Great personalities do not come from the genes

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Personality is plastic

Personality is affected by thousands of genes, but the effects of genes are not deterministic. I will argue here that personality is primarily shaped by the environment. To say that personality is hereditary is not much more accurate than to say that basketball talent is hereditary just because taller babies are more likely to be talented basketballers.

There is no limit set on personality by non-deleterious genes

Without the bias coming from our gene-obsessed culture and the effects of the Human Genome Project, we could say that the wisdom of John Watson from 1930 still holds true:

Give me a dozen healthy infants, well-formed, and my own specified world to bring them up in and I'll guarantee to take any one at random and train him to become any type of specialist I might select – doctor, lawyer, artist, merchant-chief and, yes, even beggar-man and thief, regardless of his talents, penchants, tendencies, abilities, vocations, and race of his ancestors

Watson's words seem obvious to everyone who studies learning, conditioning, or behavior. It is pretty obvious to experienced parents. However, the mythology of the personality genes is omnipresent.

We marvel over the genetics. "You got eyes after your mom", or "the same smile as your dad". And yet, all those different eyes and mouths have the same function. In healthy individuals, all different mouths are equally capable of satisfying our nutritional needs.

The same universal functional commonality is true of personality and intelligence, except they are far more plastic than anything else in the body: Personality depends on the learning brain!

Genetic studies

Identical twin studies may say that heredity of personality traits takes half of the role in nature vs. nurture interplay. However, to say personality is hereditary is highly misleading. If we want to see a planet populated with happy people, we need to make sure they grow up in conditions conducive for developing a thriving personality.

Given ideal conditions for upbringing, nearly all individuals can end up with fantastic personalities. The correlations between genes and personality traits stem from the fact that minor gene variants can have major impact on personality outcomes in certain environments. A well-known deleterious mutation is phenylketonuria, which can easily be prevented with dietary modification.

The best documented variants of significant impact on cognitive ability are APOE. APOE-ε4 increases the chances of Alzheimer's. But prevention is again possibly by simple lifestyle changes.

The story is the same in the case of genes that determine personalities. For example, our modern lifestyle makes many people neurotic. Some genes may favor resilience that prevents neuroticism. However, a change to more conducive environments could help most of the population rank low on neuroticism. In particular, authoritarian parenting and coercive schooling have a powerful impact on personality. In conditions of love and freedom, genetic differences fade. Can we then say personality is hereditary? It would be more accurate to say that the resilience to negative environmental influences on personality has a strong genetic background. In nurturing environments, nearly everyone turns out curious, scrupulous, extravert and nice.

A minor genetic factor such as attractiveness should have little effect on personality. However, in conditions of coercive schooling it may play an outsized role. Being attractive at school helps being popular, and consequently extrovert, and optimistic. It is easier to keep one's self-esteem unharmed at school.

Heredity studies show that uniform, suppressive, and homogenizing shared environments, e.g. coercive school will blow up the significance of the genes! In the wild, diversity may be wider, and more dependent on environmental factors.

Suppressive environments blow up the significance of heredity

Developmental trajectory

Personalities can be measured by a personality test. We often hear that personalities run in families or that a specific characteristic is taken after a parent, or even a grandparent.

However, there is a hidden danger in adopting the view in which heredity plays a significant role in determining the personality. Heredity implies that individuals carry genetic trait variants that are largely immutable. This lessens the motivation or hope for change. In reality, all personality traits are highly plastic, and good care in childhood brings fantastic outcomes in a vast majority of individuals.

For example, all kids are born curious. Curiosity is the key to intelligence. It is an indispensable factor in human survival in most environments. At the same time, it is very easy to kill curiosity at school, or in an autocratic family where curious behaviors are penalized (see: Learned helplessness vs. learn drive).

Two horrible side effects of attributing curiosity or intelligence to heredity are:

  • kids are classified and selected as those who are more or less capable of learning
  • gradual decrease in curiosity that occurs in schooling is seen as a natural biological process (brain maturation)

The optimistic message that should come with this text is that a vast majority of kids are conceived curious, sociable, nice, and well-composed. In our not-so-healthy society, the first obstacle course is the pregnancy. The brain is shaped by the conceptualization process that begins in week 3 of gestation. The process is controlled by environmental input, and interfered with by noxious factors such as trauma, stress, toxins, nutritional deficits, infections, etc.

Given a healthy conception, a healthy mom and a healthy pregnancy, nearly all kids are born happy, curious and smart. The process of shaping a personality is largely based on destroying what's best, and to a lesser degree, amplifying the characteristics that turn out most useful in life.

As all personality traits are polygenic, I doubt we will ever discover a single personality gene whose non-detrimental variants could be detected in human behavior by an expert or by AI. The genes that play a role in shaping the temperament are all occurring in variants that introduce tiny changes in phenotypic outcomes. All those variants have their pros and cons. Those that are clearly detrimental are successively eliminated from the population.

It is the response to adversity that may differ. An abusive household will destroy a kid with certain gene variants and make another kid resilient due to another variant. Without abuse, both kids would turn out great. If we removed noxious influences, heritability might drop dramatically.

There might exist an optimum gene set that could yield the best astronaut, or the best mathematician. However, as there are no significant evolutionary pressures to generate such optimum set, we can safely assume that all healthy kids are born with a mosaic that will turn out optimum for a specific niche in the course of sampling and adaptation to specific environments.

Majority healthy kids can become astronauts or great mathematicians as long as we do not undermine their potential in achieving that goal. Even if genes form an obstacle, the kid will naturally drift towards its strength given freedom in conducive environments.

It is the environment that makes the most of the difference, and few non-deleterious alleles produce effects that can break through environmental influences. Those that make a difference, usually make a difference for the worse, and are likely to be on the decline in populations.

Brain is highly plastic, and the hand we get dealt at birth is secondary

Big Five is just a word game

A popular myth says that the Big Five has been delineated as a result of studying genetic traits. In reality, it is just a factor analysis of words used to describe personality. There are nearly 5000 such words in English. We can safely say that if a personality characteristic is important, it will find its reflection in the language (lexical hypothesis).

With the help of factor analysis, the words describing personality can be grouped into a smaller number of categories, e.g. 16 or 5 depending on the coarseness of the grouping.

In Big Five set, the words have been grouped by various researchers by similarity until five seemingly irreducible dimensions have emerged. Big Five distinguishes five prime personality variables: openness, conscientiousness, extroversion, agreeableness and neuroticism. With its easy mnemonic OCEAN, one can quickly make a systematic personality assessment on a street corner. Pity the letter N is the only one that corresponds with a characteristic that is generally not wanted: neuroticism.

A great deal of effort in determining Big Five was done by language researchers, not psychologists!

I consider the Big Five classification highly flawed. If I was to describe my own personality, I would instantly miss (pathological) optimism or (pathological) stubbornness and reactance. How about impulsivity and aggression? Is it the opposite of agreeableness? I am considered pretty aggressive in sports. I love combat sports. However, I am also instantly classified as agreeable in face-to-face interaction. What about self-esteem? People who know me better call me arrogant, that's a direct derivative of high self-esteem. Why am I still agreeable then? Because I employ heavy auto-censoring and self-deprecation. I know I can achieve more by not being hated (due to arrogance or aggression). What about amorousness? Last but not least, why is intelligence not considered part of personality? Intelligence is as trainable as the rest of traits, and it is as important when interacting with people. It determines cognitive patters and fits the definition of a personality trait. Others observed missing traits such as egoism, manipulativeness, or thrill-seeking.

