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Familial Risk (familial + risk)

Distribution by Scientific Domains

Psychology	42%
Medical Sciences	33%
Life Sciences	14%

Selected Abstracts

Cannabis use in adolescents: the impact of risk and protective factors and social functioning

DRUG AND ALCOHOL REVIEW, Issue 6 2005
DAVID BEST
Abstract The study uses a school-based sample to test the social and familial risk and protective factors relating to cannabis use. Based on a self-completion survey of 2078 14,16-year-olds (mean age of 15 years) attending seven standard state-run secondary schools in south London, an assessment was made of rates and risk factors for cannabis use. Twenty-four per cent of the total sample had ever used cannabis, with 15% having done so in the month prior to assessment. In addition to greater likelihood of illicit drug use, lifetime cannabis users were less likely to spend time regularly with both their mothers and fathers, but more likely to spend free time with friends who smoked, drank alcohol and used illicit drugs, and with friends involved in criminal activities. Among those who had ever used cannabis, frequency of cannabis use was predicted (using linear regression) by two onset factors (earlier initiation of drinking and cannabis use were both linked to more frequent use) and two social factors (more time spent with drug-using friends and less time spent with the mother). Overall, the study showed that early onset, itself predicted by social networks, is linked to more frequent use of cannabis and that this appears to be sustained by less time spent with parents and more with drug-using peers. [source]

Visual spatial attention and speech segmentation are both impaired in preschoolers at familial risk for developmental dyslexia

DYSLEXIA, Issue 3 2010
Andrea Facoetti
Abstract Phonological skills are foundational of reading acquisition and impaired phonological processing is widely assumed to characterize dyslexic individuals. However, reading by phonological decoding also requires rapid selection of sublexical orthographic units through serial attentional orienting, and recent studies have shown that visual spatial attention is impaired in dyslexic children. Our study investigated these different neurocognitive dysfunctions, before reading acquisition, in a sample of preschoolers including children with (N=20) and without (N=67) familial risk for developmental dyslexia. Children were tested on phonological skills, rapid automatized naming, and visual spatial attention. At-risk children presented deficits in both visual spatial attention and syllabic segmentation at the group level. Moreover, the combination of visual spatial attention and syllabic segmentation scores was more reliable than either single measure for the identification of at-risk children. These findings suggest that both visuo-attentional and perisylvian-auditory dysfunctions might adversely affect reading acquisition, and may offer a new approach for early identification and remediation of developmental dyslexia. Copyright © 2010 John Wiley & Sons, Ltd. [source]

Early home-based intervention in the Netherlands for children at familial risk of dyslexia

DYSLEXIA, Issue 3 2009
Sandra G. van Otterloo
Abstract Dutch children at higher familial risk of reading disability received a home-based intervention programme before formal reading instruction started to investigate whether this would reduce the risk of dyslexia. The experimental group (n=23) received a specific training in phoneme awareness and letter knowledge. A control group (n=25) received a non-specific training in morphology, syntax, and vocabulary. Both interventions were designed to take 10,min a day, 5 days a week for 10 weeks. Most parents were sufficiently able to work with the programme properly. At post-test the experimental group had gained more on phoneme awareness than the control group. The control group gained more on one of the morphology measures. On average, these specific training results did not lead to significant group differences in first-grade reading and spelling measures. However, fewer experimental children scored below 10th percentile on word recognition. Copyright © 2008 John Wiley & Sons, Ltd. [source]

Early development of children at familial risk for Dyslexia,follow-up from birth to school age

