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A scientific case for personality typology

  • Published: 06-09-2015 Edited: 07-09-2015
  • Abstract

    It is generally considered that personality-typologies are pseudoscientific and that searching for personality-types lead to a dead end lacking any empirical evidence.

    The objective of this research was to research if the old assumptions were correct or not.

    Our conclusion is that it is scientifically possible to define personality-types and also that it is scientifically valid to assume that there exists different kinds of personality-types based on individual differences in genetic attributes.

    Introduction

    A typology is a collection of types, and consists of:

    • A category for the things which can be typed.
    • A way of determining a type for a thing.
    • A word for each type that is distinct from the other types.

    Types are linguistic constructs that are cognitively useful, because they allow much information to be reduced into smaller pieces, which are somehow useful in a specific context.

    So a personality-typology is about determining types for personalities in a way which is useful for a specific context.

    This article will focus on areas such as motivation and fatigue when looking at personality from a neuroscientific perspective.

    Neuroscience

    Dopamine is a neurotransmitter, that means it is involved in transmitting signaling from one neuron to another. Dopamine is from the catecholamine and phenethylamine families. Dopamine can be seen as a lubricant because it generally increases connectivity in the area where it is in. [29, 30, 35, 36, 76]

    The current level of dopamine in a specific area is also called extracellular dopamine, which means it is free flowing between cells. In other cases when people talk about dopamine inside cells you say intracellular dopamine or dopamine in cytosol.

    You also come in contact with the words exogenous and indigenous which means if the dopamine originates from within the body or outside the body. Sometimes scientist say endogenous extracellular meaning it’s free-flowing dopamine originating from the body. Another word that is commonly used is dopaminergic which means ”related to dopamine” or ”working on dopamine”. A concept that is used a lot is the inverted-U relationship which means that the highest value is in the middle of all values and that values decrease on both ends of that middle point.

    Dopamine is involved in eight different dopaminergic pathways in the brain, which transports dopamine from one area of the brain to another. In the brains reward systems, the most important system is the mesolimbic-reward-pathway where dopamine plays a critical role. This pathway is about stimulus-predictions and also reward predictions and it affects a substantial level of differences in personality.

    Another dopamine pathway is the mesocortical-pathway which is about releasing dopamine to the prefrontal cortex and also to the cortex. These two pathways are together referred to as the mesocorticolimbic projection. There is a great overlap between the mesolimbic and mesocortical pathway.

    The effects of these two pathways on personality is so big that it possibly exceeds all other factors in defining personality, that is why this post will be lengthy about the mechanics of dopamine on personality.

    Another dopamine pathway that is involved in voluntary movements is the nigrostriatal-pathway, but it is not relevant to the scope of this article but lies in close proximity to the mesolimbic-pathway.

    Two relationship that are often used is the inverted-U relationship and U relationship. The inverted-U relationship have the highest value in the middle and low values on both sides.

    The inverted-U relationship:




    The U-relationship has highest values on the sides and lowest in the middle:



    Another word which is commonly used in genetics is allele or allelomorph which means one of a number of alternative forms of the same gene occupying a given position on a chromosome.

    Another word used is in vivo which means that something is happening under natural circumstances, opposite of in vitro.

    Other words that are commonly used is homozygotes which means that there two identical variations of a gene and heterozygotes meaning it is different variations of a gene. Both of these words determine the zygosity which is the degree of similarity of the alleles for a trait in an organism.

    Here is a diagram for the mesolimbic and mesocortical pathways, which are most relevant to individual differences in personality.

    The mesolimbic-pathway and the mesocortical-pathway:



    General about dopamine

    The dopamine-reward system is built up of:

    • Receptors

    • Family D1: receptors D1 and D5 which is influenced by the genes DRD1 and DRD5
      Family D2: receptors D2, D3 and D4 which is influences by the genes DRD2, DRD3 and DRD4

      The dopamine receptor D2 has two forms: D2Sh (D2 Short) and D2Lh (D2 Long) where D2Sh has built in feedback mechanisms and D2Lh works as a classical receptor.

      Receptors are the ones releasing dopamine into extracellular space. D1 receptors have more stable release than the D2 receptors because D2 receptors have built in feedback mechanisms which can reuptake the released dopamine either before release (presynaptic reuptake) or after release (postsynaptic reuptake). [34]

    • Transporters

    • The dopamine active transporter (DAT) influenced by the gene DAT1. Transporters catches free dopamine and transports it back to cytosol.

