Posts Tagged ‘genes’

“Free will” is further circumscribed as two genes associated with violence are identified

October 29, 2014

The range of application of human “free will” is increasingly being circumscribed as we identify genes which are associated with specific behavioural characteristics. This is not to say that any gene or set of genes makes certain specific behaviour inevitable – but it does say that that particular behaviour is more probable for that individual. Perhaps it is more accurate to say that an individual’s gene set defines (and therefore constrains) the envelope of possible behaviour. But that itself means that he can only exercise “free will” within the envelope of possible behaviour that is available to him.

A new study from Finland has identified two genes associated with violent crime. The study of 900 Finnish criminals is published in Molecular Psychiatry.

MedPage:

Variants in two genes were significantly more common in Finnish criminals convicted of multiple violent crimes compared with the general population, researchers said.

Statistical analysis indicated that 5% to 10% of all severe violent crime in Finland could be attributed to these variants, affecting the genes for monoamine oxidase A (MAOA) and CDH13, a neuronal membrane adhesion molecule, according to Jari Tiihonen, MD, PhD, of the Karolinska Institute in Stockholm, and colleagues.

Offenders who had committed 10 or more serious violent crimes were significantly more like to carry one of several loss-of-function variants in the MAOA gene (odds ratio 2.66, 95% CI 1.60-4.42) or the so-called rs11649622 variant in the CDH13 gene (OR 2.72, 95% CI 1.77-4.15), versus participants in population-based survey studies in Finland who were considered representative of the general population.

Criminal offenders with no violent crime convictions showed no increases in risk of carrying the flagged MAOA/CDH13, with an OR of 1.12-1.13 relative to the population-based sample, which did not approach statistical significance.

In their report published online in Molecular Psychiatry, they acknowledged that crime “is a complex phenomenon, and the outcome is shaped by both genetic and environmental factors.”

But that doesn’t mean that genetic contributors cannot be identified, they argued. “It is plausible that while research of the genetic background of criminal or violent behavior is hampered by many confounding factors, focusing on extreme phenotypes might yield more robust results,” Tiihonen and colleagues wrote.

J Tiihonen et al, Genetic background of extreme violent behavior, Molecular Psychiatry , (28 October 2014), doi:10.1038/mp.2014.130

This may not have much practical application yet, and there are certainly many more genes which also predispose to violence and a genetic screening for “violent” tendencies is not coming any time soon. Violent tendencies are also certainly not only due to genes and nurture surely has a very significant part to play.

AbstractIn developed countries, the majority of all violent crime is committed by a small group of antisocial recidivistic offenders, but no genes have been shown to contribute to recidivistic violent offending or severe violent behavior, such as homicide. Our results, from two independent cohorts of Finnish prisoners, revealed that a monoamine oxidase A (MAOA) low-activity genotype (contributing to low dopamine turnover rate) as well as the CDH13 gene (coding for neuronal membrane adhesion protein) are associated with extremely violent behavior (at least 10 committed homicides, attempted homicides or batteries). No substantial signal was observed for either MAOA or CDH13 among non-violent offenders, indicating that findings were specific for violent offending, and not largely attributable to substance abuse or antisocial personality disorder. These results indicate both low monoamine metabolism and neuronal membrane dysfunction as plausible factors in the etiology of extreme criminal violent behavior, and imply that at least about 5–10% of all severe violent crime in Finland is attributable to the aforementioned MAOA and CDH13 genotypes.

I conceive an individual’s genes as defining the range of behaviour available to a human and his “nurture” as then determining his actual behaviour by the exercise of what we call “free will”. What is becoming increasingly obvious though, is that any individual’s “free will” is severely circumscribed. The application of “free will” is restricted to be within the envelope of behaviour that the genes allow.

Behaviour envelopes

I envision an individual whose limits are set by his genes. He cannot think faster or run faster or behave differently to what his genes allow. Thus no amount of “free will” (or nurture) could get an individual to behave outside the envelope of his possible behaviour as set by his individual set of genes.

 

The Black Death altered European genes

February 25, 2014

A fascinating study and further support for my view that evolution is not about survival of the fittest but is about the deselection of the weakest.

Reblogged from Science magazine:

The Black Death didn’t just wipe out millions of Europeans during the 14th century. It left a mark on the human genome, favoring those who carried certain immune system genes, according to a new study. Those changes may help explain why Europeans respond differently from other people to some diseases and have different susceptibilities to autoimmune disorders.

Geneticists know that human populations evolve in the face of disease. Certain versions of our genes help us fight infections better than others, and people who carry those genes tend to have more children than those who don’t. So the beneficial genetic versions persist, while other versions tend to disappear as those carrying them die. This weeding-out of all but the best genes is called positive selection. But researchers have trouble pinpointing positively selected genes in humans, as many genes vary from one individual to the next.

