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PubMed1989

Replicating family size: does living in a single parent family matter?

"This paper examines how living in a single parent family affects intergenerational marriage patterns regarding preferred family size. Data collected from 1,300 college students at a large midwestern [U.S.] university provide further evidence of a positive relationship between number of siblings in one's family of origin and preferred marital family size. However, this relationship does not hold for all groups. Factors affecting preferred family size differ for males and females from intact and nonintact family structures. The positive relationship between size of family of orientation and family of procreation holds only for individuals from intact homes."

Americas↗

PubMed1983

Schizophrenia and the family: II. Adverse effects of family therapy.

Theoretical formulations of the past thirty years have championed the hypothesis that family interaction contributes heavily to the etiology of schizophrenia, a position that has dominated contemporary family therapy even in the absence of solid empirical confirmation. The possibility that sociogenic modeling of schizophrenia is not only incorrect but even harmful to families, and to the relationship between families and clinicians, has never been taken seriously, despite its implications for the practice of family therapy. The author describes untoward effects of the sociogenic hypothesis in his own ten-year experience with families of chronic schizophrenics and examines pertinent reports in the family therapy literature, offering the reinterpretation that many communicational aberrations are adaptations to two therapist attributes: (a) failure to absolve the family of initial causal responsibility, and (b) failure to inform the family about the nature of the illness.

Family↗

PubMedDate not supplied

A family-based program of care for women with recurrent breast cancer and their family members.

PURPOSE/OBJECTIVES: To evaluate the FOCUS Program (family involvement, optimistic attitude, coping effectiveness, uncertainty reduction, and symptom management), a family-based program of care for women with recurrent breast cancer and their family caregivers. DATA SOURCES: Randomized clinical trial. SETTING: Midwest region of the United States. DATA SYNTHESIS: The family-based program of care consisted of five components: family involvement, optimistic attitude, coping effectiveness, uncertainty reduction, and symptom management. The program was delivered in three home visits and two follow-up phone calls over a five-month period of time. CONCLUSIONS: Patients with recurrent breast cancer and their family members reported high satisfaction with the FOCUS Program. Although the FOCUS Program had a number of strengths, limitations of the program also were identified that need to be addressed in future family-based interventions. IMPLICATIONS FOR NURSING: A need exists for family-based programs of care that enable both patients and their family members to manage the multiple demands associated with recurrent breast cancer.

Adaptation, Psychological↗

PubMed2002

Genetic screening for MEN1 mutations in families presenting with familial primary hyperparathyroidism.

A large number of families with familial isolated hyperparathyroidism (FIHP) have been reported. We wanted to determine if some of these families represent early manifestations of full-blown syndromes such as multiple endocrine neoplasia type 1 (MEN-1), as early identification may alter surgical and medical management. Four small families with a family history of hyperparathyroidism without clear-cut MEN-1 features were screened for a MEN1 mutation. The 10 exons of the MEN1 gene were amplified and analyzed by single-strand conformation analysis (SSCA). Abnormal SSCA shifts were then sequenced using an automated sequencer. Two germline mutations were found: R527X and P277H. The former was detected in three members of a family consisting of two children and a mother. At the time of testing the youngest son was normocalcemic and clinically normal but subsequently developed hyperparathyroidism (HPT). Since the initial testing, the family has been confirmed to be a MEN-1 family as the mother has developed abdominal pain and an elevated serum pancreatic polypeptide and the younger brother an anterior pituitary tumor and recurrent HPT. The latter P277H mutation was identified in two of three members tested from another family. Manifestations of MEN-1 syndrome have also developed. The father now has developed diarrhea and elevated serum gastrin; and the daughter has developed recurrent HPT. Genetic screening of families who clinically have FIHP is important and may influence the type of medical and surgical treatment and follow-up, as some have MEN-1 syndrome. Long-term screening for MEN syndromes should be included in this set of patients. Positive screening may predict disease and allow early detection and appropriate treatment before initiation of symptoms.

