Genetic and environmental determinants of bone mineral density in Mexican Americans: results from the San Antonio Family Osteoporosis Study

Mitchell, Braxton D.; Kammerer, Candace M.; Schneider, Jennifer L.; Perez, Reina; Bauer, Richard L.

doi:10.1016/s8756-3282(03)00246-1

Cited by 50 publications

(59 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Residual heritability estimates in our study sample (ranging from 0.45 to 0.71) are comparable to, and in some cases higher than, those from other studies and other populations [18,28,33,35,36,40,43,64]. For example, narrow-sense heritability estimates for adult BMD from nuclear families have been reported to be between 0.53 and 0.84 [18,28,64].…”

Section: Discussionsupporting

confidence: 82%

Quantitative genetics of cortical bone mass in healthy 10-year-old children from the Fels Longitudinal Study

Duren

Sherwood

Choh

et al. 2007

Bone

View full text Add to dashboard Cite

The genetic influences on bone mass likely change throughout the life span, but most genetic studies of bone mass regulation have focused on adults. There is, however, a growing awareness of the importance of genes influencing the acquisition of bone mass during childhood on lifelong bone health. The present investigation examines genetic influences on childhood bone mass by estimating the residual heritabilities of different measures of second metacarpal bone mass in a sample of 600 10-year-old participants from 144 families in the Fels Longitudinal Study. Bivariate quantitative genetic analyses were conducted to estimate genetic correlations between cortical bone mass measures, and measures of bone growth and development. Using a maximum likelihood-based variance components method for pedigree data, we found a residual heritability estimate of 0.71 for second metacarpal cortical index. Residual heritability estimates for individual measures of cortical bone (e.g., lateral cortical thickness, medial cortical thickness) ranged from 0.47 to 0.58, at this prepubertal childhood age. Low genetic correlations were found between cortical bone measures and both bone length and skeletal age. However, after Bonferonni adjustment for multiple testing, ρ G was not significantly different from 0 for any of these pairs of traits. Results of this investigation provide evidence of significant genetic control over bone mass largely independent of maturation while bones are actively growing and before rapid accrual of bone that typically occurs during puberty.

show abstract

Section: Discussionsupporting

confidence: 82%

Quantitative genetics of cortical bone mass in healthy 10-year-old children from the Fels Longitudinal Study

Duren

Sherwood

Choh

et al. 2007

Bone

View full text Add to dashboard Cite

show abstract

“…Recruitment and data collection for the baseline phase of the SAFOS has been previously described in detail [8]. The families included for study were selected without regard for health outcomes and represent a relatively random sample of low income families from urban San Antonio.…”

Section: Subjects and Data Collectionmentioning

confidence: 99%

“…Measurements of all baseline covariates were previously described in Mitchell et al [8]; follow-up measurements of covariates were assessed identically to the baseline measures. Annualized change in BMD (ΔBMD), height, and weight was calculated as the difference between follow-up and baseline measurements divided by the exact elapsed time between clinic visits.…”

Section: Subjects and Data Collectionmentioning

confidence: 99%

“…As previously described in detail [8,21], heritability of ΔBMD was estimated using variance decomposition methods, which model phenotypic variation in ΔBMD at each bone site as a function of effects attributable to the measured covariates, additive genetic (based on expected allele sharing between pairs of relatives), and unmeasured error components. This model takes the general form where y i is the annualized ΔBMD for the ith individual, μ is the sample mean ΔBMD, X ij is the j th covariate for the i th individual, β j is the corresponding regression coefficient, g i is the additive genetic effect, and e i is the residual error effect (which includes unmeasured environmental and non-additive genetic components).…”

Section: Statistical Analysesmentioning

confidence: 99%

“…The degenerative disorder and associated fragility fractures have devastating effects on health, resulting in substantial morbidity, and increased mortality for hip and vertebral fractures [1]. Bone mineral density (BMD), as the foremost determinant of bone strength and major predictor of future fractures, has been extensively studied to help identify the environmental [2][3][4] and genetic factors [5][6][7][8] influencing risk for osteoporosis.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Genetic influences on bone loss in the San Antonio Family Osteoporosis study

et al. 2008

View full text Add to dashboard Cite

show abstract

Effects of age on genetic influence on bone loss over 17 years in women: The Healthy Ageing Twin Study (HATS)

Moayyeri

Hammond

Hart

et al. 2012

Journal of Bone and Mineral Research

View full text Add to dashboard Cite

The rate of bone loss varies across the aging period via multiple complex mechanisms. Therefore, the role of genetic factors on bone loss may also change similarly. In this study, we investigated the effect of age on the genetic component of bone loss in a large twin-based longitudinal study. During 17 years of follow-up in TwinsUK and Healthy Ageing Twin Study (HATS), 15,491 hip and lumbar spine dualenergy X-ray absorptiometry (DXA) scans were performed in 7056 twins. Out of these subjects, 2716 female twins aged >35 years with at least two scans separated for >4 years (mean follow-up 9.7 years) were included in this analysis. We used a mixed-effects randomcoefficients regression model to predict hip and spine bone mineral density (BMD) values for exact ages of 40, 45, 50, 55, 60, 65, 70, 75, and 80 years, with adjustment for baseline age, weight, height, and duration of hormone replacement therapy. We then estimated heritability of the changes in BMD measures between these age ranges. Heritability estimates for cross-sectional hip and spine BMD were high (ranging between 69% and 88%) at different ages. Heritability of change of BMD was lower and more variable, generally ranging from 0% to 40% for hip and 0% to 70% for spine; between age 40 and 45 years genetic factors explained 39.9% (95% confidence interval [CI], 25%-53%) of variance of BMD loss for total hip, 46.4% (95% CI, 32%-58%) for femoral neck, and 69.5% (95% CI, 59%-77%) for lumbar spine. These estimates decreased with increasing age, and there appeared to be no heritability of BMD changes after the age of 65 years. There was some evidence at the spine for shared genetic effects between cross-sectional and longitudinal BMD. Whereas genetic factors appear to have an important role in bone loss in early postmenopausal women, nongenetic mechanisms become more important determinants of bone loss with advanced age. ß

show abstract

Genetic and environmental determinants of bone mineral density in Mexican Americans: results from the San Antonio Family Osteoporosis Study

Cited by 50 publications

References 27 publications

Quantitative genetics of cortical bone mass in healthy 10-year-old children from the Fels Longitudinal Study

Quantitative genetics of cortical bone mass in healthy 10-year-old children from the Fels Longitudinal Study

Genetic influences on bone loss in the San Antonio Family Osteoporosis study

Effects of age on genetic influence on bone loss over 17 years in women: The Healthy Ageing Twin Study (HATS)

Contact Info

Product

Resources

About