The Nature of the Beast: How and Why It Is Created
Reverse engineering what underlies, underpins, and constitutes the antisocial pulses be they in the form of compulsive or impulsive aggression the way it is — ranging from six overlapping perspectives — down to the cells.
“First principle, Clarice. Simplicity. Read Marcus Aurelius. Of each particular thing ask: what is in itself? What is its nature? What does he do, this man you seek?”
— Hannibal Lecter, the Silence of the Lambs
Could A Perpetrator be the First Victim?
Part I: Biochemistry, Embryology, and Trans-generational Epigenesis
1) When alcohol made its way to the system
Like any other substances, when alcohol is ingested, certain organs will embark on chemical degradation or conversion as a general rule. For starter, as this alcohol makes its way to the liver to be broken down into components, an enzyme called alcohol dehydrogenase, the one responsible for transforming ethanol to a chemical compound called acetaldehyde, thereafter, is going to be further converted to acetate. Acetaldehyde, however, is in itself problematic. Acetaldehyde (AcH), the highly toxic substance of ethanol is known to have teratogenic, carcinogenic, and epileptogenic effects to the nerve cells [10]. If you think alcohol as a tool used for cleaning up a surface or used as anesthetic due to its capacity of extinguishing bacteria and germs, then the same is true when it enters one’s digestive and neuronal system. It would not hesitate to kill bacteria and cells indiscriminately, including the ones that are useful for the gut system. So as this acetate continues to travel all the way up to the brain, arriving at the gate then meet a “security guard” of the brain called blood-brain-barrier, the toxic-carrier ethanol gets passed through without reservation nonetheless. Why? Because of the solubility of water that acetate takes form of has dissolved the toxin in. Hence, undetected. What happens by the time the toxic gets snuck in to the brain? It is found that alcohol is indiscriminate toward which brain regions and areas it reins in, but does have affinity toward few that are involved in cognition, movement, learning, and memory. 1) The prefrontal cortex, responsible for consciousness, emotional and behavioral regulation, executive functions, thus may explain why people when in an inebriated state tend not to think clearly and choose to drive carelessly with no accountable reason. 2) The cerebellum, for motor regulation and movement calibration, thus may explain why a drunken individual walks in an uncoordinated manner and struggle to reach out a cup that seems effortless to do. 3) Thalamus, responsible for sensory relay information including vision, taste, touch, but smell — which, also may explain why people’s vision became distorted and blurry or tend to soak up loud music indefinitely, for example. 4) Hippocampus, responsible for learning and memory, so when in a black-out state, one may struggle to recall what happened a night before because by the time it happened the information is not being stored by the hippocampus as it was knocked out by alcohol. However, the outcome of alcohol intoxication affecting behaviors may vary depending on the intake and the frequency [15].
So at this point, how do we get to understand its link to aggression? As we have learned, the areas affected by alcohol are those who primarily are responsible for regulatory cognitive, sensory, and motor tasks. Not the ones that are responsible for the reverse, which has a lot to do with stimuli, arousal, including impulsivity. So when someone is a subject to the sedative effects of alcohol, everything seems to be driven purely by impulses to the absence of a conscious brake. Thus, when someone engaged in confrontational argument that got his or her defensive mode triggered, ethanol may make him or her respond as exaggeratedly as primitive, reactive and reflexive with a lack of self-referential thinking simply by virtue of this external stimulus has brought his or her primal nature to the light, too readily. It is due to most of areas, regions, and connectivity involved in holding those wild strings are temporarily deactivated.
2) Growing in a toxic womb
Mounting evidence from across literature with regard to alcohol and its deleterious effects on fetus is undeniably consistent. The prenatal alcohol exposure (PAE) is responsible for many of serious mental, intellectual, physical abnormalities, whether that which may or may not sustain in the long term. The imminent danger this substance will have on the developing brain can be preceded by a single mechanism: apoptosis. In molecular genetics, apoptosis can analogously be described as when cells ‘commit suicide’ in response to ethanol exposure [11]. In a series of studies, Sulik et all (2001, 2005) have demonstrated that exposure of mouse embryos to alcohol by in utero during the 7th to 9th days of gestation (equivalent to 3rd to 4th weeks of human gestation), left a marked degeneration of precursor cell populations that are critical contributors to the growth of the brain. This precursor cell population is thought to be progenitors, or in the biological context can be thought of as the parent or direct ancestor from which newborn cells are further created. So when these progenitors are already subject to apoptosis, the detrimental power of ethanol interferes the progress of new generation in meeting critical milestone of what these newborns are capable of, which mainly occurs during the time cell migration thus taking place in this very early trimester [4]. The cells that die belong to neuronal and oligo lineages. Oligos are thought to be vitally important for neuronal function and the regulation of gene expression during DNA sequencing. Within only a few hours after alcohol enters the developing brain, millions of brain cells that were on a healthy survival track, suddenly became derailed and, as mentioned, commit suicide [11]. Findings suggest that although shifts in DNA methylation (i.e., gene silencing) were once thought to be restricted to early embryonic development, studies of nutritional, chemical, and a broad range of environmental exposures occurring during pre- and postnatal development have implicated epigenetic regulation of gene expression as a critical target of experience dependent change [2]. At this point, this widespread loss of neurons, their progenitors, and the deletion of oligos during this very early and vulnerable phase suffice to explain all the rooting features and biomarkers of the Fetal Alcohol Spectrum Disorders (FASD) Syndrome[11].