Adolescent↗

PubMed1983

Familial hyper- and hypouricemias in random and hyperlipidemic recall cohorts: the Princeton School District Family Study.

Using the Princeton School Family Study, our specific aim was to estimate the prevalence of familial hyper- and hypouricemia, to estimate the proportion of probands' first-degree relatives who were similarly affected, and to evaluate the contribution of diseases, drugs, and alcohol intake (if any) to uric acid levels. We studied 379 probands and a total of 1928 subjects, 125 and 52 black probands from a randomly recalled group, 147 white and 55 black probands from a hyperlipidemic recall (top decile cholesterol and/or triglyceride) group. Familial hyper- and hypouricemias were arbitrarily identified in those kindreds having at least two first-degree relatives in the same decile as the proband, top or bottom respectively, for serum uric acid. No probands had symptomatic gout. Diseases, drugs, and alcohol intake were not consistently associated with aggregations of high and/or low uric acid levels in families, and had little relationship to uric acid levels in individuals. Of the 177 randomly recalled probands, and of the 55 black probands in hyperlipidemic recall familial hyperuricemia, with concurrent primary hyperlipoproteinemia and hypertension. Familial hypouricemia was present in 1 of 125 white and in 1 of 52 randomly recalled black kindreds, and in 3 of 147 white and 3 of 55 hyperlipidemic recall black kindreds. While familial clustering of hyperuricemia was limited, clustering of hypouricemia was much more marked. Seventy-four and 84% respectively of first-degree relatives of hypouricemic white and black probands had uric acid less than the 50th percentile. In randomly recalled probands and their first-degree relatives there were significant inverse partial correlations between uric acid and high density lipoprotein cholesterol. Inverse associations of uric acid with high density lipoprotein cholesterol and the concurrence of hyperlipoproteinemia and hypertension in hyperuricemic families points to the importance of lipoprotein and blood pressure screening in families with asymptomatic hyperuricemia. The potential ramifications of within-family clustering of hypouricemia need to be further assessed in populations, particularly in regards to uric acid nephrolithiasis.

Adolescent↗

PubMedDate not supplied

Bipolar II disorder family history using the family history screen: findings and clinical implications.

Psychiatric family history of bipolar II disorder is understudied. The aims of the current study were to find the psychiatric family history of bipolar II patients using a new structured interview, the Family History Screen by Weissman et al (2000), and to find bipolar disorders family history predicting power for the diagnosis of bipolar II. One hundred sixty-four consecutive unipolar major depressive disorder (MDD) and 241 consecutive bipolar II major depressive episode (MDE) outpatients were interviewed with the Structured Clinical Interview for DSM-IV (SCID). The Family History Screen was used. Sensitivity and specificity of predictors of the diagnosis of bipolar II (bipolar [type I and II] family history, bipolar II family history, atypical depression, depressive mixed state, many MDE recurrences, early onset) were studied. Bipolar II subjects had significantly more bipolar I, more bipolar II (50.7%), more MDE, and more social phobia in first-degree relatives than did unipolar subjects. Bipolar II subjects had many more first-degree relatives with bipolar II than with bipolar I. Among the predictors of the diagnosis of bipolar II, bipolar II family history had the highest specificity (82.8%), while early onset had the highest sensitivity. Discriminant analysis of predictor variables found that bipolar II family history and early onset were highly significant predictors. In conclusion, bipolar II family history was common in bipolar II patients, and it had high specificity for predicting bipolar II. If detected, it could reduce bipolar II misdiagnosis by inducing careful probing for a history of hypomania.

Adult↗

PubMed2003

Familial uveal melanoma: a report on two families and a review of the literature.

