I’m looking for some “genetic detective” help. I’m currently cruising on 150-250mg Testosterone per week and I’ve been using 1mg - 1.25mg Finasteride daily as a preventative measure.
I’m considering adding a DHT-derivative (specifically Primobolan or potentially Masteron), but I’m terrified of hair loss. Since Finasteride doesn’t protect against DHT-derivatives, I pulled my raw DNA data from MyHeritage to see if I have the “protective” genes or the “hair reaper” genes.
I’ve identified a few markers, but I’d love a second opinion on my overall risk profile for Male Pattern Baldness (MPB) and how “safe” I am to run Primo.
My DNA Markers (RSIDs):
rs615204 (Chr 1): TT
rs61527094 (Chr 3): GG
rs61528371 (Chr 3): AA
rs61529892 (Chr 4): TT
rs61524171 (Chr 6): CC
rs61522264 (Chr 6): CC
rs61527129 (Chr 8): CC
rs61520309 (Chr 11): CC
rs615290 (Chr 11): CC
rs61528732 (Chr 11): CT
rs61529638 (Chr 11): TT
rs61521510 (Chr 17): GG
rs61521756 (Chr 22): CC
rs615213 (Chr X): AA
rs61525850 (Chr X): CC
rs73622812 (Chr 20): AA
rs2180439 (Chr 20): CC
rs1160312 (Chr 20): AG
rs1041668 (Chr X): AA
rs5919325 (Chr X): GG
Specific questions for the experts here:
Overall MPB Risk: Based on my Chromosome 20 (rs1160312 AG / rs2180439 CC) and my X-chromosome (rs5919325 GG), how prone am I to natural MPB?
Finasteride Necessity: Given my genetics, is the Finasteride actually doing heavy lifting on my current Test dose, or am I genetically “safe” anyway?
The Primo Test: With my specific AR-gene (rs5919325 GG), can I likely get away with adding Primobolan without nuking my hairline?
I currently have a full head of hair and no noticeable recession, but I want to be smart before adding compounds that bypass the 5-alpha reductase enzyme.
I was curious about this, so I put it into Perplexity’s deep research:
Overall MPB risk from your SNPs
Let’s focus on the loci we actually understand reasonably well from GWAS:
Chromosome 20p11 – rs1160312 (AG) and rs2180439 (CC)
rs1160312: the A allele is a risk allele; each A increases odds of MPB about 1.6–1.7× in European cohorts. With AG you carry one risk copy, so you’re above baseline.
rs2180439: the T allele is the risk allele; men with one or two T alleles have ~1.8–2.2× higher odds per T compared with CC. You are CC here, which is the “protective” genotype at this particular SNP.
Both SNPs tag the same 20p11 risk locus and show strong independent association with MPB, but rs2180439’s effect is stronger; having CC reduces risk at that marker, but rs1160312[A] still contributes risk via that locus.
X‑chromosome – AR region, rs5919325 (GG)
Classic work showed that men who carry risk alleles at both the AR locus on X and the 20p11 locus have ~7‑fold increased odds of MPB versus men without those risk alleles.
However, rs5919325 specifically is not one of the canonical AR risk tag SNPs (those are things like rs6152 or tightly linked variants). There is no strong published evidence that rs5919325(GG) is either strongly protective or strongly risky; it’s essentially “uninformative” with current data.
Other listed SNPs (rs6152xx, rs61529x, etc.)
Most of those “rs6152xx / rs6152xx‑like” IDs you listed are not the classic AR rs6152 SNP; they are in different regions, and I cannot find robust MPB‑specific association data for them.
The broader GWAS literature now lists >70–350 loci affecting MPB risk, each adding small effects; any panel of 15–20 SNPs will only explain a fraction of your true genetic liability.
Net read on natural MPB risk:
You have:
One risk A allele at rs1160312 → increased risk.
Protective CC at rs2180439 → lower risk at that specific marker.
AR‑tag SNP rs5919325 with no clear, well‑quantified effect.
Taking that together with the fact that about 50% of men show some MPB by age 50 and that the known variants explain only ~30–40% of genetic risk, your profile points to non‑trivial, probably moderate‑to‑above‑average risk, not clear “low risk,” and certainly not “immune.”
A very practical indicator is your phenotype so far: at your age, full hair and no recession is a favorable sign, but with your genotype you are still not “safe for life” if you crank up androgen exposure.
2. Is finasteride “doing work” on 150–250 mg test?
Mechanistically:
Testosterone is converted to DHT by 5α‑reductase, especially type II in scalp and prostate.
DHT is more potent at the androgen receptor in hair follicles than testosterone and is the main driver of miniaturization in genetically susceptible scalps.
Finasteride inhibits type II 5α‑reductase and can significantly lower scalp DHT; clinical data at 5 mg/day for BPH show strong drops in scalp DHT, and 1 mg/day is the standard MPB dose.