Just as critical as the other two subsequent gestational periods, the first trimester in particular observed to be a period when cerebellar cells are ‘given a shot’ to constitute a brain region that would be responsible for calibration of movements and speech, i.e., the cerebellum. When ethanol is administered to the placenta ranging at low to moderate amount occurred at this period, it decreases the volume of the so-called Purkinje cells and neurons in the developing fetus, from which the cerebellar cortex of the brain fundamentally otherwise scaffolds the whole engine. Consequently, the probability that the fetus bearing cerebellar degenerative symptoms it results increases. Poor coordination, speech and language delays are the most common features attributed to which neurodegenerative abnormality would manifest postnatally [3].
Meanwhile, in the placenta (a conduit through which food provision circulated, be they metabolic nutrients, chemicals, or otherwise, to the fetus), there is barely protective barrier to restrain the rush for a couple of reasons. First, ethanol has been found to impair the transport of ethanol from the fetus to the mother for maternal metabolism, as the fetal liver function is so limited that it cannot metabolize ethanol. This hardly surprising given amniotic fluid is 98% water compared with maternal blood 92% water, so by comparison the prevailing solubility of the amniotic fluid caters better to the reservoir of ethanol, prolonging the exposure and risks of ethanol for the fetus as a result [9]. Second, ethanol-induced teratogenicity itself is already dissolved in the metabolite, making it even more loosely to cross. And as it happens, the amount of toxin embedded in the liquid, metabolized in the digestive system of the mother thus directly permeates all over the milieu of placenta and is absorbed by the fetus during trans-placental passage, as crudely.
Now, what happens in the second trimester if the fetus still at the behest of ethanol intoxication? Middle gestation is considered to be a peak of neurogenesis and synaptogenesis, in other words, it is when the neuron proliferates and synapse branches its range of neuronal communication, connectivity and networking. Neurogenesis primarily occurs in a region that is responsible for storing long-term information and memory, learning (specifically, visual-spatial), and potentiation — the hippocampus, a part of the limbic system [14]. Moderate fetal alcohol exposure, however, has also been found to decrease the hippocampal plasticity at stretching both the size and the volume, even worse, may suppress long-term potentiation of which synapses are capable devouring as many as information and cerebral features in the life of fetus [16]. The study of ethanol- induced effects of neurotransmission have identified abnormalities in N- methyl- D- aspartate (NMDA), serotonergic, cholinergic, and glycine receptors, and L- type calcium channels. Specific to gamma aminobutyric acid (GABA) neurotransmission, ethanol exposure during brain development reduces the number and/or function of NMDA receptors. These receptors play a role in synaptogenesis, stabilizing newly formed neuronal connections. Heavy alcohol exposure inhibits the NMDA system [9].
As such, the same detrimental effects also apply to offspring, whose mother, consume opioid, class A, and/or B drugs — including but not limited to — fentanyl; cocaine, heroin, MDMA (ecstasy), LSD; ketamine, amphetamine, and cannabis (marijuana), be they used recreationally or abused habitually. For instance, self-administration of cocaine and amphetamine has been assessed in rats with prenatal stress experience, may increase the likelihood of addiction, and is enhanced in male, but not female, adult rats[8]. Ample evidence from rodent experiments, shows that exposure to psychoactive drugs during which time these newborn neurons grow and proliferate can alter the rate of its development in the developing hippocampus of fetal rat brain, suggesting the fundamental goal of neurogenesis at promoting long-term behavioral, emotional, and cognitive functions for the prospective fetus are severely phased out at this cellular level due to the apoptogenic and teratogenic properties those drugs elicit, yielding the probability of long-term deficits in adulthood to become highly likely [1].
During which time, ethanol is, too, found to be affecting monoamine neurotransmitters and its enzymatic activation. Neurotransmitters are molecules whose main function is absolutely essential for neuron firing in order to keep action potentials or nerve signals (be they in the form of stimulation, inhibition, or modulation) navigated and run intact ahead of desired outcome. The activation level of monoamine oxidase (MAO) is thought to be as a biological metric to measure the functional capacity of the serotonergic and dopaminergic systems. These two systems are central in determining not only personality phenotypes like behaviors, but also in the risk factors of psychosomatic disorders including anxiety, major depressive disorder, antisocial traits, and borderline features. The link between platelet MAO activity, which is highly genetically regulated and is stable in the individual, and personality traits, has been a longstanding area of interest to understand the developing symptoms of psychopathology, especially personality disorders and its comorbidity [12]. The activity level of monoamine oxidase (MAO), chromosomal location, including gene-environment interplay and its link to symptoms of both opposing and comorbid psychiatric disorders — will be furthered discussed in the subsequent point.