PURPOSE: A total of 69 families affected by uveal melanoma have been reported in the literature. This report describes two additional families. In addition to presenting these cases, which constitute exceptions, the paper reviews the literature. MATERIAL AND METHODS: Two families, each with two affected members, were analysed in this retrospective study. The pedigree of each family has been pieced together. RESULTS: Considering the low incidence of familial uveal melanoma in the general population, it seems unlikely that inherited genetic factors are responsible for the condition; this question remains difficult to resolve. DISCUSSION: The characteristics of each family history are described and compared with the literature data. The mode of possible inheritance is discussed. Both the histopathology and anatomical location are studied, after which we discuss the body of evidence to establish whether there is an inherited cancer predisposition syndrome in patients with familial uveal melanoma. CONCLUSION: The statistical likelihood of such an uncommon tumour occurring independently in two or more family members leads us to believe that some cases of familial uveal melanoma may go unrecognized, and that reports on too few families have been published worldwide to prove the existence of a single mendelien gene. However, appropriate tissue samples, such as blood and tumour samples, should be obtained and conserved for present or future cytogenetic and molecular genetic studies.

Adult↗

PubMed2005

Familial resemblance in eating behaviors in men and women from the Quebec Family Study.

OBJECTIVE: It is commonly recognized that genetic, environmental, behavioral, and social factors are involved in the development of obesity. The family environment may play a key role in shaping children's eating behaviors. The purpose of this study was to estimate the degree of familial resemblance in eating behavioral traits (cognitive dietary restraint, disinhibition, and susceptibility to hunger). RESEARCH METHODS AND PROCEDURES: Eating behavioral traits were assessed with the Three-Factor Eating Questionnaire in 282 men and 402 women (202 families) from the Quebec Family Study. Familial resemblance for each trait (adjusted for age, sex, and BMI) was investigated using a familial correlation model. RESULTS: The pattern of familial correlation showed significant spouse correlation for the three eating behavior phenotypes, as well as significant parent-offspring and sibling correlations for disinhibition and susceptibility to hunger. According to the most parsimonious model, generalized heritability estimates (including genetic and shared familial environmental effects) reached 6%, 18%, and 28% for cognitive dietary restraint, disinhibition, and susceptibility to hunger, respectively. DISCUSSION: These results suggest that there is a significant familial component to eating behavioral traits but that the additive genetic component appears to be small, with generalized heritability estimates ranging from 6% to 28%. Thus, non-familial environmental factors and gene-gene and gene-environmental interactions seem to be the major determinants of the eating/behavioral traits.

Adolescent↗

PubMed1997

Familial resemblance for abdominal visceral fat: the HERITAGE family study.

OBJECTIVES: Abdominal visceral fat (AVF) is considered a risk factor for diabetes, atherogenic lipid profiles and hypertension. However, little is known about the genetic contribution to AVF as compared to total body fat. DESIGN: AVF was assessed by computerized tomography, and total body fat (fat mass) was assessed by underwater weighing in 86 families participating in the Heritage Family Study. All family members were sedentary at baseline examination. The familial factors underlying the variability in age-adjusted AVF, age-fat mass-adjusted AVF and age-adjusted fat mass, were assessed using a familial correlation model. RESULTS: The maximal heritability (including genetic and familial environmental effects) for AVF was comparable before (47%) and after (48%) adjusting for fat mass, and was 55% for fat mass itself in these sedentary families. Spouse correlations were significant for fat mass and for AVF prior to, but not after, adjustment for fat mass. CONCLUSIONS: These results confirm the only previous study which investigated the familial aggregation of AVF (both in pattern and magnitude), suggesting that the factors underlying AVF in these sedentary families may be similar to those in the population at large. Although both genetic and familial environmental factors probably influence each of fat mass and AVF, there appears to be a predominantly genetic etiology for the visceral component which is independent of total body fat. These findings imply that some individuals are more at risk then others because of an inherited tendency to store abdominal fat viscerally rather than subcutaneously.

Abdomen↗

PubMed2001

Race differences in the pattern of familial aggregation for dehydroepiandrosterone sulfate and its responsiveness to training in the HERITAGE Family Study.

