Heritability of Schizophrenia

1994 ◽  
Vol 164 (4) ◽  
pp. 481-486 ◽  
Author(s):  
O. Gureje ◽  
R. Bamidele ◽  
Y. A. Aderibigbe
Keyword(s):  
Family History ◽  
Affective Psychoses ◽  
First Degree Relatives ◽  
The Family ◽  
Schizophrenic Patients ◽  
Manic Patients

Thirty-six consecutively admitted patients with schizophrenia and 20 with mania were studied for the morbid risk of psychosis in their first-degree relatives. Using the family history method of ascertainment, the morbid risk for schizophrenia in the relatives of schizophrenic probands was 4.12% compared with 1.42% in the relatives of manic probands. While this difference was not statistically significant, that between the morbid risk for affective psychoses in the relatives of manic patients (7.81%) was significantly higher than for the relatives of schizophrenic patients (0%).

Assessing the risk of Alzheimer's disease in first-degree relatives of Alzheimer's disease cases

1993 ◽  
Vol 23 (4) ◽  
pp. 915-923 ◽  
Author(s):  
A. E. Korten ◽  
A. F. Jorm ◽  
A. S. Henderson ◽  
G. A. Broe ◽  
H. Creasey ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Family History ◽  
Cumulative Incidence ◽  
Dominant Gene ◽  
Lifetime Risk ◽  
First Degree Relatives ◽  
Familial Form ◽  
The Family ◽  
History Of

SynopsisFamily history of Alzheimer's disease (AD) was investigated using a telephone re-interview of 99 cases and 116 controls selected from a case–control study of 170 matched pairs. It was found that the family history method used in the initial interview was satisfactory in identifying first-degree relatives and assessing their ages of birth and death, but the number of first-degree relatives suffering from AD was probably under-estimated. Family history of AD was confirmed as a risk factor for AD. Higher estimates of cumulative incidence were obtained among case relatives than among control relatives. No evidence was found to support the hypothesis that a familial form of AD is more common in those with earlier onset AD (before age 75) in those who display early, prominent features of aphasia or apraxia, or that an AD gene may be sex-linked. The curves for cumulative incidence showed no tendency to reach an asymptote, as is implied by the theory that some forms of AD are due to the action of an autosomal dominant gene. Estimates of lifetime risk by age 90 were within the range found by other investigators. Much larger samples of the very old are needed to obtain estimates of total lifetime risk with smaller standard errors.

scholarly journals Surveillance survey of family history in children with neural tube defects

2017 ◽  
Vol 19 (6) ◽  
pp. 690-695 ◽  
Author(s):  
Esther B. Dupépé ◽  
Daxa M. Patel ◽  
Brandon G. Rocque ◽  
Betsy Hopson ◽  
Anastasia A. Arynchyna ◽  
...  
Keyword(s):  
Risk Factors ◽  
Family History ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Positive Family History ◽  
Cns Disorders ◽  
Paternal Lineage ◽  
First Degree Relatives ◽  
The Family ◽  
History Of

OBJECTIVE Although there are known risk factors for the development of neural tube defects (NTDs), little is known regarding the role of family history. The authors' goal in this study is to describe the family history in their population of patients with NTDs. METHODS Surveys were completed for 254 patients who were accompanied by their biological mother during their annual visit to the multidisciplinary Spina Bifida Clinic at Children's of Alabama. An NTD has been diagnosed in all patients who are seen in this clinic (myelomeningocele, lipomeningocele, split cord malformation, and congenital dermal sinus tract). Each mother answered questions regarding known NTD risk factors and their pregnancy, as well as the family history of NTDs, other CNS disorders, and birth defects. RESULTS The overall prevalence of family history of NTDs in children with an NTD was 16.9% (n = 43), of which 3.1% (n = 8) were in first-degree relatives. In patients with myelomeningocele, 17.7% (n = 37) had a positive family history for NTDs, with 3.8% in first-degree relatives. Family history in the paternal lineage for all NTDs was 8.7% versus 10.6% in the maternal lineage. Twenty-two patients (8.7%) had a family history of other congenital CNS disorders. Fifteen (5.9%) had a family history of Down syndrome, 12 (4.7%) had a family history of cerebral palsy, and 13 (5.1%) patients had a family history of clubfoot. Fourteen (5.5%) had a family history of cardiac defect, and 13 (5.1%) had a family history of cleft lip or palate. CONCLUSIONS The family history of NTDs was 16.9% in children with NTD without a difference between maternal and paternal lineage. This high rate of positive family history suggests that genetics and epigenetics may play a larger role in the pathogenesis of NTD in the modern era of widespread folate supplementation.