Speaking of personality and behavioral phenotypes that ethanol exposure results, during critical gestational periods, it is important to underscore that, although the likelihood of reversibility could be on the horizon, at its fundamental levels, however, the refractoriness of toxic agents may run in a continuum throughout life — nonetheless. Therefore, drawing our attention back to a life in the womb may be a good starting point to predict the offspring’s overall life expectancy — including the risk of substance dependence and incarceration in adulthood. This also could be why personality tends to be consistently as stable across time as it, at least in part, is a by-product of either the up- or down-regulation of MAO activity at synthesizing serotonin and dopamine receptors which we know is interdependently influenced by genetic coding, albeit up to a certain percentage.
In addition to the outcome of fetal alcohol exposure, moderate to acute stress is thought to be the primary precursor of maternal alcoholism leading to the very former. hyperactivity in the emotional brain region, i.e., amygdala, of the child, thus the vulnerable little one may be more prone to develop anxiety-related markers later on in life, be they in the form of psychosomatic symptoms, readily throwing heavy tantrums, or may struggle more at regulating, identifying, attuning to his or her own emotions than those whose attachment is secure, or not least continues to be present during infancy, and forward.
“[An etiological model of the “borderline-child-to-be,”] a history of stress due to mismatched parenting, the evolution of developmental deficits, and the establishment of inefficient mechanisms for coping which become pathological defenses. The early experience of these children of neglect in the presence of the mother is associated with an inability to regulate an overwhelming “stimulus barage from within,” an impaired taming of aggression, and a failure to develop positive self-esteem.”
— On the development of the “borderline-child-to-be, American Journal of Orthopsychiatry (1986)
Off to the third trimester, that hyperactivity of amygdala could’ve also been mitigated and curbed by the basolateral amygdala (BLA) only if ethanol ceased to be administered during this gestational period. The basolateral amygdala (BLA) plays a critical role in modulating emotional processing, in part, via dopamine (DA) regulation of GABA transmission. This BLA modulatory system is acquired during the first 2 weeks of postnatal life in rodents (equivalent to the third trimester of human pregnancy) [5].
The very reason why much of birth defects, neonatal impairments, mental retardation, cognitive deficits could have been avoided, at least epigenetically, if only the mother prenatally were not to neglect her own child brings us to a starting point of sniffing the components that make up for their etiologies. Substance abuse, committed by the mother in the course of pregnancy, means there is hardly proper prenatal care, including lack of maternal attachment, toward the offspring. They thus extend to be a leading factor of long-term impairments be they socially, affectively, and cognitively that the child has to endure across lifespan unless counterbalanced by marked damage control, which may look like consistent-ditch efforts of clinical treatment and interventions. That, too, is no without exhaustive feats, such as the extent to which the environmental ‘U-turn’ support of any kind and medication’s side effects one is able to get access to and is willing to tolerate. So for this reason, poor prenatal care in terms of nutrition that leads to debilitating neurocognitive delays in childhood, including those tendency of engaging in juvenile delinquency and impulsivity, whether the symptomatic markers stain permanently or not further toward adolescent period, is relative to the consistency of clinical interventions and treatment regimen itself. At this point overall, what are the takeaways we might want to pull? Well, this all comes down to the idea that most of personality disorders and neurocognitive impairments is highly likely a consequence of the interplay around chemical imbalance derived from ethanol-induced teratogens, apoptogenesis and anxiogenesis results in this so-called, ‘negative trans-generational epigenetic inheritance,’ fostered by the mother.
References
[1] Canales, J. C. (2012). Deficient Plasticity in the Hippocampus and the Spiral of Addiction: Focus on Adult Neurogenesis. In Neurogenesis and Neural Plasticity (pp. 298–301). Berlin: Springer Heidelberg.
[2] Champagne, F. A., & Curley, J. P. (2011). Chapter 10 Epigenetic Influence of the Social Environment. In Brain, Behavior, and Epigenetics (p. 186). Springer Heidelberg.
[3] Chokroborty-Hoque, A., Alberry, B., & Singh, S. M. (2014). Exploring the complexity of intellectual disability in fetal alcohol spectrum disorders. Frontiers in Pediatrics: Child and Neurodevelopemental Psychiatry, 31–35.
[4] Creeley, C. E., & Olney, J. W. (2013). Drug-Induced Apoptosis: Mechanism by which Alcohol and Many Other Drugs Can Disrupt Brain Development. Brain Sciences, 1158–1172.
