Is Genetics the Lead Role for Adolescent Crime Victims! Is this part of Human Nature, or Human Nature doesn’t exist?

(ScienceDaily (May 20, 2009)Genes trump environment as the primary reason that some adolescents are more likely than others to be victimized by crime, according to groundbreaking research led by distinguished criminologist Kevin M. Beaver of The Florida State University.The study is believed to be the first to probe the genetic basis of victimization.

“Victimization can appear to be a purely environmental phenomenon, in which people are randomly victimized for reasons that have nothing to do with their genes,” said Beaver, an assistant professor in FSU’s nationally top-10-ranked College of Criminology and Criminal Justice. “However, because we know that genetically influenced traits such as low self control affect delinquent behavior, and delinquents, particularly violent ones, tend to associate with antisocial peers, I had reasons to suspect that genetic factors could influence the odds of someone becoming a victim of crime, and these formed the basis of our study.”

Beaver analyzed a sample of identical and same-sex fraternal twins drawn from a large, nationally representative sample of male and female adolescents interviewed in 1994 and 1995 for the National Longitudinal Study of Adolescent Health. “Add Health” interviewers had gathered data on participants that included details on family life, social life, romantic relationships, extracurricular activities, drug and alcohol use, and personal victimization.

The data convinced Beaver that genetic factors explained a surprisingly significant 40 to 45 percent of the variance in adolescent victimization among the twins, while non-shared environments (those environments that are not the same between siblings) explained the remaining variance. But among adolescents who were victimized repeatedly, the effect of genetic factors accounted for a whopping 64 percent of the variance.

“It stands to reason that, if genetics are part of the reason why some young people are victimized in the first place, and genetics don’t change, there’s a good chance these individuals will experience repeat victimization,” Beaver said.

“It is possible that we detected this genetic effect on victimization because it is operating indirectly through behaviors,” Beaver said. “The same genetic factors that promote antisocial behavior may also promote victimization, because adolescents who engage in acts of delinquency tend to have delinquent peers who are more likely to victimize them. In turn, these victims are more likely to be repeatedly victimized, and to victimize others.”

Thus, write Beaver and his colleagues, victims of crime are not always innocent bystanders targeted at random, but instead, sometimes actively participate in the construction of their victimization experiences.

“However, we’re not suggesting that victimization occurs because a gene is saying ‘Okay, go get victimized,’ or solely because of genetic factors,” Beaver said. “All traits and behaviors result from a combination of genes and both shared and non-shared environmental factors.”

And environmental factors can make a difference, he noted. The social and family environment in an adolescent’s life may either exacerbate or blunt genetic effects — a phenomenon known in the field of behavioral genetics as a “gene X environment interaction.”

Co-authors are criminology graduate students Brian Boutwell and J.C. Barnes of Florida State and Jonathon A. Cooper of Arizona State University.

Journal reference:

  1. Beaver et al. The Biosocial Underpinnings to Adolescent Victimization: Results From a Longitudinal Sample of Twins. Youth Violence and Juvenile Justice, 2009; DOI: 10.1177/1541204009333830
Adapted from materials provided by Florida State University.
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Is influenza A (H1N1) as fatal as the 1957 pandemic?

ScienceDaily (May 12, 2009) Early findings about the emerging pandemic of a new strain of influenza A (H1N1) in Mexico are published in the journal Science.

Researchers from the MRC Centre for Outbreak Analysis and Modelling at Imperial College London, working in collaboration with the World Health Organisation and public health agencies in Mexico, have assessed the epidemic using data to the end of April. Their key findings are as follows:

  • The data so far is very consistent with what researchers would expect to find in the early stages of a pandemic.
  • The researchers’ best estimate is that in Mexico, influenza A (H1N1) is fatal in around 4 in 1,000 cases, which would make this strain of influenza as lethal as the one found in the 1957 pandemic. The researchers stress that healthcare has greatly improved in most countries since 1957 and the world is now better prepared.
  • The epidemic of influenza A (H1N1) is thought to have started in Mexico on 15 February 2009. The data suggests that by the end of April, around 23,000 people were infected with the virus in Mexico and 91 of these died as a result of infection. However, the figures are uncertain – for example, some mild cases may have gone unreported. The numbers infected could be as low as 6,000 people or as high as 32,000 people.
  • The uncertainty around the numbers of people who have been infected with influenza A (H1N1) in Mexico means that the case fatality ratio (CFR) of 0.4% (4 deaths per 1000) cannot be definitely established. The CFR is in the range of 0.3% to 1.5%, but at this stage the researchers believe that 0.4% is the most likely.
  • For every person infected, it is likely that there will be between 1.2 and 1.6 secondary cases. This is high compared to normal seasonal influenza, where around 10-15 percent of the population are likely to become infected. However, it is lower than would be expected for pandemic influenza, where 20-30 percent of the population are likely to become infected.
  • In an outbreak in an isolated village called La Gloria, Mexico, children were twice as likely to become infected as adults, with 61% of those aged under 15 becoming infected, compared with 29% of those over 15. This may suggest that adults have some degree of immunity against infection, because of having been previously infected with a related strain of influenza, or it may mean that children are more susceptible to infection because they interact much more closely together, for example in school, than adults.

Professor Neil Ferguson, the corresponding author of the new research from the MRC Centre for Outbreak Analysis and Modelling at Imperial College London, said: “Our study shows that this virus is spreading just as we would expect for the early stages of a flu pandemic. So far, it has been following a very similar pattern to the flu pandemic in 1957, in terms of the proportion of people who are becoming infected and the percentage of potentially fatal cases that we are seeing.

“What we’re seeing is not the same as seasonal flu and there is still cause for concern – we would expect this pandemic to at least double the burden on our healthcare systems. However, this initial modelling suggests that the H1N1 virus is not as easily transmitted or as lethal as that found in the flu pandemic in 1918,” added Professor Ferguson.

Journal reference:

  1. Christophe Fraser, Christl A. Donnelly, Simon Cauchemez, William P. Hanage, Maria D. Van Kerkhove, T. Déirdre Hollingsworth, Jamie Griffin, Rebecca F. Baggaley, Helen E. Jenkins, Emily J. Lyons, Thibaut Jombart, Wes R. Hinsley, Nicholas C. Grassly, Francois Balloux, Azra C. Ghani, Neil M. Ferguson, Andrew Rambaut, Oliver G. Pybus, Hugo Lopez-Gatell, Celia M Apluche-Aranda, Ietza Bojorquez Chapela, Ethel Palacios Zavala, Dulce Ma. Espejo Guevara, Francesco Checchi, Erika Garcia, Stephane Hugonnet, Cathy Roth The WHO Rapid Pandemic Assessment Collaboration. Pandemic Potential of a Strain of Influenza A (H1N1): Early Findings. Science, 11 May 2009 DOI: 10.1126/science.1176062
Adapted from materials provided by Imperial College London, via EurekAlert!, a service of AAAS.