| name | nutrigx_advisor |
| description | Nutrigenomics advisor — personalized nutrition guidance based on genetic profiles |
NutriGx Advisor — Personalised Nutrition from Genetic Data
Skill ID: nutrigx-advisor
Version: 0.1.0
Status: MVP
Author: David de Lorenzo (ClawBio Community)
Requires: Python 3.11+, pandas, numpy, matplotlib, seaborn, reportlab (optional)
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)
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
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 | ↓ elongation of EPA→DHA |
| 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 | Non-persistence of lactase |
| 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 |
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:
- Look up rsid in parsed data
- Return genotype string (e.g.
"AT", "TT", "AA")
- Flag as
"NOT_TESTED" if absent (common for chip-to-chip variation)
3. Risk Scoring (score_variants.py)
Each SNP is scored on a 0 / 0.5 / 1.0 scale:
0.0 — homozygous reference (lowest risk)
0.5 — heterozygous
1.0 — homozygous risk allele
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 (repro_bundle.py)
Exports to the output directory (not committed to the repo):
commands.sh — full CLI to reproduce analysis
environment.yml — pinned conda environment
checksums.txt — SHA-256 checksums of input and output files
provenance.json — timestamp and ClawBio version tag
Usage
openclaw "Generate my personalised nutrition report from genome.csv"
openclaw "Run NutriGx analysis on variants.vcf and flag any folate pathway risks"
openclaw "What does my APOE status mean for my saturated fat intake?"
python examples/generate_patient.py --run
File Structure
skills/nutrigx-advisor/
├── SKILL.md ← this file (agent instructions)
├── nutrigx_advisor.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
├── 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
└── 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.
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).
Limitations & Disclaimer
- Not a medical device. This skill provides educational, research-oriented
nutrigenomics analysis. It does not constitute medical advice.
- Common variants only. The panel covers SNPs with MAF > 1% in at least one
major population. Rare pathogenic variants are out of scope.
- Population context. Effect sizes are predominantly derived from European
GWAS cohorts. Risk estimates may not generalise equally across all ancestries.
- 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.
- Simpson's Paradox note. Population-level associations used to derive weights
may not reflect individual trajectories (see Corpas 2025, Nutrigenomics and
the Ecological Fallacy).
Roadmap
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).
- Cornelis MC et al. (2006). Coffee, CYP1A2 genotype, and risk of myocardial infarction. JAMA.
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.