---

name: nutrigx description: Personalised nutrition report from consumer genetic data (23andMe, AncestryDNA, VCF) — interrogates nutritionally-relevant SNPs and generates actionable dietary guidance, all computed locally. license: MIT metadata: version: 0.2.0 author: David de Lorenzo tags:

• nutrigenomics
• nutrition
• diet
• genetics
• 23andme
• ancestrydna
• vcf openclaw: requires: bins:
  • python3 always: false emoji: 🥦 homepage: https://github.com/ClawBio/ClawBio os:
  • darwin
  • linux install:
  • kind: pip package: pandas numpy matplotlib seaborn
  • kind: pip package: reportlab trigger_keywords:
  • personalised nutrition
  • nutrigenomics
  • diet genetics
  • MTHFR
  • APOE
  • FTO
  • vitamin D
  • caffeine metabolism
  • lactose
  • omega-3
  • folate
  • what should I eat based on my DNA
  • vitamin absorption genetics
  • gluten

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NutriGx Advisor — Personalised Nutrition from Genetic Data

Author: David de Lorenzo (ClawBio Community) Requires: Python 3.11+, pandas, numpy, matplotlib, seaborn, reportlab (optional)

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What This Skill Does

The NutriGx Advisor generates a personalised nutrition report from consumer genetic data (23andMe, AncestryDNA raw files or VCF). It interrogates a curated set of nutritionally-relevant SNPs drawn from GWAS Catalog, ClinVar, and peer-reviewed nutrigenomics literature, then translates genotype calls into actionable dietary and supplementation guidance — all computed locally.

Key outputs

• Markdown nutrition report with risk scores and recommendations
• Radar chart of nutrient risk profile
• Gene × nutrient heatmap
• Reproducibility bundle (commands.sh, environment.yml, SHA-256 checksums)

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Trigger Phrases

The Bio Orchestrator should route to this skill when the user says anything like:

• "personalised nutrition", "nutrigenomics", "diet genetics"
• "what should I eat based on my DNA"
• "nutrient metabolism", "vitamin absorption genetics"
• "MTHFR", "APOE", "FTO", "BCMO1", "VDR", "FADS1/2"
• "folate", "omega-3", "vitamin D", "caffeine metabolism", "lactose", "gluten"
• Input files: .txt or .csv (23andMe), .csv (AncestryDNA), .vcf

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Curated SNP Panel

Macronutrient Metabolism

Gene	SNP	Nutrient Impact	Evidence
FTO	rs9939609	Energy balance, fat mass, carb sensitivity	Strong (GWAS)
PPARG	rs1801282	Fat metabolism, insulin sensitivity	Moderate
APOA5	rs662799	Triglyceride response to dietary fat	Strong
TCF7L2	rs7903146	Carbohydrate metabolism, T2D risk	Strong
ADRB2	rs1042713	Fat oxidation, exercise × diet interaction	Moderate

Micronutrient Metabolism

Gene	SNP	Nutrient	Effect of risk allele
MTHFR	rs1801133	Folate / B12	↓ 5-MTHF conversion (~70%)
MTHFR	rs1801131	Folate / B12	↓ enzyme activity (~30%)
MTR	rs1805087	B12 / homocysteine	↑ homocysteine risk
BCMO1	rs7501331	Beta-carotene → Vitamin A	↓ conversion (~50%)
BCMO1	rs12934922	Beta-carotene → Vitamin A	↓ conversion (compound het)
VDR	rs2228570	Vitamin D absorption	↓ VDR function
VDR	rs731236	Vitamin D	↓ bone mineral density response
GC	rs4588	Vitamin D binding	↑ deficiency risk
SLC23A1	rs33972313	Vitamin C transport	↓ renal reabsorption
ALPL	rs1256335	Vitamin B6	↓ alkaline phosphatase activity

Omega-3 / Fatty Acid Metabolism

Gene	SNP	Nutrient	Effect
FADS1	rs174546	LC-PUFA synthesis	↑/↓ EPA/DHA from ALA
FADS2	rs1535	LC-PUFA synthesis	Modulates omega-6:omega-3 ratio
ELOVL2	rs953413	DHA synthesis	A allele: lower EPA→DHA conversion (association, not a requirement)
APOE	rs429358	Saturated fat response	ε4 → ↑ LDL-C on high SFA diet
APOE	rs7412	Saturated fat response	Combined with rs429358 for ε typing

Caffeine & Alcohol

Gene	SNP	Compound	Effect
CYP1A2	rs762551	Caffeine	Slow/Fast metaboliser
AHR	rs4410790	Caffeine	Modulates CYP1A2 induction
ADH1B	rs1229984	Alcohol	Acetaldehyde accumulation risk
ALDH2	rs671	Alcohol	Asian flush / toxicity risk

