Blackpill Truth ACTN3 is the holy grail for genetic athletic advantage

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SSG solja
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To be honest, no.

And if you feel you're not good at explosive activities you probably don't have a CC gene but I doubt you're TT either. Most people are heterozygous and w/o mutations on either allele. It's normal. Nothing to worry about really. If you're a severe lanklet/hardgainer and have a natural talent for endurance sports like marathon running/cross-country etc then maybe get the test done. But you won't be able to edit your gene. It's not that simple. Say you order a $2k DIY kit. What will you do then? You gotta know EXACTLY what to do; even the guy selling the kit demonstrated he had no clue what he did to himself after injecting.
bro can you also please respond to my pm on that gutmaxx thing. like taking an antibiotic (metronidazol) 2 weeks to kill al gut bacteria, and then take Colostrum&Probiotics 10 weeks . Msm for mercury from tuna, Sulphorane, Zoloft and eating an anti autism diet for like 6 months, also taking BPC 157 for brain-gut axis will make me feel like taking pheibut without actually taking it? I saw you once talk about GABA B but didnt make any other thread on it. it was really interesting bro. I wish you came back with those infos here tbh

im high inhib non nt asf what can i do? Gut replace therapy ? or ropemax
 
Seth Walsh

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bro can you also please respond to my pm on that gutmaxx thing. like taking an antibiotic (metronidazol) 2 weeks to kill al gut bacteria, and then take Colostrum&Probiotics 10 weeks . Msm for mercury from tuna, Sulphorane, Zoloft and eating an anti autism diet for like 6 months, also taking BPC 157 for brain-gut axis will make me feel like taking pheibut without actually taking it? I saw you once talk about GABA B but didnt make any other thread on it. it was really interesting bro. I wish you came back with those infos here tbh
All that is too much for me to answer. Why would you take an antibiotic? I'm taking a probiotic atm. Just take a probiotic to promote a healthy gut and then just live a healthy lifestyle. There's no intricacies. There's definitely some link between the GABAB receptor complex and the gut, but I haven;t read anything on it in like 8 months. It was something to do with cAMP and a second messenger pathway targeting the G-protein coupled receptors with GTPases and shit like that
 
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SSG solja
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All that is too much for me to answer. Why would you take an antibiotic? I'm taking a probiotic atm. Just take a probiotic to promote a healthy gut and then just live a healthy lifestyle. There's no intricacies. There's definitely some link between the GABAB receptor complex and the gut, but I haven;t read anything on it in like 8 months. It was something to do with cAMP and a second messenger pathway targeting the G-protein coupled receptors with GTPases and shit like that
Antibiotic to kill all bad bacterias and then probiotic to replace bad bacteria eith good idk you said it in a thread lol but it might be cope all of this cause even if we kill bad bacteria, body will replace them back cause its fucking stupid. I think microbiota gut surgery is the mogger here

Well idk either tbh my 2 last cells are screaming when i try understanding stuff like this
 
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There may well be certain proteins who can upregulate specific pathways but it is hard or too expensive to get them individually
 
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Thanks for the looksmaxxing advice OP.

I mean this whole bs thread is like syaing 6'0+ guys have easier sating lifes than shorter guys.

I mean its true but if you are not gonna share how to increase our height there is no reason.
 
GigaMogger

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Thanks for telling us how to activate it OP you banned cuck (pic unrelated)
 
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Another giga low iq thread. Lol
 
Ada Mustang

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Bump.

For anyone wanting to interpret this. This is THE BEST way to find out how good your bodybuilding genetics are.

2.2 CC = Great
2.1 CT = okay
2.2 TT = Bad
There is a 5% chance (I recall) to get myostatin mutations as a 2 × TT, so you have individuals like Oleg Zhokh and Lee Priest who can outwin everyone yet they have 2 recessive alleles.

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High iq post op.
 
sensen

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I'm pretty sure I have both if I remember correctly, would have to go check promethease again

Uncle was 2 weight professional boxing World Champion.