DYSLEXIA, Issue 3 2004
H. Lyytinen
Abstract We review the main findings of the Jyväskylä of Dyslexia (JLD) which follows the development of children at familial risk for dyslexia (N = 107) and their controls (N = 93). We will illustrate the development of these two groups of children at ages from birth to school entry in the skill domains that have been connected to reading and reading disability in the prior literature. At school entry, the highest score on the decoding task among the poorer half (median) of the at risk children,i.e. of those presumably being most likely genetically affected,is 1 SD below the mean of the control group. Thus, the familial risk for dyslexia shows expected consequences. Among the earliest measures in which group differences as well as significant predictive associations with the first steps in reading have emerged, are indices of speech processing in infancy. Likewise, various measures of early language including pronunciation accuracy, phonological, and morphological skills (but not performance IQ) show both group differences and predictive correlations, the majority of which become stronger as the reliability of the measures increases by age. Predictive relationships tend to be strong in general but higher in the at risk group because of its larger variance in both the predictor variables and in the dependent measures, such as early acquisition of reading. The results are thus promising in increasing our understanding needed for early identification and prevention of dyslexia. Copyright © 2004 John Wiley & Sons, Ltd. [source]

Association and aggregation analysis using kin-cohort designs with applications to genotype and family history data from the Washington Ashkenazi Study

GENETIC EPIDEMIOLOGY, Issue 2 2001
Nilanjan Chatterjee
Abstract When a rare inherited mutation in a disease gene, such as BRCA1, is found through extensive study of high-risk families, it is critical to estimate not only age-specific penetrance of the disease associated with the mutation, but also the residual effect of family history once the mutation is taken into account. The kin-cohort design, a cross-sectional survey of a suitable population that collects DNA and family history data, provides an efficient alternative to cohort or case-control designs for estimating age-specific penetrance in a population not selected because of high familial risk. In this report, we develop a method for analyzing kin-cohort data that simultaneously estimate the age-specific cumulative risk of the disease among the carriers and non-carriers of the mutations and the gene-adjusted residual familial aggregation or correlation of the disease. We employ a semiparametric modeling approach, where the marginal cumulative risks corresponding to the carriers and non-carriers are treated non-parametrically and the residual familial aggregation is described parametrically by a class of bivariate failure time models known as copula models. A simple and robust two-stage method is developed for estimation. We apply the method to data from the Washington Ashkenazi Study [Struewing et al., 1997, N Engl J Med 336:1401,1408] to study the residual effect of family history on the risk of breast cancer among non-carriers and carriers of specific BRCA1/BRCA2 germline mutations. We find that positive history of a single first-degree relative significantly increases risk of the non-carriers (RR = 2.0, 95% CI = 1.6,2.6) but has little or no effect on the carriers. Genet. Epidemiol. 21:123,138, 2001. © 2001 Wiley-Liss, Inc. [source]

Temperament at 7, 12, and 25 months in children at familial risk for ADHD

INFANT AND CHILD DEVELOPMENT, Issue 4 2008
Judith G. Auerbach
Abstract As part of a longitudinal investigation of infants at familial risk for attention-deficit hyperactivity disorder (ADHD), mothers and fathers independently completed temperament ratings on their infants. In this paper, we examine the 7-, 12-, and 25-month temperament of 58 boys, 36 of whom were considered at familial risk for ADHD and 22 of whom were in the comparison group. Risk for ADHD was based on self-reported ADHD symptoms in the father. In addition, the influence of informant gender on temperament ratings was examined. The ADHD risk group received significantly higher scores for activity level and anger and lower scores for attentional shift, appropriate allocation of attention and inhibitory control. Their scores were also significantly lower on a composite measure of effortful control. Taken together, these findings offer support for the view of a link between early temperament and risk for ADHD. The only informant gender difference was for the activity level; mothers rated their sons as more active than did fathers. Copyright © 2008 John Wiley & Sons, Ltd. [source]

Parenting of 7-month-old infants at familial risk for attention deficit/hyperactivity disorder,