What is also important, we cannot find a gene or even a well-define gene set for any of Big Five characteristics. It does not help that the most often cited personality gene, COMT may affect all the traits, esp. curiosity (O) and neuroticism (N).

Still, Big Five is a very useful concept backed up by thousands of publications and books. However, in my own writing, I use a terminology that is closer to real phenomena occurring in the brain. For example, I speak of the learn drive rather than hazy "openness to experience". Instead of conscientiousness or grit, I speak of easy-to-measure self-discipline.

Science of personality calls for new classifications (e.g. compare 16PF), but I can stick to the present level of imprecision and still prove the main thesis of this text beyond any doubt: personality is highly plastic.

Default personality

Happy babies

Babies are born seemingly with no personality. First smile comes in 2-3 months. But from the very first minute, little humas are curious of the world. This is their defining characteristic. It is hard to notice significant differences in curiosity in little children as they grow up.

Once the deleterious genetic variants are sorted out (perhaps below 1% cases), we may say that humans are born with the default personality that is curious, pedantic, extroverted, pensive, sociable and resilient. This means that the default human is nice, smart, stable, and fun. Default personality takes the best of all traits in right proportions with minor variations that helps adapt to specific niches of human activity.

Heritability in young children is less pronounced than in adults

Cranky babies

Genes can determine the adaptation trajectory, but they cannot determine personality. Certain gene variants might slightly increase the chance for high neuroticism score. A specific set of non-deleterious genes may significantly increase that probably. However, we often hear that a baby was born fearful or cranky. That magnifies the conviction in the significance of genes. However, we have no way of knowing if this effect is not a result of the course of pregnancy.

Babies do not get depressed. We do not diagnose depression in the first years of life. The estimate of diagnosed depression for 3-year-olds is around 1%, and then it gradually increases with each year at school.

Cranky babies or high-needs babies are supposed to be a proof of hereditary temperament. However, cranky babies have alternative explanations.

A minor mutation might cause problems with digestion, which provides the first feedback loop between the moods of (1) herself and (2) her parents. The risk of neuroticism increases. Could we call that mutation a personality gene? And this is just one of hundreds of examples in the polygenic nature of personality.

If a parent comes with a crazy idea of planning baby sleep or the feeding schedule, she is on a sure way to make major unhappy cracks in the personality. Few people understand baby circadian cycle or lack thereof in the first months (see: Baby sleep). Schedules and planning are a sure prescription for a cranky baby.

What if a parent listens to American pediatrists with their crazy idea of shoving little babies to their own cots instead of feeling safe near mom's titty. This separation from the mom might be the main cause of crankiness and a clean start into the trait of neuroticism (see: Co-sleeping).

If you swear your baby was born cranky, many things might have happened in pregnancy.

A parental myth says that it is normal that a baby cries from time to time, or even a lot, or even 3 hours per day "on average". The only healthy reason for crying is an actual problem: primarily delayed or insufficient food, or lack of closeness with mom, or various health issues. An opposite assumption is safer: if a baby is crying it got a serious reason to do so! Naturally, we can condition babies to cry too. A simple cruel way to prove it is to keep delaying food, and to deliver it instantly when the baby starts crying. This may result in crying as a conditional call for food. The same conditioning may result in crying as soon as baby suspects she might be abandoned in a cot or in a chair.

The temperament of a cranky baby has multiple alternative environmental explanations. Once born cranky, a baby may make her mom crankier, and the entire family may live in a cranky feedback loop. Once made cranky, it is hard to take the kid back to the default happy state. It is likely to keep going on a path towards marked neuroticism.

As mom is likely to share a great deal of genes with the baby, her own adaptation trajectory may be sensitive to those starting conditions. We may then have an illusion that crankiness runs in families. However, the same baby growing in a more conducive and tolerant environment may turn out a walking sunshine. Neuroticism is not set. Can we then call it hereditary?

With a healthy pregnancy and natural parenting, chances for a cranky baby should drop dramatically

Happy centenarians

Research shows that most people become more agreeable, conscientious, and less neurotic as they age. In retirement, with a newly acquired freedom, childhood curiosity can reawaken. Reverting back to the happy child-like personality might actually be one of critical aspects of longevity.

Centenarians frequently revert to happy baby personality

Cranky centenarians

This section is empty. I keep it just for symmetry. There are very few cranky centenarians. Crankiness does not serve longevity. Centenarians might be grumpy, but their life satisfaction is usually fantastic.

Plasticity of personality

With a regular inflow of data showing how genes affect personality, it is easy to have doubts about the prime message of this text, which is to pay little attention to genetics in education. It is hard to demonstrate how little actual effect individual variations have, and hard to demonstrate the resultant effects of the complex symphony of synergistic and antagonistic influences of a polygenic genetic scene.

My original dive into the myth of the power of the genes comes from understanding the plasticity of personality. The most convincing is the demonstration how plastic brain adapts to the environment, and how individual traits can be modified to suit individual needs. In addition to the power of adaptation, we also need to be aware of the power of destructive influences that stem primarily from overriding natural adaptation with human-designed personality training, drill, taming, and breaking.

The first trait of Big Factor OCEAN is O = "openness to experience". This is a wide umbrella of characteristics with the common denominator: the learn drive.

The learn drive should actually be seen as the key component of plasticity for all personality traits. The learn drive is the basis of adaptation. It can strengthen conscientiousness of a medical student or a pragmatic neglect of secondary detail in a young mother. It can power the extroversion of a politician as much as the introversion of a mathematician. It makes people agreeable in the socialization process, but it also helps develop the necessary unkind toolset to handle unkind people. Finally, it helps develop stoic personality and resilience or enter the realm of learned neuroticism or induced neuroticism.

The learn drive is the key to understanding plasticity of personality

Conceptualization curve

The first major hint at the plasticity of personality is the fact that all traits tend to follow a typical conceptualization curve typical of all learning processes. The differences between kids tends to increase over time (source):

Individual differences in most traits tend to increase with age from early childhood into early adolescence and then plateau

In the picture below, the trait is marked as the capacity reflecting the volume of adaptation memory. The occurrence of plateau is a reflection of adaptive pressures. The model graph is typical of lifelong learning with a constant inflow of knowledge (optimally managed with spaced repetition). However, adaptive pressures reflect fluctuating interests and passions. In case of personality traits, we may safely say that for a set environment, the constellation of traits stabilizes with a few years. Hence the illusion that the personality of a 30-year-old remains stable, and the illusion it might stem from the genotype.

Figure: Hypothetical course of learning and conceptualization in a fixed-size concept network. The naïve network begins the learning process at high plasticity (in red). As individual concepts form, they are consolidated and stabilized. The overall stability of the network keeps increasing (dark blue). The speed of conceptualization (in orange) is a resultant of plasticity and stability. It reaches its theoretical maximum somewhere on the way from the random graph stage to a sparse representation stage. This is the time of a large supply of concepts that may be subject to generalization, and a good balance between stabilization and forgetting. The overall problem solving capacity of the network (light blue) is negligible at first, and tends to saturate with network stabilization. Large number of well-stabilized concepts makes it harder to find new plastic network nodes for further conceptualization. The maximum capacity of the network depends on its size. Speed of learning in spaced repetition at older ages seems to indicate that the size of the concept network of the human brain is high enough to provide for lifelong learning without noticeable saturation. See: Conceptualization theory of childhood amnesia and How much knowledge can human brain hold

O: Openness to experience

Openness to experience is easiest to understand as curiosity. The popular and pop-psychological interpretation of openness to experience includes several vital components of human cognition that requires separate definition for the purpose of modelling mental computation. These separate traits are:

All those "traits" are primarily the effect of the interaction with the environment. They can be summarized as intelligence and the potential to enhance intelligence. These "traits" may be modulated and polygenic. Genes may modify the parameters of the concept network, which may, in the long run, find a reflection in the brain architecture. However, these characteristics in adults are primarily the expression of the developmental trajectory.

