ETHNICITY PHARMACOGENOMICS OF AAS: HOW DIFFERENT ETHNICITIES TOLERATE AAS DIFFERENTLY (EXTREMELY HIGH EFFORT) GTFIH!

[chang cypionate]

Saar, what about south east asians?

Closest to East Asian.

 

[Navity]

Pharmacogenomics of AAS
How Ethnic and Racial Genetic Variation Shapes Anabolic Androgenic Steroid Response, Metabolism, and Side Effect Profile

Yes I have references nigga
View attachment 5049021View attachment 5049023View attachment 5049024
​

---

Spoiler: THREAD OST

CONTENTS​

​

Spoiler: Table of Contents

• 1. Introduction
• 2. The Androgen Axis
• 3. AR CAG Repeat Polymorphism
• 4. UGT2B17 Gene Deletion
• 5. 5-Alpha Reductase (SRD5A2)
• 6. Baseline Endocrine Profiles
• 7. Differential AAS Response by Ethnicity
• 8. Anti Doping Implications
• 9. Limitations & Caveats
• 10. Conclusion and TLDR
• 11. References

​

​

---

1 ─ INTRODUCTION

​

"Anabolic-androgenic steroids (AAS) are synthetic derivatives of testosterone that exert their effects through the androgen receptor (AR), altering gene transcription responsible for muscle hypertrophy, erythropoiesis, nitrogen retention, and secondary sexual characteristics." Water you should all know this already.​

​

But what I'd say 95% of this forum doesn't know is that the response to AAS (which is determined by molecular machinery) is genetically variable between different ethnicities. No nigger I'm not talking about muh he's a hyper responder. Maybe I am, keep reading to find out faggot.​

​

Two incels can use the exact same "stack" they found on Tiktok at the exact same dosages and still have differences in:​

• Anabolic response
• Strength gain
• Hair loss progression
• Acne severity
• Estrogenic burden
• Steroid clearance rates
• Doping detectability

​

Now most of you know that people respond differently to AAS, but I'm going to cover why and also show you niggas it's mainly because of the difference in ethnicity. Chang, Chad, and Tyrone will all respond differently (most of the time, we will stop talking about/mentioning outliers from here on out).​

​

I will cover the 3 major pharmacoegonomic mechanisms that are basically responsible for these differences:​

• AR CAG repeat polymorphism, meaning androgen receptor sensitivity
• UGT2B17 deletion, meaning androgen metabolism and excretion
• SRD5A2 polymorphisms , meaning DHT conversion rate

View attachment 5049028​

---

2 ─ THE ANDROGEN AXIS: A PRIMER FOR THE GREYS

So testosterone has two options (don't worry about aromatization, can't be bothered to explain):​

• Bind directly to the androgen receptor (good, not on topic for this thread though)
• Be converted into DHT via 5α-reductase (bad, not on topic for this thread though)

DHT binds to the androgen receptor with about 3× greater affinity than testosterone itself. Woah.​

​

After exhausting its effects, androgens are metabolised primarily through glucuronidation by UGT2B17, allowing you to piss it out.​

Now genetic variation between ethnicities comes into play:​

​

• AR sensitivity
• DHT conversion
• Androgen clearance

​

THIS THEREFORE RESULTS IN MAJOR DIFFERENCES BETWEEN HOW AAS FUNCTIONS IN CHANG'S BODY COMPARED TO TYRONE'S.

---

3 ─ THE AR CAG REPEAT POLYMORPHISM

Now the little pharmacokinetic tutorials out the way we can get down to business bhenchods.​

​

The androgen receptor gene contains a polymorphic CAG repeat region.​

Two main things you should know:​

Shorter CAG repeats leads to stronger receptor transcriptional activity ​

Longer CAG repeats leads to weaker androgen signalling ​

This means that:​

• Short repeats = stronger response per mg of rat urine
• Long repeats = weaker response per mg of rat urine

To simply put, SHORT = GOOD AND LONG = BAD (think of it as negative correlation to dick size)​

​

​

View attachment 5049034​

​

Well Chang, what are the implications of this? You may ask, let me tell you: ​

Individuals (the blacks) with shorter CAG repeats may experience:​

• Greater anabolic signalling
• Higher androgenic sensitivity
• Increased acne/hair loss risk
• More pronounced response to testosterone based cycles

Spoiler

Have you ever asked yourself why after two years of lifting you still look the same as your black friend who hasn't touched a weight in his life? This genetic variance doesn't only occur when injecting exogenous hormones, it occurs naturally as well. The AAS just amplify this effect.

---

4 ─ UGT2B17 GENE DELETION

UGT2B17 is the primary enzyme responsible for testosterone glucuronidation and urinary excretion. It basically lets you excrete testosterone by peeing. ​

​

However, some niggas possess a complete deletion of this gene:​

• ins/ins = normal excretion
• ins/del = partial reduction in excretion
• del/del = near absent urinary testosterone excretion, no pissing out for you

The ethnic distribution is extremely uneven. ​

View attachment 5049038​

What does it mean for you mean if you are missing this gene?(Asians read this):​

​

• Slower steroid clearance
• Longer circulating androgen exposure
• Different pharmacokinetics from people with the gene (Caucasians and Africans)
• Reduced reliability of urinary testosterone doping tests (we'll get to this later)
• THIS IS WHY SOMETIMES PEOPLE SAY ASIANS ARE LOW T (we will get to this in more detail in the anti doping section)

This is actually one of the most important pharmacogenomic findings in anti doping science. Cuck shit anyways, muh anti doping. ​

---

5 ─ SRD5A2 / 5-ALPHA REDUCTASE POLYMORPHISMS

​

SRD5A2 controls conversion of testosterone into DHT. R/tressless lurkers look away. ​

Two major variants dominate the literature:​

​

​

View attachment 5049041​

So what does this mean for the Norwood Reaper coming to rape you?:​

Higher DHT conversion:​

• Greater hair loss acceleration (sorry you can't keep using your dreads to fraud forever)
• Higher acne burden
• More prostate stimulation
• Stronger androgenic phenotype (most masculine guys are the blacks, it should be common knowledge atp right?)

Lower conversion:​

• Reduced androgenic side effects
• Lower DHT burden
• Potentially weaker androgenic expression
• Maybe you guys have seen some videos talking about Asians experiencing the least side effects on AAS. There is financial downsides to this, it's not just butterflies and rainbows other Changs.

---

6 ─ BASELINE ENDOCRINE DIFFERENCES

Some large endocrine studies suggest that:​

• Total testosterone differences between groups are smaller than commonly assumed (over for Asians are low T copers)
• DHT differences are more significant than testosterone differences
• Black men show higher average DHT and DHT:T ratios (over for blacks trying to keep their locs or dreads forever)
• East Asian men show lower 5α-reductase activity (lifefuel for your follicles, ropefuel for wallet and dimo)
• Black men also show higher estradiol and SHBG in several datasets

View attachment 5049043​

---

7 ─ PUTTING THE BIG PICTURE TOGETHER, A LITTLE SUMMARY FOR YOU

​

Spoiler: Niggers gtfih

• Higher AR sensitivity
• Higher DHT conversion
• Potentially stronger androgenic signalling
• Greater androgenic side effect burden

​

Spoiler: Crackers gtfih

• Intermediate across most variables
• Reference population for most AAS literature
• Standard pharmacokinetic assumptions generally apply

​

Spoiler: Gooks gtfih

• Lower AR sensitivity
• Lower DHT conversion
• Much slower steroid excretion
• Reduced urinary testosterone output
• Piss tests don't work

​

​

Spoiler: Spics gtfih

• Higher testosterone in some datasets
• Elevated A49T frequency
• Potentially stronger DHT mediated androgenic response
• Sorry the studies a lot of times didn't count you guys as a separate ethnicity for some reason, just assume you're closest to the mayos

---

8 ─ ANTI-DOPING IMPLICATIONS: EXTREMELY HOMOSEXUAL BTW

The standard testosterone/epitestosterone (T/E) ratio test assumes normal UGT2B17 function. This means you piss out normally. ​

​

This assumption fails for East Asian populations.​

Individuals with the del/del genotype can administer exogenous testosterone while producing little urinary testosterone elevation. So lifefuel for Changs that want to claim natty? Not necessarily. ​

This forced WADA to move toward more innovative approaches to doping tests:​

• Athlete Biological Passports
• Longitudinal hormone tracking
• Population adjusted steroid profiling
• YOU GUYS CAN LOOK MORE INTO THIS IF YOU WANT, THIS IS ALL THE RESEARCH I'M WILLING TO DO ON ANTI DOPING CUCKS

View attachment 5049047​

---

9 ─ LIMITATIONS & CAVEATS

​

So here's some "limitations and caveats" to the studies/findings​

Important caveats:​

• Intragroup variation shouldn't be ignored, this is where most of the hyper responder shit comes from, because two people of the same ethnicity can respond differently (ethnicity is the more important factor though)
• Ethnicity isn't deterministic biology all of the time (though most of the time it is)
• Some studies examine endogenous hormones and not necessarily exogenous AAS, but we can assume the same findings apply
• Direct RCTs on ethnic AAS response are limited compared to other fitness/bodybuilding studies, because nowadays researching about ethnic and race differences get you cancelled lul

Population level trends do not predict individual outcomes with 100% certainty. But please nigga, most of you aren't genetic outliers or hyper responders. ​

---

10 ─ CONCLUSION

So second high effort thread finished, first high effort thread about actual LM related topic. ​

Hope it was an interesting read. ​

Just fyi, I used AI only to help with formatting, all other words are mine or taken directly from the studies themselves. TLDR also done by AI, if you can't be bothered to read this thread then I can't be bothered manually making you a summary. ​

Spoiler: Inb4 DNR

Different ethnic groups appear to respond to anabolic steroids differently because of genetic differences in:

• Androgen receptor sensitivity → some populations may get a stronger anabolic signal from the same amount of testosterone.
• DHT conversion → affects things like hair loss, acne, facial/body hair growth, and prostate stimulation.
• Steroid metabolism/excretion → some groups clear testosterone more slowly, meaning steroids stay active longer and may be harder to detect in urine tests.

General trends found in the literature:

• Sub-Saharan African populations tend to have higher androgen receptor sensitivity and higher DHT activity.
• East Asian populations tend to have lower receptor sensitivity, lower DHT conversion, but much slower testosterone excretion due to high UGT2B17 deletion rates.
• Europeans are generally intermediate and are the reference population for most steroid research.
• Hispanic populations may have relatively high androgen activity in some markers.

