I just did? That was basically the entire thing. What do you have an issue with? The information is right there, courtesy of grok. If you don't like it contend with Elon musk. I dindu nuffin
Don't have to, they don't seem to do well nglNow imagine if black men competed more often in strong man?
I mean the text
Here's a other gem
regarding the MSTN Gene (the gene that literally inhibits muscle/strength growth AKA THEE strength Gene)
send the textHere's a other gem
Here's the exact question I asked it. (ignore typos I used text to speech and it cuts out sometimes so I have to relaunch it again intermediately leading to choppy sentence structure.)
View attachment 4602742
And the answer? (After a whole lot of verbose)
View attachment 4602749
Boom. There you go. It doesn't get ANY clearer then that.
I live in America as well
They still slay which is all that matters.
(Again ignore typos or choppy sentence structure I used text to speech I ain't typing all dat shit out again)
Belgian blue with mutated myostatin gene leading to double ...
That still doesn't refute the point this thread is making...
Whatever helps you sleep at night. White pussies are still being flipped out. If anything, white men willingly letting this happen just makes it more cucked.
Mirin rebuttal, still couldn't refute my point.
So the pathetic race is that one who gets free stuff and white pussy? While the other race set up everything just so it can happen? I don’t think you understand how cuck dynamics work.
The population and entire system itself is deeper into this than ever before. It’s completely over.
Bet you didn't expect me to actually do it right?
now you don't know what the hell to say do you?
Is that why all Afro-Americans have 20% white DNA?
Last time I checked, 80 is more than 20. Make way for the new kings of America.
"Cuck Dynamics"
Shut up pussy, watch your kind get flat lined by the true master race and try not to leak too much precum
(Again ignore typos or choppy sentence structure I used text to speech I ain't typing all dat shit out again)
What are some very hefty and incredible jeans that exist in the human genome that are specifically designed for muscle mass and strength ability
Thought for 26s
The question appears to refer to genes (not "jeans") in the human genome that are strongly linked to increased muscle mass and strength potential. While no genes are literally "designed" for this, certain genes and their variants can dramatically influence muscle growth, fiber type, and power/strength capacity. Muscle traits are highly heritable (30–85% for strength, 50–80% for mass), but they're polygenic (many genes involved) and heavily modulated by training, diet, and environment.pmc.ncbi.nlm.nih.govpmc.ncbi.nlm.nih.gov
Here are some of the most notable and impactful genes/variants tied to "hefty" muscle mass and strength:
Other genes with notable links include IGF1 (promotes muscle growth via insulin-like growth factor) and CNTF (associated with strength in some studies), but they tend to have subtler effects compared to the above.journals.physiology.org
- MSTN (Myostatin gene)This is arguably the most "incredible" one for sheer muscle-building potential. Myostatin normally acts as a brake on muscle growth in skeletal muscles. Rare loss-of-function variants reduce or eliminate functional myostatin, leading to uncontrolled muscle hypertrophy—up to twice the usual muscle mass, significantly reduced body fat, and increased strength.The condition is called myostatin-related muscle hypertrophy (sometimes nicknamed the "Hercules gene"). It's inherited in an incomplete autosomal dominant pattern:
- Homozygotes (variants in both gene copies) show the most dramatic increases.
- Heterozygotes (one copy) have notable but lesser gains.This is extremely rare in humans but has been documented in cases with exceptional muscle size and power, without known medical downsides.medlineplus.gov
- medlineplus.gov
- ACTN3 (Alpha-actinin-3 gene)Known as the "sprinter" or "power gene." It codes for α-actinin-3, a protein found mainly in fast-twitch (Type II) muscle fibers, which excel at explosive, high-force contractions.
- The RR genotype (functional protein present) is strongly linked to strength, power, and elite performance in speed/strength sports (e.g., sprinting, weightlifting). Most elite power athletes carry this variant.23andme.com23andme.com
- The XX genotype (no functional protein) favors endurance but reduces power potential. This gene explains a small but meaningful portion (2–3%) of muscle performance differences.23andme.com
- ACE (Angiotensin-converting enzyme gene)The I/D polymorphism affects enzyme levels and muscle fiber composition.