[5] Diaz, M. R., Jotty, K., Locke, J. L., Jones, S. R., & Valenzuela, C. F. (2014). Moderate alcohol exposure during the rat equivalent to the rat equivalent to the third trimester of human pregnancy alters regulation of GABAA receptor-mediated synaptic transmission by dopamine in the basolateral amygdala. Frontiers in Pediatrics: Child and Neurodevelopemental Psychiatry, 6–7.
[6] Granato, A., & Giorgio, A. D. (2015). Experimental models of early exposure to alcohol: a way to unravel the neurobiology of mental retardation. Frontiers in Pediatrics: Child and Neurodevelopmental Psychiatry, 4–5.
[7] Huberman, A. (2022). What Alcohol Does to Your Body, Brain & Health [Motion Picture].
[8] Kosten, T. A., & Nielsen, D. A. (2014). Chapter 16 Maternal Epigenetics Inherentence and Stress During Gestation: Focus on Brain and Behavioral Disorders. In Transgenerational Epigenetics: Evidence and Debate (p. 205). Elsevier.
[9] Lopez-Arvizu, C., Bogle, C., & Belcher, H. M. (2016). Chapter 179: Neurobiology of Fetal Alcohol Spectrum Disorders. In The Neurobiology of Disease (pp. 1255–1256). Oxford University Press.
[10] Mao, J., Ma, H., Xu, Y., Su, Y., Zhu, H., Wang, R., . . . Deng, Y. (2012). Increased Levels of Monoamine-Derived in Fetal Rat Bain Exposed to Ethanol. Springer Science+Business Media New York, 356.
[11] Olney, J. W. (2014). Focus on apoptosis to decipher how alcohol and many other drugs disrupt brain development. Frontiers in Pediatrics: Child and Neurodevelopemental Psychiatry, 22–23.
[12] Oreland, L., Hallman, J., & Damberg, M. (2004). Platelet MAO and Personality — Function and Dysfunction. Bentham Science Publishers Ltd., 2007–2010.
[13] Pine, F. (1986). On The Development of the “Borderline-Child-To-Be”. American Journal of Orthopsychiatry, 450–452.
[14] Schneider, M. L., Moore, C. F., Barnhart, T. E., Larson, J. A., DeJesus, O. T., Mukherjee, J., . . . Kraemer, G. W. (2005). Moderate-Level Prenatal Alcohol Exposure Alters Striatal Dopamine System Function in Rhesus Monkey. Alcoholism: Clinical and Experimental Research, 1686.
[15] Sullivan, E. V., Harris, R. A., & Pfefferbaum, A. (2010). Alcohol’s Effects on Brain and Behavior. Alcohol Research Health.
[16] Sutherland, R. J., McDonald, R. J., & Savage, D. D. (1997). Prenatal Exposure to Moderate Levels of Ethanol Can Have Long-Lasting Effects on Hippocampal Synaptic Plasticity in Adult Offspring . Wiley-Liss, Inc., 232.
Part II: Evolutionary Psychology, Neurobiology, and Molecular Genetics
3) Summoning a grand jury: the Prefrontal Cortex as the seat of consciousness
“Nothing in biology makes sense except in the light of evolution.” The Russian-American biologist Theodosius Dobzhansky wrote in 1967 [7, 18, 24]. A statement that almost successfully curbs the intricacies of the ontogeny of the nerve system, specifically the brain. This marks the idea that most of biological system can only be understood by zooming ourselves out to the big picture in order to understand the evolution of the brain, wholly. Pressures, competitive or even volatile environment force us to push through, acclimatize and maneuver this demanding situation with a set of skill, mental toolkits and knowledge. Yet, we can ascertain, towards the future, the novelty still often leaves us with perpetual questions, cornered us perplexed at the edge of the unknown. Hazy uncertainty is dancing everywhere in our head. Hence, the usual suspect, anxiety ensues. And as we’re trapped in this echo chamber as the given pressures are enhanced strongly, there is a particular part in our brain being summoned — to respond, the prefrontal cortex. Driven by gene-environment conflicting interplay to seize contingencies, account for their risks and benefits as one goes along, adopt which fits, and proceed to adapt in real time. That, however, an oversimplification of taking the prefrontal cortex into account. As the Dutch biologist Niko Tinbergen suggest, in order to swim into the depth of any biological system, four questions we should ask beforehand as a general rule: how did it evolve (phylogeny)?; how does it promote fitness (selection)?; how does it develop (ontogeny)?; and how does it work (mechanism)? [17] Understanding a system that is hierarchically complex and multifaceted like the central nervous system — the answers to the last two questions would not get us anywhere the core of prefrontal cortex since they only concern about the how as opposed to the first two questions about why the how is. Thus, an evolutionary framework needs to be employed, as a means to an end.
