BIOCHEMICAL AND ANTHROPOMETRIC CHARACTERIZATION OF MORBID-OBESITY IN A LARGE UTAH PEDIGREE

A Utah family with morbid obesity was extended to include 122 persons in four generations for the purpose of characterizing anthropometric a nd biochemical variables in family members with and without morbid obe sity, Seventy-seven subjects had blood drawn for biochemical analyses, Of the 77 subjects, 12 were morbidly obese (greater than or equal to 44.5 kg or 100 pounds overweight), 20 were between 22.5-45.4 kg (50 an d 99 pounds) overweight and 45 were less than 22.5 kg (50 pounds) over weight, Sixty-two randomly-ascertained controls were used for comparis ons of age- and gender-adjusted study variables, Morbidly obese subjec ts had mean body mass indices (BMI) of 41.0 kg/m(2) (62 kg over ideal weight) compared to 25.3 kg/m(2) (10 kg overweight) in the < 22.5 kg f amily members (p < 0.001), The < 22.5 kg family members had lower BMI than the random controls (27.6 kg/m(2), p < 0.05), indicating clear bi modality of obesity within the pedigree, Percent body fat from bioelec trical impedance was 35% versus 24% in the morbidly obese and the < 22 .5 kg subjects, respectively, Ideal body weight was similar among the three pedigree weight groups. Hip and waist circumferences were much l arger in the morbidly obese and the waist-to-hip ratio remained signif icantly greater in the morbidly obese subjects compared to the < 22.5 kg group, Morbidly obese subjects had elevated triglycerides and VLDL- C levels, low HDL levels, and normal LDL-C levels, Pasting insulin was the best predictor of morbid obesity of all biochemical and lipid mea surements (odds ratio of 4.5), Pasting insulin levels and the insulin- to-glucose ratio were more than twice as high as control levels. Even after adjusting for differences in BMI, fasting insulin and the insuli n to glucose ratio were elevated in the morbidly obese subjects indica ting that insulin levels were inappropriately high for their weight co mpared to this relationship found in the other groups, Adjusted insuli n levels for the 22.5-45.4 kg group were similar to controls, indicati ng insulin level was at the predicted level for their weight, In concl usion, individuals with morbid obesity appeared to have greater insuli n resistance than could be explained by their weight, CHD risk from el evated LDL-C was not present, but CHD risk was increased by the so-cal led multiple metabolic syndrome (insulin resistance, high triglyceride s and low HDL-C).