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PubMed2005

How do misassigned paternities affect the estimation of heritability in the wild?

Studies of birds have recently played an important role in the increasing success of quantitative genetics applied to natural populations. However, these studies mostly base their pedigree relationships on social information, despite the known widespread genetic polygamy in avian species. Here, we study the influence of misassigned paternities, combined with the effect of pedigree size and depth, on the estimation of heritability. First, we compute simulations of a polygenic trait for two levels of heritability (0.1 and 0.4), several extra-pair paternity rates (ranging from 5% to 40%), and varying sample sizes (20, 50 and 100 broods) or pedigree depth (2 or 4 generations). We compare heritability estimates from the social and the genetic pedigree, running a restricted maximum-likelihood 'animal model'. Social pedigree underestimates heritability by an average of 0-17% for 5-20% extra-pair paternities and by up to 18% for 40% extra-pair paternities and a heritability of 0.4. Second, we identifyied extra-pair offspring using microsatellite loci in two populations of blue tits (Parus caeruleus) showing high levels of extra-pair paternities (15% and 25% of extra-pair offspring). We compare heritabilities of tarsus length and body mass estimated with pedigrees of increasing accuracy. These analyses suggest that the bias induced by misassigned paternities on heritability estimation depends on the level of heritability and the rate of paternity error. Typical rates of extra-pair paternities in birds (around 20% of offspring) should result in an underestimation of heritability of less than 15% when estimated over a minimum of 100 broods.

Animals↗
PubMed2004

Heritability estimates for carcass traits of cattle: a review.

We present estimates of heritability for carcass traits of cattle published in the scientific literature. Seventy-two papers published from 1962 to 2004, which reported estimates of heritability for carcass traits, were reviewed. The unweighted means of estimates of heritability for 14 carcass traits by slaughter end point (age, weight, and fat depth) were calculated. Among the three end points, carcass weight, backfat thickness, longissimus muscle area, and marbling score were the carcass traits with the most estimates of heritability (56 <or= n<or=66). The averages for these traits indicate that they are similarly and moderately heritable (0.40, 0.36, 0.40, and 0.37, respectively). However, heritability estimates for most traits varied greatly, which could be due to differences in breed groups, methods of estimation, effects in the model, number of records, measurement errors, sex, and management. Few studies have compared heritability estimates for carcass traits adjusted to different end points. Results from such studies have been inconsistent, although some studies revealed that heritability estimates for several carcass traits are sensitive to the covariate included in the model for the end point, implying that direct response to selection would be different for some traits depending on slaughter end point. The effect of different end points on estimates of heritability for many carcass traits has not been studied.

Animals↗
PubMed2006

Maximum likelihood estimation of human craniometric heritabilities.

This study presents univariate narrow-sense heritability estimates for 33 common craniometric dimensions, calculated using the maximum likelihood variance components method on a skeletal sample of 298 pedigreed individuals from Hallstatt, Austria. Quantitative genetic studies that use skeletal cranial measurements as a basis for inferring microevolutionary processes in human populations usually employ heritability estimates to represent the genetic variance of the population. The heritabilities used are often problematic: most come from studies of living humans, and/or they were calculated using statistical techniques or assumptions violated by human groups. Most bilateral breadth measures in the current study show low heritability estimates, while cranial length and height measures have heritability values ranging between 0.102-0.729. There appear to be differences between the heritabilities calculated from crania and those from anthropometric studies of living humans, suggesting that the use of the latter in quantitative genetic models of skeletal data may be inappropriate. The univariate skeletal heritability estimates seem to group into distinct regions of the cranium, based on their relative values. The most salient group of measurements is for the midfacial/orbital region, with a number of measures showing heritabilities less than 0.30. Several possible reasons behind this pattern are examined. Given the fact that heritabilities calculated on one population should not be applied to others, suggestions are made for the use of the data presented.

Austria↗
PubMed2005

Significance of heritability in primary and secondary pediatric hypertension.

