Genes and Family ties to Personality

You’ll notice that the personality theories we’ve discussed in Parts 1 and 2 all emphasize flexibility, open-mindedness, conscientiousness, the ability to get along with others and self-regulate emotions as key ingredients of one’s personality. But how do we become more open-minded or more outgoing? Are we born open-minded and charismatic, or do we learn it?

Ultimately, human personality seems to develop as a complex adaptive system and each dimension may be influenced by interactions between many biogenetic and environmental variables over time. For example, a genetic variant for neuroticism may interact with a gene involved in shyness to produce an individual who’s inclined to be both anxious and shy. More and more, researchers are finding polygenic or “multi-gene” involvement in personality, concluding that one gene acting alone may have little effect on personality traits, but that multiple genes acting together can produce a significant effect. In fact, many researchers believe that perhaps hundreds of genes may influence each one of our personality traits ever so slightly, and always in conjunction with various brain systems (e.g., reward-motivation circuitry) that influence how those traits manifest in a given situation.

Many of our traits appear to be at least somewhat heritable. Most studies show that heritability of human personality traits tends to fall within the range of 30% to 60% (Gestell, Broekchoven, 2003; Hosak & Hosakova, 2010; Savitz & Ramesar 2004). The non-shared rearing (e.g., non-familial) environment accounts for the remaining 40% to 70% of the variance. But interestingly, shared environmental factors are usually found to be of minor or no importance (Bouchard & Loehlin, 2001; Ebstein et al, 2002; Savitz & Ramesar, 2004).

How can this be? Twin studies always shed light on this subject. The literature has overwhelmingly shown that identical twins share about 50 percent of the same personality traits and about 50 percent of intellectual traits. And identical twins reared apart are more similar in personality to each another than are siblings or fraternal twins who are reared together. In fact, people raised in the same family are often as different as any two people you’d randomly pick off the street.

Why does upbringing appear to have so little an effect on most personality traits? There could be many explanations. One may be that siblings may have very different experiences growing up within the same family. They may be treated differently by one or both parents and by their other siblings. They also may experience key family events such as divorce or death very differently.

Here are just a few genes that we know play a role in influencing personality traits…

Twin studies consistently show that genetic factors contribute 40 – 60% of the variance in neuroticism, whereas, contribution of the shared rearing environment accounts for only 5% of the variance. At least 10-15 genes are predicted to be involved in neuroticism (Canli, 2008).

• 5-HT T. The short variant of 5-HT T — the famous “depression/anxiety gene” — has been linked to both state anxiety and the personality trait of neuroticism. People with high neuroticism tend to have a short variant of the serotonin transporter promoter allele (5-HTTLPR), a stretch of DNA that controls how much of the serotonin transporter gets made  (Lesch et al, 1996; Sen et al, 2004; Garpenstrand et al, 2001). 5-HT T is jokingly referred to as “the Woody Allen gene” for its links to anxiety, harm avoidance, instability, moodiness and negative thinking. The 5-HTT gene is thought to affect personality traits through its influence on brain development and the amygdala (the brain’s emotion/fear-processing factory) reactivity (Canli, 2008). It’s worth mentioning, however, that the long variant of this same gene has been linked to high emotional resilience. If you’re hoping that you’re one of the lucky ones who has two long gene variants, your odds are around 30 percent. Research thus far indicates that about 70 percent of us have at least one short 5-HT T gene variant, which may help explain why so many people are vulnerable to — or predisposed to — depression and anxiety.
• DRD4. The DRD4 gene produces the protein responsible for creating a key dopamine receptor. A few studies have found that people with short variants of the DRD4 gene and serotonin transporter promoter are predisposed to shyness and neuroticism; for example, infants have been found to be less responsive to stimulation and more distressed during daily routines (Auerbach et al, 1999).
• RGS2. Variants of the gene RGS2 produce higher risk for anxiety disorders. Nine different variations of RGS2 have been associated with shy, inhibited behavior in children, introverted personalities in adults, and increased activity in areas of the brain such as the amygdala and the insula, which process fear and anxiety (Smoller, 2012).
• COMT. Some variants of the COMT gene, which regulates dopamine signaling, may play a role in causing anxiety and negative emotions (Hovatta, 2008). COMT (catabolic enzyme named catechol-O-methyltransferase) encodes an enzyme that breaks down dopamine, weakening its signal. COMT’s two alleles are Val158 and Met158. People carrying two copies of the Met158 allele may find it harder to regulate emotional arousal, a sensitivity which may, in combination with other hereditary and environmental factors, make them more prone to anxiety disorders. The Met158 allele is thought to elevate levels of circulating dopamine in the brain’s limbic system, which supports memory, emotional arousal and attention. More dopamine in the prefrontal cortex can cause an “inflexible attentional focus” on unpleasant stimuli — Met158 carriers may find that they have a hard time tearing themselves away from stimuli that is negatively arousing.
• BDNF. Some good news… five studies evaluated 1633 subjects with the Val66Met polymorphism of the BDNF gene (11p) using McCrae & Costa’s NEO neuroticism scale, finding that those who have this gene variant showed significantly lower neuroticism (Frustaci et al., 2008). BDNF (brain-derived neurotrophic factor) is involved in cell survival, various neurotransmitter systems, long-term hippocampal (memory) activation, stress regulation and anxiety-related behaviors.

