From Economist http://www.economist.com/sciencetechnology/displaystory.cfm?story_id=13899022
Dr Nesse’s hypothesis is that, as pain stops you doing damaging physical things, so low mood stops you doing damaging mental ones—in particular, pursuing unreachable goals. Pursuing such goals is a waste of energy and resources. Therefore, he argues, there is likely to be an evolved mechanism that identifies certain goals as unattainable and inhibits their pursuit—and he believes that low mood is at least part of that mechanism.
It is a neat hypothesis, but is it true? A study published in this month’s issue of the Journal of Personality and Social Psychology suggests it might be. Carsten Wrosch from Concordia University in Montreal and Gregory Miller of the University of British Columbia studied depression in teenage girls. They measured the “goal adjustment capacities” of 97 girls aged 15-19 over the course of 19 months. They asked the participants questions about their ability to disengage from unattainable goals and to re-engage with new goals. They also asked about a range of symptoms associated with depression, and tracked how these changed over the course of the study.
Their conclusion was that those who experienced mild depressive symptoms could, indeed, disengage more easily from unreachable goals. That supports Dr Nesse’s hypothesis. But the new study also found a remarkable corollary: those women who could disengage from the unattainable proved less likely to suffer more serious depression in the long run.
Mild depressive symptoms can therefore be seen as a natural part of dealing with failure in young adulthood. They set in when a goal is identified as unreachable and lead to a decline in motivation. In this period of low motivation, energy is saved and new goals can be found. If this mechanism does not function properly, though, severe depression can be the consequence.
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.
“People often act on behalf of others. They do so without immediate personal gain, at cost to themselves, and even toward unfamiliar individuals. Many researchers have claimed that such altruism emanates from a species-unique psychology not found in humans’ closest living evolutionary relatives, such as the chimpanzee. In favor of this view, the few experimental studies on altruism in chimpanzees have produced mostly negative results. In contrast, we report experimental evidence that chimpanzees perform basic forms of helping in the absence of rewards spontaneously and repeatedly toward humans and conspecifics. In two comparative studies, semi–free ranging chimpanzees helped an unfamiliar human to the same degree as did human infants, irrespective of being rewarded (experiment 1) or whether the helping was costly (experiment 2). In a third study, chimpanzees helped an unrelated conspecific gain access to food in a novel situation that required subjects to use a newly acquired skill on behalf of another individual. These results indicate that chimpanzees share crucial aspects of altruism with humans, suggesting that the roots of human altruism may go deeper than previous experimental evidence suggested.”
Citation: Warneken F, Hare B, Melis AP, Hanus D, Tomasello M (2007) Spontaneous Altruism by Chimpanzees and Young Children. PLoS Biol 5(7): e184 doi:10.1371/journal.pbio.0050184
Received: February 8, 2007; Accepted: May 14, 2007; Published: June 26, 2007
FOR most people, the idea of isolation is an uncomfortable one. It interests Paul Turner, however, because it goes hand in hand with the formation of new species. Dr Turner is a biologist at Yale University, and he and his team have just become the first people to create a new biological species in a laboratory by encouraging the sort of ecological isolation that happens in the wild. Admittedly the species in question is a virus, but the proof of principle is important. Moreover, Dr Turner’s method might be adapted to examine how animal viruses jump the species barrier to become agents of human disease.
US scientist heralds ‘artificial life’ breakthrough
WASHINGTON (AFP) — Controversial celebrity US scientist Craig Venter has announced he is on the verge of creating the first ever artificial life form which he hails as a potential remedy to illness and global warming.
Venter told Britain’s The Guardian newspaper Saturday that he has built a synthetic chromosome using chemicals made in a laboratory, and is set to announce the discovery within weeks, possibly as early as Monday.
Pat Mooney, director of the Canadian bioethics organization ETC Group, told the paper that Venter was creating “a chassis on which you could build almost anything.
The chromosome which Venter and his team has created is known as Mycoplasma laboratorium and, in the final step of the process, will be transplanted into a living cell where it should “take control,” effectively becoming a new life form.
The single cell organism, which ETC has coined “Synthia,” is piloted by a chromosome with just 381 genes, the limit necessary to sustain the life of the bacteria so it can feed and reproduce.
A former student told me about the Flying Spaghetti Monster, which I did not know before. Funny, but sad (because of what it says about science education in the US).