GHK-cu and the gene expressions it modulates, and by what %

Seth Walsh

Seth Walsh

The man in the mirror is my only threat
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Gene Expression Analysis
Fibrinogen Suppression (needed to create blood clots)


Gene title​
Percent change in gene expression​
Fibrinogen alpha chain, FGA​
121%​
Fibrinogen beta chain, FGB​
−475%​


GHK also suppresses the production of the inflammatory cytokine interleukin-6 (IL-6) which is a main positive regulator of fibrinogen synthesis, through its interaction with fibrinogen genes. In cell culture systems, GHK suppresses IL-6 secretion in skin fibroblasts and IL-6 gene expression in SZ95 sebocytes.

In summary, the effects of GHK on the FGB gene plus its effects on IL-6 production imply a suppression of overall fibrinogen production.

Ubiquitin/Proteasome System
GHK stimulated gene expression in 41 UPS genes while suppressing only 1 UPS gene.


Up​
Gene title​
Percent change in gene expression​
1​
Ubiquitin specific peptidase 29, USP29​
1056%​
2​
Ubiquitin protein ligase E3 component n-recognin 2, UBR2​
455%​
3​
Gamma-aminobutyric acid (GABA) B receptor, 1 /// ubiquitin D, GABBR1 /// UBD​
310%​
4​
Ubiquitin specific peptidase 34, USP34​
195%​
5​
Parkinson protein 2, E3 ubiquitin protein ligase (parkin), PARK2​
169%​
6​
Ubiquitin-conjugating enzyme E2I (UBC9 homolog, yeast), UBE2I​
150%​
7​
Ubiquitin protein ligase E3 component n-recognin 4, UBR4​
146%​
8​
Ubiquitin protein ligase E3B, UBE3B​
116%​
9​
Ubiquitin specific peptidase 2, USP2​
104%​
10​
Ubiquitin-like modifier activating enzyme 6, UBA6​
104%​
11​
Ubiquitination factor E4B (UFD2 homolog, yeast), UBE4B​
97%​
12​
Ubiquitin-conjugating enzyme E2M (UBC12 homolog, yeast), UBE2M​
92%​
13​
Ubiquitin-like modifier activating enzyme 7, UBA7​
88%​
14​
HECT, C2 and WW domain containing E3 ubiquitin protein ligase 1, HECW1​
81%​
15​
Proteasome (prosome, macropain) 26S subunit, ATPase, 3, PSMC3​
81%​
16​
Ubiquitin-conjugating enzyme E2D 1 (UBC4/5 homolog, yeast), UBE2D1​
79%​
17​
Proteasome (prosome, macropain) subunit, beta type, 2, PSMB2​
79%​
18​
Ubiquitin protein ligase E3 component n-recognin 5, UBR5​
77%​
19​
Ubiquitin specific peptidase 21, USP21​
76%​
20​
OTU domain, ubiquitin aldehyde binding 2, OTUB2​
76%​
21​
Proteasome (prosome, macropain) inhibitor subunit 1 (PI31), PSMF1​
75%​
22​
Ubiquitin-conjugating enzyme E2H (UBC8 homolog, yeast), UBE2H​
73%​
23​
Ubiquitin-conjugating enzyme E2N (UBC13 homolog, yeast), UBE2N​
72%​
24​
Ubiquitin carboxyl-terminal hydrolase L5, UCHL5​
71%​
25​
Proteasome (prosome, macropain) 26S subunit, non-ATPase, 13, PSMD13​
70%​
26​
Ubiquitin associated protein 1, UBAP1​
70%​
27​
Ubiquitin-conjugating enzyme E2B (RAD6 homolog), UBE2B​
69%​
28​
TMEM189-UBE2V1 readthrough /// ubiquitin-conjugating enzyme E2 variant 1, TMEM189-UBE2V1 /// UBE2V1​
67%​
29​
Proteasome (prosome, macropain) 26S subunit, non-ATPase, 1, PSMD1​
64%​
30​
Proteasome (prosome, macropain) 26S subunit, non-ATPase, 3, PSMD3​
64%​
31​
Ariadne homolog, ubiquitin-conjugating enzyme E2 binding protein, 1 (drosophila), ARIH1​
61%​
32​
BRCA1 associated protein-1 (ubiquitin carboxy-terminal hydrolase), BAP1​
60%​
33​
Ubiquitin interaction motif containing 1, UIMC1​
60%​
34​
Ubiquitin associated protein 2-like, UBAP2L​
57%​
35​
Ubiquitin protein ligase E3 component n-recognin 7 (putative), UBR7​
56%​
36​
Ubiquitin-conjugating enzyme E2G 1 (UBC7 homolog, yeast), UBE2G1​
54%​
37​
Itchy E3 ubiquitin protein ligase homolog (mouse), ITCH​
54%​
38​
Ubiquitin-conjugating enzyme E2D 4 (putative), UBE2D4​
51%​
39​
Proteasome (prosome, macropain) 26S subunit, non-ATPase, 10, PSMD10​
50%​
40​
WW domain containing E3 ubiquitin protein ligase 1, WWP1​
50%​
41​
Ubiquitin-like 3, UBL3​
50%​
Down​
Gene title​
Percent change in gene expression​
1​
Ubiquitin associated and SH3 domain containing A, UBASH3A​
−89%​


DNA Repair Genes
GHK was primarily stimulatory for DNA repair genes (47 UP, 5 DOWN).