In addition to being associated with compulsive behaviors such as gambling and alcohol addiction, certain variants of the DRD4 gene have repeatedly been linked to novelty-seeking, sensation-seeking, thrill-seeking behaviors.

• Novelty-seeking or shy? Several studies have found that people with the longer variants of the dopamine receptor gene DRD4 are predisposed to novelty-seeking behavior — the opposite of shyness, which is associated with the shorter variants (Hosak & Hosakova, 2010; Auerbach et al, 1999), including the C-521T polymorphism (Munafó et al, 2008). One study that evaluated subjects with Robert Cloninger’s 4 personality traits (novelty seeking, harm avoidance, reward dependence and persistence) found that many subjects with high novelty-seeking scores had a slightly longer form of the D4 dopamine receptor (D4DR) gene than the deliberate, reflective subjects (Ebstein et al, 1996). Another study conducted at the NIMH which evaluated subjects on Allport’s Big Five personality factors found that novelty-seeking was associated with the long version of the gene. Researchers caution, however, that the D4DR gene variant may only account for about 10 percent of the influence on the trait of novelty-seeking.Cloninger suggests that each personality trait is modified by other traits. Thus, a thrill-seeker who is also biologically inclined to be reward-dependent, persistent, and optimistic may be a successful business executive, while a thrill-seeker who is low in both reward dependence and anxiety may be more likely to turn to criminal pursuits (Cloninger et al, 1996).
• Chasing Thrills & Chills. Several studies have linked variants of the gene DRD4 to thrill-seeking. But why do some of us enjoy scary horror flicks while others don’t? One study required both horror movie-haters and horror movie-lovers to rate their emotions while watching clips of scary films. All reported similar levels of fear while watching the clips, but the horror movie-lovers actually processed the scariest scenes as the most pleasant ones (Cohen & Eduardo, 2007)! Psychologist Marvin Zuckerman, in developing his Alternate Five-Factor personality model, had previously found that high sensation-seekers enjoy morbid curiosity in general and horror movies in particular.
• Sexual promiscuity, DRD4  and the dopamine rush. One study found that people with the thrill-seeking variant of DRD4 (7R+ genotype) were about twice as likely to have a history of uncommitted sex, including one-night stands and infidelity or cheating. (Half of those with this variant reported committing infidelity in the past, compared with 22 percent of those without the variant.) DRD4, which produces the protein responsible for creating a key dopamine receptor, interacts with the brain’s dopamine reward system, which provides the motivation, impulsivity and libido that influences sexual behaviors, especially when high-risk, high-reward opportunities are involved (Garcia et al, 2010).