- The DD genotype (higher enzyme levels) is associated with a higher proportion of fast-twitch fibers, greater power, speed, and strength potential.It's one of the most studied genes for athletic performance, often paired with ACTN3 in discussions of strength vs. endurance.medlineplus.gov
These genes highlight how genetics can predispose someone to exceptional muscle-building potential, but they don't guarantee outcomes—training and lifestyle are crucial. If you're interested in genetic testing (e.g., via 23andMe), it can reveal variants in ACTN3 or others, though MSTN mutations are too rare for most consumer tests. Let me know if you'd like more details on any!
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Of the ones listed which it would you consider to be the most substantial to have the biggest difference if it's possessed by a person
Thought for 14s
MSTN (the myostatin gene) stands out as by far the most substantial among the ones I listed for creating the biggest difference in muscle mass and strength when someone possesses the favorable (loss-of-function) variant.
Here's why it's in a league of its own:
- Dramatic, transformative effect: Rare mutations that reduce or eliminate functional myostatin remove the natural "brake" on muscle growth. This can lead to extreme muscle hypertrophy—often doubling muscle mass (or more), exceptional strength, very low body fat, and a highly muscular physique even without intense training. Documented human cases include infants and children with near-superhuman muscle development from birth, sometimes called "Hercules gene" or myostatin-related muscle hypertrophy. These individuals show significantly greater muscle size and power compared to the average person, with no major health downsides reported in known cases.
‘Superboy’ Gets His Muscles From Rare Disorder
This image shows a young boy with a rare myostatin-related condition, displaying unusually pronounced muscle definition for his age—illustrating the gene's potent impact.
MSTN's influence is monogenic and large-effect (one gene, huge outcome when mutated), while ACTN3 and ACE are polygenic/common variants with smaller, additive contributions. In genetic studies, myostatin mutations produce the most striking outliers in human muscle mass.
- Comparison to the others:
- ACTN3 (RR genotype): This is the most well-known for power/strength sports. It promotes fast-twitch fibers and is enriched in elite sprinters and weightlifters, potentially boosting explosive strength and muscle performance by a noticeable but modest amount (e.g., better response to power training, perhaps 5–15% edge in relevant metrics). It's common and explains a small portion of variance in population studies, but it doesn't cause wholesale body recomposition like MSTN.
- ACE (DD genotype): Associated with a shift toward fast-twitch fibers and better anaerobic performance/power output. Again, meaningful for athletic potential (especially when combined with ACTN3), but the effect is incremental—not revolutionary.
To highlight how powerfully myostatin regulates muscle in mammals (direct analogy to humans), here are examples from animals with natural or induced myostatin disruptions:
A Belgian Blue bull with myostatin mutation—extreme "double muscling" typical of the breed.
Where are the myostatin inhibitors? | PeterBond.org
Myostatin-knockout mice (right) vs. normal (left), showing massive hypertrophy.
These visuals demonstrate the gene's outsized role. In humans, such mutations are extremely rare (only a handful of families documented), but when present, they create the most profound natural advantage for muscle mass and strength potential—far beyond what ACTN3 or ACE alone can achieve. Training and lifestyle still matter enormously, but MSTN flips the ceiling highest. If you're curious about genetic testing or specific cases, let me know!
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What are the very I mean the mutations within the mstn gene that make it become so expressed like that
The mutations in the MSTN gene (myostatin gene) that lead to the dramatic muscle hypertrophy (extreme muscle mass and strength, often called myostatin-related muscle hypertrophy or the "Hercules gene" effect) are loss-of-function variants. These disrupt the gene's ability to produce functional myostatin protein, which normally acts as a strong inhibitor ("brake") on skeletal muscle growth. When functional myostatin is reduced or absent, muscle cells proliferate and grow unchecked, resulting in significantly increased muscle fiber number (hyperplasia) and size (hypertrophy).
The most well-documented and impactful mutation causing this in humans is:
Other rare loss-of-function mutations have been implied in isolated cases or families, but details are sparse beyond this primary splice-site variant. No widespread "double muscling" like in Belgian Blue cattle (11-bp deletion in exon 3) or Piedmontese cattle (missense C313Y) has been commonly replicated in humans—human cases are far rarer and mostly trace to splice disruptions or similar null alleles.
