The genetically ideal person according to ChatGPT-5

 

Optimal Genetic Profile – Simulated Genome Data

Overview

This report presents a simulated genome file (23andMe-style raw data) representing a hypothetical “optimal” genetic profile as of 2025. We curated variants across multiple categories – disease prevention, health-related traits, pharmacogenomics, infectious disease resistance, lifestyle traits, pigmentation, and physical performance – selecting alleles associated with beneficial or protective effects. The following sections provide the raw genotype data and a summary of key variants with their expected phenotypic effects.

Synthetic Genome Raw Data

Below is the simulated raw genotype data. Each line lists a SNP rsID, chromosome, position, and genotype (using the plus-strand notation). This profile includes protective alleles for single-gene diseases, cardiometabolic health, drug metabolism, infection resistance, lifestyle traits, pigmentation, and fitness-related traits:

rs67608943    1    55512222    C G
rs4988235     2    136608646   A A
rs333         3    46414947    DD
rs113993960   7    117199646   II
rs328         8    19819724    G G
rs4986893     10   96540410    G G
rs4244285     10   96541616    G G
rs1799853     10   96702047    C C
rs1057910     10   96741053    A A
rs334         11   5248232     A A
rs1815739     11   66328095    C C
rs671         12   112241766   G G
rs12913832    15   28365618    G G
rs1426654     15   48426484    A A
rs121907954   15   72642859    G G
rs9923231     16   31107689    C C
rs1805007     16   89986117    C C
rs386833395   17   41276047    II
rs429358      19   45411941    T T
rs7412        19   45412079    C C
rs601338      19   49206674    A A
rs3892097     22   42524947    G G

(Key: “I” = insertion allele, “D” = deletion allele in indel genotypes. For example, rs333 3 … DD denotes homozygous CCR5-Δ32 deletion, and rs113993960 7 … II denotes no ΔF508 deletion in CFTR.)

Curated Variant Summary and Effects

 