​

@Revan @framepill @Nectar @nigHT.143 @pleasevanity

---

11 ─ REFERENCES​

Spoiler: References

Jakobsson, J. et al. (2006). Large differences in testosterone excretion in Korean and Swedish men are strongly associated with a UDP-glucuronosyl transferase 2B17 polymorphism. Journal of Clinical Endocrinology and Metabolism. https://pubmed.ncbi.nlm.nih.gov/16332934/

Litman, H.J. et al. (2006). Serum androgen levels in Black, Hispanic, and White men. Journal of Clinical Endocrinology and Metabolism, 91(11), 4326–4334. https://academic.oup.com/jcem/article/91/11/4326/2656429

Giovannucci, E. et al. (1999). Racial differences in the androgen/androgen receptor pathway in prostate cancer. PMC. https://pmc.ncbi.nlm.nih.gov/articles/PMC2608588/

Nakagawa, H. et al. (2010). Potentially harmful advantage to athletes: a putative connection between UGT2B17 gene deletion polymorphism and renal disorders with prolonged use of anabolic androgenic steroids. PMC. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877023/

PMC. (2016). Impact of UGT2B17 gene deletion on the steroid profile of an athlete. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760435/

PMC. (2013). UGT2B17 Genotype and the Pharmacokinetic Serum Profile of Testosterone during Substitution Therapy with Testosterone Undecanoate. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3725801/

PMC. (2024). Associations of CAG repeat polymorphism in the androgen receptor gene with steroid hormone levels and anthropometrics among men: the role of the ethnic factor. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10926003/

ResearchGate. (2025). Ethnic Variation in Allele Distribution of the Androgen Receptor (AR) (CAG)n Repeat / AAS Adverse Effects Review. https://www.researchgate.net/publication/51150922

Grönberg, H. et al. (2007). Serum estrogen, but not testosterone, levels differ between Black and White men in a nationally representative sample of Americans. Journal of Clinical Endocrinology and Metabolism, 92(7), 2519. https://academic.oup.com/jcem/article/92/7/2519/2598282

Wu, A.H. et al. (1995). 5 Alpha Reductase Metabolites & Genotype in Healthy Men (NIH Grant R01-CA068593). https://grantome.com/grant/NIH/R01-CA068593-01

ScienceDirect Topics. SRD5A2. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/srd5a2

Ellis, L. & Nyborg, H. (1992). Racial/ethnic variations in male testosterone levels: a probable contributor to group differences in health. Steroids, 57(2), 72–75. PubMed ID: 1621259

Lamont, B.T. et al. (2009). The age-testosterone relationship in Black, White, and Mexican-American men, and reasons for ethnic differences. Aging Male, 12(2–3). https://www.tandfonline.com/doi/full/10.1080/13685530903071802

NCBI StatPearls. (2026). Anabolic Steroid Use Disorder. https://www.ncbi.nlm.nih.gov/books/NBK538174/

PMC. (2025). Impact of Anabolic-Androgenic Steroid Abuse on the Cardiovascular System: Molecular Mechanisms and Clinical Implications. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12652398/

PMC. (2024). Essential blood testing in the patient using androgenic anabolic steroids: a clinical practice guideline for primary care. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10962511/

Journal of Clinical Endocrinology and Metabolism. (2007). Clinical Relevance of Racial and Ethnic Differences in Sex Steroids. https://academic.oup.com/jcem/article/92/7/2433/2598039

PMC. (2012). Racial Differences in Androgen Receptor (AR) and AR Splice Variants Expression. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10044992/

​

Great thread, will read in a bit

 

[LookzMaxxerSyn]

@LookzMaxxerSyn did u see the joseph shin + adam yu reference?

i did see and im proud

also reading thru rn

 

[Punjabi Waffen]

Pharmacogenomics of AAS
How Ethnic and Racial Genetic Variation Shapes Anabolic Androgenic Steroid Response, Metabolism, and Side Effect Profile

Yes I have references nigga
View attachment 5049021View attachment 5049023View attachment 5049024
​

---

Spoiler: THREAD OST

CONTENTS​

​

Spoiler: Table of Contents

• 1. Introduction
• 2. The Androgen Axis
• 3. AR CAG Repeat Polymorphism
• 4. UGT2B17 Gene Deletion
• 5. 5-Alpha Reductase (SRD5A2)
• 6. Baseline Endocrine Profiles
• 7. Differential AAS Response by Ethnicity
• 8. Anti Doping Implications
• 9. Limitations & Caveats
• 10. Conclusion and TLDR
• 11. References

​

​

---

1 ─ INTRODUCTION

​

"Anabolic-androgenic steroids (AAS) are synthetic derivatives of testosterone that exert their effects through the androgen receptor (AR), altering gene transcription responsible for muscle hypertrophy, erythropoiesis, nitrogen retention, and secondary sexual characteristics." Water you should all know this already.​

​

But what I'd say 95% of this forum doesn't know is that the response to AAS (which is determined by molecular machinery) is genetically variable between different ethnicities. No nigger I'm not talking about muh he's a hyper responder. Maybe I am, keep reading to find out faggot.​

​

Two incels can use the exact same "stack" they found on Tiktok at the exact same dosages and still have differences in:​

• Anabolic response
• Strength gain
• Hair loss progression
• Acne severity
• Estrogenic burden
• Steroid clearance rates
• Doping detectability

​

Now most of you know that people respond differently to AAS, but I'm going to cover why and also show you niggas it's mainly because of the difference in ethnicity. Chang, Chad, and Tyrone will all respond differently (most of the time, we will stop talking about/mentioning outliers from here on out).​

​

I will cover the 3 major pharmacoegonomic mechanisms that are basically responsible for these differences:​

• AR CAG repeat polymorphism, meaning androgen receptor sensitivity
• UGT2B17 deletion, meaning androgen metabolism and excretion
• SRD5A2 polymorphisms , meaning DHT conversion rate

View attachment 5049028​

---

2 ─ THE ANDROGEN AXIS: A PRIMER FOR THE GREYS

So testosterone has two options (don't worry about aromatization, can't be bothered to explain):​

• Bind directly to the androgen receptor (good, not on topic for this thread though)
• Be converted into DHT via 5α-reductase (bad, not on topic for this thread though)

DHT binds to the androgen receptor with about 3× greater affinity than testosterone itself. Woah.​

​

After exhausting its effects, androgens are metabolised primarily through glucuronidation by UGT2B17, allowing you to piss it out.​

Now genetic variation between ethnicities comes into play:​

​

• AR sensitivity
• DHT conversion
• Androgen clearance

​

THIS THEREFORE RESULTS IN MAJOR DIFFERENCES BETWEEN HOW AAS FUNCTIONS IN CHANG'S BODY COMPARED TO TYRONE'S.

---

3 ─ THE AR CAG REPEAT POLYMORPHISM

Now the little pharmacokinetic tutorials out the way we can get down to business bhenchods.​

​

The androgen receptor gene contains a polymorphic CAG repeat region.​

Two main things you should know:​

Shorter CAG repeats leads to stronger receptor transcriptional activity ​

Longer CAG repeats leads to weaker androgen signalling ​

This means that:​

• Short repeats = stronger response per mg of rat urine
• Long repeats = weaker response per mg of rat urine

To simply put, SHORT = GOOD AND LONG = BAD (think of it as negative correlation to dick size)​

​

​

View attachment 5049034​

​

Well Chang, what are the implications of this? You may ask, let me tell you: ​

Individuals (the blacks) with shorter CAG repeats may experience:​

• Greater anabolic signalling
• Higher androgenic sensitivity
• Increased acne/hair loss risk
• More pronounced response to testosterone based cycles

Spoiler

Have you ever asked yourself why after two years of lifting you still look the same as your black friend who hasn't touched a weight in his life? This genetic variance doesn't only occur when injecting exogenous hormones, it occurs naturally as well. The AAS just amplify this effect.

---

4 ─ UGT2B17 GENE DELETION

UGT2B17 is the primary enzyme responsible for testosterone glucuronidation and urinary excretion. It basically lets you excrete testosterone by peeing. ​

​

However, some niggas possess a complete deletion of this gene:​

• ins/ins = normal excretion
• ins/del = partial reduction in excretion
• del/del = near absent urinary testosterone excretion, no pissing out for you

The ethnic distribution is extremely uneven. ​

View attachment 5049038​

What does it mean for you mean if you are missing this gene?(Asians read this):​

​

• Slower steroid clearance
• Longer circulating androgen exposure
• Different pharmacokinetics from people with the gene (Caucasians and Africans)
• Reduced reliability of urinary testosterone doping tests (we'll get to this later)
• THIS IS WHY SOMETIMES PEOPLE SAY ASIANS ARE LOW T (we will get to this in more detail in the anti doping section)

This is actually one of the most important pharmacogenomic findings in anti doping science. Cuck shit anyways, muh anti doping. ​

---

5 ─ SRD5A2 / 5-ALPHA REDUCTASE POLYMORPHISMS

​

SRD5A2 controls conversion of testosterone into DHT. R/tressless lurkers look away. ​

Two major variants dominate the literature:​

​

​

View attachment 5049041​

So what does this mean for the Norwood Reaper coming to rape you?:​

Higher DHT conversion:​

• Greater hair loss acceleration (sorry you can't keep using your dreads to fraud forever)
• Higher acne burden
• More prostate stimulation
• Stronger androgenic phenotype (most masculine guys are the blacks, it should be common knowledge atp right?)

Lower conversion:​

• Reduced androgenic side effects
• Lower DHT burden
• Potentially weaker androgenic expression
• Maybe you guys have seen some videos talking about Asians experiencing the least side effects on AAS. There is financial downsides to this, it's not just butterflies and rainbows other Changs.