Impulsivity, or action without foresight, is a factor in many pathological behaviors including suicide, aggression, and addiction, but it’s also only fair to point out that it can be of value in an emergency where a quick decision must be made or in situations where risk-taking is favored. You’ll notice that impulsivity shares common some genetic roots with neuroticism, novelty-seeking and aggressive, antisocial behavior.

• Ability to delay action. Do some genetic influences kick in later? One longitudinal twin study evaluating the ability to delay action found that heritability increased from 30 − 51% from age 12 to 14, suggesting an increasing role of genetic influence with age (Anokhin, Golosheykin et al, 2011).
• DRD4. One study found that the DRD4 gene may account for around 45% of the variance in impulsivity (Canli, 2008). Another study linked the C-521T polymorphism of the DRD4 gene to impulsivity (Munafó et al, 2008).
• MAOA. One study found that deficient activity of the MAOA gene, can cause severe impulsivity (Bruner et al, 1993). Brunner discovered an MAOA “stop codon” (C936T), or genetic code that halts expression of a gene, which produces complete deficiency of MAOA activity and contributes to causing severe impulsivity. The MAOA gene, which plays a key role in modulating aggression, has been associated with impulsive violence in several other studies, especially in males. One study found that people with the MAOA-L variant show reduced volume and activity of the cingulate cortex, a brain area responsible for inhibiting behavior and regulating impulsive aggression. When viewing frightening scenes or faces perceived as angry, they showed increased amygdala activity and reduced amygdala-regulating activity (Meyer-Lindenberg et al, 2006). In other words, they were unable to control overreactions to angry or frightening stimuli.

Most twin and adoption studies seeking answers to the nature-nurture question have found heritability of adult antisocial behavior to fall between 40 − 60% (Jacobson, 2005). Genetic factors appeared to be particularly important for the development of more severe, life-course persistent patterns of antisocial behavior, but, as you’ll see, individual adverse environmental experiences may actually trigger later genetic vulnerability to antisocial behavior.

• MAOA, the “aggression gene.” The MAOA gene (encoding monoamine-oxidase A), an enzyme that metabolizes neurotransmitters involved in stress regulation, famously plays a role in modulating aggression (Bruner et al, 1993). MAOA is believed to influence how the brain is wired during development. MAOA enzymes break down key mood-regulating chemical messengers, most notably serotonin. MAOA has two known variants that influence aggression and impulsiveness: the violence-related MAOA-L version and the MAOA-H version, which triggers less enzyme activity, thus leaves higher levels of serotonin circulating in the brain (Pezawas et al, 2005).
• MAOA and the role of environment. Other large studies of males from birth to adulthood have sought to determine why some kids who are mistreated grow up to develop antisocial behavior, whereas others do not (Caspi et al, 2002; Ducci et al, 2007) Caspi et al found that mistreated kids with the long MAOA-H variant (which confers higher levels of serotonin) moderated the effect of maltreatment and made these kids less likely to develop antisocial problems. The short MAOA-L gene variant, on the other hand, may make children more vulnerable to maltreatment, a sensitivity that can spark anxiety, hyperactivity, impulsivity, or aggression — all behaviors that help set the stage for antisocial behavior. This study illustrates how even a relatively heritable genetic effect may still need to interact with psychosocial environmental in order to produce abnormal behavior. In other words, by itself, MAOA-L doesn’t necessarily make people violent, but it may bias the brain toward impulsive, aggressive behavior.
• HTR2B. A multinational study of violent offenders led by David Goldman at the National Institutes of Health revealed that a single DNA change that switches off a gene known as HTR2B can lead to highly impulsive behavior. On average, the prisoners had committed 5 violent crimes apiece, 94 percent of which occurred under the influence of alcohol and were typically an overreaction to a minor incident and impulsive rather than premeditated. The study also revealed that 70 percent of these prisoners with the HTR2B mutation had displayed suicidal behavior. The HTR2B gene contains the instructions for a serotonin receptor found all over the brain, especially in the frontal lobe, which is the seat of impulse control. The mutation in HTR2B is a misplaced “stop codon,” or snippet of genetic code that prevents the expression of the serotonin receptor. Serotonin is a neurotransmitter involved in regulating self-control. Low serotonin levels have been consistently associated with aggression and impulsivity; in particular, as manifested in impulsive aggression and impulsive suicides (Virkkunen & Linnoila, 1993).
• NRXN3. New studies of the two variants of the gene NRXN3, previously linked to nicotine and alcohol dependence, opiate addiction and obesity, suggests that impulsivity is the common denominator. In men, but not women, having a particular variant of NRXN3 increased the risk of alcoholism 2.5-fold. Having a different variant of NRXN3 was associated with impulsivity, in men but not in women (Stoltenberg et al, 2011).