Percent change in gene expression​
Genes up​
Genes down​
50%–100%​
41​
4​
100%–150%​
2​
1​
150%–200%​
1​
0​
200%–250%​
2​
0​
250%–300%​
1​
0​

The most affected DNA repair genes.

Up​
Gene title​
Percent change in gene expression​
1​
Poly (ADP-ribose) polymerase family, member 3, PARP3​
253%​
2​
Polymerase (DNA directed), mu, POLM​
225%​
3​
MRE11 meiotic recombination 11 homolog A MRE11A​
212%​
4​
RAD50 homolog (S. cerevisiae), RAD50​
175%​
5​
Eyes absent homolog 3 (Drosophila), EYA3​
128%​
6​
Retinoic acid receptor, alpha, RARA​
123%​
Down​
Gene title​
Percent change in gene expression​
1​
Cholinergic receptor, nicotinic, alpha 4, CHRNA4​
−105%​

Antioxidant Genes
Among the 13,424 available genes in the Broad Institute data, we were able to identify 14 antioxidant genes in which GHK stimulates as well as two prooxidant genes that GHK suppresses. GHK increases the expression of the oxidative/inflammatory gene NF-κB2 103% but also increases the expression of two inhibitors of NF-κB, TLE1 by 762% and IL18BP by 295%, thus possibly inhibiting the activity of the NF-κB protein.


Up​
Genes​
Percent change in gene expression​
Comments​
1​
TLE1​
762%​
Inhibits the oxidative/inflammatory gene NF-κB.​
2​
SPRR2C​
721%​
This proline-rich, antioxidant protein protects outer skin cells from oxidative damage from ROS. When the ROS level is low, the protein remains in the outer cell membrane but when the ROS level is high, the protein clusters around the cell’s DNA to protect it.​
3​
ITGB4​
609%​
Upregulation of ITGB4 promotes wound repair ability and antioxidative ability.​
4​
APOM​
403%​
Binds oxidized phospholipids and increases the antioxidant effect of HDL.​
5​
PON3​
319%​
Absence of PON3 (paraoxonase 3) in mice resulted in increased rates of early fetal and neonatal death. Knockdown of PON3 in human cells reduced cell proliferation and total antioxidant capacity.​
6​
IL18BP​
295%​
The protein encoded by this gene is an inhibitor of the proinflammatory cytokine IL18. IL18BP abolished IL18 induction of interferon-gamma (IFNgamma), IL8, and activation of NF-κB in vitro. Blocks neutrophil oxidase activity.​
7​
HEPH​
217%​
Inhibits the conversion of Fe(2+) to Fe(3+). HEPH increases iron efflux, lowers cellular iron levels, suppresses reactive oxygen species production, and restores mitochondrial transmembrane potential.​
8​
FABP1​
186%​
Reduces intracellular ROS level. Plays a significant role in reduction of oxidative stress.​
9​
PON1​
149%​
PON1 (paraoxonase 1) is a potent antioxidant and a major anti-atherosclerotic component of high-density lipoprotein.​
10​
MT3​
142%​
Metallothioneins (MTs) display in vitro oxyradical scavenging capacity, suggesting that they may specifically neutralize hydroxyl radicals. Metallothioneins and metallothionein-like proteins isolated from mouse brain act as neuroprotective agents by scavenging superoxide radicals.​
11​
PTGS2​
120%​
Produces cyclooxygenase-II (COX-II) which has antioxidant activities.​
12​
NF-κB2​
103%​
NF-κB, an oxidative/inflammatory protein, is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens.​
13​
NFE2L2​
56%​
Nuclear respiratory factor 2 helps activate antioxidant responsive element regulated genes which contribute to the regulation of the cellular antioxidant defense systems.​
14​
PTGS1​
50%​
Produces cyclooxygenase-I (COX-I) which has antioxidant activity.​
Down​
Genes​
Percent change in gene expression​
Comments​
1​
IL17A​
−1018%​
This strongly suppressed cytokine can stimulate the expression of IL6 and cyclooxygenase-2 (PTGS2/COX-2), as well as enhancing the production of nitric oxide (NO). High levels of this cytokine are associated with several chronic inflammatory diseases including rheumatoid arthritis, psoriasis, and multiple sclerosis (NCBI GENE entry).​
2​
TNF​
−115​
GHK suppresses this prooxidant TNF gene which inhibits the antioxidant IL18.​



