To examine whether dietary patterns are associated with obesity phenotypes.
We recruited 664 participants aged between 18 and 55 years. Dietary data were collected from a food frequency questionnaire. A factor analysis was performed to derive dietary patterns. Body mass index (BMI), weight and waist girth were recorded using standard procedures. Fat mass and fat-free mass were assessed by electrical bioimpedance. Obesity was defined as having a BMI> or =30 kg m(-2) and a positive FHO (FHO+) as having at least one obese first-degree relative.
Two dietary patterns were identified; Western and Prudent. The Western pattern was mainly characterized by a higher consumption of refined grains, French fries, red meats, condiments, processed meats and regular soft drinks whereas the Prudent pattern was mainly characterized by a higher consumption of non-hydrogenated fat, vegetables, eggs and fish and seafood. Subjects in the top tertile of the Western pattern had higher BMI, weight, waist girth, waist-to-hip ratio and fat mass than those in the lower tertile. In contrast, subjects in the top tertile of the Prudent pattern had lower BMI, weight, waist girth, fat mass, HDL-cholesterol levels, and lower triglyceride levels than those in the lowest tertile. Individuals in the upper tertile of the Western pattern were more likely to be obese (obesity was defined as having a BMI> or =30 kg m(-2)) (OR=1.82, 95% CI 1.16-2.87) whereas those in the upper tertile of the Prudent pattern were less likely to be obese (OR=0.62, 95% CI 0.40-0.96). These latter significant associations were only observed among those with FHO+. No such association was observed among FHO- individuals.
Individuals having a high score of Western pattern were more likely to be obese and those having a high score of the Prudent pattern were less likely to be obese, and this is particularly among individuals with an FHO+.
Several candidate genes have been associated with obesity, but very few studies have tested more than one gene simultaneously.
In this study, 15 polymorphisms in 10 candidate genes of obesity were tested for association with changes in adiposity measured over a period of 6-10 years in a maximum of 332 adult subjects with a wide range of adiposity (17.5or=40 years).
In the whole sample, the variance in age-related adiposity changes explained by the candidate gene polymorphisms ranged from 3.1% (BMI, P
The evidence for common familial factors underlying total fat mass (estimated from underwater weighing) and abdominal visceral fat (assessed from CT scan) was examined in families participating in phase 2 of the Québec Family Study (QFS) using a bivariate familial correlation model. Previous QFS investigations suggest that both genetic (major and polygenic) and familial environmental factors influence each phenotype, accounting for between 55% to 71% of the phenotypic variance in fat mass, and between 55% to 72% for abdominal visceral fat. The current study suggests that the bivariate familial effect ranges from 29% to 50%. This pattern suggests that there may be common familial determinants for abdominal visceral fat and total fat mass, as well as additional familial factors which are specific to each. The relatively high spouse cross-trait correlations usually suggest that a large percent of the bivariate familial effect may be environmental in origin. However, if mating is not random, then the spouse resemblance may reflect either genetic or environmental causes, depending on the source [i.e., through similar genes or cohabitation (environmental) effects]. Finally, there are significant sex differences in the magnitude of the familial cross-trait correlations involving parents, but not offspring, suggesting complex generation (i.e., age) and sex effects. For example, genes may turn on or off as a function of age and sex, and/or there may be an accumulation over time of effects due to the environment which may vary by sex. Whether the common familial factors are genetic (major and/or polygenic), environmental, or some combination of both, and whether the familial expression depends on sex and/or age warrants further investigation using more complex models.
The purpose of this study was to determine the familial risk of obesity and of an android profile of fat distribution in the general Canadian population. A sample of 15,245 participants aged 7-69 years from 6,377 households from the Canada Fitness Survey of 1981 was used. The body mass index (BMI), sum of five skinfolds (SF5), ratio of trunk-to-extremity skinfolds, adjusted for SF5, and waist circumference, adjusted for BMI were used as indicators of obesity and central fat distribution. Age- and sex-standardized risk ratios (SRRs) for spouses and first-degree relatives of obese probands indicate that there is significant familial risk for obesity and an android fat distribution in the Canadian population. SRRs for spouses and first-degree relatives of probands exceeding the 99th percentile are 3.01 and 4.96 for BMI, 7.36 and 4.15 for SF5, 1.41 and 3.18 for ratio of trunk-to-extremity skinfolds, adjusted for SF5, and 1.02 and 2.18 for waist circumference, adjusted for BMI, respectively. The SRRs are smaller for less extreme obesity (lower percentile cutoffs) than for more extreme obesity. The SRRs are greater in spouses than in first-degree relatives for SF5; however, the risk for BMI and an android fat distribution was greater among first-degree relatives than among spouses, suggesting a greater role for genetic factors.
Blood pressure (BP), an important risk factor for coronary heart disease, is a complex trait with multiple genetic etiologies. While some loci affecting BP variation are known (eg, angiotensinogen), there are likely to be novel signals that can be detected with a genome scan approach.
A genome-wide scan was performed in 125 random and 81 obese families participating in the Québec Family Study. A multipoint variance-components linkage analysis of 420 markers (353 microsatellites and 67 restriction fragment length polymorphisms) revealed several signals (P:
Comment In: Circulation. 2000 Oct 17;102(16):1877-811034931
Parental eating behavior traits have been shown to be related to the adiposity of their young children. It is unknown whether this relationship persists in older offspring or whether rigid or flexible control are involved. The objective of this study was to test the hypothesis that parental eating behavior traits, as measured by the Three-Factor Eating Questionnaire (TFEQ), are related to offspring body weight.
Cross-sectional anthropometric and TFEQ data from phase 2 and 3 of the Québec Family Study generated 192 parent-offspring dyads (offspring age range: 10-37 years). Relationships were adjusted for offspring age, sex and reported physical activity, number of offspring per family and parent body mass index (BMI).
In all parent-offspring dyads, parental rigid control and disinhibition scores were positively related to offspring BMI (r=0.17, P=0.02; r=0.18, P
Spousal similarities in 7-year changes in obesity and obesity-related phenotypes were examined in a subsample of 376 pairs of spouses from a sample of 1487 participants in the 1988 Campbell's Survey follow-up of the 1981 Canada Fitness Survey.
Indicators of body fatness included the body mass index (BMI), the sum of five skinfolds (SF5), and waist circumference (WAIST), whereas those for relative adipose tissue (AT) distribution included the ratio of two trunk to three extremity skinfolds, adjusted for SF5 (TERadj), and WAIST adjusted for BMI (WAISTadj).
Spouse correlations were 0.17, 0.17, and 0.17 for the BMI (p