The learn drive explains the monumental role of curiosity for human well-being:

  • it defines the adaptability to the environment
  • it defines the plasticity of other personality traits
  • it determines human intelligence
  • it is the best warranty of health and longevity
  • it is the foundation of the joy of living

The learn drive is the most plastic of the Big Five characteristics. A powerful learn drive is its own best amplifier. All healthy kids are well equipped from birth, but their drive to learn can be easily suppressed. The main suppressors are maternal separation, inept daycare, authoritarian parenting, and coercive schooling. Later in life, with the arrival of freedom, the learn drive tends to return. However, once suppressed, it can easily be kept in check by adversities of modern life such as corporate culture, social media, dysfunctional family, and more.

The learn drive is the most important personality characteristics that determines human well-being

C: Conscientiousness

Grit

Angela Duckworth popularized the word "grit", esp. in reference to conscientious study at school (see: Angela Duckworth is wrong about grit). Angela is blind to the harms of schooling, which she revealed in her answer to the audience here: Talks at Google (after 33 min). The key to healthy self-discipline (or grit) is passion. Schools destroy passions and rely on unhealthy grit instead. When a graduate asked what to be gritty about, he hinted that school makes it easy to be gritty, while real life leaves you with a post-school passionless void ("How to be gritty if the cost of wrong choices is so high"). Angela separated (1) interests (understood as childhood passions) and (2) purpose (understood as moral guidelines). This shows she does not realize that the only healthy passion is the one in where the two are networked and blended seamlessly. No wonder. She admits climbing the ladder of opportunity, searching for the next area to employ grit (esp. in education). A true passion begins early in life and keeps growing by accruing experiences and valuations (see: Knowledge valuation network). It is possible to build passions later in life, but they are rarely well integrated with the entirety of the knowledge network. Adaptation is a continual process, and changes of direction later in life will always leave a form of residue ballast unless the changes were sparked naturally in the course of life in response to events. Schools and colleges leave millions of graduates crippled for life due to robbing them of childhood passions (see: 100 bad habits learned at school). As a result, we live in unhappy societies driven by grit and self-discipline that quarrels with Self.

Angela is then right in diagnosing the problem:

Most of us do not even know what passion is until we find one

Duckworth's recommendation of grit is dangerous for mental health

When Scott Galloway advises people to ignore "follow your passion" advice, he is right only in that the advice is unworkable in most adults who have been washed out of passions and interests (primarily in the period of coercive schooling). See: Scott Galloway does not understand talent

"Follow your passions" is a great advice if given early enough

E: Extroversion

A healthy mind is never extrovert or introvert. It adapts. I explained my point previously: Are extroverts more creative?.

Here I will only tell my own story that ultimately made me write the present text.

A few years ago (2018), I played with Eysenck Personality Questionnaire. I was curious how I might score. One answer kept popping up over and over again: "it depends on the time of day". Could a "most cited" psychologist mis-conceive his test (Hans Eysenck)? The clarity of the flaws of the test might have come to me from the fact that I religiously free run my sleep and have developed a uniquely regular circadian cycle that favors biphasic life. I see that few people stick to this kind of "circadian religion". This results in lives that are more chaotic and harder to study. Psychology might reflect this fact. How can I possibly answer the question "Do you like to talk?". In the morning, I never open a mouth. I am locked. My connections with the world are severed. I ruminate my own ideas and quickly transition to creative work. On most of the days, I might utter my first words at midday or later. And then within a span of 1-2 hours I become a talking machine. I talk to anyone I meet in my sports slot. Today (Oct 19, 2024), after swimming, I spoke to an octogenarian German couple who did not speak English. We mixed four languages to exchange the ideas. It was riveting. We spoke of health and longevity. I love to talk. But then again, back at home, I close myself in my own world and might not speak for another 3-4 hours (siesta time). I do a great deal of work late in the night. Most of the world around is asleep. So, I do not talk. On extremely rare occasions, I connect with other continents to discuss important idea relevant to my research, school reform, or SuperMemo. What should then be my answer to the question: Do you like to talk?? It is affirmative, but true only for 1-2 hours per day. In psychology tests, my extroversion comes out maximized, but I spend most of my days "talking" only to myself in my mind.

At just about the same time, I watched a couple of Susan Cain lectures (incl. Talks at Google and TED Talk). She made me realize that, along her definition, I am as good an introvert as I am an extrovert (more details here). The only difference is time of day (which determines the context). Life would be sad and ineffectual without these two modes of action. My wild guess is that people who cannot cool down their extroverted side may never classify themselves as introvert. Similarly, what we often call a true introvert might just be a conditioned defensive response in social interactions. I do not believe in extroversion as a fixed trait (E). If you believe I am wrong, let me know.

A healthy mind can adapt to both the introvert and the extrovert mode

A

N: Neuroticism

Neuroticism is a tendency to experience negative emotions such as anger, anxiety, fear or depression.

Neuroticism and intelligence

Neuroticism may have a negative impact on one's problem-solving capacity. However, intelligence may help mitigate the effects of neuroticism by providing better coping strategies in stressful situations. An intelligent person may be better equipped to manage anxiety or emotional volatility (source).

High levels of neuroticism are often associated with anxiety, which can impair cognitive performance. Stress can trigger the release of cortisol, which can impair cognitive functions such as memory, attention, and problem-solving. Neuroticism often involves self-doubt and lower self-esteem. Individuals high in neuroticism may engage in rumination, or persistent, negative thinking about their performance or potential outcomes. This rumination can be mentally exhausting and distract from the task at hand. Individuals who are more anxious may avoid challenging cognitive tasks or educational opportunities, which could limit the development of their intellectual abilities.

Neurotic personality does not serve intelligence

Neuroticism and mental health

Neurotic personality may be the first step towards mental disease.

Neuroticism is linked to lower brain volume in specific areas because chronic stress and negative emotional states, which are common in neurotic individuals. Chronic psychological stress and negative emotional states may contribute to neurodegeneration, leading to reductions in brain volume. Neurotic individuals, due to their heightened stress responses, are more likely to experience neuroinflammation, which can accelerate age-related brain decline. The pathological process is primarily driven by the effects of chronic stress, and the influence of cortisol on brain regions such as the hippocampus, and prefrontal cortex.

The amygdala is hyperactive in neurotic individuals. While the amygdala itself may not show reduced volume, its hyperactivity could influence other brain regions negatively, particularly those responsible for regulating emotions. With a reduced function of the prefrontal cortex, one may have a harder time inhibiting negative emotional reactions, leading to a feedback loop where neuroticism is both a cause and a consequence of brain changes. Maternal separation and other forms of chronic stress can be used in animal studies to increase emotional reactivity typical of human neuroticism.