Primitive design: automatic nervous system as the precursor of evolution
Back around 1932, known as the father of neurology thanks to his seminal contribution to the matter of epilepsy, John Hughlings Jackson, has made an attempt to get around the confusion surround the nervous system, in Evolution and Dissolution of the Nervous System [15, 20]. By means of Darwinian logic, he echoed and deploy the Spencerian evolutionary framework. It is suggested that long prior to the modern anthropoid, the nerves primitively mechanized the evolutionary road from the most simple to the most complex — which, Spencer argued, regression, evolution, heterogeneity, complexity and progress are the frictions from which natural selection mobilizes onwards:
“If the doctrine of evolution is true, the inevitable implication is that mind can be understood only by observing how the mind is evolved.”
— Herbert Spencer
Spencer’s general evolutionary law, stated: “the progress from a state of indefinite, incoherent homogeneity to a state of definite, coherent heterogeneity.” [15] Early on, nerve centers are at first poorly organized and the information processing is arduously required to be structured as evolved. This Darwinian framework is akin to foraging model in the ancestral times. By purpose of fulfilling a basic biological pressure to survive, suppose a forager hunts for food out in the wilderness. The catch is, it gives room for predators to get in the forager’s way at a given time and place. This inevitable danger certainly will put him at risk that may result his body in switching to defense mode, when necessary. The sympathetic nervous system as often is associated with fight-or-flight mode that takes form of fear, once an air of danger is detected to the point of a real danger, is going to immediately secrete hormones associated with stress from adrenal glands and release energy by ramping up one’s heart rate, blood pressure, sweat glands, lowering saliva and the activity of digestive system — as for preparatory counterattack rushing straight from automatic system to the motor system, and eventually some physical altercation proceeds. This basic survival mode involves hand-eye coordination, only. And given how involuntary, directed and immediate with no conscious thinking required during which time the sensory-signal input altered to motor-enactment output, Jackson thus associated this most simple with automatism [15, 20]. From this scenario alone, we can infer that the nervous system in the prehistoric period evolved to ‘react’ immediately against threat, hence individuals back in those days have stronger propensity for reflexive and reactive behaviors. They are almost always wired to fight to the point of becoming an autopilot, considering the volatility of their environment predisposes them to be 24/7 alert, if not programmed by evolution as such [15, 20].
The Dawn of Consciousness: Order amid Chaos
Still, bear in mind, the frontal cortex is responsible for selecting, filtering, inhibiting sensory stimuli from automatic nervous system. And for all those obvious reasons, they are the antithesis of automatism. For more than 3 million years tilting further away from the savagery of Stone Age to today we step in at the age where artificial consciousness starts tinkering [13], it is not unreasonable to ascertain that homo sapiens have incrementally yet painstakingly ascended from low- to higher-leveled hierarchy of the brain. And because the junction between stages is so imperfect and complex, Jackson argued, this transition zone being a space between order and disorder leads to how natural selection plays its own part. Adaptation processing in the face of disorienting chaos ensues. This adaptive system can be thought of when bottom-up meets top-down [20, 21]. So in the foraging example, that incipient threatening signal detected by the sympathetic nervous system in the form of sensory stimulus leading to motor reaction i.e., physical altercation is when bottom-up stage takes place. It compels an agent to react in real time as a result. But now and then, considering the misfortune of such unwanted events, more so having experienced this degree of danger in this particular territory, would the forager risk his life twice by the same level of jeopardy on the next round? Of course, something needs to change. The word ‘change’ is central for the transition from bottom-up to top-down. The forager, given the circumstances, may start reconsidering the choice of the hunting area, or the kind of weapon he could and should have equipped himself with as to keep the predators at bay, or perhaps the timing issues. This degree of abstraction involves learning and memory.
Chaos, in the sense of disorderliness that entails event and uncertainty surrounding the pre-event, bolsters the brain to integrate and coordinate which best action should it be generated as to preemptively anticipate the best and worst outcome. For this reason, chaos can also be thought of as the precursor for order, which the frontal cortex has gradually and imperfectly long evolved to reconcile the past and the future. It is the episodic memories of the past event that have been stored, whose information is retrieved for assessing risks-and-benefits before the possible and probable outcomes being predicted for the upcoming scenario (the future) [22]. That feedback-loop processing also known as top-down modulation, which inextricably is dependent on and influenced by what causes it. Not only by principle, is it argued by evolutionary biologists to be the source of many philosophical problems, causation, also often argued to be preceding the effects [7, 16]. As the name suggest by the very theoretical conceptualization, it is known as ‘downward causation’, especially in the context of biological system, which stated as following: “All processes at the lower levels of a hierarchy are restrained by and act in conformity to the laws of the higher levels.” [7]
“Right between the two extremes… at a kind of abstract phase transition called the edge of chaos, you also find complexity: a class of behaviors in which the components of the system never quite lock into place, yet never dissolve into turbulence, either. These are the systems that are both stable enough to store information, and yet evanescent enough to transmit it. These are systems that can be organized to perform complex computations, to react to the world, to be spontaneous, adaptive, and alive.”