Food Sensitivities

Gene	SNP	Sensitivity	Effect
MCM6	rs4988235	Lactose intolerance	Risk allele G (GRCh38 plus / -13910C) is non-persistence; persistence allele A (-13910T) is dominant
HLA-DQ2	Proxy SNPs	Coeliac / gluten	HLA-DQA1/DQB1 risk haplotypes

Antioxidant & Detoxification

Gene	SNP	Pathway	Effect
SOD2	rs4880	Manganese SOD	↓ mitochondrial antioxidant
GPX1	rs1050450	Selenium / GSH-Px	↓ glutathione peroxidase
GSTT1	Deletion	Glutathione-S-trans	Null genotype → ↑ oxidative risk
NQO1	rs1800566	Coenzyme Q10	↓ CoQ10 regeneration
COMT	rs4680	Catechol / B vitamins	Met/Val → methylation load

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Algorithm

1. Input Parsing (parse_input.py)

Accepts:

• 23andMe .txt or .csv (tab-separated: rsid, chromosome, position, genotype)
• AncestryDNA .csv
• Standard VCF (extracts GT field)

Auto-detects format from header lines. Normalises alleles to forward strand using a hard-coded reference table (avoids requiring external databases).

2. Genotype Extraction (extract_genotypes.py)

For each SNP in the panel:

1. Look up rsid in parsed data
2. Return genotype string (e.g. "AT", "TT", "AA")
3. Flag as "NOT_TESTED" if absent (common for chip-to-chip variation)

Palindromic SNPs. Three panel SNPs are palindromic, so strand cannot be told from the genotype: rs9939609 (FTO, T/A), rs12934922 (BCMO1, A/T) and rs1801282 (PPARG, C/G). Their calls are read as reported on the plus strand, which is how 23andMe and AncestryDNA export them. A file on the minus strand would score these three the wrong way round without warning.

3. Risk Scoring (score_variants.py)

Each SNP is scored on a 0 / 0.5 / 1.0 scale by default:

• 0.0 — homozygous reference (lowest risk)
• 0.5 — heterozygous
• 1.0 — homozygous risk allele

Lactose (rs4988235) uses inheritance: dominant_protective. One copy of the persistence allele is enough, so AA and AG score as persistent (0.0) and only GG scores as non-persistence (1.0).

Composite Nutrient Risk Scores (0–10) are computed per nutrient domain by summing weighted SNP scores. Weights are derived from reported effect sizes (beta coefficients or OR) in the primary literature.

Risk categories:

• 0–3: Low risk — standard dietary advice applies
• 3–6: Moderate risk — dietary optimisation recommended
• 6–10: Elevated risk — consider testing and targeted supplementation

Important caveat: These are polygenic risk indicators based on common variants. They are not diagnostic. Rare pathogenic variants (e.g. MTHFR compound heterozygosity with high homocysteine) require clinical confirmation.

4. Report Generation (generate_report.py)

Outputs a structured Markdown report with:

• Executive summary (top 3 personalised findings)
• Per-nutrient sections: genotype table → interpretation → recommendation
• Radar chart (matplotlib) of nutrient risk scores
• Gene × nutrient heatmap (seaborn)
• Supplement interactions table
• Disclaimer section
• Reproducibility block

5. Reproducibility Bundle (nutrigx_repro_bundle.py)

Delegates to the shared clawbio.common.reproducibility layer and exports to <output_dir>/reproducibility/ (not committed to the repo):

• commands.sh — full CLI to reproduce analysis
• environment.yml — pinned conda environment
• checksums.sha256 — SHA-256 checksums of output files, labelled relative to the output directory (verify with cd <output_dir> && sha256sum -c reproducibility/checksums.sha256); files that fail to generate abort the bundle rather than being silently omitted
• provenance.json — timestamp, ClawBio version tag, and SHA-256 checksums of the input file and SNP panel

