Biochemical and Anthropometric Characterization of Morbid Obesity in a Large Utah Pedigree

Steven Hunt, Roger R. Williams, Ted D. Adams

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A Utah family with morbid obesity was extended to include 122 persons in four generations for the purpose of characterizing anthropometric and biochemical variables in family members with and without morbid obesity. Seventy‐seven subjects had blood drawn for biochemical analyses. Of the 77 subjects, 12 were morbidly obese (≥44.5 kg or 100 pounds overweight), 20 were between 22.5–45.4 kg (50 and 99 pounds) overweight and 45 were less than 22.5 kg (50 pounds) overweight Sixty‐two randomly‐ascertained controls were used for comparisons of age‐ and gender‐adjusted study variables. Morbidly obese subjects had mean body mass indices (BMI) of 41.0 kg/m2 (62 kg over ideal weight) compared to 25.3 kg/m2 (10 kg overweight) in the <22.5 kg family members (p<0.001). The <22.5 kg family members had lower BMI than the random controls (27.6 kg/m2, p<0.05), indicating clear bimodality of obesity within the pedigree. Percent body fat from bioelectrical 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 larger in the morbidly obese and the waist‐to‐hip ratio remained significantly 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. Fasting insulin was the best predictor of morbid obesity of all biochemical and lipid measurements (odds ratio of 4.5). Fasting 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 insulin to glucose ratio were elevated in the morbidly obese subjects indicating that insulin levels were inappropriately high for their weight compared to this relationship found in the other groups. Adjusted insulin levels for the 22.5–45.4 kg group were similar to controls, indicating insulin level was at the predicted level for their weight. In conclusion, individuals with morbid obesity appeared to have greater insulin resistance than could be explained by their weight. CHD risk from elevated LD L‐C was not present, but CHD risk was increased by the so‐called multiple metabolic syndrome (insulin resistance, high triglycerides and low HDL‐C). 1995 North American Association for the Study of Obesity (NAASO)

Original languageEnglish
Pages (from-to)165s-172s
JournalObesity Research
Issue number2 S
Publication statusPublished - 1995
Externally publishedYes



  • body mass index
  • genetics
  • insulin
  • percent fat
  • triglycerides

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Endocrinology, Diabetes and Metabolism
  • Food Science
  • Endocrinology
  • Public Health, Environmental and Occupational Health

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