Psychiatric Illness in First-Degree Relatives of Patients with Paranoid Psychosis, Schizophrenia and Medical Illness

1985 ◽  
Vol 147 (5) ◽  
pp. 524-531 ◽  
Author(s):  
Kenneth S. Kendler ◽  
Catherine C. Masterson ◽  
Kenneth L. Davis
Keyword(s):  
Personality Disorder ◽  
Psychiatric Illness ◽  
Delusional Disorder ◽  
Medical Illness ◽  
Schizotypal Personality ◽  
First Degree Relatives ◽  
The Family ◽  
Paranoid Personality Disorder ◽  
Schizophrenic Patients ◽  
Paranoid Psychosis

This study examines the respective morbid risk for psychiatric illness determined by the family history method in the first-degree relatives of medical controls and patients with delusional disorder (paranoid psychosis) and schizophrenia. The morbid risk for schizophrenia and schizoid-schizotypal personality disorder was significantly greater in the relatives of the schizophrenic patients than in those of the delusional disorder or medical control patients, but no difference in the risk for affective illness or alcoholism was found in the three groups of relatives. Paranoid personality disorder was significantly more common in the relatives of the delusional disorder patients than in those of the medical controls. These results support the familial independence of delusional disorder and schizophrenia.

scholarly journals How should we construct psychiatric family history scores? A comparison of alternative approaches from the Dunedin Family Health History Study

2008 ◽  
Vol 38 (12) ◽  
pp. 1793-1802 ◽  
Author(s):  
B. J. Milne ◽  
T. E. Moffitt ◽  
R. Crump ◽  
R. Poulton ◽  
M. Rutter ◽  
...  
Keyword(s):  
Family History ◽  
Genetic Research ◽  
Family Health ◽  
Significant Family History ◽  
First Degree Relatives ◽  
Health History ◽  
Public Health Screening ◽  
The Family ◽  
History Of ◽  
Strength Of Association

BackgroundThere is increased interest in assessing the family history of psychiatric disorders for both genetic research and public health screening. It is unclear how best to combine family history reports into an overall score. We compare the predictive validity of different family history scores.MethodProbands from the Dunedin Study (n=981, 51% male) had their family history assessed for nine different conditions. We computed four family history scores for each disorder: (1) a simple dichotomous categorization of whether or not probands had any disordered first-degree relatives; (2) the observed number of disordered first-degree relatives; (3) the proportion of first-degree relatives who are disordered; and (4) Reed's score, which expressed the observed number of disordered first-degree relatives in terms of the number expected given the age and sex of each relative. We compared the strength of association between each family history score and probands' disorder outcome.ResultsEach score produced significant family history associations for all disorders. The scores that took account of the number of disordered relatives within families (i.e. the observed, proportion, and Reed's scores) produced significantly stronger associations than the dichotomous score for conduct disorder, alcohol dependence and smoking. Taking account of family size (i.e. using the proportion or Reed's score) produced stronger family history associations depending on the prevalence of the disorder among family members.ConclusionsDichotomous family history scores can be improved upon by considering the number of disordered relatives in a family and the population prevalence of the disorder.

scholarly journals Endoscopic screening of relatives of patients with colorectal cancer