- IVS1+5G>A (also written as g.IVS1+5G>A or c.373+5G>A, sometimes referenced as rs397515373).This is a splice-site mutationin intron 1 (at the boundary with exon 2). It disrupts normal RNA splicing, causing abnormal inclusion of part of intron 1 into the mRNA. This leads to a frameshift and premature stop codon, producing a severely truncated, non-functional myostatin protein (or very little/no protein at all).
- Reported in a famous 2004 case: A German infant boy with both copies mutated (homozygous) showed gross muscle hypertrophy at birth—enlarged thigh and arm muscles, nearly double the normal cross-sectional area in some muscles, and exceptional strength (e.g., holding his arms out horizontally for extended periods). His mother (heterozygous, one copy mutated) was a professional athlete with increased but less extreme muscle mass.
- This variant is extremely rare (prevalence around 0.0004% or less in populations studied) and inherited in an autosomal recessive pattern for the full dramatic effect (homozygous), though heterozygotes show moderate gains. No major health downsides were noted in the documented family.
Common polymorphisms in MSTN (not true loss-of-function mutations causing extreme hypertrophy):
In summary, the very hefty, incredible muscle phenotype you asked about earlier comes almost exclusively from rare, severe loss-of-function mutations like IVS1+5G>A that essentially knock out myostatin production. These are not common polymorphisms but true disruptive changes, explaining why such super-muscular builds are exceptionally rare in humans (only a handful of documented families worldwide). Genetic testing (e.g., targeted MSTN sequencing) can detect them if suspected, but they're not part of standard consumer panels due to rarity.
- K153R (rs1805086, c.458A>G, p.Lys153Arg): A missense change in exon 2. The rare R allele has mixed associations—some studies link it to slightly better hypertrophic response to training, greater muscle mass in certain groups (e.g., athletes or elderly), or power phenotypes, but others show neutral or even negative effects (e.g., reduced peak power in jumps). It's not responsible for the profound, congenital hypertrophy seen in true loss-of-function cases.
- Others like A55T, intronic deletions (e.g., rs11333758, c.373+90delA), or E164K/P198A/I225T: These are mostly common variants with subtle or inconsistent effects on muscle traits, often tied more to endurance than extreme strength/mass.
If you'd like details on how these compare to animal mutations or potential therapeutic implications (e.g., myostatin inhibitors for muscle-wasting diseases), let me know!
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Why is it that certain West African groups have a higher prevalence of these mutations if not outright have mutations within this Gene that are seen in no other group
Thought for 33s
The premise in your question—that certain West African groups have a higher prevalence (or unique) mutations in the MSTN gene specifically causing the extreme muscle hypertrophy we discussed earlier—is partially accurate but needs clarification. The rare, severe loss-of-function mutations (e.g., the IVS1+5G>A splice-site variant in the German family case) that lead to profound, "double-muscling"-like hypertrophy are extremely rare globally and not enriched in West African or any specific population. They appear sporadically across ethnicities as private mutations and are not linked to West African ancestry in documented cases.pmc.ncbi.nlm.nih.gov
What is true is that certain common polymorphisms (single-nucleotide variants) in MSTN occur at much higher frequencies in sub-Saharan African populations (including West African groups like Yoruba in Nigeria) compared to non-African populations. These are not the null mutations causing dramatic congenital hypertrophy but subtler variants that may mildly reduce myostatin activity or alter its regulation, potentially contributing to advantages in muscle strength, mass, or performance.
Key Variants with Higher Prevalence in Sub-Saharan Africans
These variants are located in the propeptide region of the myostatin precursor protein (residues 1–266), which helps regulate the active mature myostatin.
- K153R (rs1805086, A2246G; Lys153Arg): The minor R allele frequency is ~22% in Africans (vs. ~3% in Caucasians/Europeans). The RR genotype (homozygous) is rare overall (<1–3%) but more common in African-ancestry groups.pmc.ncbi.nlm.nih.gov
- A55T (G163A): Minor allele frequency 8–29% in sub-Saharan groups (e.g., ~8% in Yoruba, higher in some Bantu) vs. 0–5% outside Africa.pmc.ncbi.nlm.nih.gov
- Other SNPs (e.g., 2379 A>G): Minor alleles 11–31% in African Americans (reflecting West/Central African ancestry) vs. <5% in Caucasians.pmc.ncbi.nlm.nih.gov
Frontiers | Beyond the Big Five: Investigating Myostatin Structure ...