On 150–250 mg/week of testosterone:
You are running supraphysiologic testosterone, meaning more substrate for DHT; without finasteride, scalp DHT would likely be substantially above natural levels in a susceptible person.
Finasteride does not block testosterone’s own AR binding, but it lowers the amplification step (T → DHT) in the scalp, which is usually where MPB acceleration shows up on cycle.
Genetically:
Your SNPs do not indicate any clear “DHT resistance” in hair follicles; you carry at least one risk allele at a strong MPB locus (rs1160312 A), and your AR tag SNP isn’t clearly protective.
Population studies show that DHT‑lowering with finasteride improves or stabilizes hair in a large fraction of men who already show MPB, which implies that if you ever develop MPB, DHT is very likely to be part of the causal chain for you as well.
So in your context, it is very likely that finasteride is meaningfully reducing your hair risk from the elevated testosterone, not just a redundant add‑on. It does not make you invincible, but given your risk allele and the high androgen environment, it is probably doing “real work.”
3. Adding Primobolan (DHT‑derived) with your genetics
Key points about Primo/Mast and hair:
DHT‑derived AAS (Primo, Masteron, Winstrol, etc.) are already 5α‑reduced or have modifications that mean they do not require 5α‑reductase to reach full androgenic activity.
Because of that, finasteride does not meaningfully reduce their local androgenic impact in the scalp; you’re bypassing the step finasteride blocks.
Hair loss from DHT‑derivatives is essentially “genetic susceptibility × total androgen load at the follicle.” If follicles are sensitive, a DHT‑like compound binding AR in the dermal papilla can still trigger miniaturization even with perfect DHT suppression from finasteride.
Where your genotype fits:
You have at least one strong MPB risk allele at 20p11 (rs1160312 A), which is associated with earlier/more frequent balding independent of the AR locus.
The AR tag you provided (rs5919325 GG) does not carry a known major protective effect; it also doesn’t mark the classic high‑risk AR haplotype, so we cannot cleanly say “you are low AR‑risk” or “high AR‑risk.” The best we can say is uncertain for AR and known elevated risk at 20p11.
Large GWAS show that dozens of additional loci influence risk; a panel limited to a few SNPs simply cannot tell us whether your follicles are, in practice, “forgiving” to DHT‑class drugs.
Given all that, the real‑world expectation for you with Primo is:
Risk is absolutely non‑zero. You do not have a clearly protective profile; you have at least one established risk variant, and you are already in a high‑androgen environment.
Finasteride will not protect you from Primo/Mast; its benefit is mainly against DHT produced from your testosterone dose.
On the other hand, your current lack of recession suggests your phenotype “tolerates” androgens reasonably well up to now; some men with similar genotypes tolerate modest Primo doses with only slowed shedding or no visible change, but others see rapid thinning. This is not predictable from rs1160312/rs5919325 alone.
If you decide to test Primo despite the above, the genetically cautious approach would be:
Start at the lowest effective dose and shortest duration rather than jumping to a high “blast” dose.
Track:
Shedding (comb/ shower count) week by week.
Macro photos of hairline and vertex under consistent lighting.
Be prepared to abort early if shedding spikes or visible miniaturization appears; once follicles miniaturize deeply, reversal is much harder, even if you increase finasteride or add dutasteride.
From a geneticist’s risk perspective, you are not someone I would call “safe to ignore hair risk” with DHT derivatives. You’re in a caution / watch‑closely zone, not a “go wild” zone.
4. Direct answers to your three questions
Overall MPB risk (rs1160312 AG / rs2180439 CC / rs5919325 GG)
rs1160312 AG = one risk allele → higher odds of MPB than GG.
rs2180439 CC = non‑risk genotype → this is favorable at that locus.
rs5919325 GG is not a validated major risk or protective marker.
Overall: moderate‑to‑elevated genetic risk compared to population baseline, not clearly low, but not the worst possible either.
Finasteride necessity on 150–250 mg test
On supraphysiologic testosterone, finasteride is almost certainly lowering scalp DHT substantially and therefore reducing your hair risk, because your genetics do not suggest special resistance to MPB.
You are not genetically “safe enough” that I’d say finasteride is pointless; if you care about hair, it is likely doing meaningful “heavy lifting” in your current setup.
The Primo test with rs5919325 GG
That AR SNP doesn’t confer any clearly documented high protection, and you already carry a risk allele at a major MPB locus.
Primo (and Masteron) bypass 5α‑reductase, so finasteride won’t shield you from their hair‑related androgenic effect.
Based on genetics plus pharmacology, you should assume real hair‑loss risk if you run Primo, especially at higher doses or for long periods; you might “get away with it,” but there is no genetic signal here strong enough to call that likely or safe.