    • Enzymes

    • Degradation enzymes: monoamine oxidase (MAO), aldehyde dehydrogenase (ALDH) or catechol o-methyltransferase (COMT)
      Synthesizing enzymes: Biopterin-dependent aromatic amino acid hydroxylase (AAAH), Aromatic L-amino acid decarboxylase (AAAD).
      Enzymes synthesize and degrade dopamine.


    The D2 receptors have highest density in the striatum. [37]

    Dopamine is synthesized chemically in the brain from L-Phenylalanine to L-Tyrosine to L-DOPA to Dopamine. Dopamine is also itself a precursor in the synthesis of norepinephrine and epinephrine which are other important chemicals in the brain.

    After synthesis dopamine is transported from cytosol into synaptic vesicles of dopamine receptors with the help of the protein vesicular monoamine transporter 2 (VMAT2).

    Once there it can be released into the synaptic cleft for two reasons:

    1. an action potential occurs and causes the vesicles to release their contents directly into the synaptic cleft through a process called exocytosis.
    2. however, dopamine receptors which are colocalized with the protein Trace amine-associated receptor 1 (TAAR1) can release dopamine into the synapse in the presence of sufficient concentrations of endogenous phenethylamine.

    Once released to the synaptic cleft, dopamine binds to and activates dopamine receptors, which can be located either on postsynaptic target cells or on the membrane of the presynaptic dopamine-releasing cell itself (i.e., D2 Short auto receptors). Once here you call the dopamine receptor binded or unavailable.

    After an action potential, the dopamine molecules quickly become unbound from their dopamine receptors and become extracellular. They are then absorbed back into the presynaptic cell, via reuptake mediated either by the high-affinity dopamine transporter (DAT) or by the low-affinity plasma membrane monoamine transporter (PMAT). Once back in the cytosol, dopamine is subsequently repackaged into vesicles by VMAT2, making it available for future release.

    In most areas of the brain and also the basal ganglia and striatum, dopamine is inactivated by the reuptake of dopamine transporters (DAT) and then broken down by the enzyme monoamine oxidase (MAO). But in the prefrontal cortex (PFC) there are few dopamine transporters (DAT) and dopamine is instead inactivated by the reuptake of norepinephrine transporter (NET) and then broken down by the enzyme catechol o-methyltransferase (COMT). Since the inactivation of DAT is much faster than the inactivation from COMT, prefrontal dopamine decreases slower than striatal dopamine.

    In humans, the COMT gene contains a functional polymorphism that codes for the substitution of valine (Val) by methionine (Met) at codon 158. Due to the fact that the COMT protein containing methionine (Met) is relatively thermolabile, its activity is lower at body temperatures than the COMT valine (Val) protein, which is fully active at body temperature. Because of this, individuals with two copies of the met allele (Met/Met) have 25–75% reduction in COMT enzyme activity compared to individuals with two copies of the val allele (Val/Val), and therefore presumptively more baseline synaptic dopamine in the prefrontal cortex. [67, 68, 69] This gene polymorphism are often called Val158Met, Val108/158Met or rs4680.

    Image of dopamine degradation (from Wikipedia):


    The amount of receptors influence how much dopamine that can be released in a period of time and the amount of transporters influence how much dopamine can be inactivated in a period of time. The dopamine-level in the brain will also influence how many dopamine receptors are available and how many are binded or unavailable.

    Image of synapse releasing neurotransmitter (from Wikipedia):


    The mesolimbic-reward-pathway

    In the mesolimbic-reward-pathway people often talk about tonic and phasic dopamine. Phasic is transient and released in response to salience or cues of predicted reward while tonic is the baseline level which is controlled by the prefrontal cortex. [4, 6, 18] Prefrontal cortex can also modulate phasic dopamine. [8] Especially if stimuli is associated with fear, the PFC and amygdala can modulate the phasic dopamine release. [39] Self-motivating behavior is essentially the prefrontal cortex which increases the tonic striatal dopamine release in absent of rewarding stimuli. [19] Tonic dopamine is released in regular bursts while phasic dopamine is released in intermittent bursts at high frequencies. [18] The prefrontal cortex can also inhibit the release of phasic dopamine with behavior-inhibition [19]. The prefrontal cortex can inhibit the release of dopamine from D2-like receptors. [21]

    Prefrontal dopamine-levels is sometimes called cortical dopamine and striatal dopamine are sometimes called limbic dopamine.