---

6 ─ BASELINE ENDOCRINE DIFFERENCES

Some large endocrine studies suggest that:​

• Total testosterone differences between groups are smaller than commonly assumed (over for Asians are low T copers)
• DHT differences are more significant than testosterone differences
• Black men show higher average DHT and DHT:T ratios (over for blacks trying to keep their locs or dreads forever)
• East Asian men show lower 5α-reductase activity (lifefuel for your follicles, ropefuel for wallet and dimo)
• Black men also show higher estradiol and SHBG in several datasets

View attachment 5049043​

---

7 ─ PUTTING THE BIG PICTURE TOGETHER, A LITTLE SUMMARY FOR YOU

​

Spoiler: Niggers gtfih

• Higher AR sensitivity
• Higher DHT conversion
• Potentially stronger androgenic signalling
• Greater androgenic side effect burden

​

Spoiler: Crackers gtfih

• Intermediate across most variables
• Reference population for most AAS literature
• Standard pharmacokinetic assumptions generally apply

​

Spoiler: Gooks gtfih

• Lower AR sensitivity
• Lower DHT conversion
• Much slower steroid excretion
• Reduced urinary testosterone output
• Piss tests don't work

​

​

Spoiler: Spics gtfih

• Higher testosterone in some datasets
• Elevated A49T frequency
• Potentially stronger DHT mediated androgenic response
• Sorry the studies a lot of times didn't count you guys as a separate ethnicity for some reason, just assume you're closest to the mayos

---

8 ─ ANTI-DOPING IMPLICATIONS: EXTREMELY HOMOSEXUAL BTW

The standard testosterone/epitestosterone (T/E) ratio test assumes normal UGT2B17 function. This means you piss out normally. ​

​

This assumption fails for East Asian populations.​

Individuals with the del/del genotype can administer exogenous testosterone while producing little urinary testosterone elevation. So lifefuel for Changs that want to claim natty? Not necessarily. ​

This forced WADA to move toward more innovative approaches to doping tests:​

• Athlete Biological Passports
• Longitudinal hormone tracking
• Population adjusted steroid profiling
• YOU GUYS CAN LOOK MORE INTO THIS IF YOU WANT, THIS IS ALL THE RESEARCH I'M WILLING TO DO ON ANTI DOPING CUCKS

View attachment 5049047​

---

9 ─ LIMITATIONS & CAVEATS

​

So here's some "limitations and caveats" to the studies/findings​

Important caveats:​

• Intragroup variation shouldn't be ignored, this is where most of the hyper responder shit comes from, because two people of the same ethnicity can respond differently (ethnicity is the more important factor though)
• Ethnicity isn't deterministic biology all of the time (though most of the time it is)
• Some studies examine endogenous hormones and not necessarily exogenous AAS, but we can assume the same findings apply
• Direct RCTs on ethnic AAS response are limited compared to other fitness/bodybuilding studies, because nowadays researching about ethnic and race differences get you cancelled lul

Population level trends do not predict individual outcomes with 100% certainty. But please nigga, most of you aren't genetic outliers or hyper responders. ​

---

10 ─ CONCLUSION

So second high effort thread finished, first high effort thread about actual LM related topic. ​

Hope it was an interesting read. ​

Just fyi, I used AI only to help with formatting, all other words are mine or taken directly from the studies themselves. TLDR also done by AI, if you can't be bothered to read this thread then I can't be bothered manually making you a summary. ​

Spoiler: Inb4 DNR

Different ethnic groups appear to respond to anabolic steroids differently because of genetic differences in:

• Androgen receptor sensitivity → some populations may get a stronger anabolic signal from the same amount of testosterone.
• DHT conversion → affects things like hair loss, acne, facial/body hair growth, and prostate stimulation.
• Steroid metabolism/excretion → some groups clear testosterone more slowly, meaning steroids stay active longer and may be harder to detect in urine tests.

General trends found in the literature:

• Sub-Saharan African populations tend to have higher androgen receptor sensitivity and higher DHT activity.
• East Asian populations tend to have lower receptor sensitivity, lower DHT conversion, but much slower testosterone excretion due to high UGT2B17 deletion rates.
• Europeans are generally intermediate and are the reference population for most steroid research.
• Hispanic populations may have relatively high androgen activity in some markers.

​

@Revan @framepill @Nectar @nigHT.143 @pleasevanity

---

11 ─ REFERENCES​

Spoiler: References

Jakobsson, J. et al. (2006). Large differences in testosterone excretion in Korean and Swedish men are strongly associated with a UDP-glucuronosyl transferase 2B17 polymorphism. Journal of Clinical Endocrinology and Metabolism. https://pubmed.ncbi.nlm.nih.gov/16332934/

Litman, H.J. et al. (2006). Serum androgen levels in Black, Hispanic, and White men. Journal of Clinical Endocrinology and Metabolism, 91(11), 4326–4334. https://academic.oup.com/jcem/article/91/11/4326/2656429

Giovannucci, E. et al. (1999). Racial differences in the androgen/androgen receptor pathway in prostate cancer. PMC. https://pmc.ncbi.nlm.nih.gov/articles/PMC2608588/

Nakagawa, H. et al. (2010). Potentially harmful advantage to athletes: a putative connection between UGT2B17 gene deletion polymorphism and renal disorders with prolonged use of anabolic androgenic steroids. PMC. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877023/

PMC. (2016). Impact of UGT2B17 gene deletion on the steroid profile of an athlete. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760435/

PMC. (2013). UGT2B17 Genotype and the Pharmacokinetic Serum Profile of Testosterone during Substitution Therapy with Testosterone Undecanoate. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3725801/

PMC. (2024). Associations of CAG repeat polymorphism in the androgen receptor gene with steroid hormone levels and anthropometrics among men: the role of the ethnic factor. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10926003/

ResearchGate. (2025). Ethnic Variation in Allele Distribution of the Androgen Receptor (AR) (CAG)n Repeat / AAS Adverse Effects Review. https://www.researchgate.net/publication/51150922

Grönberg, H. et al. (2007). Serum estrogen, but not testosterone, levels differ between Black and White men in a nationally representative sample of Americans. Journal of Clinical Endocrinology and Metabolism, 92(7), 2519. https://academic.oup.com/jcem/article/92/7/2519/2598282

Wu, A.H. et al. (1995). 5 Alpha Reductase Metabolites & Genotype in Healthy Men (NIH Grant R01-CA068593). https://grantome.com/grant/NIH/R01-CA068593-01

ScienceDirect Topics. SRD5A2. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/srd5a2

Ellis, L. & Nyborg, H. (1992). Racial/ethnic variations in male testosterone levels: a probable contributor to group differences in health. Steroids, 57(2), 72–75. PubMed ID: 1621259

Lamont, B.T. et al. (2009). The age-testosterone relationship in Black, White, and Mexican-American men, and reasons for ethnic differences. Aging Male, 12(2–3). https://www.tandfonline.com/doi/full/10.1080/13685530903071802

NCBI StatPearls. (2026). Anabolic Steroid Use Disorder. https://www.ncbi.nlm.nih.gov/books/NBK538174/

PMC. (2025). Impact of Anabolic-Androgenic Steroid Abuse on the Cardiovascular System: Molecular Mechanisms and Clinical Implications. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12652398/

PMC. (2024). Essential blood testing in the patient using androgenic anabolic steroids: a clinical practice guideline for primary care. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10962511/

Journal of Clinical Endocrinology and Metabolism. (2007). Clinical Relevance of Racial and Ethnic Differences in Sex Steroids. https://academic.oup.com/jcem/article/92/7/2433/2598039

PMC. (2012). Racial Differences in Androgen Receptor (AR) and AR Splice Variants Expression. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10044992/

​

THERE YOU GO NIGGA

FUCKING MIRINNN, GOOD THRRAD, GOOD TOPIC

 

[Awest]

THERE YOU GO NIGGA

FUCKING MIRINNN, GOOD THRRAD, GOOD TOPIC

but he ranked asians the lowest. how come?

 

[chang cypionate]

but he ranked asians the lowest. how come?

Did you read the thread? Lowest in terms of gear effectiveness yes, but that also means less side effects and the ability to run more gear. There's pros and cons. More gear with less side effects is a pro, but the cons are needing to spend more to achieve the same results on less gear, but that someone on less gear may experience more side effects. It's a balance.

 

[Awest]

Did you read the thread? Lowest in terms of gear effectiveness yes, but that also means less side effects and the ability to run more gear. There's pros and cons. More gear with less side effects is a pro, but the cons are needing to spend more to achieve the same results on less gear, but that someone on less gear may experience more side effects. It's a balance.

its fine brother I am just kidding at this point

 

[whatevenislm]

Pharmacogenomics of AAS
How Ethnic and Racial Genetic Variation Shapes Anabolic Androgenic Steroid Response, Metabolism, and Side Effect Profile

Yes I have references nigga
View attachment 5049021View attachment 5049023View attachment 5049024
​

---

Spoiler: THREAD OST

CONTENTS​

​

Spoiler: Table of Contents

• 1. Introduction
• 2. The Androgen Axis
• 3. AR CAG Repeat Polymorphism
• 4. UGT2B17 Gene Deletion
• 5. 5-Alpha Reductase (SRD5A2)
• 6. Baseline Endocrine Profiles
• 7. Differential AAS Response by Ethnicity
• 8. Anti Doping Implications
• 9. Limitations & Caveats
• 10. Conclusion and TLDR
• 11. References

​

​

---

1 ─ INTRODUCTION

​

"Anabolic-androgenic steroids (AAS) are synthetic derivatives of testosterone that exert their effects through the androgen receptor (AR), altering gene transcription responsible for muscle hypertrophy, erythropoiesis, nitrogen retention, and secondary sexual characteristics." Water you should all know this already.​

​

But what I'd say 95% of this forum doesn't know is that the response to AAS (which is determined by molecular machinery) is genetically variable between different ethnicities. No nigger I'm not talking about muh he's a hyper responder. Maybe I am, keep reading to find out faggot.​

​

Two incels can use the exact same "stack" they found on Tiktok at the exact same dosages and still have differences in:​

• Anabolic response
• Strength gain
• Hair loss progression
• Acne severity
• Estrogenic burden
• Steroid clearance rates
• Doping detectability

​

Now most of you know that people respond differently to AAS, but I'm going to cover why and also show you niggas it's mainly because of the difference in ethnicity. Chang, Chad, and Tyrone will all respond differently (most of the time, we will stop talking about/mentioning outliers from here on out).​

​

I will cover the 3 major pharmacoegonomic mechanisms that are basically responsible for these differences:​

• AR CAG repeat polymorphism, meaning androgen receptor sensitivity
• UGT2B17 deletion, meaning androgen metabolism and excretion
• SRD5A2 polymorphisms , meaning DHT conversion rate

View attachment 5049028​

---

2 ─ THE ANDROGEN AXIS: A PRIMER FOR THE GREYS

So testosterone has two options (don't worry about aromatization, can't be bothered to explain):​

• Bind directly to the androgen receptor (good, not on topic for this thread though)
• Be converted into DHT via 5α-reductase (bad, not on topic for this thread though)

DHT binds to the androgen receptor with about 3× greater affinity than testosterone itself. Woah.​

​

After exhausting its effects, androgens are metabolised primarily through glucuronidation by UGT2B17, allowing you to piss it out.​

Now genetic variation between ethnicities comes into play:​

​

• AR sensitivity
• DHT conversion
• Androgen clearance

​

THIS THEREFORE RESULTS IN MAJOR DIFFERENCES BETWEEN HOW AAS FUNCTIONS IN CHANG'S BODY COMPARED TO TYRONE'S.

