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nutrigx-advisor营养顾问

Agent Skill

nutrigx-advisor 用于查找、检索和筛选相关信息,适合在 OpenClaw 中需要根据关键词、任务场景或来源线索快速定位候选结果时使用。可结合来源仓库、安装命令和原始 README 继续核验具体用法。安装前建议确认权限范围、维护状态,以及是否会触发联网、命令执行或文件读写。

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MIT-0

最后核验

2026-05-01

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复制提示词发给支持本地命令或 Skills 的 AI 助手,先确认命令和权限,再让它执行。

请帮我安装这个 Agent Skill:nutrigx-advisor(营养顾问)
来源仓库:https://github.com/manuelcorpas/nutrigx-advisor
安装命令:
openclaw skills install nutrigx-advisor
安装前请先检查当前环境是否支持对应 CLI,并向我确认将要执行的命令、安装目录、联网范围和文件读写权限;确认后再执行。

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openclaw skills install nutrigx-advisor

简介

根据消费者基因数据分析关键 SNP 生成个性化营养报告,以提供可行的饮食和补充剂指导。

SKILL.md

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

GeneSNPNutrient ImpactEvidence
FTOrs9939609Energy balance, fat mass, carb sensitivityStrong (GWAS)
PPARGrs1801282Fat metabolism, insulin sensitivityModerate
APOA5rs662799Triglyceride response to dietary fatStrong
TCF7L2rs7903146Carbohydrate metabolism, T2D riskStrong
ADRB2rs1042713Fat oxidation, exercise × diet interactionModerate

Micronutrient Metabolism

GeneSNPNutrientEffect of risk allele
MTHFRrs1801133Folate / B12↓ 5-MTHF conversion (~70%)
MTHFRrs1801131Folate / B12↓ enzyme activity (~30%)
MTRrs1805087B12 / homocysteine↑ homocysteine risk
BCMO1rs7501331Beta-carotene → Vitamin A↓ conversion (~50%)
BCMO1rs12934922Beta-carotene → Vitamin A↓ conversion (compound het)
VDRrs2228570Vitamin D absorption↓ VDR function
VDRrs731236Vitamin D↓ bone mineral density response
GCrs4588Vitamin D binding↑ deficiency risk
SLC23A1rs33972313Vitamin C transport↓ renal reabsorption
ALPLrs1256335Vitamin B6↓ alkaline phosphatase activity

Omega-3 / Fatty Acid Metabolism

GeneSNPNutrientEffect
FADS1rs174546LC-PUFA synthesis↑/↓ EPA/DHA from ALA
FADS2rs1535LC-PUFA synthesisModulates omega-6:omega-3 ratio
ELOVL2rs953413DHA synthesis↓ elongation of EPA→DHA
APOErs429358Saturated fat responseε4 → ↑ LDL-C on high SFA diet
APOErs7412Saturated fat responseCombined with rs429358 for ε typing

Caffeine & Alcohol

GeneSNPCompoundEffect
CYP1A2rs762551CaffeineSlow/Fast metaboliser
AHRrs4410790CaffeineModulates CYP1A2 induction
ADH1Brs1229984AlcoholAcetaldehyde accumulation risk
ALDH2rs671AlcoholAsian flush / toxicity risk

Food Sensitivities

GeneSNPSensitivityEffect
MCM6rs4988235Lactose intoleranceNon-persistence of lactase
HLA-DQ2Proxy SNPsCoeliac / glutenHLA-DQA1/DQB1 risk haplotypes

Antioxidant & Detoxification

GeneSNPPathwayEffect
SOD2rs4880Manganese SOD↓ mitochondrial antioxidant
GPX1rs1050450Selenium / GSH-Px↓ glutathione peroxidase
GSTT1DeletionGlutathione-S-transNull genotype → ↑ oxidative risk
NQO1rs1800566Coenzyme Q10↓ CoQ10 regeneration
COMTrs4680Catechol / B vitaminsMet/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:

  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)

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

# 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

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

  1. Not a medical device. This skill provides educational, research-oriented

nutrigenomics analysis. It does not constitute medical advice.

  1. Common variants only. The panel covers SNPs with MAF > 1% in at least one

major population. Rare pathogenic variants are out of scope.

  1. Population context. Effect sizes are predominantly derived from European

GWAS cohorts. Risk estimates may not generalise equally across all ancestries.

  1. 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.

  1. 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

  • [ ] 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)

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.

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