other than a "copper peptide", and it's benefits and uniqueness extremely likely don't come from being just a "copper peptide".

There's too much stuff on the internet about Lysine and Histone modification. the -cu just helps absorption. I'd take a deeper look into the GHK make-up, especially the l-Lys part.

 

[Deleted member 3990]

They're incomparable if they can't modify the way DNA is read. Copper peptides are still cool, but I'm coming to realize GHK-cu is many things other than a "copper peptide", and it's benefits and uniqueness extremely likely don't come from being just a "copper peptide".

There's too much stuff on the internet about Lysine and Histone modification. the -cu just helps absorption. I'd take a deeper look into the GHK make-up, especially the l-Lys part.

I am learning through the exposure effect

Such things are not talked about on here, do you know some sites where I could dive in in all these transcription and pathway things (maybe a forum)

 

[SurgerySoon]

Yes holy shit, do like 0.3mg max

And 0.3mg is enough for all the benefits.

Thanks, but Ben Greenfield actually published an article on his site in which he said that 1.5 mg per day or possibly more could be safe and effective. Just out of curiosity, why do you recommend such a low dose?

Link to article (do keyword search for GHK):

The Little-Known Russian Wonder Compound & The Fringe Future Of Anti-Aging Medicine - Ben Greenfield Life - Health, Diet, Fitness, Family & Faith

How To Use Peptides: The Little-Known Russian Wonder Compound & The Fringe Future Of Anti-Aging Medicine

bengreenfieldfitness.com

 

[Seth Walsh]

I am learning through the exposure effect

Such things are not talked about on here, do you know some sites where I could dive in in all these transcription and pathway things (maybe a forum)

Nope, I don't know of anywhere unfortunately.

EGCG is also an Aromatic L-Amino Acid Decarboxylase inhibitor (AAAD), which helps prevent the synthesis of Serotonin and Dopamine outside of the brain. AAAD inhibitors can't pass the Blood Brain Barrier and only prevent the conversions of L-Dopa/Phenylalinine/Tyrosine to Dopamine, and 5-HTP/Tryptophan to Serotonin when outside of the brain (ie: in the gut). So that could help avoid buildup of Serotonin and Dopamine outside of the brain, possibly encouraging more of the precursors to pass the BBB to be synthesized in the brain, because that's the only place they can be synthesized.

Thanks, but Ben Greenfield actually published an article on his site in which he said that 1.5 mg per day or possibly more could be safe and effective. Just out of curiosity, why do you recommend such a low dose?

Link to article (do keyword search for GHK):

The Little-Known Russian Wonder Compound & The Fringe Future Of Anti-Aging Medicine - Ben Greenfield Life - Health, Diet, Fitness, Family & Faith

How To Use Peptides: The Little-Known Russian Wonder Compound & The Fringe Future Of Anti-Aging Medicine

bengreenfieldfitness.com

I just heard that was a good dose. Don't really have a reason. I heard it was effective at 0.3mg per day and you wanna get your money's worth.

 

[Cope]

Have you done any research on Selank? @Seth Walsh I’m trying to look for an anxiolytic (preferably a GABAergic one) that isn’t addictive/low tolerance threshold.

 

[Seth Walsh]

Have you done any research on Selank? @Seth Walsh I’m trying to look for an anxiolytic (preferably a GABAergic one) that isn’t addictive/low tolerance threshold.

None at all

 

[Summer]

@Seth Walsh
Hey! You did any further discoveries on this ? You experimented with an HDAC inhibitor yet?

 

[Seth Walsh]

@Seth Walsh
Hey! You did any further discoveries on this ? You experimented with an HDAC inhibitor yet?

I use GHK-cu almost everyday but no further discoveries on it being a HDAC inhibitor. It really is great though. Especially for the skin and anti aging.

 

[Summer]

I use GHK-cu almost everyday but no further discoveries on it being a HDAC inhibitor. It really is great though. Especially for the skin and anti aging.

Social deficits in Shank3-deficient mouse models of autism are rescued by histone deacetylase (HDAC) inhibition - Nature Neuroscience

Qin et al show that autism-like social deficits in Shank3-deficient mice arise from β-catenin-mediated transcriptional upregulation of histone deacetylase 2 (HDAC2) and are persistently alleviated by brief treatment with HDAC inhibitor romidepsin.

www.nature.com

Do you think inhibiting HDAC 2 via Vorinostat could be a potential cure for autism disorder? What is your take on this one

I actuslly made a thread about this as well lol

https://looksmax.org/threads/the-cu...tomes-reversed-by-an-anti-cancer-drug.250770/

Also ecgc works as an inhibitor as well?

 

[Soalian]

Social deficits in Shank3-deficient mouse models of autism are rescued by histone deacetylase (HDAC) inhibition - Nature Neuroscience

Qin et al show that autism-like social deficits in Shank3-deficient mice arise from β-catenin-mediated transcriptional upregulation of histone deacetylase 2 (HDAC2) and are persistently alleviated by brief treatment with HDAC inhibitor romidepsin.

www.nature.com

Do you think inhibiting HDAC 2 via Vorinostat could be a potential cure for autism disorder? What is your take on this one

I actuslly made a thread about this as well lol

https://looksmax.org/threads/the-cu...tomes-reversed-by-an-anti-cancer-drug.250770/

Also ecgc works as an inhibitor as well?

I've been experimenting with HDAC inhibitors for fear exctinction benefits.

Can only report subjectively though.

Am now certified fearless slayer.

 

[Summer]

I've been experimenting with HDAC inhibitors for fear exctinction benefits.

Can only report subjectively though.

Am now certified fearless slayer.

What is your ED routine ?

 

[GarixTheChad]

you can buy it now my nigga

 

[GarixTheChad]

so if i would inject it for some of the time it would benefit in me being fearless and more high iq?

 

[Soalian]

What is your ED routine ?

Not daily, more like three weeks on /six weeks off:

Ketogenic diet (Beta-hydroxybutyrate)

Lots of Butyrate (Inulin/Sodium Butyrate)

Vorinostat (150 mg every three days)

Resveratrol

Nigella Sativa (Thimoquinone)

Green tea Extract (EGCG)

Sulforaphane (Broccoli sprout Extract, with mustard seeds, for myrosinase)

Curcumin extract.

 

[Soalian]

so if i would inject it for some of the time it would benefit in me being fearless and more high iq?

Yes, absolutely.





















Not.

 

[GarixTheChad]

Yes, absolutely.





















Not.

its over

 

[Soalian]

its over

But it may benefit you in others areas though.

 

[GarixTheChad]

But it may benefit you in others areas though.

what areas nigga tell me

 

[gymislife]

I use GHK-cu almost everyday but no further discoveries on it being a HDAC inhibitor. It really is great though. Especially for the skin and anti aging.

Do you still use it? And do you use it along with retinoid? How's your skin like?