    In the mesolimbic-reward-pathway, dopamine is primarily sent from the ventral tegmental area (VTA) to the nucleus accumbens in the ventral striatum, hippocampus and amygdala which releases it in response to salience or rewarding-cues, which could be external or internal, anything that is experienced as interesting or novel or important. [16, 17] It can also be released as a means of self-motivation. [19] Hippocampus dopamine is associated with memory-function so reward plays an important role in memory-function. [37]

    Some of that dopamine is also transported out of the mesolimbic-pathway up to the prefrontal cortex where it is used and inactivated by the COMT enzyme. Another part of it is inactivated quickly in the striatum by the dopamine transporters (DAT) before it reaches the PFC. If dopamine release in the striatum gets transported out of the striatum you call it striatal dopamine efflux.

    Depending on differences in receptors, transporters and the COMT enzyme people will have differences in the dopaminergic system which influence personality substantially. [38]

    Striatal phasic dopamine release can be seen as a mechanism for development where rewards as expected or incorrect predictions of rewards lead to lesser phasic dopamine release than baseline and more rewards than predicted lead to higher phasic dopamine than the baseline. [27] Dopamine increases plasticity and is required for accessing and modifying memory. [27] Dopamine can be seen as a mechanism which regulates the seeking and learning from rewards and punishments. [27]

    The production of dopamine from the VTA is accompanied of a feeling of reward. The reward is basically an affect which motivates behavior. Some studies link the emotions of liking and motivation to different parts of the striatum. [20]

    When dopamine is high in the striatum we feel: [12, 22]

    • Anticipation.
    • Excitement.
    • Motivation.
    • Salience.
    • Arousal.
    • .. something unexpected just happened.


    Image of mesolimbic-pathway, mesocortical-pathway and the nigrostriatal-pathway:



    The mesocortical-pathway

    In the mesocortical-pathway, dopamine is sent from the ventral tegmental area (VTA) to the prefrontal cortex and to the frontal lobe.

    When dopamine is high in the prefrontal cortex we: [32]

    • Have the ability to plan, visualize, prevent interruptions. and use proactive cognitive control.
    • Have high ability of working memory.
    • Have high behavior inhibition.
    • Have the ability to resist salient or incentive stimuli.
    • .. can use metacognition to guide behavior.

    For working-memory, higher is not always better because working memory capacity has an inverted-U relationship with dopamine-level so that a medium amount of dopamine in the prefrontal cortex gives the highest ability for working-memory. [31]

    Low and high levels of dopamine in the prefrontal cortex is associated with the highest level of error-monitoring. [34] Medium level of dopamine is associated with lowest level of error-monitoring and also highest working-memory. [34]

    The dopamine level in the prefrontal cortex can also efflux into the striatum and influence ventral striatal reactivity.

    It is theorized that low prefrontal tonic levels of DA (associated to the COMT Val158Met Val/Val allele) lead to an amplification of the phasic dopamine response in the striatum. [77]

    Image of the mesocortical-pathway, mesolimbic-pathway and nigrostriatal-pathway:


    The mesocorticolimbic projection

    Individual differences in the mesolimbic and mesocortical pathways affect a lot of differences in personality.

    Image of dopamine release, reuptake and uptake:


    Differences in personality is to a big extent influenced by:

    • How fast dopamine is inactivated in the PFC, depending on the genotypes of the COMT Val158Met enzyme. [3] Val/Val genotype creates fast inactivation, Val/Met genotype creates moderate inactivation and Met/Met genotype creates slow inactivation.
    • How many dopamine receptors exists in the striatum, also called dopamine receptor density or dopamine receptor binding, affects how much dopamine that can be released in response to events, is caused by the genotypes of DRD genes. [5]
    • How many dopamine transporters exists in the striatum affects how much dopamine can be inactivated in the striatum, depending on the genotypes of DAT genes. [3]


    Personality-traits

    Most personality traits show non-linear associations with parts of the dopaminergic system. When studies make associations between one part of the dopaminergic system (receptor, COMT Val158Met genotype, transporters) and a personality trait they often find inconsistent results. Once multiple attributes are taken into account the associations gets more consistent, still there exists few clear association for any contemporary personality-trait with neurobiology except:

    • Reactive vs Proactive cognitive control by Braver et al.
    • Reward-Sensitivity by Jeffrey Alan Gray.

