Health family trees: a tool for finding and helping young family members of coronary and cancer prone pedigrees in Texas and Utah.

Williams, Roger R.; Hunt, Steven C.; Barlow, Gary K.; Chamberlain, Robert M.; Weinberg, Armin D.; Cooper, H. Paul; Carbonari, Joseph P.; Gotto, Antonio M.

doi:10.2105/ajph.78.10.1283

Cited by 74 publications

(40 citation statements)

References 5 publications

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“…21 Early cardiovascular disease was defined as the onset of at least one of the following conditions before the age of 56 years for males or before the age of 66 years for females: myocardial infarction (MI), coronary bypass surgery (CABG), coronary angioplasty (PTCA) and unstable angina pectoris.…”

Section: Subjectsmentioning

confidence: 99%

A genome scan for loci influencing anti-atherogenic serum bilirubin levels

et al. 2002

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Epidemiological studies have shown an association of decreased serum bilirubin levels with coronary artery disease. Two segregation analyses in large pedigrees have suggested a major gene responsible for high bilirubin levels occurring in about 12% of the population. Based on a recessive model from a previous segregation analysis, we performed a genome scan using 587 markers genotyped in 862 individuals from 48 Utah pedigrees to detect loci linked to high bilirubin levels. As a complementary approach, non-parametric linkage (NPL) analysis was performed. These two methods identified four regions showing evidence for linkage. The first region is on chromosome 2q34 -37 with multipoint LOD and NPL scores of 3.01 and 3.22, respectively, for marker D2S1363. This region contains a previously described gene, uridine diphosphate glycosyltransferase 1, which has been associated with high bilirubin levels. A polymorphism in the promoter of this gene was recently shown to be responsible for Gilbert syndrome which is associated with mild hyperbilirubinemia. The other regions were found on chromosomes 9q21, 10q25 -26, and 18q12 with maximum NPL scores of 2.39, 1.55, and 2.79, respectively. Furthermore, we investigated in these pedigrees the association between bilirubin levels and coronary artery disease. One-hundred and sixty-one male and 41 female subjects had already suffered a coronary artery disease event. Male patients showed significantly lower bilirubin concentrations than age-matched controls. This association, however, was not observed in females. These results provide evidence that loci influencing bilirubin variation exist on chromosomes 2q34 -37, 9q21, 10q25 -26, and 18q12 and confirms the association of low bilirubin levels with coronary artery disease in males.

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Section: Subjectsmentioning

confidence: 99%

A genome scan for loci influencing anti-atherogenic serum bilirubin levels

et al. 2002

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“…The first source included female subjects identified from a population-based family history database of over 100,000 families collected from the parents of high school students (7,18). Health information reported by the families includes the report of "usual weight," categorized as: Slender or average; 4.5-22.4 kg overweight; 22.5-45.4 kg overweight; or over 45.4 kg overweight.…”

Section: Subjectsmentioning

confidence: 99%

Pregnancy Weight Retention in Morbid Obesity

et al. 1995

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Recent hypotheses suggest that for women who develop morbid obesity, increases in weight associated with pregnancy may represent a significant contribution to their obesity status. The effects of multiple pregnancies on weight gain were studied in 96 morbidly obese women (<13.6 kg over ideal weight a t ages 20-24 or before an earlier first pregnancy and currently >44.5 kg over ideal weight) and 115 random control women from the Utah population. Selfreported weights for each pregnancy included: prepregnancy, greatest during pregnancy, and 6 weeks following delivery, which were validated against available hospital records. Mean number of pregnancies in each group were similar (4.2 and 4.3), ranging from 1 to 9. Mean current age was 46 and mean weight gain since ages 20-24 was 46.0 kg in the morbidly obese and 14.1 kg in controls. Regression of current weight on total number of pregnancies, adjusting for weight a t ages 20-24, showed a 1.3 kgpregnancy increase in current weight (p=0.03) with no difference between groups (p=O.6). Weight gain subsequent to the last pregnancy was not related to the number of pregnancies (p=0.2). Morbidly obese women gained more weight during pregnancy than controls only for the first pregnancy. Gains were similar for all other pregnancies. Morbidly obese women had smaller weight losses after delivery than the controls, but these differences were not significant. For the first pregnancy, morbidly obese women had a net weight retention that was 4.0 kg greater than the controls at 6 weeks post-partum and a n average of 1.6 kglpregnancy greater retention for the remaining pregnancies. Pregnancy weight gains for each pregnancy subsequent to the first pregnancy were constant. These findings suggest: 1) women who develop morbid obesity have slightly less weight loss after delivery and greater between-pregnancy weight gains than controls; 2) the number of pregnancies does not affect the amount of weight gained after the last pregnancy; and 3) while multiparity m y augment weight gain in morbidly obese women, it is probably not a primary factor in the later development of morbid obesity.