Dad was Track star, Baseball, Hockey player who destroyed ACL Junior year then came back Senior year and destroyed it again, thereby ruining any hope for pro sports in the mid 1980s.

Last time I played basketball I could grab rim and hang, almost dunk at 5'9. And that's without lifting, and being skinny as a fucking rail. I've always been much faster sprinter than 95% of other kids of any race too. But with that, I have extremely bad genetics for endurance. I get fatigued very easy, and I'd honestly give up some explosiveness for more endurance any day.
 
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Henry_Gandy

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I'm pretty sure I have both if I remember correctly, would have to go check promethease again

Uncle was 2 weight professional boxing World Champion.

Dad was Track star, Baseball, Hockey player who destroyed ACL Junior year then came back Senior year and destroyed it again, thereby ruining any hope for pro sports in the mid 1980s.

Last time I played basketball I could grab rim and hang, almost dunk at 5'9. And that's without lifting, and being skinny as a fucking rail. I've always been much faster sprinter than 95% of other kids of any race too. But with that, I have extremely bad genetics for endurance. I get fatigued very easy, and I'd honestly give up some explosiveness for more endurance any day.
just take EPO, you get the best of both worlds
 
samm735

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prob have tbh, explosive and fast as fuck as a kid sprinting in comparison to others, did 100m 400m 200m, was a winger in football and rugby, did long jump, could jump high af too, always found it relatively easy to put muscle on as my dad is also naturally muscular.

idk if i wanna give my dna to a company like 23andme to find out though lol
 
Hero of the Imperium

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It's pretty rare yeah.

About 16-17% of professional athletes who would have an advantage having C:C, have C:C. So 82-83% of the top flight professionals don't have C:C.

Well under 1% of the population would have C:C. It'd be in the 1 in thousands or 1 in tens of thousands range.
From Promethease data, that is not the case. CC ranges from ~20% in Utahn Europeans to 40% in Denver Chinese Americans to almost 80% in Yoruba West Africans
 
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100% don't have this
My 40 year dash and 100m peaked 2 years ago
 
antiantifa

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100% have this, can't do endurance for shit, easy sprinting all day long high speed
 
antiantifa

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"Association studies have identified dozens of genetic variants linked to training responses and sport-related traits. However, no intervention studies utilizing the idea of personalised training based on athlete's genetic profile have been conducted. Here we propose an algorithm that allows achieving greater results in response to high- or low-intensity resistance training programs by predicting athlete's potential for the development of power and endurance qualities with the panel of 15 performance-associated gene polymorphisms. To develop and validate such an algorithm we performed two studies in independent cohorts of male athletes (study 1: athletes from different sports (n = 28); study 2: soccer players (n = 39)). In both studies athletes completed an eight-week high- or low-intensity resistance training program, which either matched or mismatched their individual genotype. Two variables of explosive power and aerobic fitness, as measured by the countermovement jump (CMJ) and aerobic 3-min cycle test (Aero3) were assessed pre and post 8 weeks of resistance training. In study 1, the athletes from the matched groups (i.e. high-intensity trained with power genotype or low-intensity trained with endurance genotype) significantly increased results in CMJ (P = 0.0005) and Aero3 (P = 0.0004). Whereas, athletes from the mismatched group (i.e. high-intensity trained with endurance genotype or low-intensity trained with power genotype) demonstrated non-significant improvements in CMJ (P = 0.175) and less prominent results in Aero3 (P = 0.0134). In study 2, soccer players from the matched group also demonstrated significantly greater (P < 0.0001) performance changes in both tests compared to the mismatched group. Among non- or low responders of both studies, 82% of athletes (both for CMJ and Aero3) were from the mismatched group (P < 0.0001). Our results indicate that matching the individual's genotype with the appropriate training modality leads to more effective resistance training. The developed algorithm may be used to guide individualised resistance-training interventions."
 
patricknotstar

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Actenin Alpha 3 activation is what you need to maximize your chances of making it as someone who can excel in athletics, college football, having the genetics to pack on muscle naturally and stay lean; ie, have a higher chance of becoming a "Chad". 75%+ of all top flight professional sports stars have an active ACTN3, ranging across many many sports such as soccer, American football, basketball, tennis, swimming, sprinting etc. Under 17% of already athletically fit athletes have an active ACTN3.