    There is in general weak support for associations between any contemporary personality-traits with neurobiological attributes this includes traits in contemporary personality theories such as:

    • TCI / TPG by Cloninger et al.
    • EPQ by Hans Jürgen Eysenck and Sybil B. G. Eysenck.
    • Big–5 personality-traits (including NEO-PI)
    • MBTI
    • Introversion / Extraversion

    Neuroticism

    Neuroticism is a personality-trait defined as characterized by anxiety, fear, moodiness, worry, envy, frustration, jealousy, and loneliness or characteristic of security-monitoring stressful external environments.

    Neuroticism is a trait which is included in the five-factor model or the big-five personality traits.

    A higher density of dopamine D2 receptors in the striatum are associated with higher score on neuroticism and psychiatric morbidity. [34]

    Since dopamine D2 receptors have the ability to reuptake dopamine in presence of negative feedback a higher amount of them enable a more sensitive releasing of dopamine and therefore also behavior.

    Sensation-seeking, novelty-seeking and reward-dependence

    The trait sensation-seeking is defined as the search for experiences and feelings, that are varied, novel, complex and intense, and by the readiness to take physical, social, legal, and financial risks for the sake of such experiences. It is a construct created by Cloninger for TPQ and TCI.

    The trait sensation-seeking has an inverted-U relationship with the amount of dopamine receptors in the striatum, where the maximum binding potential is related to highest score of sensation-seeking. Sensation-seeking is negatively correlated with the reactivity gain of dopamine or striatal dopamine efflux. [11] Binding potential is the degree of how much dopamine can be binded to receptors.

    Sensation-seeking are influenced by greater dopaminergic responses to cues of upcoming rewards in the striatum. [9]

    Sensation-seeking might be associated to the level of dopamine-gain from rewarding-stimulus, so that lower endogenous DA levels and higher density of receptors increases score in sensation-seeking. [10]

    The density of available dopamine-receptors in the striatum have an inverted-U relationship to sensation-seeking where the highest sensation-seekers have moderate density of available receptors in the striatum. [11]

    The trait novelty-seeking is defined as make decisions quickly based on incomplete information, lose temper quickly, easily bored, thrive in conditions that seem chaotic to others. This trait is also constructed by Cloninger et al. for TPQ and TCI.

    Novelty-seeking is negatively associated with the binding potential in the insular cortex. [66]

    Novelty-seeking is positively associated with striatum dopamine efflux. [73]

    Low scores on novelty-seeking represents temperamental rigidity, reflection, reserve, and regimentation. [72]

    Novelty-seeking is inversely associated with D2-like dopamine receptor availability in the mid-brain. That means that D2-like binding of dopamine receptors in the mid-brain are associated with novelty-seeking trait. [40]

    The trait reward-dependence is characterized as a tendency to respond markedly to signals of reward, particularly to verbal signals of social approval, social support, and sentiment, and learning to maintain and pursue behaviors which were previously associated with such rewards.

    The COMT Val158Met genotype Val/Val is associated with highest novelty-seeking, sensation-seeking and reward-dependence and Met/Met with lowest. [70]

    Fluid intelligence

    Fluid intelligence (Gf) is defined as the capacity to think logically and solve problems in novel situations, independent of acquired knowledge. It is the ability to analyze novel problems, identify patterns and relationships that underpin these problems and the extrapolation of these using logic. Fluid intelligence is a construct created by Raymond Cattell.

    Slower dopamine synthesis in the striatum is associated with higher response-inhibition and flexible problem-solving which are traits related to fluid-intelligence. [25]

    Fast inactivation in the prefrontal cortex by COMT Val158Met genotype (Val/Val) are associated with higher cognitive flexibility but not intelligence. [24]

    Slow inactivation in the prefrontal cortex by COMT Val158Met genotype (Met/Met) is associated with higher fluid intelligence. [41]

    Error-processing and adaptive behavior

    Error-processing is the ability to reevaluate behavior after a error has been found. Error-processing is a crucial component of adaptive behavior.