— Mitchell Waldrop, Complexity: The Emerging Science at the Edge of Order and Chaos (1992)
So as we know from evolutionary perspectives, an adaptation is a trait that has been modified by natural selection over evolutionary time for the function of the trait [2]. The quality of error-reductions and the speed of informational processing streaming from lower to higher level hierarchy, as alluded, has so much bearing on how strategically agile and shrewd an agent responds to frictions at the brink of chaos.
High-Ordered Control: Executive Function and Hierarchical Representations
It now becomes more reasonable to ascertain this painstaking journey towards the seat of consciousness — moving from lower, organized, homogenous, coherent, simple upwards to higher, unorganized, heterogeneous, complex neural mechanism. A steep and prolonged ladder with sequences of friction where each step gives a room for natural selection. This is when incoming stimuli and automatic flow over time hindered by the skepticism of feedback-loop records laid on the table. The more complex is the task for the frontal cortex to integrate and coordinate the excitatory rush coming from automatic lower nervous system into the inhibitory brakes located in the higher strata of the cerebral, the more advanced is the representation the cognitive function tackles. Jackson thus encapsulates Spencerian mind evolution as following:
‘(1) Evolution is a passage from the most to the least organized. “Highly organised” is frequently used synonymously with ‘very complex’: but by degrees of organisation I mean degrees of perfection of union and certainty of action of nervous elements with one another. Using the term organised in this sense I say that the highest cerebral centres are the least organised (the “most helpless centres”), although they are the most complex, whereas the lowest centres are the most organized, although the least complex. In other words, we may say (2) that the evolutionary ascent is from the least to the most modifiable. If the highest centres were not modifiable, we should be very simple machines; we should make no new acquirements. If the lowest (“vital”) centres were to become modifiable as the highest are, life would cease.’
— J. H. Jackson (1932), Evolution in the Brain, Evolution in the Mind: The Hierarchical Brain and the Interface between Psychoanalysis and Neuroscience.
“Higher centres” means to encapsulate the so-called executive function. The advanced, sophisticated, and most conscious of the human mind, where it takes place in the sub-regions of, including but not limited to, all the hubs that are tightly connected with the prefrontal cortex. For most of executive functioning ability involves working memory, decision-making, problem solving, adaptive functioning, suggestibility, planning, managing goal-directed behaviors and actions [12, 17]. There are two ranks of hierarchy divided: the empathy center and the rational center. Empathy, in the context of theory of mind, is measured by the ability to attune, micromanage, infer a wide range of affect, externally or internally, thus as the name suggests ‘emotional executive function.’ Rationality, on the other hand, by the capacity of getting around complex problems, inferring logic and detached reasoning, generating short-term contingency within a scheme of long-term planning — which, lies even higher in the hierarchical system than does the emotional. Thus, ‘meta-cognitive executive function’ [3]. Functionally, however, both are not mutually exclusive. Relative to the individual’s preference or genetic predisposition toward how to approach life, in order to govern optimally and make the rulings adaptive and appropriate, the prefrontal cortex couldn’t have done these weighing pros and cons without its connectivity with milieus rooted from beyond. Admittedly, although cognition and emotion can be intertwined and involved inseparably especially when an important decision-making has to be made under fire, it requires more hierarchically complex thus is extremely rare to get that balance stroke. To simplify, caudal areas (bottom), such as the limbic system, responsible for emotions, motivation, long-term memory; the cerebellum, for movement and motor-related coordination; while the non-caudal orbitofrontal cortex, for visceral sentiments in the form of olfactory, gustatory, somatosensory, and visual perceptions. As mentioned, the relationship in between is tightly reciprocal that their way of interacting can be described as communicating feedbacks constantly from lower to higher and back to lower order [17, 19]. Since many of the frontal job also involves repeating neural representation systemized in a hierarchical order, thereby top-down ruling essentially is about selecting and filtering, if not suppressing, whatever internal and external influences that are not admissibly relevant to the means of a goal, since it can interfere the best-predicted outcome [17]. By means of hierarchical representation, this whole system and mechanism, evolutionary and ontogenically, is also about one moving from primary sensory to higher order areas, reaching for the most complex pattern in the prefrontal cortex [15]. As John Hughlings Jackson, never tired of saying: it is a profound mistake to take the brain to be a ‘solid mind’ [21].
To understand the logic of neural representation, hierarchy, and which brain connectivity or region involved in, imagine this following scenario:
A group of Nazis hunts the Jews in one specific territory. There is a possibility of hiding Jews in that territory, thus resulting soldiers to proceed an enhanced operation by cleaning up the areas. They broke down every hut and house where the usual suspects are suspected to be inside. As they wander around, a sound of crying baby caught to their ears. The mother of the baby is apparently not alone with the baby per se. She is with company, having five people with her including friends, neighbors, and relatives, hiding discreetly underneath the wooden floor of a hut. She caught between a rock and a hard place as to how resolve such a dilemma. She has two options:
(1) Saving five — at the expense of the baby — killed by the Nazis — less likely.
(2) Keeping one baby — at the expense of the five Jews (including the mother and possibly the baby) — killed by the Nazis — more likely.