2.6. Insulin and Insulin-Like System
GHK stimulates 3 genes in this system and suppresses 6 genes.


Up​
Gene title​
Percent change in gene expression​
1​
Insulin-like 6, INSL6​
188%​
2​
Insulin-like growth factor 2 mRNA binding protein 3, IGF2BP3​
136%​
3​
Insulin-like growth factor binding protein 3, IGFBP3​
82%​
Down​
Gene title​
Percent change in gene expression​
1​
Insulin-like growth factor 1 (somatomedin C), IGF1​
−522%​
2​
Insulin receptor-related receptor, INSRR​
−437%​
3​
Insulin, INS​
−289%​
4​
Insulin-like 3 (Leydig cell), INSL3​
−188%​
5​
Insulin-like growth factor binding protein 7, IGFBP7​
−110%​
6​
Insulin-like 5, INSL5​
−101%​


Summary:

Fibrinogen
Fibrinogen, the protein which is used to make blood clots, is also a strong predictor of mortality in cardiovascular patients. After vascular incidents, such as myocardial infarction, fibrinogen concentrations increase sharply. The free, unclotted fibrinogen protein increases the “stickiness” of red blood cells which stack together forming rouleaux. This increases the time of the “solid” blood state which decreases blood flow through the microcirculation where blood flows like a thixotropic fluid, switching between a solid phase and a liquid phase, somewhat like toothpaste. As a solid, it stops oxygen and nutrient flow to the tissues. This, in itself, can cause tissue damage.

The gene data on GHK’s suppression of FGB (the fibrinogen beta chain) combined with its actions on lowering IL-6 secretion on fibroblasts and sebocytes appears to be sufficient to explain its lowering effect on fibrinogen.

Ubiquitin Proteasome System
The ubiquitin proteasome system (UPS) functions in the removal of damaged or misfolded proteins. Aging is a natural process that is characterized by a progressive accumulation of unfolded, misfolded, or aggregated proteins. In particular, the proteasome is responsible for the removal of normal as well as damaged or misfolded proteins. Recent work has demonstrated that proteasome activation by either genetic means or use of compounds retards aging.

In our screening of UPS genes with a percent change of at least ±50%, GHK increased gene expression in 41 UPS genes while suppressing 1 UPS gene. Thus, it should have a positive effect on this system.

DNA Repair
It is estimated that normal metabolic activities and environmental factors such as UV light and radiation can cause DNA damage, resulting in somewhere between 1000 and as many as 1 million individual molecular lesions per cell per day. Lack of sufficient DNA repair is considered a cause of cell senescence, programmed cell death, and unregulated cell division, which can lead to the formation of a tumor that is cancerous.

GHK was stimulatory for DNA repair genes (47 stimulated, 5 suppressed) suggesting an increased DNA repair activity.


Antioxidant Defense
Free radicals and toxic end products of lipid peroxidation are linked to atherosclerosis, cancer, cataracts, diabetes, nephropathy, Alzheimer’s disease, and other severe pathological conditions of aging. Reactive oxygen species (ROS) and reactive carbonyl species (RCS) are produced in cells in small quantities under physiological conditions and play an important role in cell signaling and immune defense. A robust antioxidant network maintains balance between free radical production and scavenging, ensuring that the overall damage from free radicals is low. However, in the course of aging and in pathological conditions such as inflammation, the balance may shift toward free radical accumulation that can lead to oxidative stress and eventually to cell death.

GHK increases gene expression of 14 antioxidant genes and suppresses the expression of 2 prooxidant genes. It increases the expression of the oxidative/inflammatory gene NF-κB2 103% but also increases the expression of two inhibitors of NF-κB, TLE1 by 762% and IL18BP by 295%; thus, it possibly inhibits the activity of the NF-κB protein.

GHK also possesses antioxidant activities in cell culture and in vivo.

In dermal wound healing in rats, GHK, attached to biotin to bind it to collagen pads covering wounds, produced a higher production of protein antioxidants in the wound tissue. Superoxide dismutase was increased 80% while catalase was increased 56%. GHK reduced gastric mucosal damage by 75% against lipid peroxidation by oxygen-derived free radicals induced by acute intragastric administration of ethanol.

Interleukin 1 beta can induce serious oxidative damage to cultured cells. GHK markedly reduced oxidative damage by interleukin 1-beta to cultured insulin secreting pancreatic cells.

In another study, GHK entirely blocked the extent of in vitro Cu(2+)-dependent oxidation of low density lipoproteins (LDL). Treatment of LDL with 5 microM Cu(2+) for 18 hours in phosphate buffered saline (PBS) resulted in extensive oxidation as determined by the content of thiobarbituric acid reactive substances. Oxidation was entirely blocked by GHK. In comparison, copper, zinc-superoxide dismutase provided only 20% protection.

