Mutation and psychosis: a suggested explanation of seasonality of birth

Crow, Timothy J.

doi:10.1017/s0033291700000611

Cited by 22 publications

(7 citation statements)

References 67 publications

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“…both Book (1953) and Lewis (1958) suggested a role for new mutations in the etiology of schizophrenia, but the idea was discounted because human mutation rates were considered to be too low to account for the prevalence of schizophrenia (Huxley et al 1964;Penrose 1968). To the contrary, recent data show that mutations are common in humans; we may acquire 100 mutations per individual per generation, including several deleterious mutations, one or two of which may persist in the gene pool (Crow 1999;Eyre-Walker et al 1999). The noted geneticist, James F. Crow, has written extensively on the nature and outcome of human mutations and has proposed that a high spontaneous mutation rate could present a genetic risk for the future human population (Crow 1997(Crow , 1999.…”

Section: New Mutationsmentioning

confidence: 99%

“…To the contrary, recent data show that mutations are common in humans; we may acquire 100 mutations per individual per generation, including several deleterious mutations, one or two of which may persist in the gene pool (Crow 1999;Eyre-Walker et al 1999). The noted geneticist, James F. Crow, has written extensively on the nature and outcome of human mutations and has proposed that a high spontaneous mutation rate could present a genetic risk for the future human population (Crow 1997(Crow , 1999.…”

Section: New Mutationsmentioning

confidence: 99%

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Paternal Factors and Schizophrenia Risk: De Novo Mutations and Imprinting

Malaspina¹

2001

Schizophrenia Bulletin

147

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There is a strong genetic component for schizophrenia risk, but it is unclear how the illness is maintained in the population given the significantly reduced fertility of those with the disorder. One possibility is that new mutations occur in schizophrenia vulnerability genes. If so, then those with schizophrenia may have older fathers, because advancing paternal age is the major source of new mutations in humans. This review describes several neurodevelopmental disorders that have been associated with de novo mutations in the paternal germ line and reviews data linking increased schizophrenia risk with older fathers. Several genetic mechanisms that could explain this association are proposed, including paternal germ line mutations, trinucleotide repeat expansions, and alterations in genetic imprinting in one or several genes involved in neurodevelopment. Animal models may be useful in exploring these and other explanations for the paternal age effect and they may provide a novel approach for gene identification. Finally, it is proposed that environmental exposures of the father, as well as those of the mother and developing fetus, may be relevant to the etiology of schizophrenia.

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Section: New Mutationsmentioning

confidence: 99%

Section: New Mutationsmentioning

confidence: 99%

Paternal Factors and Schizophrenia Risk: De Novo Mutations and Imprinting

Malaspina¹

2001

Schizophrenia Bulletin

147

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“…Wright et al (1993) suggested the maternal immune response to the infection yielded antibodies to fetal brain proteins. Crow (1987) proposed that some viral species insert genes into vulnerable individuals with existing genetic predispositions.…”

Section: Epidemiological Studiesmentioning

confidence: 99%

Glucocorticoid Hormones and Early Brain Development in Schizophrenia

Koenig

Kirkpatrick

Lee

2002

Neuropsychopharmacology

181

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While genetic factors play a role in the etiology of schizophrenia, environmental factors contribute to the etiology of the disorder as well. If a woman is exposed during the second trimester of gestation to stressors such as the death of a loved one, influenza infection, or natural and man-made disasters, her baby has an increased risk of developing schizophrenia later in life. A common mechanism may mediate the effects of these diverse risk factors: a stress response during a restricted period of gestation may affect fetal brain development and, given the appropriate genetic predisposition, result in schizophrenia in adult life. Findings in animals exposed to prenatal stress strengthen the hypothesis that exposure to high glucocorticoid levels and/or other components of the stress response increases the risk of schizophrenia. These clinical and preclinical studies could be used to develop hypotheses that could then be tested in patients with schizophrenia.

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“…Studies along these lines might contribute to our knowledge of the interrelationships of affective and eating disorders. They might also be helpful in disentangling the confounded influences of sociocultural, geophysical and genetic factors (Aschoff, 1981;Rosenthal et al, 1983;Scott, 1986;Crow, 1987).…”

Section: Analyses In This Study Indicate a Season Of Onset Of An Withmentioning

confidence: 99%

Seasonal variation in anorexia nervosa? Some preliminary findings from a neglected area of research

Nielsen

1992

Int. J. Eat. Disord.

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A review of the literature on normal development and on psychiatric disorders related to seasonal variation, suggests that this phenomenon is probable to occur in anorexia nervosa. A search of the available literature is entirely negative with respect to seasonal variation in anorexia nervosa. Preliminary analysis suggests the existence of a season of onset, a season of birth, and also oi a season of admission in Danish female anorexia nervosa patients. A formally correct analysis for seasonal variation supports the existence of a season of onset in a selected sample, maximum is in May, amplitude 50%. A season of birth is found in an unselected nationwide sample of patients aged 15 years or older at first psychiatric admission for anorexia nervosa. Maximum late in April, amplitude 40% in the period 1963–1968. Season of admission could not be modelled as a sine wave, but the data suggested a pulse structure (a minimum in one month, followed by a maximum in the next month). Two annual pulses: December/January and July/August. Peak of onset is at a time of the year with maximum increase in height, and peak of other psychiatric conditions. Pattern of birth is similar to that reported for schizophrenia and mania. Replications of this preliminary study should be done in larger countries, at different latitudes and continents. Geophysical, demographic, and climatological variables should be controlled.

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Mutation and psychosis: a suggested explanation of seasonality of birth

Cited by 22 publications

References 67 publications

Paternal Factors and Schizophrenia Risk: De Novo Mutations and Imprinting

Paternal Factors and Schizophrenia Risk: De Novo Mutations and Imprinting

Glucocorticoid Hormones and Early Brain Development in Schizophrenia

Seasonal variation in anorexia nervosa? Some preliminary findings from a neglected area of research

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