• One study of 7 800 U.S. Caucasian twins found that genetic factors that influence individual variation in extroversion and neuroticism appear to account entirely for the genetic liability to social phobia and agoraphobia, suggesting that both low extroversion and high neuroticism are personality traits heavily involved in social phobia and agoraphobia (Bienvenu et al, 2007).
• A study of 238 Japanese subjects found that those with the C5178A genotype showed significantly higher extroversion than those with the C5178C genotype (Kato et al, 2004).

• COMT. One study of 17,375 European adults found that conscientiousness is altered in people who have the genetic variation (the val158met genotype) of the COMT gene, which is also generally associated with neuroticism. Conscientiousness and agreeableness were significantly correlated in people with this COMT variant, but not neuroticism, suggesting that this COMT variant’s ability to affect both dopamine and epinephrine regulation may allow it to rebalance these systems to increase positive personality traits such as conscientiousness and agreeableness (Hall et al, 2014).
• KATNAL2. These researchers found that the KATNAL2 gene is associated with conscientiousness and, in fact, may be a novel gene for personality (deMoor, Costa et al, 2012).

• RASA1. One study of 17,375 European adults showed that the RASA1 gene was associated with openness to experience (deMoor, Costa et al, 2012).

• One study of identical and fraternal twins found that a shared rearing environment had considerably more influence on Agreeableness than on Openness to Experience, or Conscientiousness (21% for Agreeableness versus 6% and 11%, respectively). Genetic influences in non-shared environments accounted for 40%, 12%, and 29% of the variance in Openness to Experience, Agreeableness, and Conscientiousness, respectively (Bargeman et al, 2003).

• DRD4. One study of 200 male subjects found that a variant of the DRD4 gene was strongly associated with Self-Transcendence. Results suggested that “spiritual acceptance” may be the most highly correlated personality trait with the DRD4 gene. Researchers believed that this result may be a function of the high concentration of the dopamine D4 receptor in the cortical areas, especially the frontal cortex (Comings et al, 2000).
• VMAT2. Another study conducted by Dean Hamer, geneticist, director of gene research at the NIMH and author of The God Gene (2004), found that people with a particular variant of the VMAT2 gene (single nucleotide polymorphism A33050C) scored significantly higher on self-transcendence.

Why do some of us turn out to be saints and others turn out to be serial killers? The influence of genes on behavior, after all, is indirect and complex — genes acting in concert with other genes. The main job of genes is to build and organize the physical structures of the body, including the brain. These structures interact with the environment to produce behavior.

Throughout our lives, genes “express” themselves in different ways — they may switch on or off. Some genes are only expressed or “turned on” in response to stimuli from the outside world, such as environmental influences, lifestyle and geography. Like light switches, genes must receive electrical current to turn on and express their particular proteins. So yes, genes may create risk factors in varying degrees, but by themselves, they simply make proteins.