Family and Parenting 3-Book Bundle - Michael Reist

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same gene, making them heterozygous. In these cases, the two alleles can interact in a number of ways, the most famous of which was discovered by an Austrian monk named Gregor Mendel. Mendelian genetics divides alleles into dominant and recessive types. When an individual possesses both a dominant and a recessive allele of the same gene, the result is not a compromise between the two. An individual with one brown eye allele and one blue eye allele will not develop murky blue irises, or one brown eye and one blue eye.[14] Rather, the dominant trait supersedes the recessive trait, which lies unexpressed in the gene, awaiting the opportunity to perhaps show itself in a subsequent generation. In the case of eye colour, blue eyes are recessive and brown eyes are dominant.[15] A man with one brown-eye allele (symbolized by a capital B) and one blue-eye allele (symbolized by a lower case b)[16] will have brown eyes. Say that man meets a brown-eyed woman who also has a recessive blue-eye allele, and together they have a child. The child’s eye colour genes could look one of four ways. She could be homozygous for the brown-eye allele (BB), heterozygous for the brown and blue-eye alleles (Bb or bB, depending on which allele comes from which parent), or homozygous for the blue-eye allele (bb). In the first three cases, the child, like her parents, will have brown eyes, as the presence of the dominant allele (B) overpowers that of the recessive allele (b). In the latter case, though, the dominant allele is not present, and so the child will have blue eyes.

      Very few traits (including the one in our example) truly fit the Mendelian mould of single-gene origin and dominant/recessive binary.[17] Most traits require multiple genes to develop, and some single gene traits vary in their degrees of expressivity, or the extent to which the “dominant” trait dominates. Still others are co-dominant, meaning that neither allele overwhelms the other. Nevertheless, Mendel’s insights were remarkable, considering all he had to work with were a few pea plants and his own powers of observation. With these humble tools, Mendel documented the first evidence of genetic inheritance, paving the way for what would become arguably the biggest scientific undertaking of the 20th century: mapping the human genome.

      DRD4

      As we’ve already learned, DRD4 (the gene) codes for DRD4 (the receptor), and DRD4 allows the human brain to dole out jolts of positive reinforcement in the form of dopamine. Its connections to drug addiction and depression seem obvious — drugs being a pharmacological shortcut to euphoria, and depression being a chemical imbalance precluding one’s ability to experience pleasure — but what links DRD4 to ADHD, heart disease, or any of the other conditions to which it is accused of contributing? Moreover, why DRD4 and not DRD3 or DRD5? The answer lies in the allele.

      Within the third exon (or section of codeable, non-“junk” DNA) of DRD4 sits a nucleotide sequence 48 base pairs long. This sequence repeats from 2 to 10 times, depending on the allele, contributing to DRD4’s reputation for being one of the most variable genes in the human genome. The 48 base-pair repeat is not the only repeated sequence in DRD4, nor is it the longest, but it is nevertheless the focus of a great deal of scientific scrutiny.

      The most common number of repeats found in DRD4 are 3 and 4, but for susceptibility to depression, addiction, and a host of other maladies, 7 seems to be the magic number. For reasons that continue to elude us, the 7-repeat allele increases a person’s predisposition toward risk-seeking behaviour, which includes typical “high-risk” activities, such as drug use, illicit sex, and gambling, but also extends to extreme sports and high-pressure business decisions. This creates an odd schism in public opinion on the 7-repeat allele. While considered an albatross around the necks of junkies and problem gamblers, it can be seen as a positive attribute when possessed by athletes and successful business people, both of whom thrive in high-risk environments.

      5-HTTLPR

      We’ve already thanked dopamine for our ability to experience pleasure; it’s only fair we now give serotonin its due.