Acrolein, a well-known carbonyl toxin, is produced by lipid peroxidation of polyunsaturated fatty acids. GHK directly blocks the formation of 4-hydroxynonenal and acrolein toxins created by carbonyl radicals that cause fatty acid decomposition. GHK also blocks lethal ultraviolet radiation damage to cultured skin keratinocytes by binding and inactivating reactive carbonyl species such as 4-hydroxynoneal, acrolein, malondialdehye, and glyoxal.

Iron has a direct role in the initiation of lipid peroxidation. An Fe(2+)/Fe(3+) complex can serve as an initiator of lipid oxidation. The major storage site for iron in serum and tissue is ferritin and the superoxide anion can promote the mobilization of iron from ferritin which can catalyze lipid peroxidation. GHK : Cu(2+) produced an 87% inhibition of iron release from ferritin by apparently blocking iron’s exit channels from the protein.


Insulin and Insulin-Like Pathways
The insulin/IGF-1-like receptor pathway is a contributor to the biological aging process in many organisms. The gene expression data suggests that GHK suppresses this system as 6 of 9 of the affected insulin/IGF-1 genes are suppressed.

Insulin/IGF-1-like signaling is conserved from worms to humans. In vitro experiments show that mutations that reduce insulin/IGF-1 signaling have been shown to decelerate the degenerative aging process and extend lifespan in many organisms, including mice and possibly humans. Reduced IGF-1 signaling is also thought to contribute to the “antiaging” effects of calorie restriction.
 
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:cool::what::love:
 
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Accidentally put this in "offtopic"
 
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That shit isnt so cheap but when i read this what u write about it i have no doubt i will buy it soon
 
3Gamma-aminobutyric acid (GABA) B receptor, 1 /// ubiquitin D, GABBR1 /// UBD
310%​
First takeaway. 310% upregulation of the metabotropic GABA-B receptor which Phenibut and Baclofen work on. Not much is known about the GABA-B complex compared to GABA-A.

GHK-cu will likely make you more responsive to anything with a gabaergic effect on the -B receptor. Not many drugs are known to work on this. While thousands work on GABA-A.

This shows a possible indirect anxiolytic effect of GHK-cu when combined with healthy living/lifestyle.

Personally I've never came across anything other than Fasoracetam to upregulate the GABA B receptor. But GHK-cu upregulates it by 310%!
6Retinoic acid receptor, alpha, RARA
123%​
Takeaway #2.

123% upregulation of the RARA receptor (retinoic acid receptor A).

As we know Retin-A works on this receptor, whilst Adapalene works on the Beta and Gamma receptors.

This leads me to believe that GHK-cu use will make Retin-A more effective at what it does, due to the huge upregulation of the receptor that Retin-A agonizes.
First takeaway. 310% upregulation of the metabotropic GABA-B receptor which Phenibut and Baclofen work on. Not much is known about the GABA-B complex compared to GABA-A.

GHK-cu will likely make you more responsive to anything with a gabaergic effect on the -B receptor. Not many drugs are known to work on this. While thousands work on GABA-A.

This shows a possible indirect anxiolytic effect of GHK-cu when combined with healthy living/lifestyle.

Personally I've never came across anything other than Fasoracetam to upregulate the GABA B receptor. But GHK-cu upregulates it by 310%!

Takeaway #2.

123% upregulation of the RARA receptor (retinoic acid receptor A).

As we know Retin-A works on this receptor, whilst Adapalene works on the Beta and Gamma receptors.

This leads me to believe that GHK-cu use will make Retin-A more effective at what it does, due to the huge upregulation of the receptor that Retin-A agonizes.
Takeaway #3 and warning for teens.

-522% change in gene expression of the IGF-1 gene. Reduced levels of IGF1 in tissues.

Pros:
Decreases risk of diabeties.
May help people achieve better proteostasis and have longevity benefits through modulation of the insulin/IGF1 pathway.

Cons:
May negatively impact the potential for growth in those who are still growing.

Pro/Con: Decrease in insulin. Will be easier to lose fat. Increased insulin sensitivity. The huge drop in IGF1 and insulin levels may push your body to release more Growth Hormone. However, heightmaxers. High GH levels coupled with significantly lower IGF1 levels will not help you grow taller. Wincel and I showed this and it was one of the things we both agreed on, due to the evidence available. Being on the polar sides of the "heightmaxing" idea as well.

You should be aware that increased growth hormone DOES increase IGF1 IN THE PRESENCE OF ADEQUATE LEVELS OF INSULIN. GHK-cu supresses IGF1 gene expression, increases the amount of IGF binding proteins, further lowering IGF1, and significantly lowers insulin levels.