BACKGROUND: Patient weight and family history are significant risk factors for the development of hypertension in children. Multiple genetic factors have been identified in primary (essential) hypertension in adults; however, the delineation of genetic factors in the separate populations of children with primary or secondary hypertension are not well understood. Heritability is the proportion of observed variation in a particular trait that can be attributed to an inherited genetic factor in contrast to environmental factors. In the consideration of hypertension, heritability can be assessed in terms of an underlying continuous gradient of the liability for developing hypertension. With this assumption it is possible to compute heritability using hypertension incidence among relatives and described by Falconer. Heritability values range from 0 (no genetic contribution) to 1 (complete genetic contribution). The aim of this study was to determine the genetic contribution to primary and secondary hypertension in a pediatric population through heritability analysis. METHODS: This was a retrospective case-control analysis of medical records of children (n=276) followed in the Pediatric Nephrology Clinic over a 4-year period from 1999 to 2002. There were 192 children and adolescents with primary hypertension (124 male, 68 female, age 0 to 21 years) and 84 children and adolescents with secondary hypertension (46 male, 38 female, age 0 to 21 years). Each hypertensive group served as the control for the other. Estimates of heritability were made using Falconer's method 2. The model assumes independence between the environment and genetic factors and that the joint distribution of liabilities between parent and child are normally distributed. Problems can arise from computing heritability due to dominance within loci, correlations between nongenetic familial effects, or the presence of a major gene. RESULTS: Of the children and adolescents with primary hypertension, 49% had parents with primary hypertension; and of the children and adolescents with secondary hypertension, 24% had parents with primary hypertension. Of the children and adolescents with primary hypertension, 10% had parents with secondary hypertension; and of the children and adolescents with secondary hypertension, 46% had parents with secondary hypertension. The estimated heritability for primary hypertension was 0.84 (SE=0.21). The estimated heritability for secondary hypertension was 1.14 (SE=0.21). As the value was >1, this indicates that the fit of the liability model is poor and that a few genes, or even one major gene, were significantly involved in the causes of secondary hypertension in the children and adolescents studied. CONCLUSIONS: The results suggest that primary and secondary hypertension do not share the same type of genetic profile. Primary hypertension in children and adolescents is likely due to a large number of additive contributions of genes, although a highly correlated environmental component can not be excluded. The continuous liability model is inappropriate for secondary hypertension because the estimate was substantially greater than one. This study supports the model that secondary hypertension in children and adolescents may be related to just a few genes.

Adolescent↗
PubMed2004

Heritability of individual depressive symptoms.

BACKGROUND: In attempting to understand the familial basis of depression, most studies have focused on broad indices of depression and mood change. Broad indices may not adequately reflect the heritable basis of depression because of an unexplored possibility that not all symptoms are heritable. METHODS: The heritability of individual depressive symptoms was estimated from a sample of 343 general population volunteer twin pairs who completed the Beck Depression Inventory, the Centre for Epidemiologic Studies Depression Scale and items from the Symptom Checklist assessing depressive symptoms. Principal component analysis of the items extracted 14 factors that represented a wide range of depressive symptomatology. RESULTS: The factors were differentially heritable (h2 range: 0.0-35.0%). The factors that have a heritable basis described endogenous or physiological functions (e.g. loss of appetite, libido/pleasure). Symptoms such as negative affect or tearfulness did not have a heritable basis, suggesting that these symptoms are responses to negative life events/experiences or a learned association to changes in physiologic function. LIMITATIONS: Relatively small size of the sample. CONCLUSIONS: Depressive symptoms are differentially heritable and the results suggest that future research, such as genotyping studies, separates heritable and non-heritable symptom clusters prior to analysis. This will help identify which genes are involved and what their function in depression may be, leading to the development of more targeted and effective therapies.

Adolescent↗
PubMed1993

Heritabilities of growth curve parameters and age-specific expression of genetic variation under two different feeding regimes in Japanese quail (Coturnix coturnix japonica).