      Though a neurotransmitter much like dopamine, serotonin is principally found in the gut, where it regulates intestinal movements. In the brain, it serves a very different function, facilitating feelings of happiness and well-being. The link between digestion and contentment may seem tenuous, but from an evolutionary standpoint, it’s actually quite logical. If one considers pleasure outside its cultural trappings, it’s ultimately an incentive for continued survival. Pleasure has become far more decadent in modern society, where basic necessities are freely available. But at its humble roots, pleasure is derived from activities necessary for the propagation of our species: sex, warmth, sleep, and, most importantly, food. As a result, we are genetically inclined to feel a sense of contentment when these needs are met, and a drive to meet them when they’re not. Serotonin helps us achieve this end.

      Studies have linked serotonin levels to food availability, which, in social animals, also relates to one’s place in the social hierarchy. When injected with excess serotonin, animals with diminutive statuses in the hierarchy display uncharacteristically aggressive behaviour. In normal circumstances, a crayfish, when faced with a bigger opponent, will perform a supplicating tail-flip gesture that forces it backward, allowing it to flee. However, when injected with serotonin, it becomes more aggressive and attacks its opponent. Curiously, the opposite is true of dominant crayfish. When they receive a boost of serotonin, their behaviour becomes more fearful.

      With this in mind, it is interesting to note the number of studies that link 5-HTT to a host of behavioural disorders in humans and other primates, including both anxiety and excess aggression. There is a wide gulf of evolutionary difference between people and prawns! But the effect of certain chemicals on the neurological system can be remarkably similar across species. The connection is purely speculative, but worth considering.

      Unlike DRD4, 5-HTT is not itself a gene, but only a section of one. It sits on the promoter region of SLC6A4, which codes for a group of serotonin transporters. They affect the efficiency with which the human body can reabsorb and reuse serotonin after it has sent its first chemical message to the receptors. Since 5-HTT codes for the SLC6A4 promoter, it decides how much serotonin the body can reclaim. There are only two allelic variations — long (l) and short (s) — but they work in conjunction. Each person has two alleles of any one gene. With two copies of the gene and two possible forms the gene can take — long and short — there are four possible combinations a person can have: long/long, long/short, short/long, and short/short. For the sake of brevity, we will refer to these as l/l, l/s, and s/s (l/s and s/l amount to the same thing, so there is no point in distinguishing between them).

      MAO-A

      Though less of a key player than either DRD4 or 5-HTT, the MAO-A gene bears consideration, especially since its function is tied into that of the other two genes. MAO-A codes for monoamine oxidase A, an enzyme that breaks down neurotransmitters like serotonin and dopamine. Its function, or lack thereof, directly affects the amount of dopamine and serotonin in the human body.

      Like DRD4, MAO-A has multiple allelic variations based on the number of times it repeats a particular sequence of nucleotides — in this case, one 30 base-pairs long. Humans can have anywhere from 2 to 5 repeats. Of these, the 4-repeat allele is considered high reactive, meaning it devours serotonin and dopamine more readily than its low-reactive counterparts.

      MAO-A has been dubbed “the warrior gene,” as recent studies have discovered a correlation between its low-reactive allele and aggressive behaviour in response to provocation. Researchers Rose McDermott and Dustin Tingley devised a study to document the interaction between a person’s MAO-A genotype and his response to a perceived wrongdoing. Or, more accurately, a man’s MAO-A genotype. As MAO-A sits on the X chromosome, focusing the study solely on males reduced the list of possible genotypes to either high or low. Girls have two X chromosomes, making their MAO-A alleles significantly more complicated (instead of high or low, you have h/h, h/l, and l/l). We do not currently know if one or both of women’s MAO-A genes function at any one time, or whether a high-reactive allele trumps a low-reactive allele, or vice versa. As a result, our knowledge of MAO-A-by-environment interactions pertains only to men.

      Ostensibly, men completed vocabulary tests in exchange for financial rewards. However, these tests were only a pretext for a subsequent game, during which an anonymous opponent could steal a certain amount of the man’s earnings. In retaliation, men were given the ability to inflict on the thief a somewhat bizarre punishment: making them

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