Using a familial correlation model to assess familial influences, baseline dehydroepiandrosterone sulfate (DHEAS) and its change (post-training minus baseline) in response to a 20-week endurance exercise training program were analyzed in 85 black families who participated in the HERITAGE Family Study (HERITAGE). Baseline levels were adjusted for a polynomial in age, and the training response was adjusted for a polynomial in age, as well as the baseline values, within 4 sex-by-generation groups before genetic analysis. We found that the maximal heritability for baseline DHEAS reached 66% (with no sex and generation differences) in black families, which is slightly (but not significantly) higher than the estimate (58%) reported previously in 99 white families in HERITAGE. Whereas weak, but significant, familial effects (26%) for the training response were previously reported for whites in HERITAGE, they were undetectable in the present study. Furthermore, we found heterogeneity in the pattern of familial aggregation (primarily due to different spouse and parent-offspring correlations) for both the baseline and its training response between blacks and whites. In conclusion, baseline DHEAS levels in blacks were also determined by substantial familial factors (just as for whites), independent of the effects of age and sex. Genetic and nongenetic familial components influencing baseline DHEAS levels in both races may be different.

Adolescent↗

PubMed1983

Some KpnI family members are associated with the Alu family in the human genome.

The structures of the termini and their flanking regions of two human KpnI family members were investigated. The two differed in length, but the starting sequence at one terminal (defined as the 5' terminal) was found to be common to both members. The Alu family sequence was found in the 5' flanking regions. The KpnI family sequence started several base-pairs downstream from the 3' end of the Alu family sequence. In both cases, the Alu family sequence was not flanked by the direct repeat sequence common to the Alu family. These two members showed no sequence homology in 3' terminal regions. Interestingly, the Alu family plus the KpnI family unit was found to be flanked by a direct repeat sequence of several base-pair length. Based on these findings, relationship between the Alu family and KpnI family is discussed.

Base Composition↗

PubMed2001

Marital interaction, family organization, and differences in parenting behavior: explaining variations across family interaction contexts.

Family systems theories remind us that, in two-parent families, children encounter their parents in multiple family configurations, including parent-child dyads and mother-father-child triads, or whole families. There are, however, relatively few empirical investigations of differences in parenting behavior which tend to emerge when a dyad is transformed into a whole family unit. Using a sample of 82 families with a kindergarten-age child, the present study offers support to earlier studies reporting that mothers' and fathers' parenting behavior differs when observed in dyadic and whole family interaction sessions. The present study then turns to examining explanations for these differences in parenting behavior. Limited support was found for the hypothesis that observations of marital interaction are associated with differences in parenting behavior across family interaction contexts. Family level assessment of adaptive organization was found to explain differences in fathers' parenting in the dyad and when the entire family is together, but not differences in mothers' parenting behavior. The clinical and methodological implications of these findings are discussed.

Adult↗

PubMed1992

Risk estimation in familial adenomatous polyposis using DNA probes linked to the familial adenomatous polyposis gene.

The familial adenomatous polyposis gene has recently been assigned to the long arm of chromosome five through linkage to several 5q DNA probes. These probes can now be used to trace inheritance of the disease gene in affected families. In this study, DNA samples from 152 members of 10 Australian familial adenomatous polyposis families have been examined for restriction fragment length polymorphisms detected by DNA probes C11P11, ECB27, and YN5.48. Linkage analysis confirmed linkage between the familial adenomatous polyposis gene and each probe with a maximum combined LOD score of 2.82 for C11P11, 2.90 for ECB27 and 5.49 for YN5.48 all at a recombination fraction of zero. Risk estimates were determined for the 51 at risk individuals in these families based on their restriction fragment length polymorphism data alone or in addition by including the effect of age dependent penetrance. Thirty two of those at risk (63%) could be assigned specific high (greater than or equal to 95%) or low (less than or equal to 5%) risks of developing familial adenomatous polyposis on the basis of their probe results. When the effect of age dependent penetrance was included, 26 (51%) fell at the extremes of risk (greater than or equal to 99% or less than or equal to 1%). Such estimates provide a sound basis for planning sigmoidoscopic screening of at risk family members and will thus facilitate surveillance in familial adenomatous polyposis families.

Adenomatous Polyposis Coli↗

PubMed2002

Nationwide prevalence of sporadic and familial idiopathic pulmonary fibrosis: evidence of founder effect among multiplex families in Finland.