INFANT MENTAL HEALTH JOURNAL, Issue 2 2010
Rivka Landau
Patterns of interaction between parents and 7-month-old boys at familial risk for attention deficit/hyperactivity disorder (ADHD) and a comparison group were studied during a warm-up and two play episodes. The sample included 78 (47 at-risk, 31 comparison) mother,child and 45 (27 at-risk, 18 comparison) father,child dyads. A coding system developed by G. Kochanska (1997, 1998) was used. Infants in the risk group did not differ from the comparison group in the rate of emission of infant-related events. However, they received less adequate responsivity from both their fathers and their mothers to these events, and specifically to negative emotions or distress, than did the comparison group. Maternal psychopathology did not account for these findings. Mothers were more adequately responsive than were fathers, especially for physiological needs. The association between nonoptimal interaction in infancy and the development of ADHD is discussed. [source]

Parental lung cancer as predictor of cancer risks in offspring: Clues about multiple routes of harmful influence?

INTERNATIONAL JOURNAL OF CANCER, Issue 3 2006
Kari Hemminki
Abstract The carcinogenic effects of active smoking have been demonstrated for many sites, but the effects of passive smoking and exposures during pregnancy and breastfeeding are less well documented. We examined whether 0,70-year-old offspring of parents with lung cancer are at a risk of cancer that cannot be explained by their smoking or familial risk. It was assumed that known target sites for tobacco carcinogenesis would be affected, if any. The nationwide Swedish Family-Cancer Database with cancers recorded from 1958 to 2002 was used to calculate age-specific standardized incidence ratios (SIRs). Among offspring of affected mothers, increased risks were observed for upper aerodigestive (SIR 1.45), nasal (2.93), lung (1.71) and bladder (1.52) cancers and for kidney cancer (6.41) in one age group. The risk of bladder cancer was found in younger age groups than that of lung cancer. Cancers at many of these sites, but not the kidney or the bladder, were in excess in offspring of affected fathers. Nasal cancer was even increased when either parent was diagnosed with lung cancer; the highest risk was for nasal adenoid cystic carcinoma (7.73). The data suggest that passive smoking during childhood is associated with an increase risk of nasal cancer. For bladder and kidney cancers, a contribution by tobacco carcinogens is implicated through breastfeeding and in utero exposure. © 2005 Wiley-Liss, Inc. [source]

Depressive symptoms among cognitively normal versus cognitively impaired elderly subjects

INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 5 2001
Yan-sheng Li
Abstract Objectives The present cross-sectional study analyzed the prevalence and severity of depressive symptoms among patients with Alzheimer's disease (DAT), vascular dementia (VAD), and among the cognitively normal elderly. Putative risk factors contributing to depression were likewise evaluated. Methods Seventy-six DAT patients, 51 VAD patients, and 121 cognitively normal subjects were admitted to the study. Questionnaires concerning demography and their vascular and familial risk factors together with results of neuropsychological testing by combined Mini-Mental Status Examinations (MMSE), Cognitive Capacity Screening Examinations (CCSE), and Hamilton Depression Rating Scales (HDRS) were obtained so that resulting data would be statistically analyzed. Results Prevalence of depressive symptoms among VAD, DAT, and cognitively normal elderly were 31.4%, 19.9%, and 13.2%, respectively. 25.5% of VAD and 13.2% of DAT patients had depression of mild to moderate degrees. Regression analysis revealed that diagnosis of VAD and DAT, heart disease, and past history of depression was significantly associated with high HDRS scores. There was no correlation between degree of depression and severity of cognitive impairments. Conclusion Mild to moderate depression is a common comorbidity with organic dementia, especially VAD, but associated depression is independent of severity of cognitive impairments. Copyright © 2001 John Wiley & Sons, Ltd [source]

The rate of urinary cortisol excretion at work is persistently elevated in women at familial risk for breast cancer

AMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 4 2008
Gary D. James
We recently reported that healthy women at familial risk for breast cancer (FH+) have higher urinary cortisol levels at work than women without familial risk (FH,). The purpose of this study was to evaluate whether this group difference persisted over a 1-month period. Subjects were healthy women (FH+, N = 42, age = 37.6 ± 9.3, FH,, N = 93, age 38.4 ± 9.0) employed primarily in clerical or technical positions at three medical centers in New York City who collected timed urine samples in three contrasting daily environments, at work (,11AM,3PM), home (,6PM,10PM) and during sleep (,10PM,6AM) on 2 mid-week workdays ,1 month apart. Two-way repeated measures ANOVA revealed that cortisol excretion differed across the environments (P < 0.001), and that there was also a significant interaction between daily environment and family history group (P < 0.049), such that FH+ women maintained higher cortisol excretion at work over the 2 days than FH, women. A Bland,Altman plot showed that both overall and by family history group, the rate of cortisol excretion at work was generally reproducible, although there was a heteroscadasticity in the relationship that likely reflected excessive stressfulness on one of the study days in a small minority of subjects. These results suggest that the presence of a potent background stressor (familial breast cancer risk) can influence more acute cortisol responses in daily life over time. Am. J. Hum. Biol., 2008. © 2008 Wiley-Liss, Inc. [source]

Familial associations of rheumatoid arthritis with autoimmune diseases and related conditions

ARTHRITIS & RHEUMATISM, Issue 3 2009
Kari Hemminki
Objective In the era of genome-wide association studies, familial risks are used to estimate disease heritability and the likelihood of candidate-gene identification. This study was undertaken to estimate associations of rheumatoid arthritis (RA) with any of 33 autoimmune diseases and related conditions among parents and offspring, singleton siblings, twins, and spouses. Methods The Multigeneration Register in Sweden was used as a reliable source of information on Swedish families throughout the last century. Data on autoimmune diseases in individual family members were obtained through linkage to the Hospital Discharge Register. The standardized incidence ratio (SIR) was calculated as a measure of the relative risk of RA in family members of patients with RA or any of 33 other autoimmune diseases or related conditions, as compared with the relative risk of RA in those lacking an affected family member. Results Among a total of 447,704 patients, 47,361 were diagnosed as having RA. The SIRs for RA were 3.02 in offspring of affected parents, 4.64 in siblings, 9.31 in multiplex families, 6.48 in twins, and 1.17 in spouses. Significant associations with the familial risk of RA in offspring according to parental proband were observed for ankylosing spondylitis (SIR 2.96), localized scleroderma (SIR 2.40), Sjögren's syndrome (SIR 2.25), systemic lupus erythematosus (SIR 2.13), systemic sclerosis (SIR 1.65), Hashimoto thyroiditis/hypothyroidism (SIR 1.54), pernicious anemia (SIR 1.53), sarcoidosis (SIR 1.40), psoriasis (SIR 1.36), Wegener's granulomatosis (SIR 1.34), and asthma or polymyalgia rheumatica (SIR 1.32). Conclusion This is the first study to compare the familial risks of RA in relation to a large number of autoimmune diseases and related conditions using data from a single population. The high discordant familial risks in this population suggest that there is extensive genetic sharing between RA and the associated diseases. [source]

A common genetic background for inflammatory bowel disease and ankylosing spondylitis: A genealogic study in Iceland