---

3 ─ THE AR CAG REPEAT POLYMORPHISM

Now the little pharmacokinetic tutorials out the way we can get down to business bhenchods.​

​

The androgen receptor gene contains a polymorphic CAG repeat region.​

Two main things you should know:​

Shorter CAG repeats leads to stronger receptor transcriptional activity ​

Longer CAG repeats leads to weaker androgen signalling ​

This means that:​

• Short repeats = stronger response per mg of rat urine
• Long repeats = weaker response per mg of rat urine

To simply put, SHORT = GOOD AND LONG = BAD (think of it as negative correlation to dick size)​

​

​

View attachment 5049034​

​

Well Chang, what are the implications of this? You may ask, let me tell you: ​

Individuals (the blacks) with shorter CAG repeats may experience:​

• Greater anabolic signalling
• Higher androgenic sensitivity
• Increased acne/hair loss risk
• More pronounced response to testosterone based cycles

Spoiler

Have you ever asked yourself why after two years of lifting you still look the same as your black friend who hasn't touched a weight in his life? This genetic variance doesn't only occur when injecting exogenous hormones, it occurs naturally as well. The AAS just amplify this effect.

---

4 ─ UGT2B17 GENE DELETION

UGT2B17 is the primary enzyme responsible for testosterone glucuronidation and urinary excretion. It basically lets you excrete testosterone by peeing. ​

​

However, some niggas possess a complete deletion of this gene:​

• ins/ins = normal excretion
• ins/del = partial reduction in excretion
• del/del = near absent urinary testosterone excretion, no pissing out for you

The ethnic distribution is extremely uneven. ​

View attachment 5049038​

What does it mean for you mean if you are missing this gene?(Asians read this):​

​

• Slower steroid clearance
• Longer circulating androgen exposure
• Different pharmacokinetics from people with the gene (Caucasians and Africans)
• Reduced reliability of urinary testosterone doping tests (we'll get to this later)
• THIS IS WHY SOMETIMES PEOPLE SAY ASIANS ARE LOW T (we will get to this in more detail in the anti doping section)

This is actually one of the most important pharmacogenomic findings in anti doping science. Cuck shit anyways, muh anti doping. ​

---

5 ─ SRD5A2 / 5-ALPHA REDUCTASE POLYMORPHISMS

​

SRD5A2 controls conversion of testosterone into DHT. R/tressless lurkers look away. ​

Two major variants dominate the literature:​

​

​

View attachment 5049041​

So what does this mean for the Norwood Reaper coming to rape you?:​

Higher DHT conversion:​

• Greater hair loss acceleration (sorry you can't keep using your dreads to fraud forever)
• Higher acne burden
• More prostate stimulation
• Stronger androgenic phenotype (most masculine guys are the blacks, it should be common knowledge atp right?)

Lower conversion:​

• Reduced androgenic side effects
• Lower DHT burden
• Potentially weaker androgenic expression
• Maybe you guys have seen some videos talking about Asians experiencing the least side effects on AAS. There is financial downsides to this, it's not just butterflies and rainbows other Changs.

---

6 ─ BASELINE ENDOCRINE DIFFERENCES

Some large endocrine studies suggest that:​

• Total testosterone differences between groups are smaller than commonly assumed (over for Asians are low T copers)
• DHT differences are more significant than testosterone differences
• Black men show higher average DHT and DHT:T ratios (over for blacks trying to keep their locs or dreads forever)
• East Asian men show lower 5α-reductase activity (lifefuel for your follicles, ropefuel for wallet and dimo)
• Black men also show higher estradiol and SHBG in several datasets

View attachment 5049043​

---

7 ─ PUTTING THE BIG PICTURE TOGETHER, A LITTLE SUMMARY FOR YOU

​

Spoiler: Niggers gtfih

• Higher AR sensitivity
• Higher DHT conversion
• Potentially stronger androgenic signalling
• Greater androgenic side effect burden

​

Spoiler: Crackers gtfih

• Intermediate across most variables
• Reference population for most AAS literature
• Standard pharmacokinetic assumptions generally apply

​

Spoiler: Gooks gtfih

• Lower AR sensitivity
• Lower DHT conversion
• Much slower steroid excretion
• Reduced urinary testosterone output
• Piss tests don't work

​

​

Spoiler: Spics gtfih

• Higher testosterone in some datasets
• Elevated A49T frequency
• Potentially stronger DHT mediated androgenic response
• Sorry the studies a lot of times didn't count you guys as a separate ethnicity for some reason, just assume you're closest to the mayos

---

8 ─ ANTI-DOPING IMPLICATIONS: EXTREMELY HOMOSEXUAL BTW

The standard testosterone/epitestosterone (T/E) ratio test assumes normal UGT2B17 function. This means you piss out normally. ​

​

This assumption fails for East Asian populations.​

Individuals with the del/del genotype can administer exogenous testosterone while producing little urinary testosterone elevation. So lifefuel for Changs that want to claim natty? Not necessarily. ​

This forced WADA to move toward more innovative approaches to doping tests:​

• Athlete Biological Passports
• Longitudinal hormone tracking
• Population adjusted steroid profiling
• YOU GUYS CAN LOOK MORE INTO THIS IF YOU WANT, THIS IS ALL THE RESEARCH I'M WILLING TO DO ON ANTI DOPING CUCKS

View attachment 5049047​

---

9 ─ LIMITATIONS & CAVEATS

​

So here's some "limitations and caveats" to the studies/findings​

Important caveats:​

• Intragroup variation shouldn't be ignored, this is where most of the hyper responder shit comes from, because two people of the same ethnicity can respond differently (ethnicity is the more important factor though)
• Ethnicity isn't deterministic biology all of the time (though most of the time it is)
• Some studies examine endogenous hormones and not necessarily exogenous AAS, but we can assume the same findings apply
• Direct RCTs on ethnic AAS response are limited compared to other fitness/bodybuilding studies, because nowadays researching about ethnic and race differences get you cancelled lul

Population level trends do not predict individual outcomes with 100% certainty. But please nigga, most of you aren't genetic outliers or hyper responders. ​

---

10 ─ CONCLUSION

So second high effort thread finished, first high effort thread about actual LM related topic. ​

Hope it was an interesting read. ​

Just fyi, I used AI only to help with formatting, all other words are mine or taken directly from the studies themselves. TLDR also done by AI, if you can't be bothered to read this thread then I can't be bothered manually making you a summary. ​

Spoiler: Inb4 DNR

Different ethnic groups appear to respond to anabolic steroids differently because of genetic differences in:

• Androgen receptor sensitivity → some populations may get a stronger anabolic signal from the same amount of testosterone.
• DHT conversion → affects things like hair loss, acne, facial/body hair growth, and prostate stimulation.
• Steroid metabolism/excretion → some groups clear testosterone more slowly, meaning steroids stay active longer and may be harder to detect in urine tests.

General trends found in the literature:

• Sub-Saharan African populations tend to have higher androgen receptor sensitivity and higher DHT activity.
• East Asian populations tend to have lower receptor sensitivity, lower DHT conversion, but much slower testosterone excretion due to high UGT2B17 deletion rates.
• Europeans are generally intermediate and are the reference population for most steroid research.
• Hispanic populations may have relatively high androgen activity in some markers.

​

@Revan @framepill @Nectar @nigHT.143 @pleasevanity

---

11 ─ REFERENCES​

Spoiler: References

Jakobsson, J. et al. (2006). Large differences in testosterone excretion in Korean and Swedish men are strongly associated with a UDP-glucuronosyl transferase 2B17 polymorphism. Journal of Clinical Endocrinology and Metabolism. https://pubmed.ncbi.nlm.nih.gov/16332934/

Litman, H.J. et al. (2006). Serum androgen levels in Black, Hispanic, and White men. Journal of Clinical Endocrinology and Metabolism, 91(11), 4326–4334. https://academic.oup.com/jcem/article/91/11/4326/2656429

Giovannucci, E. et al. (1999). Racial differences in the androgen/androgen receptor pathway in prostate cancer. PMC. https://pmc.ncbi.nlm.nih.gov/articles/PMC2608588/

Nakagawa, H. et al. (2010). Potentially harmful advantage to athletes: a putative connection between UGT2B17 gene deletion polymorphism and renal disorders with prolonged use of anabolic androgenic steroids. PMC. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877023/

PMC. (2016). Impact of UGT2B17 gene deletion on the steroid profile of an athlete. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760435/

PMC. (2013). UGT2B17 Genotype and the Pharmacokinetic Serum Profile of Testosterone during Substitution Therapy with Testosterone Undecanoate. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3725801/

PMC. (2024). Associations of CAG repeat polymorphism in the androgen receptor gene with steroid hormone levels and anthropometrics among men: the role of the ethnic factor. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10926003/

ResearchGate. (2025). Ethnic Variation in Allele Distribution of the Androgen Receptor (AR) (CAG)n Repeat / AAS Adverse Effects Review. https://www.researchgate.net/publication/51150922

Grönberg, H. et al. (2007). Serum estrogen, but not testosterone, levels differ between Black and White men in a nationally representative sample of Americans. Journal of Clinical Endocrinology and Metabolism, 92(7), 2519. https://academic.oup.com/jcem/article/92/7/2519/2598282

Wu, A.H. et al. (1995). 5 Alpha Reductase Metabolites & Genotype in Healthy Men (NIH Grant R01-CA068593). https://grantome.com/grant/NIH/R01-CA068593-01

ScienceDirect Topics. SRD5A2. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/srd5a2

Ellis, L. & Nyborg, H. (1992). Racial/ethnic variations in male testosterone levels: a probable contributor to group differences in health. Steroids, 57(2), 72–75. PubMed ID: 1621259

Lamont, B.T. et al. (2009). The age-testosterone relationship in Black, White, and Mexican-American men, and reasons for ethnic differences. Aging Male, 12(2–3). https://www.tandfonline.com/doi/full/10.1080/13685530903071802

NCBI StatPearls. (2026). Anabolic Steroid Use Disorder. https://www.ncbi.nlm.nih.gov/books/NBK538174/

PMC. (2025). Impact of Anabolic-Androgenic Steroid Abuse on the Cardiovascular System: Molecular Mechanisms and Clinical Implications. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12652398/

