A recent study conducted by W.I.T. has determined that many of the behavioral traits typically ascribed to liberalism are caused by a hereditary chromosomal defect. The chromosomal abnormality, located on the seventeenth pair of autosome chromosomes, has a severe and profound impact on normal brain development and function. The new disease, Blacks Disorder, is named after Dr. Amanda Black, who first discovered the chromosomal replication abnormality and later headed the research project at W.I.T.’s applied genetics department examining this defect.

While doing population demographic and genetic research, Dr. Black noted that a high percentage of individuals who self-identified as possessing a “liberal” political ideology, within the genetically sequenced research group, seemed to possess the same hereditary autosomal defect. Specifically, when undergoing mitosis in the early critical junction of cell division a transcription error occurs that shortens one of the chromosome Q arms so that the total genes contained within it is reduced from its normal 1672 genes to 1670. Another three genes within the chromosome undergo minute transcription abnormalities which result in a specific mutation. These genetic omissions and errors cumulatively effect neural function in several identifiable and consistent ways.

One of the biggest changes involves the brains overproduction of the hormone Oxytocin. This overproduction leads to a increase in ethnocentric behavior and an increase in trust and empathy disassociated from sociological inputs. Ethnocentric behavior is characterized by judging another group or culture solely by the values and standards of ones own culture. Individuals with Blacks disease tend to be highly intolerant of viewpoints and ideas that do not conform to those of their self-identified group. It is also characteristic for individuals possessing this disorder to exhibit elevated signs of aggression and a propensity to attack when their group convictions are challenged. Sufferers of Blacks Disease are also prone to utilize emotional based thinking as opposed to rational thinking; very seldom being able to change their beliefs based on rational inputs and evidence. Their emotional attachment to their convictions and beliefs appear to overwhelm their ability to be objective. The aforementioned is coupled with a increase of trust and group bonding in the group they belong to. This results in those they consider to be “in their group” being fiercely protected even when they act in a injurious fashion toward the well being of the group as a whole. All of these symptoms are directly tied to the overabundance of Oxytocin present in those who suffer from this affliction.

The second major and identifiable changes relating to Blacks Disease involve parts of the brain involved in instinctual motivation and responsibility. Researchers noted that one of the transcription errors causes by Blacks Disease detrimentally effects function of the mesolimbic region of the brain, as well as effecting tertiary functions relating to learning in the hippocampus and medial temporal lobe. Cumulatively these detrimental abnormalities effect suffers of Blacks Disease ability to utilize reward anticipation functions. This leads to a breakdown of basic understanding within the brain to the connection between task and reward: the basis for neuro-functional motivation. This lack of effective processing of emotional motivation in response to task/reward scenarios has a negative impact on individual responsibility. Individuals with Blacks Disease are literally unable to understand the connection between task preformed and reward gained. This renders them largely unable to understand and function in a optimally responsible manner.

Researchers noted that even offspring of those raised by sufferers of Blacks Disease, who did not possess the chromosomal abnormality associated with, were still highly prone to engaging in the same type of nonfunctional behaviors. Researchers posit that learned behavioral patterns are the cause in individuals not effected by Blacks Disease. This offers the hope that early intervention and remediation therapy can be used to save those without the actual chromosomal abnormality from its effect. Full findings to be published in next quarters issue of The American Journal Of Human Genetics.