Neurotic personality does not serve mental health

Advantages of neuroticism

What is considered positive about neuroticism is a side effect of passion and drive. Neuroticism, often associated with emotional instability, anxiety, and vulnerability to stress. It is then generally viewed as a negative trait. However, certain aspects of neuroticism may offer adaptive or beneficial qualities within a population. I do not fully appreciate those aspects, and I quote here mostly what I read from other authors. If there are genes that favor developing a neurotic personality, they are probably having some positive side effects. Vigilance is an example. However, in need, you can be highly vigilant without being neurotic. Being scared may be justified. Attention to detail is also an expression of passion that requires a bit of scrupulousness. Motivation to improve is a universal characteristic of a healthy mind. Does neuroticism increase it? I am not sure. Empathy and social awareness are trainable and also highly beneficial. I tend to be empathetic and yet there is no trace of neuroticism in the fact. Artistic expression in neuroticism may indeed differ from a creativity of a cooler mind. Again, I rather tend to see neuroticism as an acquired and not-so-positive characteristic. Polygenetic influences might only modify the trajectory that might have an accelerated course in sensitive people.

Heritability

Twin studies show a strong correlation between genes and neuroticism. This is why nearly all researchers claim neurotic personality is hereditary. In the section devoted to genes, we see that higher levels of methylation at the S allele for the serotonin transporter can reduce its already low expression, potentially exacerbating the allele’s effects on emotional reactivity and stress sensitivity.

However, more detailed analysis of the heredity shows that traits are polygenic, and the genes that can be identified have good and bad sides. In contrast, personality traits are clearly delineated as an expression of personality quality. For example, being open to new experience is generally considered a good thing. We want people to be curious and creative. However, in some cultures, curiosity is unwelcome, while creativity in a classroom may result in ADHD diagnosis.

Similarly, being neurotic is rarely considered a good thing in popular language. At the same time, Big Five is a product of factor analysis on personality description adjectives. If we look at specific genes that favor neuroticism, we may see their positive aspects. For example, increased sensitivity to stimuli may be a distraction in some contexts and a benefit in other context.

It is not personality that it hereditary, but it is the susceptibility to the deterioration of personality in set circumstances that may be strongly influenced by gene variants!

From each parent we get a big bunch of genes that may modify the developmental trajectory that shapes the personality; however, it is a safe to say we are all born with qualities needed to develop a personality optimal for the target environment. It is the environment that shapes that ultimate outcome. All traits are plastic. Some people may be more resilient to change or more sensitive to potential deterioration.

The claims of adaptability by Watson are a motto for this text. Experiments with Little Albert showed how anxieties and fears can be conditioned. This might have determined Watson's thinking. He was able to induce neurotic characteristics in a child.

We are born with a set of genes that provide an excellent ground for developing a fantastic personality

Personal experience

Personal anecdote. Why use anecdotes?
I claim to be rather stoic. However, in my own life I can demonstrate a striking example of conditioning a substantial fear and then deconditioning it out entirely.

I was an early swimmer (perhaps 6-7). My bro would toss me to water from a diving tower at depths and I would love it. I enjoyed the "admiration of the audience". I had an episode of drowning in the sea at a very young age (perhaps 5-6). While diving passionately, I approached the groynes and lost my ground. I could see the surface of the water coming closer and further while I tried to catch a breath. The beach was crowded and some guy pulled me out by my hand. My mom failed to pay attention. Amazingly, the episode left no scares. I would swim lakes and rivers and jump to water from heights.

However, upon watching Jaws (at the age of 15), I lost that fearlessness. In the sea, I started imaging a shark attack. In lakes I had memories of a horse head at the dark bottom swarming with eels. I did not want to be swarmed in cold darkness. Those fears keep building up until I stopped my swimming adventures.

Then again, at the age of 42, I started swimming a lot with focus on performance. When my brain shifted from fears to other things (e.g. surviving an exhausting distance), I incrementally took more and more risks, to the point when I totally lost my fear of water. I would learn to combat currents, big waves, cold water, winds, darkness, and even ice.

This loss of fear evolved to a point when dying in water might be my prime risk of death today. A 10 B storm in winter feels like a fun challenge. Diving in super-cold water in darkness feels ecstatic. I love scary waters. My openness to experience has always been high. My neuroticism negligible. But for 30 years, I was too anxious to open myself to the exploration of the sea or even a local lake. Cold water is my favorite narcotic drug. It is powerful. I learned and unlearned a significant fear in the course of a single lifetime (in the span of 40 years)

Neuroticism is a side effect

We can now conclude that neuroticism is a result of conditioning or a side effect of rapid adaptation. We can see that it is predominantly disadvantageous. I would then rather consider neuroticism not as a trait that serves a spectrum of adaptations. It does not seem to be a healthy product of evolution. I would rather see it as a side effect of our maladaptation to rapid change of the civilization. Why is it then part of the Big Five analysis. I think it landed there only as a result of its importance and its obvious effect on personality. As mentioned elsewhere in this text: Big Five is just a word game.

Jordan Peterson claims that if you are unlucky to experience a mismatch of temperament and environment, your life will be miserable (source (after 4th minute)). He is right. The mismatch will leave you neurotic.

However, he should rather say that dramatic changes in the environment with insufficient adaptation time may result in a slide into neuroticism. This should rather be seen as a pathological side effect of a failed attempt to adapt. You can easily avoid the mismatch if you begin your adaptation early and with no constraints.

Traumatic life events can also have similar side effect: death of a parent or a child, loss of a job, divorce, homelessness, etc. More often, however, a childhood with limited freedom is enough to limit adaptability

Jordan notoriously overestimates the power of the gene and underestimates the beauty of the life on the planet.

Neuroticism is a byproduct of the rapid changes brought about by modern civilization

Unschoolers

When I speak to young unschoolers, or kids who approximate unlimited freedom of development, their answers to my personality test questions are invariably the same: "it depends". It is a great expression of the flaws of the Big Five approach and its genetic bias.

Let me here list only a single example of adaptability per trait:

  • O: curiosity depends on the domain
  • C: conscientiousness depends on the priority
  • E: extroversion depends on the social context
  • A: agreeableness depends on the individual engaged in the interaction
  • N: neuroticism depends on past experiences for the context

The main difference between a young unschooled personality and an average adult in modern western societies is lack of schooling. This ensures that all control mechanisms responsible for charging the developmental trajectory are unaffected by coercion. The main effect of coercion is the suppression of natural instincts that drive the personality in the unhappy direction. In terms of Big Five, unfree individuals are shy, perfectionistic, introverted, unkind, and anxious (see: 100 bad habits learned at school).

I have been lucky and free for my entire life. My self-observation helps me see my own plasticity. I can be all kinds of people depending on the context. Even neuroticism has its place and advantages. Self-observation was also the starting point for this entire text. Too many claims from psychology books disagreed with my own observations.

Plasticity of personality is a reflection of mental health

Missing heritability

Where are those genes?

Turkheimer noted that the study of the genetics of personality began with tremendous promise but ended in frustration, leading to the concept of "missing heritability" (Turkheimer, E. (2014). The genetics of human behavior: Lessons from twin studies. Current Directions in Psychological Science, 23(4), 273-278).

The term "missing heritability" refers to the gap between genetic variation identified in studies and the actual heritability of traits observed in populations. It arose from studies on various traits, including personality, as researchers found that common genetic variants explained less of the heritability than expected based on twin studies.

In 1996, a furore was caused when dopamine D4 receptor was found to be associated with novelty seeking. Soon neuroticism was associated with serotonin transporter gene. It was the beginning of a new era in the study of personality. Sadly, soon the replication crisis hit. Even the proponents of genetic roots of personality admit that candidate gene research turned out to be a blind alley (e.g. [Ritchie interview link]).

Large-scale genome-wide association studies (GWAS) analyzing millions of SNPs identified only two SNPs associated with curiosity and one with conscientiousness, together accounting for just 0.2% of the variance in these traits.