This diagram shows the MSTN precursor structure: The pro-region (blue) contains sites like K153R and A55T; cleavage releases the active peptide (green) that inhibits muscle growth.
They likely cause partial (not complete) reductions in myostatin function, leading to subtle increases in muscle growth potential or strength—e.g., better hypertrophic response to training or higher baseline power output in some studies. Meta-analyses show the R allele at K153R is enriched in strength/power athletes (odds ratio ~2 for carrying it).pmc.ncbi.nlm.nih.gov
Myostatin-driven muscle hypertrophy: a double-edged sword in ...
This illustrates myostatin's inhibitory role on muscle growth via signaling pathways; variants reducing its activity could shift the balance toward more muscle synthesis.
Why Higher Prevalence in West African/Sub-Saharan Groups?
Genetic evidence points to positive natural selection acting on these variants in sub-Saharan African populations over the last ~10,000–50,000 years (recent in evolutionary terms). Key signatures include:
Proposed adaptive reasons (hypotheses from the research):
- Excess nonsynonymous (amino acid-changing) variants compared to neutral expectations.
- Long-range haplotype homozygosity around these sites.
- Negative Tajima's D values indicating recent selective sweeps.pmc.ncbi.nlm.nih.gov
These variants aren't "unique" to West Africans—they're present elsewhere but at low frequencies due to out-of-Africa bottlenecks and lack of the same selective pressure. Higher prevalence reflects ancestral adaptation in Africa, with African Americans inheriting elevated frequencies from West/Central African roots.
- Protection against muscle wasting during periods of famine or nutritional stress—common in ancestral African environments transitioning to agriculture. Mild myostatin inhibition could help preserve or build muscle more efficiently under calorie restriction.pmc.ncbi.nlm.nih.gov
- Fitness advantages in muscle-related traits—e.g., better strength/endurance for hunting, labor, or survival in physically demanding habitats. These subtle effects (not extreme hypertrophy) might have boosted reproductive success.
- No strong evidence ties them directly to sprinting dominance (that's more ACTN3 fast-twitch fiber genetics), but they could contribute additively to overall athletic potential in some contexts.pmc.ncbi.nlm.nih.gov
These are common variants with modest effects; extreme muscle phenotypes still require rare null mutations plus environment/training. If you're exploring personal genetics or athletic implications, let me know for more!
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Based on the studies in the evidence provided thus far how much of an effect percentage wise either objectively or with an educated guess would you say these gene mutations within West African populations have an effect on muscle and strength potential and growth overall
Thought for 22s
The common MSTN polymorphisms prevalent in West African (and broader sub-Saharan African) populations—primarily K153R (rs1805086), with the minor R allele at ~22% frequency vs. ~3% in Caucasians—have modest to moderate effects on muscle mass, strength potential, and hypertrophic response to training. These are not the dramatic loss-of-function mutations (like IVS1+5G>A) that can double muscle mass; instead, they are subtler variants that partially reduce myostatin inhibition, leading to incremental advantages.
Based on the key studies referenced in our conversation (e.g., meta-analyses and ethnicity-specific research):
These effects are variable—some studies show neutral or mixed results (e.g., no difference in training-induced changes in some cohorts), and the R allele is often heterozygous (KR) rather than homozygous (RR, very rare at <1–3%). Muscle traits are highly polygenic (heritability 45–82% for mass/strength), so any single variant like K153R explains only a small portion of population variance (likely 2–5%, similar to ACTN3).
- Quantitative effects from specific studies:
- In African American carriers of the R allele (reflecting West/Central African ancestry), baseline isometric muscle strength (e.g., maximum voluntary contraction) was ~29% higher (64.2 kg vs. 49.8 kg in non-carriers; P<0.05). This association was ethnicity-specific and not seen in other groups.
- Hypertrophy response to strength training: One analysis showed ~68% greater increase in leg muscle mass in KR heterozygotes vs. KK homozygotes (P=0.056, borderline significant). Other reports noted significantly larger gains in biceps/quadriceps thickness (e.g., +0.300 cm biceps, +0.421 cm quadriceps; P<0.01) in carriers.
- Peak power output (e.g., vertical jump tests): The R allele was linked to better explosive power production, though exact percentages varied.
