Fertility of the Sibs of Schizophrenic Patients

Buck, Carol; Ge, Hobbs; Simpson, H; Jm, Wanklin

doi:10.1192/bjp.127.3.235

Cited by 35 publications

(17 citation statements)

References 9 publications

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“…In traditional population genetics, the fitness of an individual has been quantified by using only his or her genotype o r phenotype. For some diseases, however, the fitness of an individual is determined not only by the disease but by other factors such as cultural and social reactions to the disorder (Reed and Neel, 1959;Lindelius, 1970;Buck et al, 1975;Yokoyama et al, 1980a,b). Therefore, the traditional population genetics approaches are not sufficient to understand evolutionary changes of human diseases a t the population level.…”

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confidence: 99%

Social selection and evolution of human diseases

Yokoyama

1983

American J Phys Anthropol

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Disease incidences in human populations depend on etiology of the disease, the fitness of individuals, and demographic changes of the population. The fitness of an individual is determined not only by the disease but also by other factors such as cultural and social reaction to the disorder and demographic changes of the population. Social selection studies the effect of the social behavior on the incidence of a trait. In studies of Huntington's disease, it has been shown that the fitness of the normal sibling of an affected individual is reduced as much as that of the affected individual himself or herself. A similar social effect has been observed for mental retardation. Thus, even if an individual has a normal genotype, mate finding and fertility may be changed considerably by the presence of affected family members. At the present time, the way in which genetic variabilities are maintained is poorly understood even for clearcut genetic diseases. Studies of social selection indicate that such information should be acquired by considering both the nature of the disease and its social effect.

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confidence: 99%

Social selection and evolution of human diseases

Yokoyama

1983

American J Phys Anthropol

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“…Yokoyama and Templeton (1979) have shown that the incidence of Huntington's disease in a population is determined mainly by its social effect, and thus, the social selection has an important role on the population dynamics of the dominant genes. Such reproductive disadvantage of a phenotypically normal individual with schizophrenic sibs has also been demonstrated by Buck et al (1975) and Lindelius (1970). Morton (1978) suggests that about one-sixth of mental retardation in matings of normal parents could be due to rare recessive genes at more than 300 loci.…”

Section: Introductionmentioning

confidence: 53%

The effect of social selection on population dynamics of rare deleterious genes

Yokoyama

1980

Heredity

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SUMMARYGenetically abnormal or phenotypically affected individuals may influence the reproductive behaviour of other members in the family, regardless of their phenotype. This social selection is modelled by considering that whenever the normal individual has at least one affected member in the nuclear family the person has a reduced chance in mating success or in fertility compared to those from the normal nuclear family. The usual individual selection has also been incorporated using a single locus with two alleles. The gene frequency change is divided into two parts: the change due to individual selection and that due to social selection. It has been shown that a low mutation rate, a small population size and strong selection at both stages lower the equilibrium frequency of deleterious genes. The possibility of extending the single locus model for common diseases is also discussed.

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“…5). One line of evidence is increased fertility of individuals in one or more category of non-affected first-degree relatives of schizophrenics, which has been reported in multiple studies (Avila et al 2001;Bassett et al 1996;Fañ anás & Bertranpetit 1995;Haukka et al 2003;McGlashen et al 2006;Srinivasan & Padmavati 1997;Waddington & Youssef 1996), although other studies report a lack of such differences (Buck et al 1975;Rimmer & Jacobsen 1976). Converse considerations apply to autistic conditions.…”

Section: Behavior and Adaptive Significancementioning

confidence: 94%

Private speech, cognitive-computational control, and the autism-psychosis continuum

Frawley¹

2008

Behav Brain Sci

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Autistic-spectrum conditions and psychotic-spectrum conditions (mainly schizophrenia, bipolar disorder, and major depression) represent two major suites of disorders of human cognition, affect, and behavior that involve altered development and function of the social brain. We describe evidence that a large set of phenotypic traits exhibit diametrically opposite phenotypes in autistic-spectrum versus psychotic-spectrum conditions, with a focus on schizophrenia. This suite of traits is inter-correlated, in that autism involves a general pattern of constrained overgrowth, whereas schizophrenia involves undergrowth. These disorders also exhibit diametric patterns for traits related to social brain development, including aspects of gaze, agency, social cognition, local versus global processing, language, and behavior. Social cognition is thus underdeveloped in autistic-spectrum conditions and hyper-developed on the psychotic spectrum.We propose and evaluate a novel hypothesis that may help to explain these diametric phenotypes: that the development of these two sets of conditions is mediated in part by alterations of genomic imprinting. Evidence regarding the genetic, physiological, neurological, and psychological underpinnings of psychotic-spectrum conditions supports the hypothesis that the etiologies of these conditions involve biases towards increased relative effects from imprinted genes with maternal expression, which engender a general pattern of undergrowth. By contrast, autistic-spectrum conditions appear to involve increased relative bias towards effects of paternally expressed genes, which mediate overgrowth. This hypothesis provides a simple yet comprehensive theory, grounded in evolutionary biology and genetics, for understanding the causes and phenotypes of autistic-spectrum and psychotic-spectrum conditions.

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Fertility of the Sibs of Schizophrenic Patients

Cited by 35 publications

References 9 publications

Social selection and evolution of human diseases

Social selection and evolution of human diseases

The effect of social selection on population dynamics of rare deleterious genes

Private speech, cognitive-computational control, and the autism-psychosis continuum

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