This study investigated genetic variation in growth and final size in relationship to differences in heritabilities under good and poor feeding conditions. Heritabilities of growth and final size were estimated for several traits under ad libitum and restricted feeding conditions. A 30% feed restriction from hatching to 44 days of age in Japanese quail chicks decreased body weight and tarsus length at 44 days of age and the length of the third primary convert feather at 24 days of age relative to controls fed ad libitum. Wing length at 44 days of age was not significantly different for ad libitum fed and restricted quail. Genetic variances for body weight and tarsus length were very large throughout growth which resulted in heritability estimates close to one for these traits. The genetic correlations among feeding treatments were low, indicating that different genes were affecting growth under the two treatments. Growth was described by the components: asymptote, growth period, and shape of the growth curve following the modified Richards growth curve model (Brisbin et al. 1986). Tarsus length, which had high heritability of the parameter 'growth period' of the model, tended to display a higher heritability under the restriction than under ad libitum feeding. Body weight and feather length, which had either no heritable or low heritable 'growth periods' estimates, tended to be more heritable under ad libitum feeding. The shape parameter of the growth curve was not heritable for any trait, except tarsus length under restricted feeding.

Age Factors↗
PubMed1993

Laboratory and natural heritabilities of male courtship song characters in Drosophila montana and D. littoralis.

We estimated heritabilities for several male courtship song characters in two Drosophila species using father-son regression under conditions where both fathers and sons had been raised in the laboratory. In D. montana the heritabilities of song characters were rather high (-0.23 to 0.80) and in most cases significant. In D. littoralis the heritabilities of song characters were generally lower (-0.33 to 0.18), and none of them was significantly larger than zero. We also estimated heritabilities regressing characters of wild-caught fathers with those of their laboratory reared sons, and used the method employed by Riska et al. to estimate the lower bound of heritabilities in nature. In D. montana most and in D. littoralis all of the across-environment heritabilities were non-significant (-0.15 to 0.43 and -0.04 to 0.15, respectively), and in some cases the across-environment heritabilities were significantly lower than the heritabilities measured under laboratory conditions. The low across-environment heritabilities appeared to be due to larger phenotypic variability of song characters in the field and in some cases also due to genotype-environment interactions.

Animals↗
PubMed2004

Heritability of ambulatory and office blood pressure phenotypes in Swedish families.

OBJECTIVE: The aim of this study was to estimate the heritability of 24-h ambulatory blood pressure and office blood pressure phenotypes in Swedish families. METHODS: We measured ambulatory and office blood pressure in 260 siblings without antihypertensive treatment from 118 families. Blood pressure heritability was estimated using standard quantitative genetic variance component analysis implemented in the 'SOLAR' software package after adjustment for significant covariates. RESULTS: Heritability values were significant for night-time systolic (37%), diastolic (32%) and mean (32%) ambulatory blood pressure (P < 0.05 for all). During daytime, systolic ambulatory blood pressure was significantly heritable (33%, P < 0.05). Twenty-four-hour systolic (30%) and diastolic (29%) ambulatory blood pressure also had significant values of heritability (P < 0.05). Pulse pressure ambulatory blood pressure was significantly heritable over 24 h (63%, P < 0.01), during daytime (53%, P < 0.01) and at night (34%, P < 0.05). None of the office blood pressure phenotypes had a significant heritability. CONCLUSIONS: We conclude that ambulatory blood pressure, in particular at night, seems better than office blood pressure to capture the heritable part of blood pressure, suggesting that ambulatory blood pressure may be a more exact estimate of an individual's true blood pressure. Genetic studies using ambulatory blood pressure as the phenotype are likely to be more powerful than those using office blood pressure. The high heritability of pulse pressure ambulatory blood pressure indicates that variation in arterial stiffness in subjects free from antihypertensive medication is strongly affected by genetic factors.

Adult↗
PubMed2004

The contribution of risk factors to blood pressure heritability estimates in young adults: the East flanders prospective twin study.

