TY - JOUR
T1 - Segregation Analysis of Body Mass Index in an Unselected French‐Canadian Sample
T2 - The Québec Family Study
AU - Rice, Treva
AU - Borecki, Ingrid B.
AU - Bouchard, Claude
AU - Ruo, RD C.
PY - 1993/7
Y1 - 1993/7
N2 - Interest in a single gene etiology for obesity, as assessed by the body mass index (BMI), has been spurred recently by reports of a putative recessive major gene for extreme values, which accounts for as much as 40% of the variance. The major gene hypothesis was evaluated here in the Québec Family Study, a random sample of 375 French‐Canadian volunteer families. This report represents one component in a more complete investigation of obesity in these families. In contrast to the recent studies, a major gene hypothesis for BMI was not verified here. Although there was a major effect, it did not conform to a Mendelian pattern of transmission. A multifactorial component (i.e., polygenic and/or common environmental factors) accounted for 42% of the phenotypic variance. In addition, evidence of heterogeneity between the generations was found. The heterogeneity was traced to the major non‐Mendelian component (which accounted for 0.01% of the variance in parents and over 40% in offspring) rather than to the multifactorial one. These results would suggest that a simple recessive gene mixed model may not be sufficient to explain the familial distribution of the BMI. Several factors which may have contributed to these results include temporal trends and surrogate effects such as those related to variation in body composition and energy balance components. (OBESITY RESEARCH 1993; 1:288–294) 1993 North American Association for the Study of Obesity (NAASO)
AB - Interest in a single gene etiology for obesity, as assessed by the body mass index (BMI), has been spurred recently by reports of a putative recessive major gene for extreme values, which accounts for as much as 40% of the variance. The major gene hypothesis was evaluated here in the Québec Family Study, a random sample of 375 French‐Canadian volunteer families. This report represents one component in a more complete investigation of obesity in these families. In contrast to the recent studies, a major gene hypothesis for BMI was not verified here. Although there was a major effect, it did not conform to a Mendelian pattern of transmission. A multifactorial component (i.e., polygenic and/or common environmental factors) accounted for 42% of the phenotypic variance. In addition, evidence of heterogeneity between the generations was found. The heterogeneity was traced to the major non‐Mendelian component (which accounted for 0.01% of the variance in parents and over 40% in offspring) rather than to the multifactorial one. These results would suggest that a simple recessive gene mixed model may not be sufficient to explain the familial distribution of the BMI. Several factors which may have contributed to these results include temporal trends and surrogate effects such as those related to variation in body composition and energy balance components. (OBESITY RESEARCH 1993; 1:288–294) 1993 North American Association for the Study of Obesity (NAASO)
UR - http://www.scopus.com/inward/record.url?scp=0001618132&partnerID=8YFLogxK
U2 - 10.1002/j.1550-8528.1993.tb00623.x
DO - 10.1002/j.1550-8528.1993.tb00623.x
M3 - Article
C2 - 16353359
AN - SCOPUS:0001618132
SN - 1071-7323
VL - 1
SP - 288
EP - 294
JO - Obesity research
JF - Obesity research
IS - 4
ER -