Activation of ACTN3 is relatively straight forward and clean in the sense that it is so specific to enhancing skeletal muscle growth potential (only skeletal muscle), and giving a better edge in competitive sports.

View attachment 116453

MSTN (the myostatin gene) on the other hand is not at all specific to enhancing growth of skeletal muscle and can cause many complications if messed with. A functioning MSTN is what most of us have. causing one or more mutations on the gene is not only biologically much harder than simply activating ACTN3, but also only prevents the myostatin gene from doing all it's tasks. Over 97% of ultra successful professional and college athletes have the normal TT homozygous allele pair on MSTN. MSTN polymorphisms do not statistically provide a genetic advantage in success with athletics. In fact there's so few accomplished athletic professionals who even have a hetrozygous or non-default homozygous allele pair on MSTN.

View attachment 116456

EDIT: Green bar in picture1 is showing Skeletal Muscle

MSTN is a regulatory gene for many very different parts of our biology. It is in no way selective to skeletal muscle modulation like ACTN3 is.
Where find this stuff?
 
FailedAbortion

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I did from child to young adult. That's my entire point.

I'm genetically not athletic. If someone could learn a kickflip in a few weeks, it took me a couple years to be able to do one with like a 20% success rate. Catching footballs. Hitting baseballs. Same thing.

It's like for people who are athletic, life moves in slower motion for them. And everything happens in a flash with me.
Fucking brutal
 
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actual9cmjawslayer

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Absolutely brutal I just got my ancestry traits test back and I'm TT for this.



rs1800497

G>A conversion, also known as TaqIA (or Taq1A), in the gene dopamine D2 receptor (DRD2).



G = DRD2*A2 = Wild-type allele

A = DRD2*A1 = Alternate allele

G:G (46.6%) = Normal levels of dopamine D2 receptors = reduced dopamine

G:A (41.7%) = Lower levels of dopamine D2 inhibitory receptors = increased dopamine

A:A (11.7%) = Lower levels of dopamine D2 inhibitory receptors = increased dopamine


I have the first (G, G) for this gene related to dopamine. What does this mean for me?
 
btsgangruling

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Actenin Alpha 3 activation is what you need to maximize your chances of making it as someone who can excel in athletics, college football, having the genetics to pack on muscle naturally and stay lean; ie, have a higher chance of becoming a "Chad". 75%+ of all top flight professional sports stars have an active ACTN3, ranging across many many sports such as soccer, American football, basketball, tennis, swimming, sprinting etc. Under 17% of already athletically fit athletes have an active ACTN3.

Activation of ACTN3 is relatively straight forward and clean in the sense that it is so specific to enhancing skeletal muscle growth potential (only skeletal muscle), and giving a better edge in competitive sports.

View attachment 116453

MSTN (the myostatin gene) on the other hand is not at all specific to enhancing growth of skeletal muscle and can cause many complications if messed with. A functioning MSTN is what most of us have. causing one or more mutations on the gene is not only biologically much harder than simply activating ACTN3, but also only prevents the myostatin gene from doing all it's tasks. Over 97% of ultra successful professional and college athletes have the normal TT homozygous allele pair on MSTN. MSTN polymorphisms do not statistically provide a genetic advantage in success with athletics. In fact there's so few accomplished athletic professionals who even have a hetrozygous or non-default homozygous allele pair on MSTN.

View attachment 116456

EDIT: Green bar in picture1 is showing Skeletal Muscle

MSTN is a regulatory gene for many very different parts of our biology. It is in no way selective to skeletal muscle modulation like ACTN3 is.
 