The heritability of blood pressure estimated in previous studies may be confounded by the influence of potential blood pressure risk factors. We applied the classical twin design to estimate the contribution of these covariates to blood pressure heritability. The study consisted of 173 dizygotic and 251 monozygotic twin pairs aged 18-34 years, randomly selected from the East Flanders Prospective Twin Survey. In a standardized examination, blood pressure and anthropometry was measured, a questionnaire was completed, and a fasting blood sample was taken. In univariate and bivariate modeling, diastolic and systolic heritability were estimated both unadjusted and adjusted for potential risk factors. Also, covariate interaction was modeled. Bivariate analysis gave heritability estimates of 0.63 (95%CI 0.55-0.59), 0.74 (95%CI: 0.68-0.79), and 0.78 (95%CI: 0.70-0.84) for diastolic, systolic, and cross-trait heritability, respectively. The remaining variances could be attributed to unique environmental influences. These heritability estimates did not change substantially in univariate analyses or after adjustment for risk factors. A sex-limitation model showed that the heritability estimates for women were significantly higher than for men, but the same genetic factors were operating across sexes. Sex and cigarette smoking appeared to be statistically significant interaction terms. The heritability of blood pressure is relatively high in young adults. Potential risk factors of blood pressure do not appear to confound the heritability estimates. However, gene by sex by smoking interaction is indicated.

Adolescent↗
PubMed1993

[Estimation of the sampling variance of co-heritability].

Formulae for the sampling variances of co-heritability and co-environment are developed from the one-fold and two-fold nested genetic analyses of variance and covariance with balanced and unbalanced data. Some potential roles of the co-heritability in breeding programs and the relationship with genetic correlation have also been investigated. The co-heritability has dual characteristics of both heritability and genetic correlation. Heritability is a special case of co-heritability with co-heritability an extended form of heritability. The use of co-heritability to express the genetic covariation between two characters will give smaller sampling errors than those of the genetic correlation (gamma A).

Analysis of Variance↗
PubMed1982

Quantitative genetics of skeletal nonmetric traits in the rhesus macaques of Cayo Santiago. III. Relative heritability of skeletal nonmetric and metric traits.

This study addresses the long-standing controversy in skeletal biology concerning the relative utility of skeletal metric and nonmetric traits for studies of biological relationship. This controversy centers on the relative heritability of these two trait sets. This paper presents heritabilities for a series of skeletal metric and nonmetric traits measured with the same sample of mother-offspring pairs from the Cayo Santiago skeletal collection of rhesus macaques. Skeletal nonmetric traits display significantly greater heritability estimates than metric traits. This difference is due primarily to the high heritability estimates of hyperostotic nonmetric traits. Foraminal traits are not significantly more heritable than skeletal metric traits. The generality of this pattern of heritability values, in which hyperostotic nonmetric traits are more highly heritable than foraminal nonmetric and metric traits, depends on future empirical study of the correlation of heritability values in populations and theoretical work.

Animals↗
PubMed2001

Time, memory and the heritability of major depression.

OBJECTIVE: Although family, twin and adoption studies have suggested that lifetime major depression (MD) is a heritable condition, nearly all these studies have relied for the diagnosis on long-term human memory, which is fallible and potentially biased. Could the estimates of heritability of MD be biased by the well-demonstrated genetic influences on memory? METHODS: Both members of 858 female-female twin pairs from a population-based registry were personally interviewed at least three times over 9 years. The interview assessed a history of depressive onsets and recoveries in the last year to the nearest month. We examine heritability of MD using four recall intervals: last year, last 6 months, last 3 months and current month. RESULTS: Examining the occurrence of one or more depressive episodes across all three interviews, heritabilities of MD (95% CI) for the four time periods were: 0.41 (0.27-0.54), 0.41 (0.26-0.55), 0.35 (0.16-0.52) and 0.34 (0.11-0.55). These heritability estimates did not differ significantly from one another. A similar pattern was found if heritability was assessed for the number of interviews in which criteria for MD were met. CONCLUSION: Modelling results suggest that the heritability of MD was not influenced by the duration of the required recall. Genetic influences on human recall do not appear to contribute substantially to estimated heritability of MD.

Adult↗
PubMedDate not supplied

Heritability of brain size and surface features in rhesus macaques (Macaca mulatta).