As philosophically conflicting as it became notoriously widely-debated, this dilemma has indeed attracted the attention of researchers and scientists to investigate the neurobiological underpinnings of each option chosen [19]. Neuroimaging evidence shows, there is a strong activation in the amygdala, insula, anterior cingulate cortex (ACC), the orbitofrontal cortex (OFC), which also sometimes called ventromedial prefrontal cortex (vmPFC), of those who go with number 2. As the ethics’ model suggests, it is hypothesized that due to the underlying emotion contributes predominantly to how they make a decision. But even when we page through back to their anatomy, it is sensibly consistent. As we have learned, the amygdala is responsible for detecting danger, this somatic marker in the form of fear then activates the so-called amygdala’s brake, anterior cingulate cortex (ACC) to reflect the feeling of sadness, anger, guilt, etc before rostrally going upward to the prefrontal cortex, specifically a part weighing the outcome of that emotion, the ventromedial prefrontal cortex (vmPFC). The temporal sound of the crying, the vulnerable and helpless look that the baby painfully transmits to the viscerally-responsive OFC enough to evoke a sense of guilt thus dissuade the morally-constrained vmPFC from smothering the baby. When the decision of not killing the baby is made despite the long-term outcome to the contrary, neuroimaging shows, this neural representation reaches only as high as the second order hierarchy [17, 19]. Hence, a re-representation of representations. They trade the lives of the collectives for the guilt they dreadfully may have to bear in the future, as the outcome, if opting for the death of a baby. Hence, the rationalization of option 2 may sound like, “Any living individual can never be a pawn.” They are less likely smother the baby irrespective of the costs of doing or not doing it because their emotion has overpowered the cognition can they otherwise opt with.
Contrary to those who go with the option 2, option 1, a stronger activation takes place in the most rational and unsentimental part of the PFC: the dorsolateral prefrontal cortex (dlPFC), who might respond to the decision made by the vmPFC, “Well yes, for the right outcome.” The dlPFC will be more than happy to disregard emotions for maximizing benefits to and acting upon the interest of the many as opposed to of the few [19]. This level of impersonality and disinterestedness makes the dorsal areas of the PFC sit at one level higher above the vmPFC (or OFC), insula, ACC, amygdala, hippocampus, including the rest of nerves associated with automatism [17, . It is when the second level representation projecting feedback from the lower order is modified to become a re-representation of the re-representation [15, 17, 20]. As the neurobiologist Robert Sapolsky in Behave viewed dlPFC as, ‘a decider of deciders,’ to the point of, as the neuroscientist Joshua Greene also profiled this particular brain area, ‘a hallmark of human cognition’ [14].
Weighing the pros and cons in the way of not only how people direct their own action but also what they are as a “human being” has been a longstanding battle between the vmPFC and the dlPFC in deciding that which whether driven by the rule of principle or by of consequence. In addition, dlPFC is also believed to be the part of the brain that matures last, and because of this, is the most recent contrary to the limbic system and least constrained by genes. Thus, it does not fully mature until the individual reach the age of 25. For it takes more or less this range for the individual rolling with the punches, and learning reversibly from non-shared environments — be it mentors, teachers, or tutors [12, 17].
4) Taking the usual suspect into account: Monoamine Oxidase A (MAOA) and the hereditary sin
Dates back in 1978, a woman walked into a hospital in the Netherlands, not because she was worried about herself but because she was worried about her family. All the men in her blood circle had a history of violent crimes. There were murders, rapes, arsons, traced back across the chain of generations. Researchers, H.G. Brunner and his colleagues, started getting DNA samples from the members of her family, and they discovered, those who had engaged in these acts of violence shared one thing in common: an astonishing abnormality in their genetic mutation. This gene known as Monoamine Oxidase A, or MAOA. It completely knocks out the DNA function making a person uncontrollably aggressive, reactive and impulsive, thus the so-called Brunner Syndrome was popularized due to the symptomology of this particular genetic disorder became pervasive even beyond the scope of the Dutch family[5, 6]. It is suggested that as MAOA gene encodes an enzyme i.e., MAO-A, whose primary job is to degrade the neurotransmitters i.e., dopamine (drive, motivation), serotonin (mood, emotion), and norepinephrine (adrenaline), the low activity of this gene expression — giving rise to less produced enzyme — thus being “understaffed”. Therefore, a great amount of those molecules are accumulated in the synapse while they should have been removed by the MAO-A enzymatic degradation or pumped by the monoaminergic reuptake to the presynaptic neuron. The 5HTT serotonin reuptake, whose job is to reabsorb those molecules, otherwise work harder at mopping them up in the synapse. And given such a case, they compensate, and as studies suggested, even overcompensating by decreasing serotonin receptor numbers instead, thereby reducing sensitivity to all that serotonin [11, 19]. So, whenever a primitive arousal and stimuli emerged out from limbic system, this signal that is supposed to be controlled by the brake system located in the frontal lobes, are not being conditioned in a kind of Pavlovian way — because that elevated level of serotonin have already enhanced the fear response of the individual through the manifestation of the reactive behavioral outcomes. The evidence has shown through several neuroimaging studies. The polymorphism influences the connectivity between the regions of the prefrontal cortex and the limbic areas, such as amygdala and hippocampus. This dynamic known as corticolimbic connectivity, which is made up of the prefrontal cortices, amygdala, hippocampus, whose main job, deploying a broad range of behavioral and cognitive function, including motor control, decision making, and emotional regulation — and yet being dysfunction due to the low-activity MAOA alleles in the MAOA gene [11].
