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(searched for: doi:10.1080/00207411.1972.11448564)
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M Abdullah Ijaz
Published: 6 February 2018
SSRN Electronic Journal; https://doi.org/10.2139/ssrn.3119070

Abstract:
The role of the neuron pathways in the behaviour of a human reflects on their importance in all human attributes including conscience. Provided that the positioning and structure of the pathways is a phenotype the genetic code of any individual becomes responsible for his behaviour. Using past research an outline has been generated showing the relationship of genetic factors and conscience.
, Jay Joseph
Published: 1 April 2013
International Journal of Health Services, Volume 43, pp 281-303; https://doi.org/10.2190/hs.43.2.f

Abstract:
This article critiques the “missing heritability” position, which calls for greater efforts and funding to identify the genetic architecture of common disorders, even if this endeavor has yet to translate into tangible prevention, diagnosis, or treatment interventions. Supporters of the position contend that genetic variants “for” common disorders, which they argue must exist based on heritability estimates (hence their “missing heritability” position), have not been found because the current state of science and technology is not adequate to the task, yet they insist that this search warrants significant societal investments. We argue, instead, that these variants have not been found because they do not exist. The thrust of the problem with the “missing heritability” position, we propose, lies in its proponents' use of faulty concepts and research methods, including reliance on twin studies, plagued with environmental confounds; on the concept of heritability, a breeding statistic and not a measure of the importance of genetic influences on phenotypes; and on the belief that genetic variations are relevant to understanding, preventing, or treating common disorders, a belief that we argue is false. We elaborate on these problems, discuss their public health implications, and suggest future directions for a critical analysis of human genetics.
Published: 24 November 2012
Journal of the History of Biology, Volume 46, pp 1-30; https://doi.org/10.1007/s10739-012-9344-6

The publisher has not yet granted permission to display this abstract.
Published: 23 April 2012
Applied Developmental Science, Volume 16, pp 65-83; https://doi.org/10.1080/10888691.2012.667343

Abstract:
The psychiatric genetics field is currently undergoing a crisis due to the decades-long failure to uncover the genes believed to cause the major psychiatric disorders. Since 2009, leading researchers have explained these negative results on the basis of the “missing heritability” argument, which holds that more effective research methods must be developed to uncover presumed missing genes. According to the author, problems with the missing heritability argument include genetic determinist beliefs, a reliance on twin research, the use of heritability estimates, and the failure to seriously consider the possibility that presumed genes do not exist. The author concludes that decades of negative results support a finding that genes for the major psychiatric disorders do not appear to exist, and that research attention should be directed away from attempts to uncover “missing heritability” and toward environmental factors and a reassessment of previous genetic interpretations of psychiatric family, twin, and adoption studies.
Jon Löve Karlsson
Published: 12 February 2009
Journal: Hereditas
Hereditas, Volume 72, pp 153-158; https://doi.org/10.1111/j.1601-5223.1972.tb01037.x

The publisher has not yet granted permission to display this abstract.
Jon L. Karlsson
Published: 14 February 2008
Journal: Hereditas
Hereditas, Volume 107, pp 59-64; https://doi.org/10.1111/j.1601-5223.1987.tb00269.x

The publisher has not yet granted permission to display this abstract.
Jon L. Karlsson
Published: 1 January 1998
Nordic Journal of Psychiatry, Volume 52, pp 453-457; https://doi.org/10.1080/08039489850139229

Abstract:
Longitudinal studies of mental illness in Iceland indicate that psychosis sometimes segregates into high- and low-rate family branches. Instances are also reported in which the disorder appears to have been derived from one parent. A large family investigation has led to extensive risk data for various classes of relatives, consistent with modified dominant transmission when delusional and affective psychoses are treated as a unit. Some carriers of the proposed psychosis gene are highly gifted, both in terms of artistic production and academic performance. Particularly striking is the number of individuals in families with psychosis who perform brilliantly in mathematics. Attempts to isolate and characterize a psychosis gene seem fully warranted.
A. Pam, S.S. Kemker, Colin A Ross, R R Golden
Acta geneticae medicae et gemellologiae: twin research, Volume 45, pp 349-360; https://doi.org/10.1017/s0001566000000945

Abstract:
The comparison of MZ-DZ twins in behavioral genetics has produced what seems like irrefutable evidence for the heritability of many psychiatric disorders. But such research depends on the validity of the EEA – the “equal environments assumption” – as an underlying premise. In this paper, several empirical studies which support the EEA are critically reviewed in terms of methodology and the way data has been processed in a mathematical model called “path analysis”. It turns out that studies investigating the EEA appear to be largely inadequate in terms of technique, as well as biased in the inferences drawn. Further, the “heritability” estimate – often taken to mean the influence of trait – specific genes – is merely a statistical abstraction derived from a matrix of correlations; this estimate encompasses many buried environmental effects so that “heritability” does not correspond to any underlying DNA structure. In conclusion, many MZ-DZ pedigree studies have dubious scientific value, given the non-viable premise of the EEA, as well as the misleading operational definition of what has been called “heritability”.
T. J. Crow
The British Journal of Psychiatry, Volume 156, pp 788-797; https://doi.org/10.1192/bjp.156.6.788

