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Table 2 Genotypes and PDT results of the independent analysis of 235 obesity families and combined analyses of a total of 603 obesity families

From: Mutation screen and association studies for the fatty acid amide hydrolase (FAAH) gene and early onset and adult obesity

SNP1

N3

Genotypes (frequency %)4

Allele frequ. %5

Transm. rate6

PDT p-value for 235 independent families

PDT p-value and GRR with 95%-CI on 603 families7

rs324420

494

CC 320 (0.648)

C: 0.802

0.47 (A)

0.14

0.02

(1.23, 1.03-1.48)

  

CA 152 (0.308)

    
  

AA 22 (0.044)

A: 0.198

   

rs324419

491

GG 350 (0.713)

G: 0.838

0.51 (A)

0.75

0.18

(0.94, 0.77-1.15)

  

GA 123 (0.251)

    
  

AA 18 (0.036)

A: 0.162

   

rs873978

494

GG 485 (0.982)

G: 0.991

0.49 (A)

0.56

0.08

(2.50, 0.97-6.44)

  

GA 9 (0.018)

    
  

AA 0 (0.000)

A: 0.001

   

rs2295632

496

GG 266 (0.536)

G: 0.732

0.483 (T)

0.32

0.03

(1.15, 0.98-1.35)

  

GT 194 (0.391)

    
  

TT 36 (0.073)

T: 0.268

   
  1. 1 all SNPs were tested for Hardy-Weinberg equilibrium (p > 0.05); 2 numbers are given according to Dunnen and Antonarakis 2001 Hum Genet 109:121-124 [33]; 3 number of obese children or adolescents of the 235 obesity families; 4 genotype frequencies in the index patients of the 235 obesity families; 5 allele frequencies in the obese children or adolescents of the 235 obesity families. These are very similar to the allele frequencies reported for the European population in the dbSNP database http://www.ncbi.nlm.nih.gov/SNP/; 6 transmission rate of minor allele in 235 obesity families; 7 p-value of the combined analyses of the 603 obesity families.