Heightmaxers you are wasting your time buying peptides and AI's. Even those who are buying real HGH and injecting, it's useless. The exogenous HGH won't raise your IGF-1 to supraphysiological levels due to the other moving parts like IGFBPs and insulin levels. Your body still naturally peters towards homeostasis. Heightmaxers would be better off injecting IGF along with HGH. Although I still wouldn't personally recommend it.
 
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@x30001 alt tbh
 
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Broad overview

*No gene in our body is intended to be inherently bad if it's expression is increased (excluding mutated and defective genes.. but incidentally, some mutated genes are just more 'silenced', with less expression... the mutation isn't increasing expression of an expression in which the gene cannot express..)

GHK-cu increases the expression of 59% of our genes, while lowering expression of 41% of our genes. This is positive. (Note, some gene's are sensors and have an indirect role. ie: genes that if their expression is increased, there may be knock on effects such as a decrease in expression of genes that aid in the release of anti-inflammatory cytokines). In short: If the expression of ALL our genes were to increase proportionately, it would be a BENEFIT to us.

Percent Change |||||||||| Genes Stimulated |||||||||| Genes Supressed
50-99% |||||||||| 1569 |||||||||| 583
100-199% |||||||||| 646 |||||||||| 469
200-299% |||||||||| 227 |||||||||| 196
300-599% |||||||||| 196 |||||||||| 207
600-899% |||||||||| 39 |||||||||| 47
900-1199% |||||||||| 8 |||||||||| 7
1200% |||||||||| 2 |||||||||| 4
Broad overview

*No gene in our body is intended to be inherently bad if it's expression is increased (excluding mutated and defective genes.. but incidentally, some mutated genes are just more 'silenced', with less expression... the mutation isn't increasing expression of an expression in which the gene cannot express..)

GHK-cu increases the expression of 59% of our genes, while lowering expression of 41% of our genes. This is positive. (Note, some gene's are sensors and have an indirect role. ie: genes that if their expression is increased, there may be knock on effects such as a decrease in expression of genes that aid in the release of anti-inflammatory cytokines). In short: If the expression of ALL our genes were to increase proportionately, it would be a BENEFIT to us.

Percent Change |||||||||| Genes Stimulated |||||||||| Genes Supressed
50-99% |||||||||| 1569 |||||||||| 583
100-199% |||||||||| 646 |||||||||| 469
200-299% |||||||||| 227 |||||||||| 196
300-599% |||||||||| 196 |||||||||| 207
600-899% |||||||||| 39 |||||||||| 47
900-1199% |||||||||| 8 |||||||||| 7
1200+% |||||||||| 2 |||||||||| 4
Next I will run a simulation using randomly generated numbers between 0-1. The amount of stimulated genes on the left columns and the amount of suppressed genes on the right columns. The first column pair is the 50-99% changers. I will be giving the lowest % on the band a weight of 0, and the highest number on the band a weight of 1. For example: 50% = 0, 99% = 1, for the first column pair. I am giving the last column pair an arbitrary cut off at 1399%, so it will be 1200-1399%. Since there are only 6 genes in this bracket, and going under the assumption that a gene can't be suppressed by 10000000% (I still don't know how expression can be reduced by more than 100% anyways, considering that 100% suppression would silence a gene entirely, even if expression of that gene is at any given level...)

I will run this simulation and repeat it 20 million times to see if there is a net increase in overall gene stimulation. (which there likely will be).

1583347950484
 
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Broad overview

*No gene in our body is intended to be inherently bad if it's expression is increased (excluding mutated and defective genes.. but incidentally, some mutated genes are just more 'silenced', with less expression... the mutation isn't increasing expression of an expression in which the gene cannot express..)

GHK-cu increases the expression of 59% of our genes, while lowering expression of 41% of our genes. This is positive. (Note, some gene's are sensors and have an indirect role. ie: genes that if their expression is increased, there may be knock on effects such as a decrease in expression of genes that aid in the release of anti-inflammatory cytokines). In short: If the expression of ALL our genes were to increase proportionately, it would be a BENEFIT to us.

Percent Change |||||||||| Genes Stimulated |||||||||| Genes Supressed
50-99% |||||||||| 1569 |||||||||| 583
100-199% |||||||||| 646 |||||||||| 469
200-299% |||||||||| 227 |||||||||| 196
300-599% |||||||||| 196 |||||||||| 207
600-899% |||||||||| 39 |||||||||| 47
900-1199% |||||||||| 8 |||||||||| 7
1200% |||||||||| 2 |||||||||| 4

Next I will run a simulation using randomly generated numbers between 0-1. The amount of stimulated genes on the left columns and the amount of suppressed genes on the right columns. The first column pair is the 50-99% changers. I will be giving the lowest % on the band a weight of 0, and the highest number on the band a weight of 1. For example: 50% = 0, 99% = 1, for the first column pair. I am giving the last column pair an arbitrary cut off at 1399%, so it will be 1200-1399%. Since there are only 6 genes in this bracket, and going under the assumption that a gene can't be suppressed by 10000000% (I still don't know how expression can be reduced by more than 100% anyways, considering that 100% suppression would silence a gene entirely, even if expression of that gene is at any given level...)

