Can sociopathy be passed down genetically
Genetic factors of aggression
Love is a miracle that is always possible
evil a fact that is always there.
It is assumed that aggressive behavior is determined by a very complex interaction between genetic makeup and environmental conditions. This interaction can be viewed under five aspects:
- Genetically conditioned: A person can be genetically particularly aggressive but also peaceful.
- Organically caused: Mental states, sensations and motives influence the aggressive behavior.
- Sociologically determined: When a hierarchy is formed or when a hierarchy breaks down, all those involved are more aggressive than when the hierarchy is established. In an anonymous group, the members react differently than among acquaintances.
- Physiologically conditioned: Hormones and neurotransmitters are involved in controlling aggressive behavior.
- Socially and ecologically conditioned: Large group density or food shortages influence aggressive behavior
In addition to these five directly effective factors, there are also historical influences:
- Tribal history: Aggressive behavior has developed differently in different species, and there are probably evolutionary differences between the human races.
- Cultural history: Aggressive behavior is culturally reshaped through ritualizations.
- Ontogenetically: Personal experiences, experiences, frustrations, fears, role models influence aggressive behavior.
The Tendency to aggression but is at least partially passed on from generation to generation, although it is always open whether through role model, upbringing or heredity. Martin Teicher (Harvard Medical School) reported in Scientific American (No. 3, 2002) on studies that showed that the hippocampus and amygdala are smaller in people who were abused or abused in childhood. Apparently, severe stress in childhood changes the molecular organization of these brain regions, such as the structure of the receptors for the neurotransmitter gamma-amino-butyric acid.
Like most character traits, aggressiveness is also hereditary to a considerable extent (around 50%), although the press also spoke of a "gene for aggressiveness". The first relevant work described eight men from a large Dutch family, all of whom were prone to unusual attacks of aggression, which, according to the authors, manifested themselves in arson and exhibitionism, among other things. In all of these men, a gene that codes for the enzyme monoamine oxidase A (MAOA) is completely inactive. Such enzymes break down monoamines, among which are neurotransmitters like dopamine and serotonin. If these are not broken down after they have transmitted their message from one nerve cell to the next, this affects the conduction of stimuli. It is known from other studies that the serotonin concentration in the brain influences aggressiveness and impulsiveness. At least 15 genes have been identified in mice that are said to have something to do with aggressiveness, including a gene for NO synthase, an enzyme that produces the versatile neurotransmitter NO. Conclusions about corresponding genes in humans are problematic, however, because the brain structure of mice and other mammals differs significantly and our society and culture are also much more complex.
But now a piece of work (Science, 297, p. 851) combines the influences of the environment and heredity. A group led by Terry Moffitt (King's College London) showed that those male subjects who had been badly treated in their childhood were on average more likely to show antisocial behavior than a control group. The expression of the MAOA gene was also examined, which showed that the inactive expression of the gene could not be detected, but a more and a less active variant was found. The less active MAOA variant seems to significantly amplify the effects of the bad childhood experiences. Of the men who were abused or severely neglected in their childhood, those with the less active MAOA variant showed behavioral disorders twice as often in adolescence as those with the more active gene version. The connection is even clearer in the case of violent crimes such as robbery or rape. In contrast, the gene expression alone - without childhood trauma - has no statistically determinable influence. This means that only an environmental factor ("stressor") allows a genetic factor to take effect. The fact that MAOA activity is particularly effective in childhood could be due to the fact that a second, similar gene (MAOB) only becomes active later in life.
Why was the analysis limited to men? First, because the MAOA gene is on the X chromosome and is therefore only available in single copies in men, which makes it easier to interpret. In women who have two X chromosomes, the effects of a less active MAOA variant are usually mitigated by the second edition of the gene on the second X chromosome. Second, because one has more experience in describing and defining anti-social aggressive behavior in men than in women. After all, as US geneticist Greg Carey noted, "the strongest genetic marker of violence is still the presence of a Y chromosome".
The gene that contains the building instructions for the enzyme monoamino oxidase A (MAOA) is also one of the Risk factors for panic disorderThere is a variant of this gene that ensures increased MAO activity, which favors the disease. A study with 369 panic patients showed that the risk gene not only causes more severe anxiety symptoms, but also reduces the success of behavior therapy, because the patients with the risk variant became less accustomed to the standardized therapy the fearful situation while the other patients learned to deal with it better. Another difference related to the activation in a certain brain region in fearful situations, from which it can be concluded that the behavioral therapy leads to different brain activation patterns in the two patient groups. The results of the study show for the first time that genetic information can be helpful in offering individually tailored psychotherapies.
source: http://idw-online.de/de/news533166 (13-05-16)
Thomas Kramar (2002). From generation to generation: genes and upbringing pass on aggressiveness. August 10th Press, Spectrum S. X.
Teicher, Martin H. (2002). Scars that Won't Heal: The Neurobiology of Child Abuse. Scietific American, 286 (3), pp. 68-75.
See Morality is in the forebrain
The sertonin level plays a role in the control of aggression, although it is reduced in the case of aggressive behavior. According to studies by Berend Olivier (University of Utrecht) there are mechanisms in the brains of humans and animals that control aggression, although this control of aggression occurs genetic prerequisites is based, but upbringing also plays an essential role in coping with aggression. The serotonin system is less active in very aggressive people than in normal people. Pharmacologists bred mice in which certain receptors in the brain had been switched off and part of the serotonin system had been disabled. As a result, these animals were no longer able to suppress their aggressions.
Irascibility and brain structure
It is known that hunger makes us more aggressive and makes us feel more angry, and also that certain gene variants influence the release of neurotransmitters and thus promote aggression and weaken impulse control. Coccaro et al. (2016) have shown in a study of people who often have barely controllable fits of anger (irascibility) that the Structure of the brain plays a role in the development of aggression, with pathological irascibility being controlled by areas in the fronto-limbic part of the brain. In the irascible, the volume of some areas in the prefrontal cortex or the amygdala is significantly smaller than in comparison groups, whereby the stronger the outbursts of aggression were, the more the gray matter was reduced in those areas that are considered to be the control centers for feelings. The tendency towards aggressive behavior in some people may therefore be related to the anatomy of the regions in the brain that control their emotions and may have less to do with their personality.
Coccaro, E. F., Fitzgerald, D. A., Lee, R., McCloskey, M. & Luan Phan, K. (2016).
Frontolimbic Morphometric Abnormalities in Intermittent Explosive Disorder and Aggression. Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, 1, 32-38.
Table of Contents
Theories to explain - genetic approach - ethological concept - Huesmann and Berkowitz - learning psychological explanation - catharsis hypothesis - psychoanalytic explanation - frustration hypothesis - digression - amok - an intercultural phenomenon - self-harm - perception in the family - family - hooliganism - media effects - media research - parents tips - Self-injurious behavior - Training program - School - Literature
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