Could it be that certain genes, unrelated to personality, still influence it? For example, a gene that causes a minor mutation leading to digestive problems in infancy could have a downstream impact on personality. If this digestive issue affects the baby’s mood, sleep, and interactions with caregivers, it could set off a cascade of environmental and psychological factors that increase the risk of developing certain personality traits, such as neuroticism. Could we then consider that mutation a 'personality gene'?

In this text I try to explain "missing heritability". Most of all, I will try to show that despite being polygenic, the ultimate personality outcome is highly plastic. We can help people grow lovely dispositions.

Genetic symphony

A massive impact of similar genes contributes to "missing heritability". The problem arises because the genetic variants identified in genome-wide association studies (GWAS) often explain only a small fraction of the heritability estimated from family and twin studies. This discrepancy suggests that there are other sources of genetic influence that GWAS might not be capturing effectively.

Personality traits are likely influenced by a large number of genes (polygenic influence), each contributing a small effect. Many of these genes might not have direct effects on personality but could affect related biological processes that influence personality indirectly. When the effects of many such genes accumulate, they could significantly shape personality traits, but each individual gene's effect might be too small to be detected in a GWAS.

Polygenic scores correlate strongly with height. They may also determine the risk of diseases such as coronary diseases or diabetes. In those risk cases nutrition and exercise can cover up for most of the difference. The same is true in reference to "nutritive environments" that foster sunny personalities, high intelligence, and pristine mental health.

Genes with indirect effects might interact with environmental factors in complex ways. For example, a gene that affects early childhood health might influence personality development through its impact on life experiences and social interactions. Such interactions are difficult to capture in GWAS, which typically look for direct associations between genetic variants and traits.

Many genes have pleiotropic effects, meaning they influence multiple traits. A gene involved in a biological process like metabolism might also influence mood, stress response, and, indirectly, personality. These pleiotropic effects might dilute the apparent direct relationship between a single gene and a specific personality trait, making it harder to detect in GWAS.

Genes that regulate other genes (e.g., through epigenetic mechanisms) could play a significant role in shaping personality traits. These regulatory genes might not be directly associated with personality in GWAS but could influence the expression of other genes that are more directly related to personality traits. An example of a gene activated by environmental interaction might be a dormant predisposition to schizophrenia that responds to environmental factors such as chronic stress or amphetamines. The suppression of resilience-incurring gene occurs via methylation of histones occurring in the hippocampus (source). This epigenetic regulatory network complexity could contribute to missing heritability.

Rare genetic variants and structural variations (like copy number variations) might have substantial effects on personality but are often missed in GWAS, which typically focus on common SNPs. If many rare variants with small effects are involved, they could collectively explain a large portion of the heritability.

The missing heritability problem comes from the complex and indirect effects of many genes, which together have a substantial influence on personality. These indirect effects, gene-environment interactions, pleiotropy, and other genetic mechanisms might not be fully captured by current GWAS approaches.

Breaking up the determinism

The de-emphasis of genetic determinism is important to eliminate problems such as poor performance at school, mental disease, addictions, and violence.

Kids that are horrible at fractions at school, and deemed dumb at math, can build rockets and bridges using state-of-art physics tools or even delve into relativity and quantum theories (using YouTube instead of a thick textbook). The old notion of math talent is just one of those old myths of the archaic school system. Tragically, teacher's perception of math talent predicts math scores (source). Those pre-determined paths and school selection are steeped in genetic mythology.

Aware of this burning problem, Oliver James went a step further in his opinion article for The Guardian (here):

Scientists call this the missing heritability. But there are strong grounds for supposing the heritability is not actually missing – it’s non-existent

Illusion of heritability

Individual genes underlying personality have never been found. Those that are known to affect personality have multiple, nuanced, or contradictory influences (see separate section in this text). In a polygenic score, gene variants may act synergistically or antagonistically. This mean that parents of high polygenic score may produce offspring where different combinations of variants cancel out each other resulting in a lower score.

Brain over brawn

The shape of the bones is malleable. Muscles, bones, and tendons can be strengthened and molded. Skin color can change under the influence of the sun. However, there is nothing more adaptable than the brain. All personality traits come from the brain. Genes have a huge influence on the developmental trajectory of personality, but it is the environment that determines the ultimate adaptation. In nurturing conditions, most kids can reach genius levels of creativity. All people can grow nice or grow nasty depending on their circumstances. Kids from Compton will all be different, but might all gravitate towards high intelligence, high propensity to violence, high creativity, and high assertiveness. It is the Compton milieu.

Harm of schooling

Uniform shared environment, e.g. coercive school will blow up the significance of heritability! In the wild, diversity may be wider, and more environmental.

What is worse, coercive schooling is likely to transform a default curious optimist into someone who has lost its curiosity and social extroversion. School makes people less agreeable and more neurotic. It converts conscientiousness into pathological perfectionism and unhealthy self-discipline. Coercive school invariably changes children for the worse (see: 100 bad habits learned at school)

Research in psychology is based on humans who have been schooled. As such it is terribly biased.

We are born with fantastic brains, and yet, due to schooling, only a few reach the level of genius

Non-personality genes that affect personality

A great way to study the link between genes and environment is to observe identical twins separated at birth and raised in drastically different environments. "The Three Identical Strangers" [link] provides a good storyline to see what happens in such cases; except, the kids in question have been separated at 6 months to the detriment to their mental health.

There is a clear correlation between genes and personality. However, genes that are completely unrelated to personality can heave a major impact on shaping personality through the interaction with the environment.

For example, the genes that make for general attractiveness make life easier, and help retain the default personality, esp. by withstanding the negative impact of pathological socialization at school.

Equally important are the genetic traits associated with ethnicity that can influence how individuals are treated in discriminatory environments. The mechanism is exactly the same as in the case of attractiveness as a mere skin color can expose a kid to more bullying, or more favoritism at school.

Those outwardly apparent human characteristics will underlie a powerful link between genes and personality, and no twin study can remedy that. Not only is twin separation unethical, but it is also impossible to find opposite discriminatory vectors without implicit harm to children. It would not be nice to place a skinny kid in a culture that loves round shapes.

Conducting experiments that involve placing individuals in families of different racial or ethnic backgrounds can raise significant ethical concerns, especially regarding informed consent and the potential for harm.

We know many cases of adoption of non-white kids in white families. A more interesting are cases where white kids are raised in black communities (e.g. in Africa).

In there, white children may experience a form of reverse discrimination, if they are perceived as "other" in an African setting. Their skin color can make them stand out and depending on local attitudes toward race and colonial history, they may be treated with suspicion, alienation, or targeted for negative attention. On the other hand, in some African cultures, lighter skin can carry connotations of beauty, and success.

There were rare cases where white children have been adopted by African families. In such cases, white children might still experience a degree of social discrimination related to their skin color when interacting with the community. Missionary families often have lived in African villages, and their children, often white, were raised alongside local African children. The treatment of these children depended heavily on the cultural values of the village and the relationship between the local community and the missionaries.

Ultimately, whether white skin is treated as a cause for discrimination or a source of privilege in African communities depends on the specific cultural, economic, and historical context.

Genes that affect appearance will influence the personality

Divergence in identical twins

Identical twins will diverge in personality based on minor differences stemming from accidental disparate events. One twin may become interested in crime novels, the other in football. Football may favor time outdoors and exercise which will help neurogenesis. This serves well openness and curiosity. On the other hand, crime novels will have a similar but likely less pronounced effect.