I will run this simulation and repeat it 20 million times to see if there is a net increase in overall gene stimulation. (which there likely will be).

View attachment 294424
1583350938998

This is incredible. Now to run this 20Million+ times to get a more accurate mean, var and stdev
 
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@x30001 Rest in Peace Lil Peep, may the gods forgive every word I spoke badly of him.
Please, for the love of the others, drop the Anti-aging pill.

thx bro
 
View attachment 294480
This is incredible. Now to run this 20Million+ times to get a more accurate mean, var and stdev
1583351061153

Trial 2. So far it seems it increases gene activity by x950-980. Will automate the simulation and get a huge sample. The weights will be completely randomized each time, as they already are.
Broad overview

*No gene in our body is intended to be inherently bad if it's expression is increased (excluding mutated and defective genes.. but incidentally, some mutated genes are just more 'silenced', with less expression... the mutation isn't increasing expression of an expression in which the gene cannot express..)

GHK-cu increases the expression of 59% of our genes, while lowering expression of 41% of our genes. This is positive. (Note, some gene's are sensors and have an indirect role. ie: genes that if their expression is increased, there may be knock on effects such as a decrease in expression of genes that aid in the release of anti-inflammatory cytokines). In short: If the expression of ALL our genes were to increase proportionately, it would be a BENEFIT to us.

Percent Change |||||||||| Genes Stimulated |||||||||| Genes Supressed
50-99% |||||||||| 1569 |||||||||| 583
100-199% |||||||||| 646 |||||||||| 469
200-299% |||||||||| 227 |||||||||| 196
300-599% |||||||||| 196 |||||||||| 207
600-899% |||||||||| 39 |||||||||| 47
900-1199% |||||||||| 8 |||||||||| 7
1200% |||||||||| 2 |||||||||| 4

Next I will run a simulation using randomly generated numbers between 0-1. The amount of stimulated genes on the left columns and the amount of suppressed genes on the right columns. The first column pair is the 50-99% changers. I will be giving the lowest % on the band a weight of 0, and the highest number on the band a weight of 1. For example: 50% = 0, 99% = 1, for the first column pair. I am giving the last column pair an arbitrary cut off at 1399%, so it will be 1200-1399%. Since there are only 6 genes in this bracket, and going under the assumption that a gene can't be suppressed by 10000000% (I still don't know how expression can be reduced by more than 100% anyways, considering that 100% suppression would silence a gene entirely, even if expression of that gene is at any given level...)

I will run this simulation and repeat it 20 million times to see if there is a net increase in overall gene stimulation. (which there likely will be).

View attachment 294424
 
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No pill for your:

"entire life motivation and drive to actually achieve physical achievements through effort with the will-power and the unhypocritical function of your own mind to strive towards living a better life for nothing other than your own first-hand happiness."
 
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A normal person would do their research on a peptide before they spend their money on it
 
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No pill for your:

"entire life motivation and drive to actually achieve physical achievements through effort with the will-power and the unhypocritical function of your own mind to strive towards living a better life for nothing other than your own first-hand happiness."
thx bro
 
Fuarkkkk I can't wait for my GHK-Cu to arrive

Gonna buy the powder for cheap on Amazon and snort lines of the shit off my gf's tits
 
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Fuarkkkk I can't wait for my GHK-Cu to arrive

Gonna buy the powder for cheap on Amazon and snort lines of the shit off my gf's tits
inb4 it gives some rare type of cancer
 
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Fuarkkkk I can't wait for my GHK-Cu to arrive

Gonna buy the powder for cheap on Amazon and snort lines of the shit off my gf's tits
Honestly I was so low inhib today wtf was a fucking personality Chad in college. GHK-cu apparently has opiate like effects and does something with opioid receptors. Look it up!

Also the GABA B receptor upregulation is already confirmed, so it could just be that.
 
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Honestly I was so low inhib today wtf was a fucking personality Chad in college. GHK-cu apparently has opiate like effects and does something with opioid receptors. Look it up!

Also the GABA B receptor upregulation is already confirmed, so it could just be that.
Just from a touch of the serum?
 
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Honestly I was so low inhib today wtf was a fucking personality Chad in college. GHK-cu apparently has opiate like effects and does something with opioid receptors. Look it up!

Also the GABA B receptor upregulation is already confirmed, so it could just be that.
When i read you niggas talking about it i feel like its some golden drug.
 