Enter Mihai Netea, an immunologist at Radboud University Nijmegen Medical Centre in the Netherlands. He realized that in his home country, Romania, the existence of two very distinct ethnic groups provided an opportunity to see the hand of natural selection in the human genome. A thousand years ago, the Rroma people—commonly known as gypsies—migrated into Europe from north India. But they intermarried little with European Romanians and thus have very distinct genetic backgrounds. Yet, by living in the same place, both of these groups experienced the same conditions, including the Black Plague, which did not reach northern India. So the researchers sought genes favored by natural selection by seeking similarities in the Rroma and European Romanians that are not found in North Indians.

Celebrating differences. The migration of gypsies from India 1000 years ago (see map) set the stage for a telling study about how diseases can influence the genome.

Celebrating differences. The migration of gypsies from India 1000 years ago (see map) set the stage for a telling study about how diseases can influence the genome.

Netea; evolutionary biologist Jaume Bertranpetit of Pompeu Fabra University in Barcelona, Spain; and their colleagues looked for differences at more than 196,000 places in the genomes of 100 Romanians of European descent and 100 Rroma. For comparison, the researchers also cataloged these differences in 500 individuals who lived in northwestern India, where the Rroma came from. Then they analyzed which genes had changed the most to see which were most favored by selection.

Genetically, the Rroma are still quite similar to the northwestern Indians, even though they have lived side by side with the Romanians for a millennium, the team found. But there were 20 genes in the Rroma and the Romanians that had changes that were not seen in the Indians’ versions of those genes, Netea and his colleagues report online today in the Proceedings of the National Academy of Sciences. These genes “were positively selected for in the Romanians and in the gypsies but not in the Indians,” Netea explains. “It’s a very strong signal.”

Those genes included one for skin pigmentation, one involved in inflammation, and one associated with susceptibility to autoimmune diseases such as rheumatoid arthritis. But the ones Netea and Bertranpetit were most excited about were a cluster of three immune system genes found on chromosome 4. These genes code for toll-like receptors, proteins which latch on to harmful bacteria in the body and launch a defensive response. “We knew they must be important for host defense,” Netea says.

What events in history might have favored these versions of the genes in gypsies and Romanians, but not in Indians? Netea and his colleagues tested the ability of the toll-like receptors to react to Yersinia pestis, the bacterium that caused the Black Death. They found that the strength of the immune response varied depending on the exact sequence of the toll-like receptor genes.

Netea and Bertranpetit propose that the Rroma and European Romanians came to have the same versions of these immune system genes because of the evolutionary pressure exerted byY. pestis. Other Europeans, whose ancestors also faced and survived the Black Death, carried similar changes in the toll-like receptor genes. But people from China and Africa—two other places the Black Death did not reach—did not have these changes. (There have been multiple plagues throughout history around the world, but none have been so deadly as the Black Death, which killed an estimated one in every four Europeans, and so exerted very strong selection.) The similarities in the other genes were likely caused by other conditions experienced by Rroma and Europeans, but not Indians.

“The use of two populations living in the same geographic area is very clever,” says human population geneticist Oscar Lao of Erasmus MC in Rotterdam, the Netherlands, who was not involved in the study. “This experimental evidence is very important,” he adds. It shows that the Black Death bacterium does indeed interact with the proteins coded for by the genes favored by natural selection. “That should be the goal for all those type of analyses.”

“It’s a nice hypothesis that they are putting forward,” agrees Lluis Quintana-Murci, a human population geneticist at the Pasteur Institute in Paris who was not involved in the study. The genetic changes may have modern-day effects. “The presence of these particular versions of these genes may give the evolutionary basis for why certain populations are more at risk” for certain types of diseases, says Douglas Golenbock, an immunologist at the University of Massachusetts Medical School in Worcester. “The side effect seems to be that the Europeans have a more proinflammatory immune system than those who have never experienced Black Death.”

However, Lao and Quintana-Murci wonder if the convergence in these genes might be explained another way. It’s possible that these favorable versions were introduced into the Rroma by interbreeding between the Rroma and the Romanians, they suggest. Additional sequencing of the converged genetic regions should answer this question, Quintana-Murci says. It’s also important to check how these toll-like receptors respond to other deadly bacteria to see if other diseases might have been the cause of the changes. That will likely happen, Quintana-Murci adds. “This will inspire other labs to see if other bacterial infections could also explain the [selection].”

I am but a prisoner of my genes

January 20, 2014

I’d like to fly but but my genes don’t agree

And they determine how tall I will be,

I am but a lowly prisoner of my genes,

My apparent freedom is not quite what it seems.

But thanks to my genes I’m not a chimpanzee.

All abnormal behaviour is illness, says DSM-five,

Just following precisely what our genes do contrive.

Our genomes hold us tightly captive,

As slaves in their battle to survive,

So it matters not how much we strive.


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