PMC. (2024). Essential blood testing in the patient using androgenic anabolic steroids: a clinical practice guideline for primary care. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10962511/

Journal of Clinical Endocrinology and Metabolism. (2007). Clinical Relevance of Racial and Ethnic Differences in Sex Steroids. https://academic.oup.com/jcem/article/92/7/2433/2598039

PMC. (2012). Racial Differences in Androgen Receptor (AR) and AR Splice Variants Expression. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10044992/

​

nigger forgot about arabs/west asians

 

[buccalfatremoval]

Pharmacogenomics of AAS
How Ethnic and Racial Genetic Variation Shapes Anabolic Androgenic Steroid Response, Metabolism, and Side Effect Profile

Yes I have references nigga
View attachment 5049021View attachment 5049023View attachment 5049024
​

---

Spoiler: THREAD OST

CONTENTS​

​

Spoiler: Table of Contents

• 1. Introduction
• 2. The Androgen Axis
• 3. AR CAG Repeat Polymorphism
• 4. UGT2B17 Gene Deletion
• 5. 5-Alpha Reductase (SRD5A2)
• 6. Baseline Endocrine Profiles
• 7. Differential AAS Response by Ethnicity
• 8. Anti Doping Implications
• 9. Limitations & Caveats
• 10. Conclusion and TLDR
• 11. References

​

​

---

1 ─ INTRODUCTION

​

"Anabolic-androgenic steroids (AAS) are synthetic derivatives of testosterone that exert their effects through the androgen receptor (AR), altering gene transcription responsible for muscle hypertrophy, erythropoiesis, nitrogen retention, and secondary sexual characteristics." Water you should all know this already.​

​

But what I'd say 95% of this forum doesn't know is that the response to AAS (which is determined by molecular machinery) is genetically variable between different ethnicities. No nigger I'm not talking about muh he's a hyper responder. Maybe I am, keep reading to find out faggot.​

​

Two incels can use the exact same "stack" they found on Tiktok at the exact same dosages and still have differences in:​

• Anabolic response
• Strength gain
• Hair loss progression
• Acne severity
• Estrogenic burden
• Steroid clearance rates
• Doping detectability

​

Now most of you know that people respond differently to AAS, but I'm going to cover why and also show you niggas it's mainly because of the difference in ethnicity. Chang, Chad, and Tyrone will all respond differently (most of the time, we will stop talking about/mentioning outliers from here on out).​

​

I will cover the 3 major pharmacoegonomic mechanisms that are basically responsible for these differences:​

• AR CAG repeat polymorphism, meaning androgen receptor sensitivity
• UGT2B17 deletion, meaning androgen metabolism and excretion
• SRD5A2 polymorphisms , meaning DHT conversion rate

View attachment 5049028​

---

2 ─ THE ANDROGEN AXIS: A PRIMER FOR THE GREYS

So testosterone has two options (don't worry about aromatization, can't be bothered to explain):​

• Bind directly to the androgen receptor (good, not on topic for this thread though)
• Be converted into DHT via 5α-reductase (bad, not on topic for this thread though)

DHT binds to the androgen receptor with about 3× greater affinity than testosterone itself. Woah.​

​

After exhausting its effects, androgens are metabolised primarily through glucuronidation by UGT2B17, allowing you to piss it out.​

Now genetic variation between ethnicities comes into play:​

​

• AR sensitivity
• DHT conversion
• Androgen clearance

​

THIS THEREFORE RESULTS IN MAJOR DIFFERENCES BETWEEN HOW AAS FUNCTIONS IN CHANG'S BODY COMPARED TO TYRONE'S.

---

3 ─ THE AR CAG REPEAT POLYMORPHISM

Now the little pharmacokinetic tutorials out the way we can get down to business bhenchods.​

​

The androgen receptor gene contains a polymorphic CAG repeat region.​

Two main things you should know:​

Shorter CAG repeats leads to stronger receptor transcriptional activity ​

Longer CAG repeats leads to weaker androgen signalling ​

This means that:​

• Short repeats = stronger response per mg of rat urine
• Long repeats = weaker response per mg of rat urine

To simply put, SHORT = GOOD AND LONG = BAD (think of it as negative correlation to dick size)​

​

​

View attachment 5049034​

​

Well Chang, what are the implications of this? You may ask, let me tell you: ​

Individuals (the blacks) with shorter CAG repeats may experience:​

• Greater anabolic signalling
• Higher androgenic sensitivity
• Increased acne/hair loss risk
• More pronounced response to testosterone based cycles

Spoiler

Have you ever asked yourself why after two years of lifting you still look the same as your black friend who hasn't touched a weight in his life? This genetic variance doesn't only occur when injecting exogenous hormones, it occurs naturally as well. The AAS just amplify this effect.

---

4 ─ UGT2B17 GENE DELETION

UGT2B17 is the primary enzyme responsible for testosterone glucuronidation and urinary excretion. It basically lets you excrete testosterone by peeing. ​

​

However, some niggas possess a complete deletion of this gene:​

• ins/ins = normal excretion
• ins/del = partial reduction in excretion
• del/del = near absent urinary testosterone excretion, no pissing out for you

The ethnic distribution is extremely uneven. ​

View attachment 5049038​

What does it mean for you mean if you are missing this gene?(Asians read this):​

​

• Slower steroid clearance
• Longer circulating androgen exposure
• Different pharmacokinetics from people with the gene (Caucasians and Africans)
• Reduced reliability of urinary testosterone doping tests (we'll get to this later)
• THIS IS WHY SOMETIMES PEOPLE SAY ASIANS ARE LOW T (we will get to this in more detail in the anti doping section)

This is actually one of the most important pharmacogenomic findings in anti doping science. Cuck shit anyways, muh anti doping. ​

---

5 ─ SRD5A2 / 5-ALPHA REDUCTASE POLYMORPHISMS

​

SRD5A2 controls conversion of testosterone into DHT. R/tressless lurkers look away. ​

Two major variants dominate the literature:​

​

​

View attachment 5049041​

So what does this mean for the Norwood Reaper coming to rape you?:​

Higher DHT conversion:​

• Greater hair loss acceleration (sorry you can't keep using your dreads to fraud forever)
• Higher acne burden
• More prostate stimulation
• Stronger androgenic phenotype (most masculine guys are the blacks, it should be common knowledge atp right?)

Lower conversion:​

• Reduced androgenic side effects
• Lower DHT burden
• Potentially weaker androgenic expression
• Maybe you guys have seen some videos talking about Asians experiencing the least side effects on AAS. There is financial downsides to this, it's not just butterflies and rainbows other Changs.

---

6 ─ BASELINE ENDOCRINE DIFFERENCES

Some large endocrine studies suggest that:​

• Total testosterone differences between groups are smaller than commonly assumed (over for Asians are low T copers)
• DHT differences are more significant than testosterone differences
• Black men show higher average DHT and DHT:T ratios (over for blacks trying to keep their locs or dreads forever)
• East Asian men show lower 5α-reductase activity (lifefuel for your follicles, ropefuel for wallet and dimo)
• Black men also show higher estradiol and SHBG in several datasets

View attachment 5049043​

---

7 ─ PUTTING THE BIG PICTURE TOGETHER, A LITTLE SUMMARY FOR YOU

​

Spoiler: Niggers gtfih

• Higher AR sensitivity
• Higher DHT conversion
• Potentially stronger androgenic signalling
• Greater androgenic side effect burden

​

Spoiler: Crackers gtfih

• Intermediate across most variables
• Reference population for most AAS literature
• Standard pharmacokinetic assumptions generally apply

​

Spoiler: Gooks gtfih

• Lower AR sensitivity
• Lower DHT conversion
• Much slower steroid excretion
• Reduced urinary testosterone output
• Piss tests don't work

​

​

Spoiler: Spics gtfih

• Higher testosterone in some datasets
• Elevated A49T frequency
• Potentially stronger DHT mediated androgenic response
• Sorry the studies a lot of times didn't count you guys as a separate ethnicity for some reason, just assume you're closest to the mayos

---

8 ─ ANTI-DOPING IMPLICATIONS: EXTREMELY HOMOSEXUAL BTW

The standard testosterone/epitestosterone (T/E) ratio test assumes normal UGT2B17 function. This means you piss out normally. ​

​

This assumption fails for East Asian populations.​

Individuals with the del/del genotype can administer exogenous testosterone while producing little urinary testosterone elevation. So lifefuel for Changs that want to claim natty? Not necessarily. ​

This forced WADA to move toward more innovative approaches to doping tests:​

• Athlete Biological Passports
• Longitudinal hormone tracking
• Population adjusted steroid profiling
• YOU GUYS CAN LOOK MORE INTO THIS IF YOU WANT, THIS IS ALL THE RESEARCH I'M WILLING TO DO ON ANTI DOPING CUCKS

View attachment 5049047​

---

9 ─ LIMITATIONS & CAVEATS

​

So here's some "limitations and caveats" to the studies/findings​

Important caveats:​

• Intragroup variation shouldn't be ignored, this is where most of the hyper responder shit comes from, because two people of the same ethnicity can respond differently (ethnicity is the more important factor though)
• Ethnicity isn't deterministic biology all of the time (though most of the time it is)
• Some studies examine endogenous hormones and not necessarily exogenous AAS, but we can assume the same findings apply
• Direct RCTs on ethnic AAS response are limited compared to other fitness/bodybuilding studies, because nowadays researching about ethnic and race differences get you cancelled lul

Population level trends do not predict individual outcomes with 100% certainty. But please nigga, most of you aren't genetic outliers or hyper responders. ​

---

10 ─ CONCLUSION

So second high effort thread finished, first high effort thread about actual LM related topic. ​

Hope it was an interesting read. ​

Just fyi, I used AI only to help with formatting, all other words are mine or taken directly from the studies themselves. TLDR also done by AI, if you can't be bothered to read this thread then I can't be bothered manually making you a summary. ​

Spoiler: Inb4 DNR

Different ethnic groups appear to respond to anabolic steroids differently because of genetic differences in:

• Androgen receptor sensitivity → some populations may get a stronger anabolic signal from the same amount of testosterone.
• DHT conversion → affects things like hair loss, acne, facial/body hair growth, and prostate stimulation.
• Steroid metabolism/excretion → some groups clear testosterone more slowly, meaning steroids stay active longer and may be harder to detect in urine tests.

