Familial Aggregation of Morbid Obesity

Abstract

Recent studies have shown major gene effects for obesity in randomly ascertained families. To investigate the familial aggregation of a specific subset of obesity, which is particularly prone to medical complications, families with morbid obesity were studied. This condition occurs in 1%-2%of the population and is defined as 45.5 kg (100 pounds) or more over ideal weight. First-degree relatives of 221 morbidly obese probands (1560 adults) were identified, and height and weight (current and greatest) were obtained from each family member. Morbid obesity occurred in the family members of the probands 8 times more often than in the general population. Of the morbidly obese probands, 48% had one or more first-degree relatives who were also morbidly obese compared to a 6% population estimate. By the ages of 20-24, 12% of the morbidly obese probands were already 45.5 kg or more overweight, and 45% were 22.7 kg (50 pounds) or more overweight. There was little difference in the prevalence of familial morbid obesity by the gender of the probands: 47% of the male probands and 48% of the female probands had another morbidly obese relative, while 67% and 53% of the early onset (before age 25) male and female probands, respectively, had one or more firstdegree relatives who were also morbidly obese. In addition to the extreme degree of familial aggregation, the prevalence of morbid obesity in parent-offspring sets was calculated within the morbidly obese families. Morbidly obese families who have one or two morbidly obese parents have a 2.6 times

Obesity related phenotypes in families selected for extreme obesity and leanness

“…56 Almost half of the extremely obese individuals in the current study had a very early age at onset (onset age`10 y). In a different study which ascertained families through a single extremely obese proband, rates of early-onset obesity were much lower than the rates in this study (12% compared with 42% in the current report 57 ). The high rates of early-onset obesity seen in these family members may re¯ect the increased in¯uence of genes in determining the phenotypes of these multiplex families.…”

Metabolic syndrome and ADRB3 gene polymorphism in severely obese patients from South Italy

“…This study was carried out in a population of severely obese patients, where a strong polygenic component is expected (Price et al, 1990;Adams et al, 1993) thus representing a target population for genetic studies in human obesity (Clement et al, 1995;Oksanen et al, 1996). The prevalence of the ADRB3 Trp64Arg polymorphism in our obese subjects did not differ from that in the control subjects or from the prevalence already identified in adult male employers of the Olivetti plant in South Italy (Strazzullo et al, 2001).…”

“…Morbid obesity (BMI 440 kg/m 2 ), which is increasing in adults and children (Flegal et al, 2002), has a strong genetic component (Price et al, 1990;Adams et al, 1993). Consequently, there patients may represent a good sample in which to evaluate the role of ADRB3 polymorphisms in obesity predisposition.…”

20 YEARS OF LEPTIN: Leptin at 20: an overview

“…That there is a substantial genetic contribution to obesity is also supported by adoption and familial aggregation studies (Stunkard et al 1986, Adams et al 1993. However, while some fraction of obesity can be attributed to the aforementioned Mendelian defects as well as variation in genes identified in GWAS studies such as FTO, there is a reason to expect that many new genes remain to be discovered (Fawcett & Barroso 2010).…”