Experiment on genetically identical mice shows the divergence in a rich shared environment: How Identical Twins Develop Different Personalities. The excerpt is abbreviated:

Researcher Julia Freund began with 40 genetically-identical young female mice. These mice were housed in a custom-built mouse paradise.

Though the mice at the start all demonstrated a similar level of wanderlust, by the end of the experiment their travel patterns were decidedly different. While some mice hung around a home area, others spent equal parts of time in all the cage’s corners. The mice’s wanderlust at the end of the experiment was correlated with how many new neurons they’d added in their hippocampus.

It’s been known that physical activity promotes neurogenesis, but in this case the researchers found it didn’t fully explain the differences. Mice that were very active but in a limited range showed less neuron-creation than mice that wandered over a greater area. The researchers thus concluded that the mice’s divergent experiences of their environment were driving their brain changes. In the end, about one-fifth of the differences in neurogenesis between the mice was attributable to how far the mice wandered.

Thus identical twins, though they start with the same genes, likely develop different personalities in the same environment partially based on how they interact with their environment. This lived experience, in turn, probably changes their genes: Previous research has found that human identical twins accumulate epigenetic changes as they age, making them more dissimilar over time. In this way small initial personality differences could snowball—changing behavior, which changes brain—and result in our colorful, unique selves

Personality trajectories are chaotic even if the genes and environments are identical

Conjoined twins have different personalities and preferences despite sharing the immediate environment and even their body parts. See: What Twins Can Teach Us About Genetic and Environment Influences

Butterfly effect

Consider a wildly simplified theoretical model of a developmental trajectory for personality.

If the game theory insists that a stable coherent social group is likely to have only one alpha (dominant individual), we might (1) produce identical copies of two humans, and (2) flip one nitrogenous base in the DNA at random. This "mutation" (genetic variation) might then be hailed as responsible for alpha-proneness!

This illustrates the butterfly effect in genetics, where a seemingly insignificant genetic variation, in interaction with environmental factors, could lead to significant phenotypic differences. Those variations do not need to be in any way related to the trait, or might even produce opposite outcomes in different environments.

Small irrelevant genetic variations can have significant phenotypic outcomes

Power of a gene

A human is considered smarter than a monkey. The genetic differences between a chimp and a human baby make a world of difference. However, within Homo sapiens population, genes have much less influence over personality than is popularly believed. We all form a huge interchangeable gene pool, and genes that do not serve adaptation tend to slowly disappear from the population. Humans are all different, but their adaptability is largely the same.

Twin studies will make you believe that 40% of personality is hereditary, however, if you look for specific genes (e.g. with GWAS), you will find just a handful with microscopic influences. Ironically, of 12,000 genes that contribute to height, each is having an impact on personality.

Diminished height had a huge impact on the personality of Putin. Conversely, Michael Jordan would be a very different person had he been born as short as Putin.

Lives of Danny DeVito (1.47 m) or Shaquille O’Neal (2.16 m) will tell you that despite disadvantages of being very tall or very short, the genes that moderately contribute to height will not be eliminated from the population due to height alone.

Same truths affect thousands of genes that affect personality. If they all conspire to make you neurotic, your chances of passing the bunch to the next generation diminish slightly. We want populations that are diversified via adaptability with lesser variability being advantageous population-wide in identical environments.

It is clear what variations of Big Five are considered advantageous in set circumstances. This is why the population genetics will generally drive towards the optimum default with a high degree of adaptability (see: Are extroverts more creative?)).

Geneticists are adamant that genes determine personality (to a large degree). Behaviorists believe in the incredible plasticity of the brain. I study adaptability, which might make me a tad biased. However, I also study the brain, and molecular aspects of memory. It is memory that determines who we are. It is the brain architecture that determines the impact of memories on personality and behavior. Our current knowledge of the brain speaks a lot of adaptability, and nearly nothing about genetically determined parameters that might sway adaptation trajectory one way or another.

If you ask geneticists and behaviorists about personality, you may get different answers

Heritability does not limit Adaptability

Eric Turkheimer says that in inbred rats you may find heritability of 0, while in rats held in solitude in perfectly identical cages you might find heritability of 1. The most influential "identical cages" in human lives are the "depository" institutions of the youth: daycare, preschool, kindergarten, and coercive school.

By flattening the impact of the environment through coercive upbringing, we amplify the butterfly effect of the genes and increase the illusion of heritability. School seems to segregate humans into genetic categories providing a corset on adaptability.

Turkheimer put is best (source):

Heritability does not constrain malleability (Turkheimer)

However, the environment can constrain heritability. Geneticist Richard Lewontin noticed that in times of plenty, height is highly heritable, while in times of famine, it is largely flattened. In contrast, psychologists such as Arthur Jensen and Robert Plomin consider heritability to be inseparable from the trait.

As individuals grow older, the influence of genetic factors on traits tends to become more pronounced, regardless of the environment. In controlled or restricted environments, individuals are more subject to external influences, which can limit the expression of their genetic potential. Environmental factors play a significant role in shaping outcomes.

When individuals have the freedom to choose their environments, they can align their experiences with their genetic predispositions, which allows for greater expression of their inherent traits and abilities.

The Debunker: Dr Jay Joseph

Jay Joseph is a psychotherapist who is a serial debunker of genetic aspects of intelligence, personality and mental disorders. In his practice, he can see the effects of abuse, oppression and discrimination. This provides rich direct evidence on the power of the environment.

Joseph's opponent, Robert Plomin himself noticed that psychological traits might vary across ethnic or gender groups not because of genetics, but due to factors like discrimination (source):

The causes of average differences,” he says, “aren’t necessarily related to causes of individual differences. So that’s why you can say heritability can be very high for a trait, but the average differences between groups – ethnic groups, gender – could be entirely environmental [Plomin]

Media and textbooks are all soaked in genetic myths that pervade our culture. It is common knowledge that schizophrenia tends to run in families. Joseph found little evidence of genetic predisposition to schizophrenia (see: 'Schizophrenia' and heredity: Why the emperor (still) has no genes)(pdf). He found no reliable evidence from identical twins raised apart in mental disorders studies!

Big Farma promotes genetic basis of mental disease, as it is easy to derive the need and the demand from a specific neurotransmitter profile that might be rooted in the genes (neurochemical phenotype).

Non-genetic approach to mental disease favors prevention and behavioral therapies over drugs. A skeptic might argue that the non-genetic interpretation of personality serves the interest of a psychotherapist (except Jay's evidence is rock-solid).

Vested interests of Big Pharma, psychotherapy, etc. contribute to the obfuscation in the nature-vs-nurture debate

Interestingly, Joseph also debunked another popular myth: there is not criminality wired into the genes.

I recommend this fantastic fact-packed interview: No Evidence of Genetics Behind Psychiatric Disorders

Developmental unpredictability

If science says there is a 40-50% heritability of personality traits (with all Big Five contributing to a similar degree), the science is right about numbers. Genes and traits correlate. But the conclusion drawn from numbers is dead wrong. It is highly misleading to say, "personality is hereditary". It is more accurate to say that, to a microscopic degree, genes nudge developmental trajectories. Personality is entirely plastic (in free and rich environments). It is only that the exact same environmental influences may result in significantly different outcomes.

Using a spaceflight metaphor, genes act like microscopic thrusters, subtly guiding the developmental journey, where even the smallest adjustments can lead to vastly different destinations.

Given a precise genotype, we have nearly no way of predicting the outcome of personality development

Known genes

In a cognitive contest between humans and apes, humans usually win when employing human criteria. The difference between the two groups is hidden in the genes. However, in contests between humans, gene play far less significant role.