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“…Initially, 67 subjects were identified from apopulationbased family history database of over 100,000 families collected from the parents of high school students (4,12). Using two school semesters from the year 1988 (database contains 20 total semesters) all families with one or more morbidlyobesemembers (reportedtobe45.5 kgormoreover ideal weight) were identifed.…”

Section: Subjectsmentioning

confidence: 99%

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

Hunt

Williams

Adams³

1995

Obesity Research

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HUNT,STEVEN C,ROGERRWILLIAMS AND TED D ADAMS. Biochemical and anthropometric characterizationofmorbidobesityinalarge Utahpedigree. ObesRes.AUtahfamilywithmorbidobesitywas extendedtoinclude 122personsinfourgenerationsforthepurposeof characterizing anthropometric and biochemicalvariables in family members with and without morbid obesity. Seventyseven subjects had blood drawnforbiochemicalanalyses. Ofthe77 subjects, 12weremorbidlyobeseQ44.5kgor 100 pounds overweight), 20 were between22.5-45.4 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 studyvariables.Morbidly obesesubjects hadmean body mass indices (BMI)of41.0 kg/m2 (62kgoveridealweight)comparedto 25.3 kg/m2 (10 kg overweight) in the ~2 2 . 5 kg family members @<0.001). The <22.5 kg family members had lower BMIthan the random controls (27.6 kg/mz,p<0.05), indicating clear bimodality of obesity within the pedigree. Percent body fat from bioelectricalimpedance was 35% versus 24% in the morbidly obese and the <22.5 kg subjects,respectively. Idealbodyweightwas similar among thethree pedigreeweight groups. Hip andwaist circumferences weremuchlargerinthemorbidly obese and thewaistto-hip ratio remained significantly greaterin themorbidly obese subjects compared to the ~2 2 . 5 kg group.Morbidly obese subjects hadelevatedtriglycerides and VLDL-C levels,low HDL-levels,andnormalLDGC levels. Fasting insulin was the best predictor of morbid obesity of allbiochemical andlipidmeasurements (odds ratio of 4.5). Fasting insulin levels and theinsulin-to-glucose ratio were 1995;3(~~ppl2): 165s-172s. Copynght 01995 NAASO more than twice as high as control levels. Even after adjusting for differences in BMI, fasting insulin and the insulin to glucoseratio were elevated inthemorbidly obese subjects indicating that insulin levels were inappropriately high for theirweight compared to this relationship foundin the other groups. Adjustedinsulinlevelsforthe 22.5-45.4 kg group were similar to controls, indicating insulin levelwas at the predicted level for their weight.In conclusion, individuals with morbid obesity appeared to have greater insulin resistance than could be explained by theirweight. CHD riskfrom elevatedLDG C wasnotpresent,but CHD riskwasincreasedbythesocalled multiple metabolic syndrome (insulin resistance, high triglycerides andlow HDGC).

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Health family trees: a tool for finding and helping young family members of coronary and cancer prone pedigrees in Texas and Utah.

Cited by 74 publications

References 5 publications

A genome scan for loci influencing anti-atherogenic serum bilirubin levels

A genome scan for loci influencing anti-atherogenic serum bilirubin levels

Pregnancy Weight Retention in Morbid Obesity

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

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