Behave: The Biology of Humans at Our Best and Worst

In this chapter, Sapolsky provides an introduction to the science of genetics and coverage of how our individual genome influences our behavior. For those unfamiliar with genetics, Sapolsky suggests reading Appendix 3.

Genes from the Bottom Up

Genes are hugely important to how the human body is organized, but the cultural conversation around genetics often exaggerates their importance to the idea that genes decide everything about us. In fact, environment plays a large role in “deciding” what genes “decide.”

Genes specify the shape, structure, and function of proteins, which are the building blocks of the human body. However, genes do not themselves decide when to “turn on” and start building. Instead, genes are turned on by transcription factors (TFs) which bind to “promoters,” the on switch at the head of the gene on the DNA strand. TFs activate due to environmental factors including those local to the gene, inside the whole of the organism, and the outside world. This can be understood in terms of an if/then clause: “If you smell your baby, then activate the oxytocin gene” (227), which triggers milk release in the breast. If you don’t smell the baby, no oxytocin, no milk release. Environmental inputs also cause TFs to be blocked from binding to promoters, setting genes to permanent on/off states that can be inherited by offspring. This is the phenomenon of Epigenetics.

 In a discussion of genes from the “bottom up,” Sapolsky outlines the core behavior of genes in organisms and highlights the importance of environmental triggers in shaping what genes do. This is an argument against “genetic determinism,” a style of thinking about organisms that suggests everything about their bodies and behavior is caused by genes. By showing how genes depend on environment, Sapolsky reminds us of the importance of avoiding a reductive approach to biology and foreshadows the importance of culture in determining behavior that he will delve into in the next chapter.

Genes from the Top Down

Before genetics was studied in terms of DNA (because DNA had not yet been discovered), it was studied in terms of traits: If relatives share traits, these traits must be genetic. However, when using families to learn about genetic traits, a confound exists: The families share the same environment, which can also cause the expression of traits.

Twin studies became an important innovation. Studies of identical (aka monozygotic, MZ) twins, who share 100% of their genes, and fraternal (aka dizygotic, DZ) twins, who share 50%, help scientists determine the influence of genes on individual traits. If traits are more often shared in MZ twins, they are understood to be more controlled by genetics, not environment. Studies on siblings separated at birth, and more rarely even twins separated at birth, is another method.

These studies show genuine genetic influences on several domains including IQ, propensity to specific mental disorders, and personality. This suggests the truth of a “genetic determinist” worldview: Everything about us depends on our genes. Overall, these studies “inflate the perceived importance of genes” in deciding our traits (240). This is evidenced via Sapolsky’s discussion of the science of heritability scores.

Geneticists examining traits of organisms produce “heritability scores” (241), a measure of the percentage of total variation of a trait that is determined by genetics. Sapolsky makes the argument that heritability scores are consistently inflated by geneticists because they only study organisms in controlled environments and are unable to gather inference on the total variability of the organism in different environments. For instance, if geneticists look at the heritability of the trait of height in three plants produced in a lab, they might see only minimal height variation between the plants, which suggests high heritability of the height trait. However, if they were to raise one of those plants in the desert or jungle, it would have a massive height difference, suggesting low heritability of the height trait. Sapolsky’s argument of the importance of multiple contexts for the science of genetics again highlights ethology over behaviorism: Reducing all the data to one universal context ignores all the potential variability environment produces.

Environments can impact organisms’ expressed traits, but they can also impact their actual genes or their genes’ effects, a phenomenon known as gene/environment (G/E) interaction. These forms of interaction make genuine assessment of genetic control over traits nearly impossible and make scientists realize the following: It is not relevant to ask “what does a gene do?”; it is only relevant to ask “what are genes likely to do in specific environments?”

Genes’ Effects on Our Best and Worst Behaviors

Genes related to serotonin, dopamine, and oxytocin/vasopressin have been linked to behaviors including aggression, generosity, promiscuity, and several other behaviors.

Multiple genes control for the creation, degradation, removal, and reception of serotonin. According to studies based on the presence or absence of these genes in individuals, scientists have equally purported that high aggression is linked to low serotonin and high serotonin, or due to the presence of one but not the others of these genes. One gene, MAO-A, which degrades serotonin, has even been termed the warrior gene and so deeply (and falsely) linked to predisposition to aggressive behavior that criminal sentences have been lessened for at least two individuals due to the presence of this gene. Of course, these genes’ effects on aggression are a product of multiple factors. MAO-A is a G/E interactive gene, with exposure to aggression in childhood a crucial trigger for its activation, as is coupling with high testosterone levels. Genetics is not as simple as cause and effect.

Genes that produce lower dopamine signaling are associated with pleasure and thrill-seeking. One dopamine-related gene, known as the 7R form of DRD4, produces a specific dopamine receptor that is relatively unresponsive to dopamine. It has been linked to predispositions to promiscuity, gambling, ADHD, and generosity, but in each case the development of these traits depends on G/E interactive factors.

Similar gene/environment interactions rule the day for genes modulating the expression of oxytocin, vasopressin, testosterone, and estrogen. The key takeaway: The effects of genes on behavior depend on environmental interaction with the gene both in the context of other genes in the body and external stimulus. In fact, hundreds of individual genes control for seemingly simple traits, but all of these genes interact with each other to form the trait’s final product. However, scientists are still only capable of investigating the interactions of a few genes at a time. All of this boils down to what is called “nonspecificity” (264). Genes have plenty to do with behavior, and all behavioral traits are impacted in some degree by our genetics. However, our predictive power in their exact associations is limited. “Genes aren’t about inevitability. Instead, they’re about context dependent tendencies, propensities, potentials, and vulnerabilities” (265). In an argument foregrounding his work in Chapter 16, Sapolsky outlines a genuine social consequence of the genetic determinist style of thinking. If we think all traits are controlled for by genes, we are liable to ignore steps we could take to avoid these effects by properly structuring our human environments. For instance, if we trace predisposition to violence to a singular gene, but then see this gene is a G/E interaction gene triggered by experience of violence, we now have scientific evidence that diminishing violence in the home lives of children will help our society to become less violent in generations to come.