General trends found in the literature:

• Sub-Saharan African populations tend to have higher androgen receptor sensitivity and higher DHT activity.
• East Asian populations tend to have lower receptor sensitivity, lower DHT conversion, but much slower testosterone excretion due to high UGT2B17 deletion rates.
• Europeans are generally intermediate and are the reference population for most steroid research.
• Hispanic populations may have relatively high androgen activity in some markers.

​

@Revan @framepill @Nectar @nigHT.143 @pleasevanity

---

11 ─ REFERENCES​

Spoiler: References

Jakobsson, J. et al. (2006). Large differences in testosterone excretion in Korean and Swedish men are strongly associated with a UDP-glucuronosyl transferase 2B17 polymorphism. Journal of Clinical Endocrinology and Metabolism. https://pubmed.ncbi.nlm.nih.gov/16332934/

Litman, H.J. et al. (2006). Serum androgen levels in Black, Hispanic, and White men. Journal of Clinical Endocrinology and Metabolism, 91(11), 4326–4334. https://academic.oup.com/jcem/article/91/11/4326/2656429

Giovannucci, E. et al. (1999). Racial differences in the androgen/androgen receptor pathway in prostate cancer. PMC. https://pmc.ncbi.nlm.nih.gov/articles/PMC2608588/

Nakagawa, H. et al. (2010). Potentially harmful advantage to athletes: a putative connection between UGT2B17 gene deletion polymorphism and renal disorders with prolonged use of anabolic androgenic steroids. PMC. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877023/

PMC. (2016). Impact of UGT2B17 gene deletion on the steroid profile of an athlete. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760435/

PMC. (2013). UGT2B17 Genotype and the Pharmacokinetic Serum Profile of Testosterone during Substitution Therapy with Testosterone Undecanoate. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3725801/

PMC. (2024). Associations of CAG repeat polymorphism in the androgen receptor gene with steroid hormone levels and anthropometrics among men: the role of the ethnic factor. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10926003/

ResearchGate. (2025). Ethnic Variation in Allele Distribution of the Androgen Receptor (AR) (CAG)n Repeat / AAS Adverse Effects Review. https://www.researchgate.net/publication/51150922

Grönberg, H. et al. (2007). Serum estrogen, but not testosterone, levels differ between Black and White men in a nationally representative sample of Americans. Journal of Clinical Endocrinology and Metabolism, 92(7), 2519. https://academic.oup.com/jcem/article/92/7/2519/2598282

Wu, A.H. et al. (1995). 5 Alpha Reductase Metabolites & Genotype in Healthy Men (NIH Grant R01-CA068593). https://grantome.com/grant/NIH/R01-CA068593-01

ScienceDirect Topics. SRD5A2. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/srd5a2

Ellis, L. & Nyborg, H. (1992). Racial/ethnic variations in male testosterone levels: a probable contributor to group differences in health. Steroids, 57(2), 72–75. PubMed ID: 1621259

Lamont, B.T. et al. (2009). The age-testosterone relationship in Black, White, and Mexican-American men, and reasons for ethnic differences. Aging Male, 12(2–3). https://www.tandfonline.com/doi/full/10.1080/13685530903071802

NCBI StatPearls. (2026). Anabolic Steroid Use Disorder. https://www.ncbi.nlm.nih.gov/books/NBK538174/

PMC. (2025). Impact of Anabolic-Androgenic Steroid Abuse on the Cardiovascular System: Molecular Mechanisms and Clinical Implications. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12652398/

PMC. (2024). Essential blood testing in the patient using androgenic anabolic steroids: a clinical practice guideline for primary care. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10962511/

Journal of Clinical Endocrinology and Metabolism. (2007). Clinical Relevance of Racial and Ethnic Differences in Sex Steroids. https://academic.oup.com/jcem/article/92/7/2433/2598039

PMC. (2012). Racial Differences in Androgen Receptor (AR) and AR Splice Variants Expression. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10044992/

​

Good read from your fellow Arab acetate

 

[buccalfatremoval]

nigger forgot about arabs/west asians

 

[true juan]

Closest to East Asian.

what ab mexicans bhai

 

[chang cypionate]

what ab mexicans bhai

There is a short section on Hispanics .

 

[Finncelchud]

Read every molecule

 

[spermiel]

Pharmacogenomics of AAS
How Ethnic and Racial Genetic Variation Shapes Anabolic Androgenic Steroid Response, Metabolism, and Side Effect Profile

Yes I have references nigga
View attachment 5049021View attachment 5049023View attachment 5049024
​

---

Spoiler: THREAD OST

CONTENTS​

​

Spoiler: Table of Contents

• 1. Introduction
• 2. The Androgen Axis
• 3. AR CAG Repeat Polymorphism
• 4. UGT2B17 Gene Deletion
• 5. 5-Alpha Reductase (SRD5A2)
• 6. Baseline Endocrine Profiles
• 7. Differential AAS Response by Ethnicity
• 8. Anti Doping Implications
• 9. Limitations & Caveats
• 10. Conclusion and TLDR
• 11. References

​

​

---

1 ─ INTRODUCTION

​

"Anabolic-androgenic steroids (AAS) are synthetic derivatives of testosterone that exert their effects through the androgen receptor (AR), altering gene transcription responsible for muscle hypertrophy, erythropoiesis, nitrogen retention, and secondary sexual characteristics." Water you should all know this already.​

​

But what I'd say 95% of this forum doesn't know is that the response to AAS (which is determined by molecular machinery) is genetically variable between different ethnicities. No nigger I'm not talking about muh he's a hyper responder. Maybe I am, keep reading to find out faggot.​

​

Two incels can use the exact same "stack" they found on Tiktok at the exact same dosages and still have differences in:​

• Anabolic response
• Strength gain
• Hair loss progression
• Acne severity
• Estrogenic burden
• Steroid clearance rates
• Doping detectability

​

Now most of you know that people respond differently to AAS, but I'm going to cover why and also show you niggas it's mainly because of the difference in ethnicity. Chang, Chad, and Tyrone will all respond differently (most of the time, we will stop talking about/mentioning outliers from here on out).​

​

I will cover the 3 major pharmacoegonomic mechanisms that are basically responsible for these differences:​

• AR CAG repeat polymorphism, meaning androgen receptor sensitivity
• UGT2B17 deletion, meaning androgen metabolism and excretion
• SRD5A2 polymorphisms , meaning DHT conversion rate

View attachment 5049028​

---

2 ─ THE ANDROGEN AXIS: A PRIMER FOR THE GREYS

So testosterone has two options (don't worry about aromatization, can't be bothered to explain):​

• Bind directly to the androgen receptor (good, not on topic for this thread though)
• Be converted into DHT via 5α-reductase (bad, not on topic for this thread though)

DHT binds to the androgen receptor with about 3× greater affinity than testosterone itself. Woah.​

​

After exhausting its effects, androgens are metabolised primarily through glucuronidation by UGT2B17, allowing you to piss it out.​

Now genetic variation between ethnicities comes into play:​

​

• AR sensitivity
• DHT conversion
• Androgen clearance

​

THIS THEREFORE RESULTS IN MAJOR DIFFERENCES BETWEEN HOW AAS FUNCTIONS IN CHANG'S BODY COMPARED TO TYRONE'S.

---

3 ─ THE AR CAG REPEAT POLYMORPHISM

Now the little pharmacokinetic tutorials out the way we can get down to business bhenchods.​

​

The androgen receptor gene contains a polymorphic CAG repeat region.​

Two main things you should know:​

Shorter CAG repeats leads to stronger receptor transcriptional activity ​

Longer CAG repeats leads to weaker androgen signalling ​

This means that:​

• Short repeats = stronger response per mg of rat urine
• Long repeats = weaker response per mg of rat urine

To simply put, SHORT = GOOD AND LONG = BAD (think of it as negative correlation to dick size)​

​

​

View attachment 5049034​

​

Well Chang, what are the implications of this? You may ask, let me tell you: ​

Individuals (the blacks) with shorter CAG repeats may experience:​

• Greater anabolic signalling
• Higher androgenic sensitivity
• Increased acne/hair loss risk
• More pronounced response to testosterone based cycles

Spoiler

Have you ever asked yourself why after two years of lifting you still look the same as your black friend who hasn't touched a weight in his life? This genetic variance doesn't only occur when injecting exogenous hormones, it occurs naturally as well. The AAS just amplify this effect.

---

4 ─ UGT2B17 GENE DELETION

UGT2B17 is the primary enzyme responsible for testosterone glucuronidation and urinary excretion. It basically lets you excrete testosterone by peeing. ​

​

However, some niggas possess a complete deletion of this gene:​

• ins/ins = normal excretion
• ins/del = partial reduction in excretion
• del/del = near absent urinary testosterone excretion, no pissing out for you

The ethnic distribution is extremely uneven. ​

View attachment 5049038​

What does it mean for you mean if you are missing this gene?(Asians read this):​

​

• Slower steroid clearance
• Longer circulating androgen exposure
• Different pharmacokinetics from people with the gene (Caucasians and Africans)
• Reduced reliability of urinary testosterone doping tests (we'll get to this later)
• THIS IS WHY SOMETIMES PEOPLE SAY ASIANS ARE LOW T (we will get to this in more detail in the anti doping section)

This is actually one of the most important pharmacogenomic findings in anti doping science. Cuck shit anyways, muh anti doping. ​

---

5 ─ SRD5A2 / 5-ALPHA REDUCTASE POLYMORPHISMS

​

SRD5A2 controls conversion of testosterone into DHT. R/tressless lurkers look away. ​

Two major variants dominate the literature:​

​

​

View attachment 5049041​

So what does this mean for the Norwood Reaper coming to rape you?:​

Higher DHT conversion:​

• Greater hair loss acceleration (sorry you can't keep using your dreads to fraud forever)
• Higher acne burden
• More prostate stimulation
• Stronger androgenic phenotype (most masculine guys are the blacks, it should be common knowledge atp right?)

Lower conversion:​

• Reduced androgenic side effects
• Lower DHT burden
• Potentially weaker androgenic expression
• Maybe you guys have seen some videos talking about Asians experiencing the least side effects on AAS. There is financial downsides to this, it's not just butterflies and rainbows other Changs.