A gene variant or a non-deleterious mutation can modify the adaptation vectors. This means that an adaptation trajectory may differ between individuals. Some may adapt slower but are more able to reverse the course. Others become very rigid once adapted. Yet others show fantastic plasticity despite multiple adaptation efforts. The value of a given vector shows up only in a subset of circumstances. This way having a large variety of adaptation trajectories, humans can successfully inhabit multiple adaptation niches. We differ. But we all have all necessary adaptation capacities in the cognitive sphere. If not limited by physical or organic factors, we all learn to walk, speak, count and read. We can play chess, enjoy music, or learn programming. We can be nice or mean. It is all a matter of adaptation and adaptation is the effect of exposure over time.

For example, a tiny genetic variant may make one slide faster into neuroticism or introversion or aggression. However, the variants only change the adaptation targets if environment sampling is possible. They also change the adaptation trajectory, which can outwardly be seen mostly as adaptation speed. Genetic variants do not deprive individuals of adaptation options. The brain is universally plastic and this affect personality as well.

Genetic variants modulate adaptation trajectories. They do not block adaptability

Heredity factor

Around 1 in 50 people are affected by a known single-gene disorder. Approximately half of the population will experience some kind of health problem rooted in genetics over the course of their life. In other words, not everyone is "perfectly healthy" at conception. At birth, around 1-2% of people may have an organic defect in control systems that affect personality or behavior.

This suggests that the optimistic message of this text may not fully apply to as many as 3-5% of children. When a child exhibits signs of neuroticism or other challenges from birth, their path to adulthood may not be as bright as portrayed here.

Variability at birth is less likely to be caused by genetic variants of normal genes and more often the result of deleterious mutations. More commonly, however, such outcomes are shaped by maternal stress, trauma, infections, poor nutrition, disease, toxic exposures, or other factors during pregnancy that can lead to developmental issues or birth defects.

A small proportion of kids are born less fortunate, and may find it harder to thrive

Eugenic origins

As I write these words, Oct 7, 2024, Donald Trump rants about immigration that brings in thousands of murderers to the country, with an emphasis on the claim that "murder goes in the genes". This illustrates the potential harm of the theory of personality genes.

Trump's claims about immigrants "poisoning our blood" is part of a long tradition of eugenic rhetoric that dates back to Henry Goddard (1912). With his interest in IQ, Goddard "pioneered" precise classification of "morons, imbeciles and idiots"! By his account, roughly 80% of immigrants were feeble-minded (incl. Jews, Russians, and the like).

Goddard sought to apply Gregor Mendel's principles to human traits, including intelligence. Goddard's research on the so-called "feebleminded" fed into a broader fascination with the idea that undesirable traits, such as low intelligence, criminality, and even promiscuity, were inherited. This pseudoscientific belief laid the groundwork for social policies that targeted immigrants, particularly from non-European countries, as genetically predisposed to criminal behavior. Trump's rhetoric echoes these earlier ideas by suggesting that criminality is a genetic trait carried by certain groups, reinforcing harmful stereotypes that have been debunked but still resonate in political discourse today.

See also: Myth: Blacks are less intelligent than whites

Polygenic nature of personality

While it is difficult to identify individual genes that affect personality, polygenic analysis has shown that more and more loci are correlated with individual traits, mental disorders, or intelligence.

Single genes rarely explain complex traits like personality or intelligence. Instead, polygenic analysis, which examines the combined effect of many genes, has found increasing numbers of specific locations on genes that are associated with these traits. The effect of any one locus is usually microscopic, and environmental factors play an oversized role. We have found already a link between the genes and dog ownership [link] !

In the end, as research becomes more precise, we may conclude that through the butterfly effect, all genes play some role, and polygenic scores function as a form of phenotypic pattern recognition, with a distant connection to Mendelian genetics.

In words of Nathaniel Comfort (here):

If all you have is a polygenic score, everything looks like a gene!

This justifies the claim that genes affect personality, but the practical meaning of polygenicity is that we should focus on environmental influences, and their impact on the health of society. We can debate nature-vs-nurture ad nauseam, while all solutions to social mental status like in the environments we open to kids on their way from the uterus to an independent existence.

The figure below illustrates the proliferation of genetic links in schizophrenia, which can be contrasted with a horrific early interpretations:

Dispute over schizophrenia's genetic basis has been ferocious. This is hardly surprising given that Swiss psychiatrist Ernst Rüdin — an early proponent of the argument that the condition is a single-gene disorder — advocated the view that people with mental illnesses should not have children, and justified the sterilization and murder of people with schizophrenia source

Figure: We have gone a long way from the single-gene interpretation of mental disease to today's polygenic view. The former was the basis of the claim we should sterilize mentally ill. The latter provides ground for understanding the value of diversity. The figure illustrates the proliferation of known genes that can be linked to schizophrenia. Source

DRD4

Dopamine receptor D4 (DRD4) has long been associated with traits like thrill-seeking, risk-taking, and creativity. Earlier research suggested that this gene might have a profound effect on personality, linking it to novelty-seeking behavior. This would then be the magic driver of the learn drive in humans. It would allegedly separate those more and less curious, and in the long run, those more and less intelligent.

The idea gained prominence in the late 1990s, particularly with a study published in 1996 by Benjamin et al. in Nature Genetics (Population and familial association between the D4 dopamine receptor gene and measures of Novelty Seeking). This study linked the 7-repeat allele of the DRD4 gene to novelty-seeking, which sparked significant interest in the potential for single genes to influence broad personality traits. 7-repeat allele occurs in 1% of Asian, but up to 50% Native American populations (it may have undergone positive selection in migratory populations).

However, newer studies emphasize that while DRD4 may influence such traits, personality is shaped by a complex interplay of many genes and environmental factors. 7-repeat allele might explain only about 3-4% of the variance in novelty-seeking traits.

COMT

The most well-documented and prominent gene associated with personality and intelligence is COMT (Catechol-O-Methyltransferase). The COMT gene encodes an enzyme that degrades dopamine, particularly in the prefrontal cortex, which is crucial for cognitive functions like decision-making, reasoning, and executive control.

The most studied variation in COMT is the Val158Met (rs4680) polymorphism, where a substitution of methionine (Met) for valine (Val) affects enzyme activity. Individuals with the Met variant have lower enzyme activity, leading to higher dopamine levels in the prefrontal cortex. This is associated with better working memory and cognitive flexibility but also a higher risk of anxiety. Studies show that individuals with the Met/Met variant tend to perform better on tasks requiring executive functions, particularly under low stress conditions (perhaps a gain of 1-2 IQ points). The COMT gene is linked to traits like emotional stability and stress response, influencing personality traits like neuroticism and resilience.

While other genes, such as BDNF, DRD4, and APOE, also play roles in cognitive and personality-related traits, the COMT gene is particularly well-documented in relation to both personality and intelligence.

The Met variant is associated with better cognitive performance under low-stress conditions, but under high-stress conditions, the same individuals often experience cognitive overload and heightened anxiety. This is due to the more sustained activation of the prefrontal cortex, which can become counterproductive under stress.

Variants of COMT meet the trade-off between executive function and resilience

BDNF

BDNF (Brain-Derived Neurotrophic Factor) is a protein essential for neurogenesis, synaptogenesis, and synaptic plasticity. Higher levels are associated with faster brain development (which isn't always a good thing; see the precocity paradox). As a result, BDNF plays a key role in adaptability and stress resilience.