Shako Mako

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Actenin Alpha 3 activation is what you need to maximize your chances of making it as someone who can excel in athletics, college football, having the genetics to pack on muscle naturally and stay lean; ie, have a higher chance of becoming a "Chad". 75%+ of all top flight professional sports stars have an active ACTN3, ranging across many many sports such as soccer, American football, basketball, tennis, swimming, sprinting etc. Under 17% of already athletically fit athletes have an active ACTN3.

Activation of ACTN3 is relatively straight forward and clean in the sense that it is so specific to enhancing skeletal muscle growth potential (only skeletal muscle), and giving a better edge in competitive sports.

View attachment 116453

MSTN (the myostatin gene) on the other hand is not at all specific to enhancing growth of skeletal muscle and can cause many complications if messed with. A functioning MSTN is what most of us have. causing one or more mutations on the gene is not only biologically much harder than simply activating ACTN3, but also only prevents the myostatin gene from doing all it's tasks. Over 97% of ultra successful professional and college athletes have the normal TT homozygous allele pair on MSTN. MSTN polymorphisms do not statistically provide a genetic advantage in success with athletics. In fact there's so few accomplished athletic professionals who even have a hetrozygous or non-default homozygous allele pair on MSTN.

View attachment 116456

EDIT: Green bar in picture1 is showing Skeletal Muscle

MSTN is a regulatory gene for many very different parts of our biology. It is in no way selective to skeletal muscle modulation like ACTN3 is.
What does this mean boss?
rs1805086(A;G)
rs397515373(G;G)
:fuk::fuk:
 
uglygoyim

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Actenin Alpha 3 activation is what you need to maximize your chances of making it as someone who can excel in athletics, college football, having the genetics to pack on muscle naturally and stay lean; ie, have a higher chance of becoming a "Chad". 75%+ of all top flight professional sports stars have an active ACTN3, ranging across many many sports such as soccer, American football, basketball, tennis, swimming, sprinting etc. Under 17% of already athletically fit athletes have an active ACTN3.

Activation of ACTN3 is relatively straight forward and clean in the sense that it is so specific to enhancing skeletal muscle growth potential (only skeletal muscle), and giving a better edge in competitive sports.

View attachment 116453

MSTN (the myostatin gene) on the other hand is not at all specific to enhancing growth of skeletal muscle and can cause many complications if messed with. A functioning MSTN is what most of us have. causing one or more mutations on the gene is not only biologically much harder than simply activating ACTN3, but also only prevents the myostatin gene from doing all it's tasks. Over 97% of ultra successful professional and college athletes have the normal TT homozygous allele pair on MSTN. MSTN polymorphisms do not statistically provide a genetic advantage in success with athletics. In fact there's so few accomplished athletic professionals who even have a hetrozygous or non-default homozygous allele pair on MSTN.

View attachment 116456

EDIT: Green bar in picture1 is showing Skeletal Muscle

MSTN is a regulatory gene for many very different parts of our biology. It is in no way selective to skeletal muscle modulation like ACTN3 is.
same result on ancestry im too lazy to find the screenshot
Screenshot 20220704 054138 Chrome
 

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CRISPR editing for ACTN3 gene activation when?
 
Bitchwhipper2

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It does not matter that much for strength atleast

Im just as strong as my brother whose been gymcelling with high - intensity and frequency for 2 years, despite only going to the gym with low intensity once a week for 2 months

Our 23andme test results were
Me: CT
Him: CC

My age: 18
His age: 21

My weight: 67kg
His weight: 71kg

My bf: 13-16%
His bf: 18-20%
 
Seth Walsh

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Looking back, I don't think it matters much if you got the homozygous Cytosine alleles or the heterozygous pair. Having the Thymine dinucleotide is the only thing that's a hindrance aesthetically.

If you've got the CC polymorphism, DO NOT try get as big as possible. Use it to your advantage so you'll hold more muscle while leanmaxxing. Look at it as an advantage from an anti-catabolic standpoint rather than being able to grow bigger muscles.

Leanmaxxing is one of the core tenants. A lot of gymcelled boyos with CC will cope by getting bigger and bigger and not realise that they need to lose weight, more specifically, lose FAT.