The extent of heritability for overall brain size and regional cortical surface features such as sulcus lengths is important for demonstrating a genetic component to the observed phenotypic differences among individuals and for evaluating the potential for evolutionary change in response to selection. Although the genetics of brain size has been extensively considered, the detailed morphology of the cortical surface has not previously been subjected to genetic analysis. We estimated the heritability of brain size and cortical sulcus lengths using 438 endocranial casts taken from skeletons of rhesus macaques (Macaca mulatta) from the Cayo Santiago population. Estimates were obtained both by mother-offspring regression and symmetric-differences-squared (SDS) methods. Brain size, measured as cranial capacity, was highly and significantly heritable in this population, confirming results of previous studies with laboratory mice. Overall, cortical sulcus lengths were also heritable, with 35% of the sulci significantly heritable at the 5% level in the mother-offspring analysis. The average mother-offspring heritability estimate, 0.31, was the same as the average heritability obtained previously from a series of 56 cranial metric characters. The SDS analyses generally corresponded to the findings based on mother-offspring regressions, although the significance test appeared more conservative. Both gross and detailed morphology of the brain are heritable.

Animals↗
PubMed2005

Distinct heritable patterns of angiographic coronary artery disease in families with myocardial infarction.

BACKGROUND: Coronary artery disease (CAD) and myocardial infarction (MI) are significantly determined by genetic background. Whether distinct angiographic features of CAD are affected by inherited factors has never been investigated. Thus, we analyzed comprehensively the extent to which various aspects of CAD, including disease severity, distribution of lesions, presence of coronary calcification, morphology of stenoses, and anatomic characteristics, are under genetic control. METHODS AND RESULTS: We retrospectively studied the coronary angiograms of 882 siblings with CAD from 401 families. These families were ascertained through index patients defined by MI before the age of 60 years and at least 1 sibling with MI or coronary revascularization procedures. Heritability calculations were performed with variance-component analysis. Additionally, recurrence risks to siblings were analyzed. Traditional cardiovascular risk factors and age at the first coronary event displayed significant heritable components. After adjustment for age and sex, significant heritabilities were identified for proximal stenoses, in particular, left main CAD (h2=0.49+/-0.12; P=0.01), coronary calcification (h2=0.51+/-0.17; P=0.001), and ectatic coronary lesions (h2=0.52+/-0.07; P=0.001). In contrast, no heritability was found for distal disease (h2=0.05+/-0.19; NS), the pattern of coronary arterial blood supply, or the number of diseased vessels. Calculation of recurrence risks in siblings largely confirmed the heritability estimates. CONCLUSIONS: Distinct morphological characteristics associated with CAD show different degrees of heritability. Notably, the most hazardous localizations, like left main or proximal disease, display a high heritability. In contrast, some features of coronary morphology, such as distal disease, do not appear to be markedly influenced by heritable factors.

Analysis of Variance↗
PubMed2001

Heritability of resistance to individual contaminants and to contaminant mixtures in the sheepshead minnow (Cyprindon variegatus).

Resistance heritability (the additive genetic variance out of the total phenotypic variance, signifying a population's potential to genetically adapt to detrimental levels of contamination) was quantified in the sheepshead minnow (Cyprinodon variegatus). Heritability was estimated for tolerance to individual contaminants (phenanthrene, zinc) and to contaminant mixtures (phenanthrene plus zinc, and a complex mixture with three metals and three polycyclic aromatic hydrocarbons). Estimates were obtained from resemblances between relatives, both parent-offspring pairs, and families of sibs and half-sibs. Heritabilities determined from parent-offspring regressions averaged only 0.08 (scale, 0-1), whereas resemblance among full sibs yielded heritabilities averaging 0.85. The half-sib analysis yielded heritabilities of -0.01 (sire component) and 0.77 (dam component). This pattern in the magnitude of heritabilities indicates that heritabilities for the resistance of C. variegatus to these chemicals are low (with the high resemblances among sibs being due to common environmental and dominance genetic variation rather than additive genetic variation). The parent-offspring regressions provide evidence that heritabilities may be lower if more contaminants are involved. Our results mean, then, that C. variegatus in contaminated environments is not likely to become resistant to these contaminants very rapidly, and that resistance may develop even more slowly as more contaminants become involved.

Adaptation, Physiological↗
PubMed1995

Contribution of heritable disorders to mortality in the pediatric intensive care unit.