    The COMT Val158Met genotype affects individual differences in error-processing, where Val/Val show highest level of error-processing. Low and high prefrontal dopamine is associated with error-processing. If dopamine is increased in people with Met/Met they show higher error-processing, but if dopamine is increased in people with Val/Val they show decreased error-processing. [33]

    The COMT Val158Met genotypes Val/Val and Val/Met are associated with increased performance in teamwork situations compared to the Met/Met genotype. [49]

    The COMT Val158Met genotype Val/Val is associated with increased cooperativeness over the Met/Met. [50]

    The COMT Val158Met genotype Val/Val is associated with highest egalitarian behavior, Val/Met with moderate and Met/Met with lowest but all genotypes show more egalitarian behavior after given a COMT inhibitor which increases prefrontal dopamine. [50]

    The COMT Val158Met genotype Met/Met is associated with least flexible behavior due to a increased corticolimbic connectivity. [70]

    Exploration vs Exploitation

    The COMT Val158Met genotype (Val/Val) is associated with lowest exploration due to uncertainty, (Val/Met) is associated with moderate exploration due to uncertainty and (Met/Met) is associated with highest exploration due to uncertainty. [2]

    Proactive cognitive control

    Proactive cognitive-control is a construct created by Braver et al. for the DMC-model.

    Proactive cognitive control is associated with COMT Val158Met genotypes which has slower inactivation of prefrontal dopamine like COMT (Met/Met). [45] Met/Met genotypes are associated with having higher ability for sustained attention and working-memory.

    Reactive cognitive control

    Proactive cognitive-control is another construct created by Braver et al. for the DMC-model.

    Reactive cognitive control is associated with COMT Val158Met genotypes which has faster inactivation of prefrontal dopamine like Val/Val. [45] Val/Val genotypes are associated with having higher cognitive flexibility.

    Differences in brain connectivity

    The dopamine transporter gene affects connectivity in task-positive networks and task-negative networks, but also depending on state. People have differences in connectivity depending on state and DAT genes. [47] This includes connectivity with frontopolar, orbitofrontal, task-positive network, default-mode network and more.

    The availability of midbrain dopamine D3 receptors affect connectivity in large-scale networks in the brain. [48]

    Temporal discounting, reward sensitivity, impulsivity, intertemporal choice, immediate rewards, reward responsiveness

    A region of the DAT-gene, 40bp variable number of tandem repeats (VNTR) polymorphism in the 30 untranslated region of the DAT gene (DAT1), affect dopamine transporter density and therefore also dopamine availability.

    DAT1 9-repeat allele has lower density of dopamine transporters than the DAT1 10-repeat allele and is associated with higher impulsivity and ventral striatal reactivity. [1]

    The DAT 10-repeat allele is associated with 50%–90 elevated density of transporters compared to the DAT 9-repeat allele. [63]

    A deletion variant of a single nucleotide polymorphism (SNP) in the promoter region (–141C insertion/deletion, Ins/Del) of the DRD2 gene decreases ventral striatal reactivity compared to the Ins/Ins genotype due to decreased DRD2 expression. [1, 64]

    A DRD2 Taq1A polymorphism, a C/T SNP (rs1800497) located in the ankyrin repeat and kinase-domain containing 1 (ANKK1) gene. The T (A1) allele show higher has been associated with increased DA signaling, increased striatal glucose metabolism and reactivity to reward than the C (A2) allele. [14]

    There is relatively greater ventral striatal reactivity associated with the 7-repeat allele of a 48bp VNTR in the third exon of the DRD4 gene, which leads to reduced DRD4-mediated inhibitory postsynaptic effects. [1]

    By taking dopamine receptors, dopamine transporters and the COMT Val158Met enzyme one can get the best understanding of striatal reactivity. [14]

    Reward-sensitivity is defined as the degree of impulsivity when approaching a goal.. It is a construct created by Jeffrey Alan Gray for his Gray’s biopsychological theory of personality and his Reinforcement Sensitivity Theory (RST).

    Ventral striatal reactivity is strongly associated with reward-sensitivity in individuals with the DAT 10-repeat allele but not in individuals with the DAT 9-repeat allele. [15]

    Temporal discounting is the ability to discount delayed rewards, that means to associate less value with rewards which are further away in time. This is also called delayed discounting.

