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Stands on its own.
Nothing else here links to this position yet — but the page above is the point: what the
research found, what each genotype means, and where it came from, in language you can
read. Links to conditions, drugs and the senses appear automatically if we write them.
Strength of the evidence
1 / 4
Its strongest genetic-study result is p = 10−8, with 1 associations in the GWAS Catalog.
How this is scored
4: ClinVar disease-causing, reviewed by an expert panel or a guideline (3–4 stars). 3: ClinVar, several labs agreeing (2 stars), or a genetic study at p ≤ 10−50. 2: ClinVar from one lab (1 star), or p ≤ 10−20. 1: ClinVar submitted without criteria (0 stars), or genome-wide significance (p ≤ 5×10−8). The higher of the two counts. It says how solid the evidence is, not whether it matters for a particular person.
What the study found
Who was studied 630,117 European ancestry individuals.
The effect
Each copy of the A allele shifted the measure 0.0319 lower (95% confidence interval 0.021-0.043); p = 8 × 10−9.
How common The A allele had a frequency of about 5% in the people studied.
Where it sits Chromosome 6, band 6p22.3 — in an intron of CDKAL1.
What each result means
A/ATwo copies of the version the research linked to Serum urate levels. That is the strongest link of the three results. A link in a study is not a diagnosis.
A/GOne copy of the version the research linked to Serum urate levels. That is a smaller link than two copies.
G/GNo copy of the version the research linked to Serum urate levels. This is the starting point the study compared everyone against.
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