OBJECTIVES: To determine the percentage of patients dying in the pediatric intensive care unit (PICU) who have heritable disorders and to compare vital statistics classification of underlying cause of death with underlying heritable disorder identified from medical record review. DESIGN: Retrospective medical record review. SETTING: The PICU of a university-affiliated hospital. METHODS: Medical records were reviewed for all deaths occurring in the PICA over a 5-year period. Further review, including hospital course, clinical findings, and the presence or absence of a genetic evaluation, was accomplished for those patients found to have a chromosome abnormality, recognized syndrome, single major malformation, or unrecognized syndrome. Underlying cause of death classification obtained from the Center for Health Statistics, Arkansas Department of Health was reviewed to determine the frequency with which the underlying heritable disorder was recorded. RESULTS: Fifty-one of 268 (19%) deaths during the study period were in patients with heritable disorders. Of these 51 patients, eight (16%) had chromosome abnormalities, 17 (33%) had a recognized syndrome, 15 (29%) had a single primary defect in development, and 11 (22%) had an unrecognized syndrome. Genetic evaluation was carried out on 45% of patients, with the frequency of evaluation differing between categories of patients with heritable conditions. When underlying cause of death from vital statistics classification was reviewed, 21 of 51 (41%) records did not include the underlying heritable disorder. CONCLUSIONS: Heritable disorders are a frequent cause of mortality in the PICU. Vital statistics classification of underlying cause of death in this population often fails to identify heritable disorders, leading to an underascertainment of these conditions in mortality statistics. Improved cause of death classification procedures will be necessary to target public health interventions to etiology-specific populations.

Child, Preschool↗
PubMed2005

Dipping and variability of blood pressure and heart rate at night are heritable traits.

BACKGROUND: Blunted nocturnal blood pressure dipping (NBPD) as well as high variability in blood pressure (BPV) and low variability in heart rate (HRV), are associated with increased cardiovascular morbidity and mortality. The aim of this study was to determine whether these traits are heritable. METHODS: We studied 260 healthy siblings without antihypertensive drugs from 118 Swedish families. The BPV and HRV were defined as the standard deviation of BP and heart rate values recorded during 24 h, daytime (6 am to 10 pm), and night-time (10 pm to 6 am). The NBPD was defined as the ratio between night-time and daytime BP. Heritability was estimated with a maximal likelihood method implemented in the Solar software package with and without adjustment for significant covariates. RESULTS: At night, significant heritability was found for systolic (33%, P < .05), diastolic (36%, P < .05), and mean (42%, P < .01) BPV. After covariate adjustment the corresponding heritability values were 23% (P = .08), 29% (P < .05), and 37% (P < .05). Daytime BPV was not heritable. The heritability of NBPD was 38% (P < .05) for systolic, 9% (P = .29) for diastolic, and 36% (P < .05) for mean BP, but after adjustment only systolic NBPD was significant (29%, P < .05). Heart rate was highly heritable both during daytime (57%, P < .001) and night-time (58%, P < .001), but the variability of heart rate, after adjustment, was only significant at night (37%, P < .05). CONCLUSIONS: Our data suggest that BPV and HRV are partially under genetic control and that genetic loci of importance for these traits could be mapped by linkage analysis.

Adult↗
PubMed2005

The heritability of inducible defenses in tadpoles.

The evolution of plastic traits requires phenotypic trade-offs and heritable traits, yet the latter requirement has received little attention, especially for predator-induced traits. Using a half-sib design, I examined the narrow-sense heritability of predator-induced behaviour, morphology, and life history in larval wood frogs (Rana sylvatica). Many of the traits had significant additive genetic variation in predator (caged Anax longipes) and no-predator environments. Whereas most traits had moderate to high heritability across environments, tail depth exhibited high heritability with predators but low heritability without predators. In addition, several traits had significant heritability for plasticity, suggesting a potential for selection to act on plasticity per se. Genetic correlations confirmed known phenotypic relationships across environments and identified novel relationships within each environment. This appears to be the first investigation of narrow-sense heritabilities for predator-induced traits and confirms that inducible traits previously shown to be under selection also have a genetic basis and should be capable of exhibiting evolutionary responses.

Adaptation, Physiological↗