Category	Variant (Gene)	Genotype	Effect / Rationale
Single-Gene Disease Prevention	CFTR ΔF508 (CFTR) rs113993960	CTT/CTT (no ΔF508)	Lacks the common ΔF508 mutation for cystic fibrosis, avoiding CF. (ΔF508 accounts for ~70% of CF cases .)
Sickle Cell (HBB) rs334	A/A (Glu/Glu)	No sickle-cell allele present (normal hemoglobin); prevents sickle-cell anemia while sacrificing malaria protection .
Tay-Sachs (HEXA) rs121907954	G/G (wild-type)	No pathogenic HEXA variant (e.g. Gly269Ser) common in Tay-Sachs carriers – reduces Tay-Sachs disease risk (especially in at-risk populations).
BRCA1 185delAG (BRCA1) rs386833395	I/I (no deletion)	Does not carry the BRCA1 185delAG frameshift mutation (a high-risk founder variant for breast/ovarian cancer ); thus, significantly lower hereditary cancer risk.
Cardiometabolic Health	PCSK9 Y142X (PCSK9) rs67608943	C/G (heterozygous)	One loss-of-function PCSK9 allele conferring ~40% lower LDL cholesterol , which is associated with significantly reduced coronary heart disease risk (mimicking the heart-healthy PCSK9 “null” phenotype).
LPL S447X (LPL) rs328	G/G (Ser447Ter)	Homozygous for LPL S447X gain-of-function variant, linked to lower triglycerides and ~22% reduced coronary artery disease risk . This variant truncates LPL, increasing its activity.
APOE ε3/ε3 (APOE) rs429358/rs7412	T/T & C/C (ε3/ε3)	APOE genotype ε3/ε3 – the “neutral” ApoE status . Avoids the APOE4 allele (Alzheimer’s and cardiovascular risk) and APOE2 issues. Promotes average lipid metabolism and brain health.
Pharmacogenomic Compatibility	CYP2C9*1 (CYP2C9) rs1799853/rs1057910	C/C & A/A (no *2 or *3)	Lacks CYP2C9*2 and *3 alleles (R144C and I359L). This CYP2C9 genotype is extensive metabolizer status, avoiding the reduced warfarin and NSAID metabolism associated with *2/*3 variants (which cause poor metabolism ).
CYP2D6*1 (CYP2D6) rs3892097	G/G (wild-type)	No non-functional CYP2D6*4 allele . Ensures normal CYP2D6 activity (avoids poor metabolizer status for many antidepressants, beta-blockers, codeine, etc.).
CYP2C19*1 (CYP2C19) rs4244285/rs4986893	G/G & G/G (no *2 or *3)	Lacks CYP2C19*2 and *3 alleles, which means normal CYP2C19 enzyme activity. Avoids the *2 allele that causes clopidogrel poor response and *3 (stop codon) common in Asians. Results in an extensive metabolizer phenotype for drugs like clopidogrel, PPIs, SSRIs.
VKORC1 –1639G>A (VKORC1) rs9923231	C/C (GG)	Lacks the VKORC1 -1639A variant associated with warfarin sensitivity . This genotype (C/C) leads to normal VKORC1 expression, avoiding excessively low warfarin dose requirements and bleeding risk .
Infectious Disease Resistance	CCR5-Δ32 (CCR5) rs333	Δ32/Δ32 (homozygous)	Homozygous for the CCR5-Δ32 deletion, which confers near-complete resistance to HIV infection (albeit with trade-offs like increased West Nile virus susceptibility). Both CCR5 alleles are the 32-bp deletion (no functional CCR5 co-receptor for HIV).
FUT2 Secretor (FUT2) rs601338	A/A (non-secretor)	Homozygous for the FUT2 nonsense allele (W143X). Non-secretor status provides resistance to certain viral infections like norovirus and rotavirus , though it slightly increases risks of some autoimmunity and alters microbiome composition. (Recessive trait – A/A means no ABO antigens in body fluids.)
Lifestyle-Convenience Traits	Lactase Persistence (MCM6) rs4988235	A/A (T/T)	Homozygous for the lactase persistence allele (−13910*T in the MCM6 enhancer). Enables lifelong lactase enzyme production – i.e. the ability to digest lactose in adulthood (common in European populations). Avoids adult lactose intolerance.
Alcohol Flush (ALDH2) rs671	G/G (no ALDH2*2)	Encodes the normal ALDH2 enzyme (no Asian flush variant). Lacks the ALDH22 (Lys504) allele that causes acetaldehyde build-up. This genotype (Glu504/Glu504) allows efficient alcohol metabolism , avoiding the facial flushing and high cancer risk associated with ALDH22 carriers .
Caffeine Metabolism (CYP1A2) rs762551	A/A	Genotype associated with fast caffeine metabolism. Homozygous CYP1A2 1F allele (−163A) leads to higher inducible enzyme activity . As a result, caffeine is metabolized quickly – conferring tolerance to caffeine and a lower risk of hypertension in coffee drinkers.
Pigmentation Traits	Eye Color (HERC2/OCA2) rs12913832	G/G (blue eyes)	Genotype linked to blue eyes. G/G at HERC2 intron rs12913832 greatly reduces OCA2 expression, resulting in blue eye color ~99% of the time . (Avoids the A allele associated with brown eyes.)
Skin Pigmentation (SLC24A5) rs1426654	A/A (Thr111)	Homozygous for the derived SLC24A5 allele (A111T). The A allele correlates with lighter skin pigmentation and is near-fixation in West Eurasian populations. This contributes to fair skin, which may aid vitamin D synthesis in low UV environments (while increasing sun sensitivity).
Hair Color (MC1R) rs1805007	C/C (Arg151)	No MC1R red-hair variant. C/C genotype (Arg151) is the wild-type, producing fully functional MC1R receptors . This avoids the loss-of-function MC1R alleles (like 151Cys) that cause red hair, increased UV sensitivity, and higher melanoma risk . The profile thus likely yields brown/black hair with better UV protection.
Physical Performance	Muscle Power (ACTN3) rs1815739	C/C (R577)	ACTN3 “power” genotype. C/C (Arg577Arg) means functional α-actinin-3 in fast-twitch muscle fibers (often called the RR genotype) . Associated with sprint/power performance and greater muscle strength; avoids the XX genotype that impairs muscle power (but aids endurance) .
Endurance (ACE) I allele rs1799752	I/I (Insertion)	ACE gene Insertion/Insertion genotype. Associated with lower ACE levels and improved endurance performance (the ACE II genotype is overrepresented in elite endurance athletes) . Also linked to certain cardioprotective effects (e.g. smaller left ventricular hypertrophy compared to D allele) .

 

Notes: This optimal-profile individual lacks known high-risk variants for dominant disorders and is not a carrier of common recessive disease alleles. They have lipid-lowering mutations (PCSK9, LPL) that protect against heart disease, and a neutral APOE status (ε3/ε3). Pharmacogenetically, they are “extensive metabolizers” for CYP2C9, CYP2C19, CYP2D6 and respond normally to warfarin (VKORC1), reducing risk of adverse drug reactions . Homozygous CCR5-Δ32 grants resistance to HIV , while FUT2 non-secretor status blocks certain GI infections . Lifestyle-friendly traits include lactase persistence for milk digestion , normal ALDH2 for alcohol tolerance , and fast caffeine metabolism . Pigmentation alleles yield fair skin, blue eyes, and dark hair, an aesthetic combination made possible by selecting specific loci (blue-eye HERC2 allele with dominant dark hair via functional MC1R). Lastly, fitness-related polymorphisms favor power athletics (ACTN3 R allele) while retaining ACE II for endurance – potentially capturing benefits of both strength and endurance.

This synthetic profile illustrates how documented “protective” alleles could coexist in one genome. In reality, such a combination is extremely rare, and some trade-offs (like higher UV sensitivity from fair skin or potential slightly elevated inflammatory responses in non-secretors) are noted. Nonetheless, this hypothetical genome serves as an educational model of how genetics can influence health and traits in beneficial ways under certain environments and contexts.

Sources: Key variant effects are drawn from current genetic research and databases (see citations). This profile is for illustration and does not guarantee any particular outcome – real-world phenotype depends on gene–gene and gene–environment interactions. All selected alleles are based on high-frequency or well-studied variants in individuals of primarily European ancestry, reflecting the bias of available research data as of 2025.

 

 Link to full work