BACKGROUND: The prevalence of sporadic and familial idiopathic pulmonary fibrosis (IPF) cases in Finland was evaluated according to the revised recommendations of the American Thoracic Society. METHODS: All Finnish pulmonary clinics (n=29) were included in the primary screening. Hospital data bases were used to identify patients with the diagnosis "alveolitis fibroticans idiopathica" (J84.1 in ICD-10 classification). The total number of patients with IPF was extrapolated based on the evaluation of random samples of case records in different centres. Families with more than one potentially affected member were identified from a questionnaire study and the diagnosis was verified from the medical records. RESULTS: Using this approach, the nationwide prevalence of IPF in Finland was estimated to be 16-18/100 000. In 90% of the patients lung involvement was assessed by high resolution computed tomographic (HRCT) scanning and in 31% a surgical biopsy specimen was available, further confirming the diagnosis. Seventeen multiplex families with 2-5 affected family members were identified, giving a prevalence of 5.9/million for familial IPF in Finland. Both multiplex and sporadic families were clustered in Eastern Finland. This clustering reflects the demographic history of Finland in the 16th century and suggests that multiplex families may share a common ancestor in the last 20-25 generations. CONCLUSION: The familial form explained 3.3-3.7% of all Finnish cases of IPF diagnosed according to the revised international guidelines. Geographical clustering of multiplex families suggests a recent founder effect in patients with familial IPF.

Aged↗

PubMed2002

German national case collection of familial pancreatic cancer - clinical-genetic analysis of the first 21 families.

BACKGROUND: The observation of a familial accumulation of ductal pancreatic adenocarcinoma (PC) and the increased risk for PC in certain hereditary tumor syndromes point to a genetic predisposition for PC. In order to evaluate the characteristics of familial PC, a German national case collection for familial pancreas cancer (FaPaCa) was established. PATIENTS AND METHODS: In FaPaCa, families of patients with PC are being collected, who have at least 1 first-degree relative with PC or with malignant melanoma. Histopathologic verification of tumor diagnoses, acquisition of clinical data, and full genetic counselling are prerequisites for the enrollment of PC families in FaPaCa. RESULTS: So far, 21 families fulfilled the criteria for partaking in FaPaCa. In 11 families, PC represented the sole tumor entity. Additional tumors included malignant melanoma in 5, breast cancer in 3, and prostatic, colon or lung cancer in 2 families. Compared to the preceding generation, a younger age at diagnosis of PC was observed in the offspring of PC patients (offspring median 53 years vs. parents median 75.5 years). CONCLUSION: The association of PC and breast cancer, and of PC and malignant melanoma suggests predisposing mutations in the BRCA2 or CDKN2A genes in about one third of the FaPaCa families. Mutational analyses in both candidate genes may help to identify individuals who are at an increased risk for developing PC. A shift towards a younger age at diagnosis in our PC families may indicate genetic anticipation and/or changes of patterns of exogenous risk factors.

Adult↗

PubMed2004

Approaches to familial aggregation: hypothesis testing and estimation when families are selected through parent probands under a variant of single ascertainment.