I think you kind of already know if you've TT. You'll feel you're a hard gainer and will be naturally skinny. That's a problem. And the solution is NOT to hop on roids ever. Steroids are a looksmin.

So if you get the 23andme and find you've CC, then look at it with the focus the anti-asthenic benefits while getting lean, rather than seeing it as an opportunity to get huge and male-gaze / buffalo / elephantsealmaxx.

Lean is law, Angular facial features are law, Bone definition is law. Bloatminning is law.
 
Lihito

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How to activate under 500$
 
Seth Walsh

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CRISPR editing for ACTN3 gene activation when?
It is possible to change the alleles right now with CRISPR. But who knows how gene expression will work after that? Gene editing is not so simple as there is no guarantee that editing the actual gene will result in the same gene expression as an unmodified gene that is theoretically "identical".
 
Seth Walsh

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How to activate under 500$
Do you know what your ACTN3 allele is at the moment? CRISPR is so experimental. I've never seen any practical benefits from it ever, especially not in the case of something like looksmaxxing.

The point of this thread I guess was to shift people's focus away from "myostatin" to point towards something which is far more significant when it comes to muscle building genetics.

Myostatin and myostatin inhibitors are cope. There seemed to be a common misconception that deletion of the MSTN gene would bridge all the difference between having a TT compared to a CC ACTN3 gene. So I made this thread to try an shed light there.

Gene editing is far past my scope. I know it is possible for sure. But DIY CRISPR is too risky and from what I've seen, "results or expectations" are heavily underwhelming or non-existent. The repercussions are completely unexplored too.
 
Lihito

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Do you know what your ACTN3 allele is at the moment? CRISPR is so experimental. I've never seen any practical benefits from it ever, especially not in the case of something like looksmaxxing.

The point of this thread I guess was to shift people's focus away from "myostatin" to point towards something which is far more significant when it comes to muscle building genetics.

Myostatin and myostatin inhibitors are cope. There seemed to be a common misconception that deletion of the MSTN gene would bridge all the difference between having a TT compared to a CC ACTN3 gene. So I made this thread to try an shed light there.

Gene editing is far past my scope. I know it is possible for sure. But DIY CRISPR is too risky and from what I've seen, "results or expectations" are heavily underwhelming or non-existent. The repercussions are completely unexplored too.
Yeah , with CRISPR i change strenght just to get a Huge penis tumor on my back and IQ drop :lul::lul::lul::lul:

Reminds me of that chinese scientist increasing twins IQ because he changed some other genes and now they are gonna be giga successful rice
hoes Running some corp in the West and having sex with chads






Life is truly a bullshit dice drop
 
Lihito

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Do you know what your ACTN3 allele is at the moment? CRISPR is so experimental. I've never seen any practical benefits from it ever, especially not in the case of something like looksmaxxing.

The point of this thread I guess was to shift people's focus away from "myostatin" to point towards something which is far more significant when it comes to muscle building genetics.

Myostatin and myostatin inhibitors are cope. There seemed to be a common misconception that deletion of the MSTN gene would bridge all the difference between having a TT compared to a CC ACTN3 gene. So I made this thread to try an shed light there.

Gene editing is far past my scope. I know it is possible for sure. But DIY CRISPR is too risky and from what I've seen, "results or expectations" are heavily underwhelming or non-existent. The repercussions are completely unexplored too.
Also thanks For telling me its not over im texting some JB rn and she loves the hell out of me (not cope)
 
edmund_brahte

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I have 0 ACTN3 expression. I’m ngmi simple as
 
Amnesia

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according to my 23and me i have two working copies of this gene. Makes sense why i can have a lot of mass as a natty and why I was the fastest sprinter in my district in HS
 
Deleted member 18439

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Also thanks For telling me its not over im texting some JB rn and she loves the hell out of me (not cope)
You're coping so hard...
 
Brian Peppers

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I'm genotype TT which is difficulty building muscle. I'm not skinny though - 85kg /5'10, overweight. Lean body mass of 64kg.
 

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