ScienceDaily (June 18, 2008) — An Italian research team, consisting of Andrea Camperio Ciani and Giovanni Zanzotto at the University of Padova and Paolo Cermelli at the University of Torino, found that the evolutionary origin and maintenance of male homosexuality in human populations could be explained by a model based around the idea of sexually antagonistic selection, in which genetic factors spread in the population by giving a reproductive advantage to one sex while disadvantaging the other.
Male homosexuality is thought to be influenced by psycho-social factors, as well as having a genetic component. This is suggested by the high concordance of sexual orientation in identical twins and the fact that homosexuality is more common in males belonging to the maternal line of male homosexuals. These effects have not been shown for female homosexuality, indicating that these two phenomena may have very different origins and dynamics.
the authors of the new study considered a range of different hypotheses for the genetic diffusion of male homosexuality. These included: the genetic maternal effects on sons, the heterozygote advantage (as is found in malaria resistance), and “sexually antagonistic selection.” The latter is a particular aspect of Darwinian evolution, in which genetic factors spread in the population by giving a reproductive advantage to one sex while disadvantaging the other. This type of evolution has been previously found in insects, birds, and some mammals, but never in humans.
They concluded that the only possible model was that of sexually antagonistic selection. The other models did not fit the empirical data, either implying that the alleles would become extinct too easily or invade the population, or failing to describe the distribution patterns of male homosexuality and female fecundity observed in the families of homosexuals. Only the model of sexually antagonistic selection involving at least two genes — at least one of which must be on the X chromosome (inherited in males only through their mother) — accounted for all the known data.
Maybe time to make use of https://www.23andme.com/ ?
“Researchers at the Max Planck Institute for Human Cognitive and Brain Sciences in Leipzig, Germany have found a genetic factor that affects our ability to learn from our errors. The scientists demonstrated that men carrying the A1 mutation, which reduces the amount of dopamine D2 receptors in the brain, are less successful at learning to avoid mistakes than men who do not carry this genetic mutation. This finding has the potential to improve our understanding of the causes of addictive and compulsive behaviors. “
Green light for hybrid research
Regulators in the UK have given scientists the green light to create human-animal embryos for research. Two centres, King’s College London and Newcastle University, will now be able to begin their work under one-year research licences. Any other centres wishing to do similar work will have to apply to the HFEA for permission, which will make a decision on a case-by-case basis.
Scientists want to create hybrid embryos by merging human cells with animal eggs in a bid to extract stem cells. The embryos would then be destroyed within 14 days.
Most people tend to learn from their mistakes and avoid making the same blunder twice. Now research reveals a genetic mutation that helps to determine the extent to which certain people are doomed to repeat history.
Drug addicts, alcoholics and compulsive gamblers are known to be more likely than other people to have this genetic mutation, which leaves them with fewer receptors of a certain type in the brain. These receptors — called D2 receptors — are activated when levels of the neurotransmitter dopamine drop.
Dopamine is responsible for signalling fun and pleasure in the brain. But dopamine also helps us learn. When we make a pleasurable decision, dopamine is a chemical treat, urging the brain to repeat the choice. Being deprived of such a treat should theoretically activate D2 receptors and encourage people not to make that same decision again.
So it had been theorized that people with fewer D2 receptors might be less capable of learning from negative reinforcement.
Cesarini David et el
Abstract: We use the classical twin design to provide estimates of genetic and environmental influences on experimentally elicited preferences for risk and altruism. Our estimates provide strong prima facie evidence that economic preferences are heritable. Approximately 30 percent of the variation in behavior is explained by genetic effects in the best-fitting models. The results suggest a modest role for common environment as a source of phenotypic variation. Based on the findings, we encourage economists to move beyond a black-box treatment of preference formation and suggest that the further study of the codetermination of preferences by genes and environment will lead to a more comprehensive economic science.