ARTHRITIS & RHEUMATISM, Issue 8 2007
Bjarni Thjodleifsson
Objective Patients with ankylosing spondylitis (AS) and ,50% of their first-degree relatives may have a genetic abnormality that results in subclinical intestinal inflammation. This study was undertaken to examine the familial occurrence and cosegregation of AS and inflammatory bowel disease (IBD) in order to determine whether there is a shared genetic risk factor in families. Methods The Icelandic genealogy database and population-wide data on all living Icelanders diagnosed as having AS (n = 205) and/or IBD (n = 1,352) were used to estimate the risk ratios of AS for relatives of patients with AS, the risk ratios of IBD for relatives of patients with IBD, and the cross-risk ratios of AS for relatives of patients with IBD or of IBD for relatives of patients with AS. The mean kinship coefficients for each disease were calculated. The control population for disease risk calculations comprised 10,000,100,000 sets of matched Icelandic subjects. Results First-, second-, and third-degree relatives of patients with AS had risk ratios of 94, 25, and 3.5, respectively, indicating an increased risk of developing AS (each P < 0.0005), while first-, second-, and third-degree relatives of patients with IBD had risk ratios for IBD of 4.4, 2.2, and 1.4, respectively (each P < 0.0001). The cross-risk ratios of IBD were 3.0 and 2.1 in first- and second-degree relatives of patients with AS, respectively, and were the same for AS in first- and second-degree relatives of patients with IBD. With the exception of Crohn's disease, the risk of having AS, ulcerative colitis, or IBD in spouses of patients with these diseases did not differ significantly from that in controls. Calculation of the kinship coefficients confirmed these patterns of familial risk. Conclusion Patients with AS or IBD in Iceland are significantly more related to each other than are randomly sampled control subjects, in terms of an increased risk of either or both conditions developing in third-degree relatives. These findings suggest that one or more undiscovered genetic variants may underlie the risk of both diseases. [source]

Sex-specific familial risks of urinary bladder cancer and associated neoplasms in Sweden

INTERNATIONAL JOURNAL OF CANCER, Issue 9 2009
Justo Lorenzo Bermejo
Abstract Male gender and a family history of cancer are established risk factors for urinary bladder neoplasms. This study used the latest update of the Swedish Family-Cancer Database, which includes 42,255 bladder cancer patients, to investigate the sex-specific incidences and types of tumors in relatives of bladder cancer patients. Men with parents or siblings affected by lung cancer did not show an increased risk of bladder neoplasms. Among women, the familial association was restricted to daughters of women with lung cancer. Brothers showed higher risks than the sons of bladder cancer patients. Men older than 54 years were at an increased risk of bladder cancer only if their fathers or siblings were diagnosed after age 65 years. The present data indicated a limited contribution of smoking to the familial clustering of bladder cancer with other neoplasms. The dependence of the relative risks on the type of familial relationship probably reflected a heterogeneous character of familial aggregation. Age-specific results suggested differential risk factors for tumors diagnosed before 50 years of age versus neoplasms detected later in life. The present data may guide the design of forthcoming gene identification studies and the interpretation of the genome-wide association studies that are about to be published. © 2008 Wiley-Liss, Inc. [source]

Quantification of the familial contribution to juvenile idiopathic arthritis

ARTHRITIS & RHEUMATISM, Issue 8 2010
Sampath Prahalad
Objective We previously demonstrated that there is familial aggregation of juvenile idiopathic arthritis (JIA). Using a large JIA cohort, we sought to identify additional clusters of JIA cases and to calculate robust estimates of the relative risk (RR) of JIA in the siblings and cousins of JIA probands. We also estimated the population attributable risk (PAR) of familial factors in JIA. Methods A probabilistic record-linking analysis was performed by matching the records of 862 patients with JIA with the records of ,7 million individuals in the Utah Population Database (UPDB), a computerized genealogic database. For each patient, 5 control subjects matched for birth year and sex were selected from the UPDB. Specialized software was used to test for familial aggregation of disease, to estimate the magnitude of familial risks, and to identify families at high risk of disease. Results We identified 22 founders who had significantly more descendants with JIA than expected (5,13 descendants; P values ranged from <0.0001 to <0.008). The PAR of familial factors for JIA was ,13%. The RR of JIA in the siblings of patients was significantly increased (11.6, 95% confidence interval [95% CI] 4.9,27.5, P < 2.59 × 10,8). The RR of JIA in first cousins was also increased (5.82, 95% CI 2.5,13.8, P < 6.07 × 10,5). Conclusion We have identified the largest sets of JIA pedigrees described to date. Approximately 13% of cases of JIA can be attributed to familial factors. Siblings and first cousins of probands with JIA have an increased risk of JIA. The observed decline in the magnitude of risk between siblings and cousins suggests that JIA is influenced by shared genetic factors. [source]