- Meta-analysis insights(from systematic review of 71 studies on K153R/rs1805086):
- The R allele (KR/RR genotypes) showed a significant association with strength/power phenotypes in athletes, with odds ratios of ~2.02–2.15 (meaning roughly double the odds of being a strength-oriented athlete vs. controls; P=0.05). Frequency was higher in athletes (12.5% KR/RR) than controls (7.9%).
- It enhances hypertrophic response to power-oriented training, but the overall impact is described as favorable for muscle mass/strength development without quantifying a single universal percentage.
Educated overall estimate:
These are not revolutionary like true myostatin knockout; they're evolutionary fine-tuning for ancestral environments (e.g., famine resistance or physical demands). Larger studies are needed for precise quantification, as effects can differ by age, sex, training status, and ethnicity. If you're considering genetic testing or training implications, these could be worth exploring!
- For individuals carrying the favorable R allele (more common in West African groups), these variants likely provide a 10–25% advantage in muscle strength potential (e.g., baseline force output) and hypertrophic growth response to training (e.g., greater mass gains under resistance load) compared to non-carriers. This is additive to other genes, training, diet, and environment.
- At the population level (higher R allele frequency), it may contribute a subtle 5–15% edge in average muscle/strength traits for West African-ancestry groups, potentially helping explain some observed athletic tendencies in power-based activities—but it's far from deterministic and much smaller than rare null mutations.
Contend with what cracker? Your sad cracker ass crying about Jews for the upteenth time? You talk about whining like a bitch and wanting handouts yet all I see is you being a bitch and crying about Jews and how they somehow affected your insignificant cracker life in anyway that you don't like.
Very good. I like what I'm seeing.
bruh don't you understand that you are making your clanker ADMIT what I just said? That blacks DO indeed have a higher prevalence of every gene/mutation I listed off? With the only difference being you training it to low-ball or reinforce caution/criticism with the numbers and effects of sed genes/mutations?
it was a pleasure educating you on black genetic superiority!
That was exactly the joke bro.
It's literally everywhere nowLol. This new trend of LARPing as another race and saying how subhuman “your race” is. Such a stupid trend.
Even like a year ago everyone was just repping their own race without doing this shit
Over 80 percent of the names he listed were ancient Greek/Roman philosophers who were influenced by the older Egyptian and Persian philosophers.... Claiming even Gandhi as part of a nonexistent "Caucasoid race" its hilarious
Imagine being so subhuman you have to make ai art of anime characters with your ethnicity to feel better about it.
North Africans and blacks are legit the same exact shii to anyone who lives near them stop the cope of a "Caucasoid" United race
Greek thought emerged from its own intellectual soil. Philosophy is literally a school of thought founded by socrates, and even before him, scientists like thales and pythagoras were doing groundbreaking works.
All the guys you named are caucasoid. Everything ever comes from Europe, MENA and South Asia.
I don't do it to feel better about my race, I do it to masturbate.
Everyone gets white pussy, blacks usually get it a lot less than other races other than chinks and Indians especially outside the US.
jfl at this proud goonercel
Like? Other than porn (fictional entertainment with fictional stories featuring paid actors, written by Jews) that only mem watch and most women (non slumwhores) dont know about nor give af about.
bbc is a subgenre, standard porn features white men. And therefore most of porn features white men, despite most frequent watchers being black men. Pretty cucked.
Thales was a natural scientist and not philosopher.Thales of Miletus - Wikipedia
en.wikipedia.org
Huge cope the first Greek philosopher was studying in Iraq and Egypt
Show your responses bruh. Why you hiding them? What are you hiding? I didn't hide mine? What are you trying to woo it into telling you? You are such a petty individual don't you know that? Even with your CLEARLY forced responses the best you could get is:
DEBUNKED
and then:
The difference is only marginal
Did you seriously not expect me to read your post? Hahaha this is absolutely fucking pathetic. I'll take this as a sign that you surrender. Hasta luego
Keep coping
Nafris in Europe are parasitic, thats undoubtable. But their certainly not on par with blacks.North Africans and blacks are legit the same exact shii to anyone who lives near them stop the cope of a "Caucasoid" United race
North Africans have the highest crime rates in any European country not a single European man in Spain, Belgium, or France ever said
"I like Nafri immigrants they're hard working I want to import more" Nafris and Somalians are basically the most hated immigrant groups in Europe no likes these niggas