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inb4 it gives some rare type of cancer
Namely the p53 and p38 genes.

Suppresses the pro oxidant TNF. Suppresses IL-6. Produces COX-I and COX-II. Lowers ROS. Stimulates PON1. Negative regulator of NLRP3 which suppresses the pro-oxidants IL-1B and IL-18.

Inhibits the conversion of Fe(2+) to Fe(3+). HEPH increases iron efflux, lowers cellular iron levels, suppresses reactive oxygen species production, and restores mitochondrial transmembrane potential.

Up-regulation of ITGB4 promotes wound repair ability and antioxidative ability.

Binds oxidized phospholipids and increases the antioxidant effect of high-density lipoproteins (HDL).

Stimulates the TLE1 gene by 762% which inhibits NF-κB which is oxidative/inflammatory.

142% Stimulation of MT3.
Metallothioneins (MTs) display in vitro free radical scavenging capacity, suggesting that they may specifically neutralize hydroxyl radicals. Metallothioneins and metallothionein-like proteins isolated from mouse brain act as neuroprotective agents by scavenging superoxide radicals.
my question is then why isnt everyone and their mom injecting it instramuscularly every day
You can apply it topically and it's effects are systemic. It passes through the stratum corneum pretty effectively. Retinoids also thin out the SC. GHK-cu also upregulates the Retinoic Acid Receptor-A by 123%, making Retin-A use more effective also.
my question is then why isnt everyone and their mom injecting it instramuscularly every day
Idk why everyone isn't using it. I don't want people to use it though.
Namely the p53 and p38 genes.

Suppresses the pro oxidant TNF. Suppresses IL-6. Produces COX-I and COX-II. Lowers ROS. Stimulates PON1. Negative regulator of NLRP3 which suppresses the pro-oxidants IL-1B and IL-18.

Inhibits the conversion of Fe(2+) to Fe(3+). HEPH increases iron efflux, lowers cellular iron levels, suppresses reactive oxygen species production, and restores mitochondrial transmembrane potential.

Up-regulation of ITGB4 promotes wound repair ability and antioxidative ability.

Binds oxidized phospholipids and increases the antioxidant effect of high-density lipoproteins (HDL).

Stimulates the TLE1 gene by 762% which inhibits NF-κB which is oxidative/inflammatory.

142% Stimulation of MT3.
Metallothioneins (MTs) display in vitro free radical scavenging capacity, suggesting that they may specifically neutralize hydroxyl radicals. Metallothioneins and metallothionein-like proteins isolated from mouse brain act as neuroprotective agents by scavenging superoxide radicals.

You can apply it topically and it's effects are systemic. It passes through the stratum corneum pretty effectively. Retinoids also thin out the SC. GHK-cu also upregulates the Retinoic Acid Receptor-A by 123%, making Retin-A use more effective also.

Idk why everyone isn't using it. I don't want people to use it though.
Also, evidence on GHK-cu's effect on myelin sheaths in brain nerves, coming soon.
 

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That's very interesting. So what is the consensus? How much of this GHK-cu should one be taking daily? How to know if it is working?
 
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That's very interesting. So what is the consensus? How much of this GHK-cu should one be taking daily? How to know if it is working?
Only 0.3mg is needed tbh. I just use a little of the cream and serum daily, so I'm not measuring out a dose. I feel the benefit after 1 day. Noticed a really weird and extreme reduction in anxiety today and kinda felt like I was on some anxiolytic drug. GHK-cu does upregulate the GABA-B receptor quite a lot, that could be part of the reason. Other possibility is placebo. I feel like I might create a placibimus surrounding GHK-cu. But day 1, so far so good. Pretty freaky how different it made me feel (or at least how it changed how I think I feel). I'll know better on how much it actually benefits me and how, once I've been taking it daily for months. Alarico is gonna start using it too so he can give his unbiased input. Made my hair and skin better instantly (or atleast made me think that), but I'm pretty sure it really did improve my skin/hair. Used a bit more than I plan on using daily because it's day 1.
 
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You forgot to mention it’s an anti-androgen you fucking Jew.
 
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Intredasting1
 
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Wait, it kills T? That is bad
 
Do you get the anxiolytic effects from topical use?

I currently take the peptide DHH-B which is a GABAA receptor agonist. Gonna try taking rapamycin before doing intranasal Ketamine in order to relieve depression symptoms as well. Btw how's your progress on the depression/anxiety guide?
 
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Do you get the anxiolytic effects from topical use?

I currently take the peptide DHH-B which is a GABAA receptor agonist. Gonna try taking rapamycin before doing intranasal Ketamine in order to relieve depression symptoms as well. Btw how's your progress on the depression/anxiety guide?
Rapamycin and Ketamine wtf haha. Yeah I felt a reduction in anxiety from topical use. It might not have been just the GHK-cu... maybe created some drug interaction. I want the depression/anxiety thread to be fully comprehensive but then again idk if I can be bothered to put in the effort. So maybe I'll just go over the important parts
 
First takeaway. 310% upregulation of the metabotropic GABA-B receptor which Phenibut and Baclofen work on. Not much is known about the GABA-B complex compared to GABA-A.