    Greater temporal discounting is associated with lower ventral striatal binding potential. [5] Lower density of dopamine D2/D3 receptors in nucleus accumbens is associated with higher impulsivity. Lower level of ventral striatal dopamine release is associated with higher temporal discounting. [5]

    Higher striatal activity is associated with preference for immediate over delayed rewards. [13] Individual differences in delayed discounting correlate positively with magnitude of ventral striatal activation in response to both positive and negative feedback. [13] Greater temporal discounting is associated with lower dopamine reactivity in the nucleus accumbens core and shell. [61]

    The COMT Val158Met genotype Val/Val genotype is associated with diminished patience and hyperactivity in dorso-lateral prefrontal cortex (DLPFC) and posterior parietal cortex (with no apparent effects in the striatum). The Val/Val genotype has also been linked to perseverative errors during reinforcement learning tasks which have been attributed to reduced levels of dopamine in prefrontal cortex. [62]

    The COMT Val158Met genotype Val/Val show increased ventral striatal activation and medial prefrontal activation for large and unexpected monetary gains compared to the Met/Met genotype. The Val/Val genotype also show higher valence activation (differences between gains and losses) than the Met/Met genotype. Maybe in Val/Val individuals the unexpected gains might have had a weaker working memory representation, and the resulting greater unexpectedness might have led to an increased response to unexpected gains in these subjects. [76]

    Higher reward-sensitivity is associated with the ability of improving working-memory in rewarding contexts. [65]

    Tonic dopamine-levels modulate the striatal dopamine efflux to the prefrontal cortex more than phasic dopamine bursts. [20] Blocking receptor reuptake (DRD2) increases striatal phasic dopamine efflux. [20]

    Individuals with the COMT Val158Met genotype Met/Met show increased reward responsiveness over the other groups and are more willing to take calculated risks when rewards were attainable. This is maybe caused by experiencing rewards as more pleasant and therefore having more reward seeking behavior. [75]

    Individuals with the COMT Val158Met genotype Met/Met show decreased immediate reward bias and show less fronto-parietal activity during decision making compared with those homozygous for the 158Val allele. This Met/Met show less temporal discounting. [74]

    Ventral striatal reactivity is mostly defined by:

    • Higher amount / density of dopamine receptors (DRD) enables higher binding potential and therefore higher release of dopamine and this is associated with lower impulsivity.
    • The degree of presynaptic and postsynaptic inhibition of dopamine via DRD2 –141C Ins/Del expression decreases reactivity, where Ins allele show higher reactivity compared to Ins/Del allele. [1, 14] This is because a higher inhibition of dopamine causes smaller binding and release.
    • The degree of postsynaptic inhibition of dopamine via DRD4 decreases reactivity, where 7-repeat allele have highest reactivity. [1, 14] This is because a higher inhibition causes smaller binding and release.
    • Higher amount / density of dopamine transporters (DAT) decreases the reactivity by inactivating the phasically released dopamine. DAT 9-repeat has lowest density, DAT 9-repeat/10-repeat has moderate and DAT 10-repeat has highest density of transporters. [1, 14]


    Summary

    So the dopamine release in the striatum can be seen as a ”carrot” of reward. Dopamine is crucially involved in all decision-making for this reason, because people make decisions primarily because of rewarding emotions.

    But if a strong reward response is present at the same time as the prefrontal cortex already have a high level of response-inhibition, the prefrontal cortex will evaluate if the reward-signal is in conflict with goals or target and if so it may use executive control to inhibit these responses to make sure they are not distracted from their target or goal. The prefrontal cortex will in that case decrease the reward-signal using top-down executive control. If the reward-signals does not conflict with goals the prefrontal cortex can decide to explore the new stimuli.

    This is why dopamine affects individual differences in traits like impulsivity, excitability but also extraversion / introversion, novelty-seeking, sensation-seeking, fluid intelligence and more as explained above.

    So we get a dual-system model of this like this:

    Image of prefrontal vs striatal:


    So how does this relate to individual differences in personality?

    If we were to categorize individual differences into boxes or types based on evidence, it could look like this:

    • COMT Val158Met genotypes create three different types of prefrontal attributes of dopamine inactivation: fast (Val/Val), moderate (Val/Met) and slow (Met/Met) = 3 permutations.
    • Connectivity can be divided into differences in connectivity depending on cognitive state with task-positive network, default mode network, frontopolar cortex, parietal cortex. [47, 48]
    • The amount of striatal D2 dopamine receptors with high and low = 2 permutations. Which would indicate the level of sensitivity towards new stimuli.


    Summary

    It seems possible to link personality-types to individual differences in genetic attributes. However a complete integration of personality-types with genetic types does not exist in any form yet.

    We can conclude that it is true to claim that personality typology can be based on scientific evidence.

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