---

6 ─ BASELINE ENDOCRINE DIFFERENCES

Some large endocrine studies suggest that:​

• Total testosterone differences between groups are smaller than commonly assumed (over for Asians are low T copers)
• DHT differences are more significant than testosterone differences
• Black men show higher average DHT and DHT:T ratios (over for blacks trying to keep their locs or dreads forever)
• East Asian men show lower 5α-reductase activity (lifefuel for your follicles, ropefuel for wallet and dimo)
• Black men also show higher estradiol and SHBG in several datasets

View attachment 5049043​

---

7 ─ PUTTING THE BIG PICTURE TOGETHER, A LITTLE SUMMARY FOR YOU

​

Spoiler: Niggers gtfih

• Higher AR sensitivity
• Higher DHT conversion
• Potentially stronger androgenic signalling
• Greater androgenic side effect burden

​

Spoiler: Crackers gtfih

• Intermediate across most variables
• Reference population for most AAS literature
• Standard pharmacokinetic assumptions generally apply

​

Spoiler: Gooks gtfih

• Lower AR sensitivity
• Lower DHT conversion
• Much slower steroid excretion
• Reduced urinary testosterone output
• Piss tests don't work

​

​

Spoiler: Spics gtfih

• Higher testosterone in some datasets
• Elevated A49T frequency
• Potentially stronger DHT mediated androgenic response
• Sorry the studies a lot of times didn't count you guys as a separate ethnicity for some reason, just assume you're closest to the mayos

---

8 ─ ANTI-DOPING IMPLICATIONS: EXTREMELY HOMOSEXUAL BTW

The standard testosterone/epitestosterone (T/E) ratio test assumes normal UGT2B17 function. This means you piss out normally. ​

​

This assumption fails for East Asian populations.​

Individuals with the del/del genotype can administer exogenous testosterone while producing little urinary testosterone elevation. So lifefuel for Changs that want to claim natty? Not necessarily. ​

This forced WADA to move toward more innovative approaches to doping tests:​

• Athlete Biological Passports
• Longitudinal hormone tracking
• Population adjusted steroid profiling
• YOU GUYS CAN LOOK MORE INTO THIS IF YOU WANT, THIS IS ALL THE RESEARCH I'M WILLING TO DO ON ANTI DOPING CUCKS

View attachment 5049047​

---

9 ─ LIMITATIONS & CAVEATS

​

So here's some "limitations and caveats" to the studies/findings​

Important caveats:​

• Intragroup variation shouldn't be ignored, this is where most of the hyper responder shit comes from, because two people of the same ethnicity can respond differently (ethnicity is the more important factor though)
• Ethnicity isn't deterministic biology all of the time (though most of the time it is)
• Some studies examine endogenous hormones and not necessarily exogenous AAS, but we can assume the same findings apply
• Direct RCTs on ethnic AAS response are limited compared to other fitness/bodybuilding studies, because nowadays researching about ethnic and race differences get you cancelled lul

Population level trends do not predict individual outcomes with 100% certainty. But please nigga, most of you aren't genetic outliers or hyper responders. ​

---

10 ─ CONCLUSION

So second high effort thread finished, first high effort thread about actual LM related topic. ​

Hope it was an interesting read. ​

Just fyi, I used AI only to help with formatting, all other words are mine or taken directly from the studies themselves. TLDR also done by AI, if you can't be bothered to read this thread then I can't be bothered manually making you a summary. ​

Spoiler: Inb4 DNR

Different ethnic groups appear to respond to anabolic steroids differently because of genetic differences in:

• Androgen receptor sensitivity → some populations may get a stronger anabolic signal from the same amount of testosterone.
• DHT conversion → affects things like hair loss, acne, facial/body hair growth, and prostate stimulation.
• Steroid metabolism/excretion → some groups clear testosterone more slowly, meaning steroids stay active longer and may be harder to detect in urine tests.

General trends found in the literature:

• Sub-Saharan African populations tend to have higher androgen receptor sensitivity and higher DHT activity.
• East Asian populations tend to have lower receptor sensitivity, lower DHT conversion, but much slower testosterone excretion due to high UGT2B17 deletion rates.
• Europeans are generally intermediate and are the reference population for most steroid research.
• Hispanic populations may have relatively high androgen activity in some markers.

​

@Revan @framepill @Nectar @nigHT.143 @pleasevanity

---

11 ─ REFERENCES​

Spoiler: References

Jakobsson, J. et al. (2006). Large differences in testosterone excretion in Korean and Swedish men are strongly associated with a UDP-glucuronosyl transferase 2B17 polymorphism. Journal of Clinical Endocrinology and Metabolism. https://pubmed.ncbi.nlm.nih.gov/16332934/

Litman, H.J. et al. (2006). Serum androgen levels in Black, Hispanic, and White men. Journal of Clinical Endocrinology and Metabolism, 91(11), 4326–4334. https://academic.oup.com/jcem/article/91/11/4326/2656429

Giovannucci, E. et al. (1999). Racial differences in the androgen/androgen receptor pathway in prostate cancer. PMC. https://pmc.ncbi.nlm.nih.gov/articles/PMC2608588/

Nakagawa, H. et al. (2010). Potentially harmful advantage to athletes: a putative connection between UGT2B17 gene deletion polymorphism and renal disorders with prolonged use of anabolic androgenic steroids. PMC. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877023/

PMC. (2016). Impact of UGT2B17 gene deletion on the steroid profile of an athlete. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760435/

PMC. (2013). UGT2B17 Genotype and the Pharmacokinetic Serum Profile of Testosterone during Substitution Therapy with Testosterone Undecanoate. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3725801/

PMC. (2024). Associations of CAG repeat polymorphism in the androgen receptor gene with steroid hormone levels and anthropometrics among men: the role of the ethnic factor. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10926003/

ResearchGate. (2025). Ethnic Variation in Allele Distribution of the Androgen Receptor (AR) (CAG)n Repeat / AAS Adverse Effects Review. https://www.researchgate.net/publication/51150922

Grönberg, H. et al. (2007). Serum estrogen, but not testosterone, levels differ between Black and White men in a nationally representative sample of Americans. Journal of Clinical Endocrinology and Metabolism, 92(7), 2519. https://academic.oup.com/jcem/article/92/7/2519/2598282

Wu, A.H. et al. (1995). 5 Alpha Reductase Metabolites & Genotype in Healthy Men (NIH Grant R01-CA068593). https://grantome.com/grant/NIH/R01-CA068593-01

ScienceDirect Topics. SRD5A2. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/srd5a2

Ellis, L. & Nyborg, H. (1992). Racial/ethnic variations in male testosterone levels: a probable contributor to group differences in health. Steroids, 57(2), 72–75. PubMed ID: 1621259

Lamont, B.T. et al. (2009). The age-testosterone relationship in Black, White, and Mexican-American men, and reasons for ethnic differences. Aging Male, 12(2–3). https://www.tandfonline.com/doi/full/10.1080/13685530903071802

NCBI StatPearls. (2026). Anabolic Steroid Use Disorder. https://www.ncbi.nlm.nih.gov/books/NBK538174/

PMC. (2025). Impact of Anabolic-Androgenic Steroid Abuse on the Cardiovascular System: Molecular Mechanisms and Clinical Implications. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12652398/

PMC. (2024). Essential blood testing in the patient using androgenic anabolic steroids: a clinical practice guideline for primary care. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10962511/

Journal of Clinical Endocrinology and Metabolism. (2007). Clinical Relevance of Racial and Ethnic Differences in Sex Steroids. https://academic.oup.com/jcem/article/92/7/2433/2598039

PMC. (2012). Racial Differences in Androgen Receptor (AR) and AR Splice Variants Expression. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10044992/

​

Mirin high effort

 

[Dewhey321]

Pharmacogenomics of AAS
How Ethnic and Racial Genetic Variation Shapes Anabolic Androgenic Steroid Response, Metabolism, and Side Effect Profile

Yes I have references nigga
View attachment 5049021View attachment 5049023View attachment 5049024
​

---

Spoiler: THREAD OST

CONTENTS​

​

Spoiler: Table of Contents

• 1. Introduction
• 2. The Androgen Axis
• 3. AR CAG Repeat Polymorphism
• 4. UGT2B17 Gene Deletion
• 5. 5-Alpha Reductase (SRD5A2)
• 6. Baseline Endocrine Profiles
• 7. Differential AAS Response by Ethnicity
• 8. Anti Doping Implications
• 9. Limitations & Caveats
• 10. Conclusion and TLDR
• 11. References

​

​

---

1 ─ INTRODUCTION

​

"Anabolic-androgenic steroids (AAS) are synthetic derivatives of testosterone that exert their effects through the androgen receptor (AR), altering gene transcription responsible for muscle hypertrophy, erythropoiesis, nitrogen retention, and secondary sexual characteristics." Water you should all know this already.​

​

But what I'd say 95% of this forum doesn't know is that the response to AAS (which is determined by molecular machinery) is genetically variable between different ethnicities. No nigger I'm not talking about muh he's a hyper responder. Maybe I am, keep reading to find out faggot.​

​

Two incels can use the exact same "stack" they found on Tiktok at the exact same dosages and still have differences in:​

• Anabolic response
• Strength gain
• Hair loss progression
• Acne severity
• Estrogenic burden
• Steroid clearance rates
• Doping detectability

​

Now most of you know that people respond differently to AAS, but I'm going to cover why and also show you niggas it's mainly because of the difference in ethnicity. Chang, Chad, and Tyrone will all respond differently (most of the time, we will stop talking about/mentioning outliers from here on out).​

​

I will cover the 3 major pharmacoegonomic mechanisms that are basically responsible for these differences:​

• AR CAG repeat polymorphism, meaning androgen receptor sensitivity
• UGT2B17 deletion, meaning androgen metabolism and excretion
• SRD5A2 polymorphisms , meaning DHT conversion rate

View attachment 5049028​

---

2 ─ THE ANDROGEN AXIS: A PRIMER FOR THE GREYS

So testosterone has two options (don't worry about aromatization, can't be bothered to explain):​

• Bind directly to the androgen receptor (good, not on topic for this thread though)
• Be converted into DHT via 5α-reductase (bad, not on topic for this thread though)

DHT binds to the androgen receptor with about 3× greater affinity than testosterone itself. Woah.​

​

After exhausting its effects, androgens are metabolised primarily through glucuronidation by UGT2B17, allowing you to piss it out.​

Now genetic variation between ethnicities comes into play:​

​

• AR sensitivity
• DHT conversion
• Androgen clearance

​

THIS THEREFORE RESULTS IN MAJOR DIFFERENCES BETWEEN HOW AAS FUNCTIONS IN CHANG'S BODY COMPARED TO TYRONE'S.

