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Genes, environment and antisocial behaviour

The science and issues

An early model: Genes vs. environment


it must be the way he was brought up . . . Im sure it runs in the family . . .

Jason is always getting into trouble

Risk factors for antisocial behaviour


Having an aggressive father Having divorced parents Poverty Subject to inconsistent discipline Being born to a teenage mother Being reared in a family of at least four children Growing up with antisocial peers or adults (a criminal father, young role models) Being thrill-seeking, interested in danger, enjoy taking risks. The right genotype?

Nature and nurture


In August 2002 a ground-breaking study was published in the prestigious American journal, Science. The research team (UK and New Zealand) reported new evidence of a "gene by environment" interaction: a genetic variant is associated with different antisocial outcomes among maltreated children. This was the first convincing evidence of the complex interplay of genetic and environmental influences on behaviour in humans. This evidence has since been supported in more than three other studies, but unsupported by one.

The new model: G x E (genes by environment)


it must be a combination of his genes and the way he was brought up

. . .

Jason is always getting into trouble

The science . . .

Backtrack: Of knock-out mice and aggressive men


Key studies in the 1990s Brunner et al (1993). Genetic and metabolic studies on a large family where males are affected by a syndrome (borderline retardation and abnormal behaviour inc. impulsive aggression). The affected males were found to have a truncated (shortened) monoamine oxidase A (MAOA) protein. Conclusion: MAOA deficiency disturbed regulation of impulsive aggression Cases et al (1995), Shih et al (1999). Created transgenic mice lacking MAOA activity (induced a deletion in the gene). Males had significant increase in brain levels of neurotransmitters serotonin and norepinephrine and exhibited enhanced aggression. Studies suggested a lack of MAOA expression in the forebrain, which could be reversed in young animals, but not in adults.

Monoamine oxidase A
Monoamine oxidases (MAOs) are enzymes which break down neurotransmitters the chemicals such as noradrenaline and serotonin which enable nerve impulses to bridge the gaps between individual nerve cells. If the enzyme that is supposed to break down neurotransmitters is missing or present at low levels, then the nerves continue to transmit the same impulse.
A computer model of monoamine oxidase. Source: Berman et al. (2000) The Protein Data Bank

X-linkage
Genetic conditions caused by changes on the X chromosome are called sex-linked (or Xlinked). Mutations on X chromosomes are consequently far more likely to affect men than women. Males have only one copy of the X chromosome, whereas females have two copies. If a change (mutation) occurs in a gene on a mans X chromosome, there is no other copy of the gene to compensate.

Source: Indigo Instruments, www.indigo.com

A gene for violence?


Researchers have attempted to find a connection between the levels of MAOA produced by individuals and behaviour such as violence, alcoholism, depression and bipolar disease. However, none of these studies was able to show a convincing link the behaviour was apparently too complex to be controlled by a single gene.

The Dunedin connection


The Dunedin Multidisciplinary Health and Development study 1037 children (52% male) born in Dunedin between April 1972 and March 1973. Subjects assessed at ages 3, 5, 7, 9, 11, 13, 15, 18, 21 and 26 years.

DNA swabs taken at age 26.


Source: Google Earth, http://earth.google.com/

The 2002 Science paper


boys who had a high risk . . . a low activity MAOA genotype on the genetic test . . . and had been maltreated, were only about 10% of the boys in the study but accounted for almost 40% of the crimes that had been committed. the boys who had been maltreated, who had the high-activity MAOA genotype seemed to be protected against maltreatment . . .
Source: Caspi et al (2002), Science, 297, 851-854; interview with co-author Professor T. Moffitt

Could the following have an effect?


Could the high MAOA activity protective effect be brought about: if children with this genotype were likely to be reared in favourable environments? No social class differences were found between males with low and high MAOA activity because of individual differences in IQ. No IQ differences were found between males with low- and high MAOA activity

Some issues about applications:


How reliable would a test be? Would a treatment have side effects? How antisocial is antisocial enough?

Who should be tested (how much maltreatment is too much?)


Could MAOA levels become a defence in court?
Source: Wellcome Trust Medical Photographic Library

Is a protected child less worthy of help after maltreatment?


Should testing be required; is there at time when benefits to society override the rights of an individual?

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