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Usage

# From 23andMe raw data
openclaw "Generate my personalised nutrition report from genome.csv"

# From VCF
openclaw "Run NutriGx analysis on variants.vcf and flag any folate pathway risks"

# Targeted query
openclaw "What does my APOE status mean for my saturated fat intake?"

# Generate a random demo patient and run the report
python examples/generate_patient.py --run

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File Structure

skills/nutrigx/
├── SKILL.md                      ← this file (agent instructions)
├── nutrigx.py                    ← main entry point
├── parse_input.py                ← multi-format parser
├── extract_genotypes.py          ← SNP lookup engine
├── score_variants.py             ← risk scoring algorithm
├── generate_report.py            ← Markdown + figures
├── nutrigx_repro_bundle.py       ← reproducibility export
├── .gitignore
├── data/
│   └── snp_panel.json            ← curated SNP definitions
├── tests/
│   ├── synthetic_patient.csv     ← fixed 23andMe-format test data (for pytest)
│   ├── test_nutrigx.py           ← pytest suite
│   └── test_repro_bundle.py      ← reproducibility bundle tests
└── examples/
    ├── generate_patient.py       ← random patient generator (demo use)
    ├── data/                     ← generated patient files land here (gitignored)
    └── output/
        ├── nutrigx_report.md     ← pre-rendered demo report
        ├── nutrigx_radar.png     ← demo radar chart (nutrient risk profile)
        └── nutrigx_heatmap.png   ← demo gene × nutrient heatmap

Note: Runtime output directories and randomly generated patient files are excluded from version control via .gitignore. Only the pre-rendered demo report in examples/output/ is committed.

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Privacy

All computation runs locally. No genetic data is transmitted. Input files are read-only; no raw genotype data appears in any output file (reports contain only gene names, SNP IDs, and risk categories).

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Limitations & Disclaimer

Symbolic links in the output path are refused. Report, figure and reproducibility files will not be written through a symlink, including a deliberately symlinked output directory; point --output at a real directory. On platforms without O_NOFOLLOW and dir_fd support (such as Windows) the same refusal is made with a less race-proof check.

1. Not a medical device. This skill provides educational, research-oriented nutrigenomics analysis. It does not constitute medical advice.
2. Common variants only. The panel covers SNPs with MAF > 1% in at least one major population. Rare pathogenic variants are out of scope.
3. Population context. Effect sizes are predominantly derived from European GWAS cohorts. Risk estimates may not generalise equally across all ancestries.
4. Gene–environment interaction. Genetic risk scores interact with baseline diet, lifestyle, microbiome, and epigenetic state. A "high risk" score does not mean a nutrient deficiency is present — it means the individual may benefit from monitoring.
5. Simpson's Paradox note. Population-level associations used to derive weights may not reflect individual trajectories (see Corpas 2025, Nutrigenomics and the Ecological Fallacy).

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Roadmap

• v0.2: Microbiome × genotype interaction module (16S rRNA input)
• v0.3: Longitudinal tracking — compare reports across time
• v0.4: HLA typing for immune-mediated food reactions (coeliac, gluten sensitivity)
• v0.5: Integration with NeoTree neonatal data for maternal nutrition risk scoring
• v1.0: Multi-omics integration (metabolomics + genomics + dietary recall)

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References

Key literature underpinning the SNP panel and scoring algorithm:

• Corbin JM & Ruczinski I (2023). Nutrigenomics: current state and future directions. Annu Rev Nutr.
• Fenech M et al. (2011). Nutrigenetics and nutrigenomics: viewpoints on the current status. J Nutrigenet Nutrigenomics.
• Stover PJ (2006). Influence of human genetic variation on nutritional requirements. Am J Clin Nutr.
• Phillips CM (2013). Nutrigenetics and metabolic disease: current status and implications for personalised nutrition. Nutrients.
• Minihane AM et al. (2015). APOE genotype, cardiovascular risk and responsiveness to dietary fat manipulation. Proc Nutr Soc.
• Frayling TM et al. (2007). A common variant in the FTO gene is associated with body mass index. Science.
• Pare G et al. (2010). MTHFR variants and cardiovascular risk. Hum Genet.
• Lecerf JM & de Lorgeril M (2011). Dietary cholesterol: from physiology to cardiovascular risk. Br J Nutr.
• Tanaka T et al. (2009). Genome-wide association study of plasma polyunsaturated fatty acids in the InCHIANTI Study. PLoS Genet (FADS1/2; ELOVL2 rs953413, minor A allele with lower DHA). PMID 19148276.
• rs953413 regulates polyunsaturated fatty acid metabolism by modulating ELOVL2 expression (2020). iScience (G allele gives higher ELOVL2 enhancer activity than A). PMID 31928966.
• Cornelis MC et al. (2006). Coffee, CYP1A2 genotype, and risk of myocardial infarction. JAMA.
• Enattah NS et al. (2002). Identification of a variant associated with adult-type hypolactasia. Nat Genet 30:233–237. PMID 11788828.

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Contributing

The SNP panel (data/snp_panel.json) is maintained by the skill author. To suggest additions or corrections, contact David de Lorenzo directly via GitHub (@drdaviddelorenzo) or open an issue tagging him in the main ClawBio repository.