GHK-cu will likely make you more responsive to anything with a gabaergic effect on the -B receptor. Not many drugs are known to work on this. While thousands work on GABA-A.

This shows a possible indirect anxiolytic effect of GHK-cu when combined with healthy living/lifestyle.

Personally I've never came across anything other than Fasoracetam to upregulate the GABA B receptor. But GHK-cu upregulates it by 310%!

Takeaway #2.

123% upregulation of the RARA receptor (retinoic acid receptor A).

As we know Retin-A works on this receptor, whilst Adapalene works on the Beta and Gamma receptors.

This leads me to believe that GHK-cu use will make Retin-A more effective at what it does, due to the huge upregulation of the receptor that Retin-A agonizes.

Takeaway #3 and warning for teens.

-522% change in gene expression of the IGF-1 gene. Reduced levels of IGF1 in tissues.

Pros:
Decreases risk of diabeties.
May help people achieve better proteostasis and have longevity benefits through modulation of the insulin/IGF1 pathway.

Cons:
May negatively impact the potential for growth in those who are still growing.

Pro/Con: Decrease in insulin. Will be easier to lose fat. Increased insulin sensitivity. The huge drop in IGF1 and insulin levels may push your body to release more Growth Hormone. However, heightmaxers. High GH levels coupled with significantly lower IGF1 levels will not help you grow taller. Wincel and I showed this and it was one of the things we both agreed on, due to the evidence available. Being on the polar sides of the "heightmaxing" idea as well.

You should be aware that increased growth hormone DOES increase IGF1 IN THE PRESENCE OF ADEQUATE LEVELS OF INSULIN. GHK-cu supresses IGF1 gene expression, increases the amount of IGF binding proteins, further lowering IGF1, and significantly lowers insulin levels.

Heightmaxers you are wasting your time buying peptides and AI's. Even those who are buying real HGH and injecting, it's useless. The exogenous HGH won't raise your IGF-1 to supraphysiological levels due to the other moving parts like IGFBPs and insulin levels. Your body still naturally peters towards homeostasis. Heightmaxers would be better off injecting IGF along with HGH. Although I still wouldn't personally recommend it.
Didnt read
 
Modulation of the antidepressant effects of ketamine by the mTORC1 inhibitor rapamycin

It's definitely not the best idea, just thought I'd throw it out there lol.
Would be too hard for me to understand. I wouldn't be able to get my head around why there's synergy between the 2 compounds. Ketamine alone provide massive anti-depressive effects because of the NMDA receptor antagonism. But rapamycin is pretty dangerous man I wouldn't touch that; and it seems really out of place and unnecessary when it comes to alleviating depression. It'll block all mTOR signalling so you'll more than likely waste away and get sick depending on how you use it. One of the riskiest drugs out there and the only thing I see it being used for imaginatively would be for anti-aging.
 
would MK677 work just as well?
 
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Would be too hard for me to understand. I wouldn't be able to get my head around why there's synergy between the 2 compounds. Ketamine alone provide massive anti-depressive effects because of the NMDA receptor antagonism. But rapamycin is pretty dangerous man I wouldn't touch that; and it seems really out of place and unnecessary when it comes to alleviating depression. It'll block all mTOR signalling so you'll more than likely waste away and get sick depending on how you use it. One of the riskiest drugs out there and the only thing I see it being used for imaginatively would be for anti-aging.
Ye, I've heard horror stories about rapamycin. Going back to K, apparently there is evidence that blockage of the NMDA receptor "enhances glutamatergic transmission preferentially engaging α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors leading to mTOR pathways activation". Ketamine activates mTOR also in dopaminergic neurons, but this activation depends on the presence of functional dopamine D3 receptors.
 
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Ye, I've heard horror stories about rapamycin. Going back to K, apparently there is evidence that blockage of the NMDA receptor "enhances glutamatergic transmission preferentially engaging α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors leading to mTOR pathways activation". Ketamine activates mTOR also in dopaminergic neurons, but this activation depends on the presence of functional dopamine D3 receptors.
Damn that's over my head lol
 
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Fuarkkkk I can't wait for my GHK-Cu to arrive

Gonna buy the powder for cheap on Amazon and snort lines of the shit off my gf's tits
Going ER if it doesn't arrive soon

Tracking link has stopped working
 
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Going ER if it doesn't arrive soon

Tracking link has stopped working
Never worked for me and took about 4 weeks to arrive.
 
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Just arrived, took less than a week

This shit smells like a hospital
 
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intredasting
 

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