Likewise, Brunner not only found a profound degree of abnormal behaviors in those men affected by the gene, but also how the lack of MAOA itself affects their cognitive functions. It manifests through borderline mental retardation in the form of lower IQ, ranging from neurocognitive to neurobehavioral disabilities, including attention-deficit/hyperactivity disorder (ADHD), conduct disorder, substance abuse, and other risky behaviors. By corollary, inattention, impulsivity, alcoholism, social deviance, may predispose the individual to committing violence [18].
So why are violent crimes committed disproportionately by men in the family? It is due to the genetic defect was located on the X chromosome. What makes it rarely the case for females committing such criminal offences, as Brunner discovered, is because females have two X chromosomes as opposed to males a single one, only. Therefore, when the defective gene is detected, it will be masked by another X chromosome in females (XX), while sadly, not in males (XY) because there is no another X that would. This explains why men are more prone to be aggressive than women, especially if they are affected. But even if females inherit this gene and may not be equally at risk as their male counterparts, they still do run the risk because the “potential” problem is preserved in her X chromosome just by being the gene’s carrier — from which her later son would highly likely embody it [5, 6]. Given how groundbreaking the discovery was, countless furthered studies since then have been developing and conducted with regard to the link between the low activity of MAOA and antisocial behaviors, which became consistent across time, even beyond to non-human-primates like in rodents which also appeared to be case.
Before going down further, it is important to underscore that we all have the MAOA gene, the line drawn between the groups of non-violent and violent in the general population has bearing on the activity level of the constituency of this gene, specifically known as platelet. Strictly speaking, the lower the activity of MAOA platelet (MAOA-L), the higher and more elevated neurotransmitters in the synapse, the individual is more prone to symptoms of antisocial behavior. The higher the activity of MAOA platelet (MAOA-H), the lower and less elevated neurotransmitter in the synapse, the individual is more prone to symptoms of major depression. This is evident based on a sample of 538 participants from the Iowa Adoption Studies [4]. Of course, the notion prone does not equate is. The former simply means potential risk. And as one study suggested, MAOA-L does not always act out in an antisocial way albeit its genetic information may contribute to the acts of antisocial behaviors. Low levels of platelet MAO activity can also be found in socially well-adjusted and creative non-criminal subjects [1], which is unsurprising given genes couldn’t care less about the outcome of either the affected or the carrier will be in life, hence a longstanding nature vs. nurture debate remains. Under the confines of DNA transcription, the alleles are competing for their slot on the chromosomes of the future generation in the gene pool, wherein consists of the combined genetic information (i.e., physical, personality phenotypes) of all the individuals of the same species in a given area (the individual’s immediate environment) which share a common group of genes. Any gene that behaves in such a way as to increase its own survival chances will tend to survive and thereby is more likely to claim its slot in the chromosome[10]. Back to the creative non-criminal subjects, it is suggested that low platelet MAO activity is linked to personality traits such as sensation seeking, impulsiveness and monotony avoidance which can be thought of as a precursor for adventurously risk-taking endeavors, which not rarely the case is independent from criminal offending. It also has been suggested that genotype, the genetic constitution of an individual organism, may influence response to environmental risk. This is where gene x environment interplays made it into discourse.
To emphasize in more details, there was another seminal research in the field of behavioral and social sciences conducted by two scientists, Terrie Moffitt and Avshalom Caspi, whose paper published in Science in 2002, found that individuals having combination of maltreatment and the low-activity MAOA genotype represented 12% of the birth cohort, accounted for 44% of those convicted of violence [8, 9]. Indeed, it may relatively not look like much but one event has a knock-on effect throughout generation. Hence, hereditary sin. According to the findings, it appears that psychosocial factors rule not out the possibility to accelerate the genetic and the biological pulses in predisposing the individual to later antisocial and violent conduct. So if someone grows up in an aversive environment, going through any form of abuse (sexual, physical, emotional), parental rejection or neglected as a child, being held back as much by their caregivers as by peers either in a household or at school, and occurred within the reach of their immediate environment on a fairly regular basis — it fosters more strongly the effects of MAOA-L genotype on the development of antisocial behavior during the course of a person’s behavioral ontogeny [8, 9].
So, could a perpetrator be the “first” victim?
Judge for yourself.
References
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