Epidemiologic approaches to testing and estimating familial aggregation of a disease consist of comparing rates of disease in relatives of individuals with the disease (known as case probands) with rates of disease in relatives of individuals without the disease (known as control probands). Gold et al. (J Am Stat Ass 1967;62: 409-420) derived an explicit mathematical model and sampling methods, under which this approach is equivalent to testing the null hypotheses that the disease risk in families is homogenous. A basic assumption of this model is that every family member has the same risk of disease and that disease status is independent among family members, although the disease risk may vary between families. When the disease is suspected of having a genetic component, rather than being purely environmental, this model has been shown to be appropriate for detecting disease aggregation in siblings, when relatives are siblings of probands. This model however is unrealistic for use in nuclear families when the affected status of offspring is not independent of the affected status of parents, and these families are selected through an affected or an unaffected parent, so that a parent is the proband and relatives are offspring of probands. We extend the Gold et al. model to allow for the disease risk in offspring to vary with the affected status of the parent. We assume that families are selected through affected and unaffected parents, under a variation of single ascertainment. Under this study design, we show that the usual test of association between affected status of probands and relatives, performed by comparing sample proportions of affected relatives of affected and unaffected probands, respectively, is no longer equivalent to a test of homogeneity of disease risk in offspring. Instead, it is equivalent to testing that the disease risk in offspring is independent of the number of affected parents. This test reduces to a test of homogeneity if and only if one assumes that the variation in disease risk in offspring, between families, is solely due to the variation in the number of affected parents. As a result, we show that under this study design, the standard chi2 test must be modified in order to obtain a valid test of familial aggregation. In addition the sample proportions of affected relatives of case and control probands, respectively, are shown to provide unbiased estimates of the expected risk of disease in an offspring given an affected/unaffected parent. We apply these results to methods of sample selection and discuss the practical implications of these findings.

Data Interpretation, Statistical↗

PubMed1997

Familial resemblance of plasma lipids, lipoproteins and postheparin lipoprotein and hepatic lipases in the HERITAGE Family Study.

The familial aggregation of lipids and lipoproteins and plasma postheparin triglyceride lipases was investigated in 86 Caucasian families participating in the HERITAGE Family study, a study investigating the role of genetic factors in the adaptation to exercise training and its relationships with cardiovascular disease risk factors. Accordingly, sedentary subjects were recruited, tested for a battery of measurements, exercise trained for 20 weeks, and were re-measured. The present report includes plasma levels of total cholesterol, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol and triglycerides, and postheparin plasma lipoprotein lipase (LPL) and hepatic lipase (HL) activities measured in 437 sedentary individuals (171 parents and 266 adult offspring) before training. Significant familial resemblance was observed for all the age-adjusted phenotypes. The pattern of familial correlations reveals no spouse correlations but significant parent-offspring and sibling correlations for total cholesterol, HDL-cholesterol and LDL-cholesterol with heritability (h2) estimates of 62%, 83%, and 50%, respectively. For plasma triglyceride concentrations (h2 = 55%) and HL activity (h2 = 40%), significant spouse correlations were found in addition to parent-offspring and sibling correlations, suggesting that common familial environment in addition to genetic factors contribute to the familial resemblance. For plasma LPL activity, there was no spouse correlation, but sex differences were found in the familial correlations with higher heritabilities in female pairs (h2 = 76%) compared to male pairs (h2 = 30%) and opposite-sex pairs (h2 = 44%). These results confirm the findings of previous family studies showing that genetic factors are major determinants of the familial resemblance in plasma lipids and lipoproteins and suggest the presence of sex differences in the heritability of postheparin LPL activity.

Adolescent↗

PubMed1998

Differences in familial segregation of FEV1 between asthmatic and nonasthmatic families. Role of a maternal component.

Studies have demonstrated familial aggregation of lung function. This study employed segregation analysis to investigate the mode of inheritance of FEV1 using regressive models for continuous traits. The study population comprised 309 families (1,163 individuals) enrolled in the Tucson Children's Respiratory Study who had both parents and at least one child with FEV1 data. Results showed significant genetic heterogeneity among the 87 families (328 individuals) with at least one member with asthma and the 222 families (835 individuals) with no asthmatic members. In families with no asthmatic members, all statistical models were rejected, indicating the absence of a major gene controlling lung function. However, a significant familial component indicated a strong polygenic/multifactorial mode of inheritance. In families with asthmatic member(s), results suggested polygenic/multifactorial inheritance with weak evidence for a Mendelian component expressed in a recessive fashion. However, while both father-offspring and mother-offspring correlations were statistically significant in families with no asthmatic members, only the mother-offspring correlation was significant in families with asthmatic members. The data suggest that lung function is inherited as a polygenic/multifactorial trait, but in asthmatic families a major element of intergenerational correlation is associated with a maternal influence, which may be genetically or environmentally mediated.

Adult↗