The most well-known variant of the BDNF gene is the Val66Met polymorphism, where valine (Val) is replaced by methionine (Met) at position 66 of the protein.

Lower levels of BDNF in the Met variant are linked to reduced stress adaptation, making people more vulnerable to adverse emotional states. Impairments in synaptic plasticity and neurogenesis can lead to reduced hippocampal volume, poorer memory, and a higher risk of mental disorders. In terms of personality, the Met variant may accelerate a tendency toward neuroticism. It's also possible that individuals with the Met variant are more likely to score higher in introversion.

The Val66Met polymorphism in the BDNF gene is relatively common worldwide. Approximately 30% of people of European descent carry at least one copy of the Met allele, while in East Asian populations, the Met allele frequency can be as high as 50%. The allele is rare in African populations.

Genetic diversity within a population is crucial for adaptability. If everyone carried only the Val variant, the population might be less adaptable to future environmental changes. A mix of individuals with different emotional profiles can enhance group dynamics.

My wild guess is that the high frequency of the Met allele indicates its contribution to the value of population neurodiversity.

Cognitive deficits linked to the Val66Met polymorphism are not substantial; memory impairments might account for a 1-3 point IQ drop. When you consider that failing to learn to read can reduce a potential IQ of 120 to zero on a test requiring reading, the Val66Met polymorphism is more of a molecular curiosity than a factor with a significant impact on people's lives.

Variants of BDNF might satisfy a different balance in the plasticity-stability trade-off

SLC6A4

Serotonin transporter gene

Altered serotonin transporter expression influences the brain’s response to stress, affecting how one perceives and reacts to stressful situations. People with lower serotonin transporter expression may exhibit a tendency toward rumination and a negative bias in processing emotional information, leading to a more pessimistic way of seeing the world. This genetic variation reflects the broader evolutionary principle that what might be a disadvantage in one environment could be an advantage in another, contributing to the complexity of human behavior, personality diversity, and neurodiversity in general.

Polygenic influences

Serotonin transporter genes have been involved in dozens of expressions of personality and mental health. A great deal of that research suffers from the usual replication problem. However, it is also important to note that each of those expressions relies on dozens if not hundreds of other genes. While we may see correlations, it is hard to build consistent model of the impact of individual alleles. For example, if we peek at the hazy concept of ADHD, we quickly realize it is a polygenic "disorder" due to the effects of genes underlying dopamine, norepinephrine, serotonin, GABA, and other neurotransmitters. Dopamine genes DRD1, DRD2, DRD4, DRD5, dopamine–beta-hydroxylase, and the dopamine transporter. Epinephrine genes ADRA2A, ADRA2C, PNMT, norepinephrine transporter, MAOA, COMT, serotonin genes TDO2, HTR1A, HTR1DA, GABA genes GABRB3, and many others (see the text by Kenneth Blum here for details).

Epigenetic mechanisms

I have already shown that the reasoning that personality is hereditary is misleading. So is the thought that epigenetics turns on specific genes that change personality.

A good understanding of plastic personality can be derived from the general principles of the conceptualization process occurring in the brain in the course of development as well as in the course of learning. Epigenetics is just a mechanism for turning on the genes that take part in modifying synaptic connections and affect the modulation of the activity of existing connections. It is part of the adaptation process in which personality characteristics are a reflection of the adaptation to a specific environment.

Metaphorically speaking, in the process of building bridges as part of improving transport routes in the country, we do not dwell over the production of bricks. Increasing the production of red bricks does not have a direct effect on transportation network of a country. Bricks are incorporated in the infrastructure where they are needed. Genes do not set the personality. Genes serve adaptations

Short and long alleles

The two main alleles, short (S) and long (L), are associated with different levels of serotonin reuptake efficiency, leading to distinct patterns of emotional regulation. The S allele is generally associated with lower transcriptional efficiency, meaning it produces less of the serotonin transporter protein compared to the L allele.

Individuals with two copies of the L allele generally have lower sensitivity to stress and are less likely to experience mood disturbances. However, they might be less attuned to potential threats or subtle social cues, which could be a disadvantage in environments where social or environmental vigilance is crucial.

Individuals with one or two copies of the S allele tend to have increased sensitivity to environmental stress, often showing higher levels of anxiety, depression, or emotional reactivity, especially in stressful situations. However, this sensitivity may be advantageous in highly social or unpredictable environments where heightened awareness of threats could enhance survival. This allele is also linked to greater empathy and social bonding under supportive conditions.

Variants of the serotonin transporter gene (5-HTTLPR) are generally considered non-deleterious, meaning they don’t typically lead to serious negative health effects. Instead, they are linked to a range of personality traits and emotional responses that reflect an evolutionary trade-off, contributing to neurodiversity.

DNA methylation

DNA methylation is a key epigenetic mechanism that can influence the expression of genes. The serotonin transporter gene, particularly its promoter region 5-HTTLPR (serotonin transporter linked polymorphic region), is one of the best-known genes associated with personality traits that can be epigenetically modified.

DNA methylation on the 5-HTTLPR have been linked to variations in how individuals respond to stress, which in turn affects personality traits such as neuroticism, anxiety, and emotional regulation. People with different epigenetic modifications in this gene may display varying levels of resilience or vulnerability to stress. Individuals with lower methylation and higher serotonin transporter expression often show greater emotional stability and resilience. Higher DNA methylation, often due to stress or adverse experiences, can lead to lower serotonin transporter expression. This is associated with higher levels of neuroticism, anxiety, and moodiness.

Increased methylation may reflect a form of plasticity where individuals become more sensitive to environmental influences. This could mean that the S allele, in particular, shows a heightened epigenetic response to life experiences, potentially amplifying both positive and negative emotional reactions. Methylation of the L allele can also reduce its expression, dampening the expected benefit of having this allele in terms of emotional stability or resilience.

For more details see: Genotype-dependent associations between serotonin transporter gene (SLC6A4) DNA methylation and late-life depression

Chronic stress

Chronic stress, trauma, or adverse childhood experiences can lead to epigenetic changes, such as increased DNA methylation at the 5-HTTLPR region. Exposure to stress increases methylation of the SLC6A4 promoter region, affecting both S and L alleles, though individuals with the S allele may be more vulnerable. This often results in reduced expression of the serotonin transporter, leading to altered serotonin levels in the brain. Exposure to negative social environments, such as bullying or social isolation, can also modulate the gene's activity through epigenetic mechanisms.

Stress does not activate the SLC6A4 gene uniformly across all cells. Instead, its activation is likely targeted to specific brain regions and neuron types where changes in synaptic connections are needed. This localized response is a sophisticated mechanism to ensure that the brain adapts appropriately to stress, potentially altering mood, cognition, and behavior as required.

Maternal care

By analogy, high quality maternal care has opposite effects to stress. It can lead to lower methylation of the SLC6A4 gene, resulting in higher expression of the serotonin transporter, which is associated with more positive emotional outcomes in later life. Over and over again we can see how environmental stressors result in a departure from the default sunny personality, while unconstrained behavioral spaces combined with love, keep the default personality intact.

It is then easy to guess than regular physical activity will result in positive epigenetic changes that may enhance serotonin transporter expression, thereby promoting resilience.

For more see: Daycare misery

OXTR

MAOA

AVPR1A

APOE

The APOE4 allele is linked to a higher risk of developing Alzheimer's. Dementia has a huge impact on personality [link: elsewhere in the text]. However, this variant falls out from the non-deleterious category. It seems evolution does not care much about older people. As long as genes are spread successfully, the fate of the organism is secondary.

Further reading