Gut ◽  
1998 ◽  
Vol 42 (1) ◽  
pp. 71-75 ◽  
Author(s):  
L M Hunt ◽  
P S Rooney ◽  
J D Hardcastle ◽  
N C Armitage
Keyword(s):  
Colorectal Cancer ◽  
Family History ◽  
Lower Risk ◽  
Flexible Sigmoidoscopy ◽  
Familial Risk ◽  
Endoscopic Screening ◽  
First Degree Relatives ◽  
The Family ◽  
Satisfactory Method ◽  
History Of

Background—The risk of colorectal cancer is higher among relatives of those affected. The neoplastic yield reported from screening such individuals varies enormously between studies and depends on the age and strength of the family history of those screened.Aims—To ascertain the neoplastic yield of endoscopic screening of first degree relatives of patients with colorectal cancer by age and familial risk.Subjects—A total of 330 individuals with a family history of colorectal cancer.Method—Endoscopic screening conducted according to a protocol.Results—Adenomas were found in 12%, and adenomas larger than 1 cm in 8%, of “high risk” individuals screened primarily by colonoscopy. Of those with neoplasia, 26% had lesions at or proximal to the splenic flexure. Neoplasia was found in 9.5% of individuals at lower familial risk, screened primarily by 60 cm flexible sigmoidoscopy, 4% of whom had neoplasia larger than 1 cm in size or cancer. Neoplastic yield was greatest in the fourth and fifth decades in those at highest risk, but increased with age in those at lower risk.Conclusions—For individuals with two or more first degree relatives, or relatives who have developed colorectal cancer at a young age, colonoscopy appears to be the only satisfactory method of screening, but 60 cm flexible sigmoidoscopy may be useful in those at lower levels of risk.

Comparison of Hospitalization Measures in Schizophrenic Patients with and without a Family History of Schizophrenia

1969 ◽  
Vol 115 (520) ◽  
pp. 321-334 ◽  
Author(s):  
L. Erlenmeyer-Kimling ◽  
Susan Nicol
Keyword(s):  
Family History ◽  
Familial Incidence ◽  
Increased Risk ◽  
The Family ◽  
Schizophrenic Patients ◽  
History Of ◽  
Open Question

It is well known that an individual with a family history of schizophrenia carries an increased risk of manifesting the disorder in comparison with members of the population at large. Also, within the population of schizophrenic patients, individuals may or may not have other members of the family affected. Obviously also, schizophrenic patients may be distinguished by gradations of severity of the illness. Whether familial incidence of schizophrenia and severity co-vary, however, remains an open question.

A controlled family history study of bulimia

1987 ◽  
Vol 17 (4) ◽  
pp. 883-890 ◽  
Author(s):  
James I. Hudson ◽  
Harrison G. Pope ◽  
Jeffrey M. Jonas ◽  
Deborah Yurgelun-Todd ◽  
Frances R. Frankenburg
Keyword(s):  
Eating Disorders ◽  
Family History ◽  
Major Depression ◽  
Psychiatric Disorders ◽  
Affective Disorder ◽  
First Degree Relatives ◽  
The Family ◽  
Alternative Hypotheses ◽  
History Of

SynopsisUsing the family history method, we assessed the morbid risk for psychiatric disorders the first-degree relatives of 69 probands with bulimia, 24 probands with major depression, and nonpsychiatric control probands. The morbid risk for major affective disorder among the first-degree relatives of the bulimic probands was 32%, significantly greater than that found in the nonpsychiatric control probands. The rate of familial major affective disorder was significantly greater in bulimic probands who had a history of major affective disorder themselves than in bulimic probands without such a history - but the latter group, in turn, displayed significantly higher rates than the nonpsychiatric control probands. Eating disorders were slightly, but not significantly, more prevalent in the families of bulimic probands than nonpsychiatric control probands. We present two alternative hypotheses which might explain these findings.

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