Abstract:
Attempts to draw a line of genetic demarcation between schizophrenic and affective illnesses have failed. It must be assumed that these diseases are genetically related. A post-mortem study has demonstrated that enlargement of the temporal horn of the lateral ventricle in schizophrenia but not in Alzheimer-type dementia is selective to the left side of the brain. This suggests that the gene for psychosis is the ‘cerebral dominance gene‘, the factor that determines the asymmetrical development of the human brain. That the psychosis gene is located in the pseudoautosomal region of the sex chromosomes is consistent with observations that sibling pairs with schizophrenia are more often than would be expected of the same sex and share alleles of a polymorphic marker at the short-arm telomeres of the X and Y chromosomes above chance expectation. That the cerebral dominance gene also is pseudoautosomal is suggested by the pattern of verbal and performance deficits associated with sex-chromosome aneuploidies. The psychoses may thus represent aberrations of a late evolutionary development underlying the recent and rapid increase in brain weight in the transition fromAustralopithecusthroughHomo habilisandHomo erectustoHomo sapiens.
Patrick Burke, Joaquim Puig-Antich
Published: 1 January 1990
The publisher has not yet granted permission to display this abstract.
Steven Taylor, Elizabeth Hinton
Published: 1 December 1987
Psychological Reports, Volume 61, pp 875-878; https://doi.org/10.2466/pr0.1987.61.3.875

Abstract:
The present article considers the recent increase in community-based support systems for psychiatric patients. Although these systems appear to offer some short-term benefits, the long-term consequences have received little attention. Here, the case is examined for such systems actually facilitating the reproductive rates and hence general incidence of genetically transmitted disorders such as schizophrenia.
Timothy J. Crow, D.John Done
Published: 30 June 1986
Psychiatry research, Volume 18, pp 107-117; https://doi.org/10.1016/0165-1781(86)90023-5

Abstract:
Original article can be found at: http://www.sciencedirect.com/science/journal/01651781 Copyright Elsevier Ltd. DOI: 10.1016/0165-1781(86)90023-5 [Full text of this article is not available in the UHRA]The possibility that schizophrenia is horizontally transmitted has been assessed in an analysis of age of onset in 264 recorded pairs of siblings with the disease. Age of onset was found to be correlated between siblings, and there was a tendency for the disease to occur at an earlier age in the younger sibling. Three explanations for this finding are considered: horizontal transmission, early detection, and ascertainment bias. An analysis by date of birth differences between siblings gives results consistent with horizontal transmission, but analysis by order of onset of illness (which shows that the age shift is not seen in elder-sibling-ill-first pairs) indicates that ascertainment bias (which arises from a tendency to include an excess of early onsets in younger siblings) is a more cogent explanation of the age shift. Although horizontal transmission is not altogether eliminated, the data suggest that age of onset is determined by genetic or prenatal factors rather than environmental precipitants in postnatal life. The retrovirus/transposon hypothesis (Crow, 1984) can accommodate the findings more readily than the gene-virus interaction hypothesis (Crow, 1983)
James P. Curran, Robert G. Sutton, , Simone Guenette
Published: 1 January 1985
The publisher has not yet granted permission to display this abstract.
Jon L. Karlsson
The British Journal of Psychiatry, Volume 140, pp 600-606; https://doi.org/10.1192/bjp.140.6.600

Abstract:
Summary: The more recent large scale family investigations of schizophrenia are reviewed, particularly studies in which the authors have compared the rates in relatives of index cases with those of the general population. The risk of psychotic illness is increased four-fold in first-degree relatives and two-and-a-half-fold in second-degree relatives over that of the population at large. The possible genetic mechanisms are evaluated, with the conclusion that modified dominant transmission, based on a single major gene, is a plausible system.
H. R. Maricq
Published: 1 October 1975
Acta Psychiatrica Scandinavica, Volume 52, pp 264-282; https://doi.org/10.1111/j.1600-0447.1975.tb00042.x

Abstract:
A two-gene model for the hereditary transmission of schizophrenia is presented involving two pairs of autosomal alleles Ss and Pp. It is hypothesized that the recessive gene can produce schizophrenia in homozygous state with a penetrance of .40. In the presence of the gene P schizophrenia can occur in the heterozygote Ss, resulting in a more serious form of the disease and having a manifestation rate of .70. The population frequencies best fitting the available data are estimated to be approximately .03 for P and .07 or .08 for s. It is also hypothesized that the reproductive fitness is .80 in manifest schizophrenics with genotype ss pp and .50 in overt schizophrenics carrying the modifier gene P. The model is proposed to cover only the so-called "process" or "nuclear" type of schizophrenia. The remaining schizophrenics of "reactive" and other types may belong to different genotypes or consist in phenocopies. The model is discussed in relation to literature observations and our own previous studies. The possibilities for increased fitness of non-schizophrenic carriers of P and s are also discussed.
Jon L. Karlsson
Published: 1 November 1973
The British Journal of Psychiatry, Volume 123, pp 549-554; https://doi.org/10.1192/bjp.123.5.549

Abstract:
At the present time there is a renewal of interest in the contribution of biological factors to schizophrenic illness. This stems in part from the success of pharmacological treatment and in part from the impressive findings in studies of foster-reared relatives of schizophrenics. While the pendulum of emphasis thus seems to be generally swinging in favour of constitutional influences, recent reports on twin studies have tended to go in the opposite direction. As will be discussed below, this development is largely attributable to a methodological error in the most recent twin investigations.
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