---

3 ─ THE AR CAG REPEAT POLYMORPHISM

Now the little pharmacokinetic tutorials out the way we can get down to business bhenchods.​

​

The androgen receptor gene contains a polymorphic CAG repeat region.​

Two main things you should know:​

Shorter CAG repeats leads to stronger receptor transcriptional activity ​

Longer CAG repeats leads to weaker androgen signalling ​

This means that:​

• Short repeats = stronger response per mg of rat urine
• Long repeats = weaker response per mg of rat urine

To simply put, SHORT = GOOD AND LONG = BAD (think of it as negative correlation to dick size)​

​

​

View attachment 5049034​

​

Well Chang, what are the implications of this? You may ask, let me tell you: ​

Individuals (the blacks) with shorter CAG repeats may experience:​

• Greater anabolic signalling
• Higher androgenic sensitivity
• Increased acne/hair loss risk
• More pronounced response to testosterone based cycles

Spoiler

Have you ever asked yourself why after two years of lifting you still look the same as your black friend who hasn't touched a weight in his life? This genetic variance doesn't only occur when injecting exogenous hormones, it occurs naturally as well. The AAS just amplify this effect.

---

4 ─ UGT2B17 GENE DELETION

UGT2B17 is the primary enzyme responsible for testosterone glucuronidation and urinary excretion. It basically lets you excrete testosterone by peeing. ​

​

However, some niggas possess a complete deletion of this gene:​

• ins/ins = normal excretion
• ins/del = partial reduction in excretion
• del/del = near absent urinary testosterone excretion, no pissing out for you

The ethnic distribution is extremely uneven. ​

View attachment 5049038​

What does it mean for you mean if you are missing this gene?(Asians read this):​

​

• Slower steroid clearance
• Longer circulating androgen exposure
• Different pharmacokinetics from people with the gene (Caucasians and Africans)
• Reduced reliability of urinary testosterone doping tests (we'll get to this later)
• THIS IS WHY SOMETIMES PEOPLE SAY ASIANS ARE LOW T (we will get to this in more detail in the anti doping section)

This is actually one of the most important pharmacogenomic findings in anti doping science. Cuck shit anyways, muh anti doping. ​

---

5 ─ SRD5A2 / 5-ALPHA REDUCTASE POLYMORPHISMS

​

SRD5A2 controls conversion of testosterone into DHT. R/tressless lurkers look away. ​

Two major variants dominate the literature:​

​

​

View attachment 5049041​

So what does this mean for the Norwood Reaper coming to rape you?:​

Higher DHT conversion:​

• Greater hair loss acceleration (sorry you can't keep using your dreads to fraud forever)
• Higher acne burden
• More prostate stimulation
• Stronger androgenic phenotype (most masculine guys are the blacks, it should be common knowledge atp right?)

Lower conversion:​

• Reduced androgenic side effects
• Lower DHT burden
• Potentially weaker androgenic expression
• Maybe you guys have seen some videos talking about Asians experiencing the least side effects on AAS. There is financial downsides to this, it's not just butterflies and rainbows other Changs.

---

6 ─ BASELINE ENDOCRINE DIFFERENCES

Some large endocrine studies suggest that:​

• Total testosterone differences between groups are smaller than commonly assumed (over for Asians are low T copers)
• DHT differences are more significant than testosterone differences
• Black men show higher average DHT and DHT:T ratios (over for blacks trying to keep their locs or dreads forever)
• East Asian men show lower 5α-reductase activity (lifefuel for your follicles, ropefuel for wallet and dimo)
• Black men also show higher estradiol and SHBG in several datasets

View attachment 5049043​

---

7 ─ PUTTING THE BIG PICTURE TOGETHER, A LITTLE SUMMARY FOR YOU

​

Spoiler: Niggers gtfih

• Higher AR sensitivity
• Higher DHT conversion
• Potentially stronger androgenic signalling
• Greater androgenic side effect burden

​

Spoiler: Crackers gtfih

• Intermediate across most variables
• Reference population for most AAS literature
• Standard pharmacokinetic assumptions generally apply

​

Spoiler: Gooks gtfih

• Lower AR sensitivity
• Lower DHT conversion
• Much slower steroid excretion
• Reduced urinary testosterone output
• Piss tests don't work

​

​

Spoiler: Spics gtfih

• Higher testosterone in some datasets
• Elevated A49T frequency
• Potentially stronger DHT mediated androgenic response
• Sorry the studies a lot of times didn't count you guys as a separate ethnicity for some reason, just assume you're closest to the mayos

---

8 ─ ANTI-DOPING IMPLICATIONS: EXTREMELY HOMOSEXUAL BTW

The standard testosterone/epitestosterone (T/E) ratio test assumes normal UGT2B17 function. This means you piss out normally. ​

​

This assumption fails for East Asian populations.​

Individuals with the del/del genotype can administer exogenous testosterone while producing little urinary testosterone elevation. So lifefuel for Changs that want to claim natty? Not necessarily. ​

This forced WADA to move toward more innovative approaches to doping tests:​

• Athlete Biological Passports
• Longitudinal hormone tracking
• Population adjusted steroid profiling
• YOU GUYS CAN LOOK MORE INTO THIS IF YOU WANT, THIS IS ALL THE RESEARCH I'M WILLING TO DO ON ANTI DOPING CUCKS

View attachment 5049047​

---

9 ─ LIMITATIONS & CAVEATS

​

So here's some "limitations and caveats" to the studies/findings​

Important caveats:​

• Intragroup variation shouldn't be ignored, this is where most of the hyper responder shit comes from, because two people of the same ethnicity can respond differently (ethnicity is the more important factor though)
• Ethnicity isn't deterministic biology all of the time (though most of the time it is)
• Some studies examine endogenous hormones and not necessarily exogenous AAS, but we can assume the same findings apply
• Direct RCTs on ethnic AAS response are limited compared to other fitness/bodybuilding studies, because nowadays researching about ethnic and race differences get you cancelled lul

Population level trends do not predict individual outcomes with 100% certainty. But please nigga, most of you aren't genetic outliers or hyper responders. ​

---

10 ─ CONCLUSION

So second high effort thread finished, first high effort thread about actual LM related topic. ​

Hope it was an interesting read. ​

Just fyi, I used AI only to help with formatting, all other words are mine or taken directly from the studies themselves. TLDR also done by AI, if you can't be bothered to read this thread then I can't be bothered manually making you a summary. ​

Spoiler: Inb4 DNR

Different ethnic groups appear to respond to anabolic steroids differently because of genetic differences in:

• Androgen receptor sensitivity → some populations may get a stronger anabolic signal from the same amount of testosterone.
• DHT conversion → affects things like hair loss, acne, facial/body hair growth, and prostate stimulation.
• Steroid metabolism/excretion → some groups clear testosterone more slowly, meaning steroids stay active longer and may be harder to detect in urine tests.

General trends found in the literature:

• Sub-Saharan African populations tend to have higher androgen receptor sensitivity and higher DHT activity.
• East Asian populations tend to have lower receptor sensitivity, lower DHT conversion, but much slower testosterone excretion due to high UGT2B17 deletion rates.
• Europeans are generally intermediate and are the reference population for most steroid research.
• Hispanic populations may have relatively high androgen activity in some markers.

​

@Revan @framepill @Nectar @nigHT.143 @pleasevanity

---

11 ─ REFERENCES​

Spoiler: References

Jakobsson, J. et al. (2006). Large differences in testosterone excretion in Korean and Swedish men are strongly associated with a UDP-glucuronosyl transferase 2B17 polymorphism. Journal of Clinical Endocrinology and Metabolism. https://pubmed.ncbi.nlm.nih.gov/16332934/

Litman, H.J. et al. (2006). Serum androgen levels in Black, Hispanic, and White men. Journal of Clinical Endocrinology and Metabolism, 91(11), 4326–4334. https://academic.oup.com/jcem/article/91/11/4326/2656429

Giovannucci, E. et al. (1999). Racial differences in the androgen/androgen receptor pathway in prostate cancer. PMC. https://pmc.ncbi.nlm.nih.gov/articles/PMC2608588/

Nakagawa, H. et al. (2010). Potentially harmful advantage to athletes: a putative connection between UGT2B17 gene deletion polymorphism and renal disorders with prolonged use of anabolic androgenic steroids. PMC. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877023/

PMC. (2016). Impact of UGT2B17 gene deletion on the steroid profile of an athlete. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760435/

PMC. (2013). UGT2B17 Genotype and the Pharmacokinetic Serum Profile of Testosterone during Substitution Therapy with Testosterone Undecanoate. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3725801/

PMC. (2024). Associations of CAG repeat polymorphism in the androgen receptor gene with steroid hormone levels and anthropometrics among men: the role of the ethnic factor. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10926003/

ResearchGate. (2025). Ethnic Variation in Allele Distribution of the Androgen Receptor (AR) (CAG)n Repeat / AAS Adverse Effects Review. https://www.researchgate.net/publication/51150922

Grönberg, H. et al. (2007). Serum estrogen, but not testosterone, levels differ between Black and White men in a nationally representative sample of Americans. Journal of Clinical Endocrinology and Metabolism, 92(7), 2519. https://academic.oup.com/jcem/article/92/7/2519/2598282

Wu, A.H. et al. (1995). 5 Alpha Reductase Metabolites & Genotype in Healthy Men (NIH Grant R01-CA068593). https://grantome.com/grant/NIH/R01-CA068593-01

ScienceDirect Topics. SRD5A2. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/srd5a2

Ellis, L. & Nyborg, H. (1992). Racial/ethnic variations in male testosterone levels: a probable contributor to group differences in health. Steroids, 57(2), 72–75. PubMed ID: 1621259

Lamont, B.T. et al. (2009). The age-testosterone relationship in Black, White, and Mexican-American men, and reasons for ethnic differences. Aging Male, 12(2–3). https://www.tandfonline.com/doi/full/10.1080/13685530903071802

NCBI StatPearls. (2026). Anabolic Steroid Use Disorder. https://www.ncbi.nlm.nih.gov/books/NBK538174/

PMC. (2025). Impact of Anabolic-Androgenic Steroid Abuse on the Cardiovascular System: Molecular Mechanisms and Clinical Implications. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12652398/

PMC. (2024). Essential blood testing in the patient using androgenic anabolic steroids: a clinical practice guideline for primary care. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10962511/

Journal of Clinical Endocrinology and Metabolism. (2007). Clinical Relevance of Racial and Ethnic Differences in Sex Steroids. https://academic.oup.com/jcem/article/92/7/2433/2598039

PMC. (2012). Racial Differences in Androgen Receptor (AR) and AR Splice Variants Expression. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10044992/

​

very nice