Family and Parenting 3-Book Bundle. Michael Reist

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      Anxious macaques and bullies have a lot in common. Both have trouble relating with other macaques in their troop. Both show signs of behavioural disorder, a fact neatly ascertained by the reaction of anxious and bully macaques to a “happy hour” test. For a one-hour period, macaques are given unrestricted access to a fruity beverage containing 9 percent alcohol. Well-adjusted macaques know their limits. They have between three and four drinks and call it quits. Anxious and bully macaques show no such moderation. They drink to excess, though each group goes about it in a different way. Anxious macaques drink more than they should, but they do so in a manner that suggests self-medication. They drink until they’re good and drunk. Bullies take it one step further. They are the frat boys of the animal kingdom, hitting the bottle as if it were an endurance contest. They drink until they are practically unconscious, their drunken bodies reeling and their blood alcohol content skyrocketing to dangerous levels.

      But perhaps the most important connection between anxious and bully macaques is their origins. Both have genetic susceptibility to problematic behaviour, but genetic cause ends precisely there. In order to activate these behaviours, young macaques must experience them during childhood. Anxious macaques came from anxious mothers, and bully macaques from bully mothers. When these macaques grow, they adopt the same parenting flaws they themselves experienced as infants and impart them on a number of their children, lending the cycle of neuroses and violence an air of inevitability. But take the neurotic or aggressive macaque away from his troublesome upbringing and foster him to a nurturing, affectionate mother, and these adverse behaviours disappear.

      The culprit, therefore, is poor parenting, though it is aided and abetted by certain high-reactive polymorphisms. If you’ve read this far, it shouldn’t surprise you that one of them goes by the name rh-5HTTLPR, the macaque equivalent of our notorious friend 5-HTT. As with 5-HTT, rh-5HTT has a long (l) and a short (s) allele; when you genotype bully macaques, guess which one you find? Consistently, the s allele makes an appearance, either paired with an l allele (l/s) or doubled up with anothers allele (s/s).

      Genetically susceptible individuals, when raised in nurturing environments, are no more likely than genetically resistant individuals to succumb to their grim, ostensibly gene-predicted fates. Genes may be the trigger, but the environment is the finger that pulls it. And different environments choose very different targets, and so trigger very different outcomes. Suomi’s genetically vulnerable macaques may become bullies when raised by bullies, or suffer chronic anxiety when raised by anxious mothers, but when they are raised in supportive environments, they don’t just do okay, they flourish.

      In a number of ways, high-reactive macaques fostered with love and affection actually exceed their low-reactive, similarly coddled peers. They consume less alcohol in happy hour tests. They become exceptionally caring mothers, their nervous energy channeled into a productive pursuit. They rise high in the social hierarchy, often becoming prize mates or matriarchs of top-ranking troops. And, on a molecular level, they process serotonin (the neurotransmitter responsible for modulating mood) roughly 10 percent more efficiently than l/l macaques, despite having the supposedly less efficient serotonin transporter gene.

      Not all primates have an exact equivalent of the 5-HTT serotonin transporter gene. In fact, only two species do: macaques and humans. Macaques may not be our closest relatives, but we and they share another trait that every other primate lacks: versatility. Apes, chimps, and bonobos are fine-tuned to their environments; attempt to relocate them even in the most tightly controlled conditions and the results will be, at best, lukewarm. Macaques are a different story. Pluck a troop of macaques from their native home and drop them just about anywhere on Earth,[24] and they will not only survive, but prosper. Given adequate resources and sufficient means to avoid predators, their numbers will steadily increase until they reach the upper limits of sustainability.

      On the Indian subcontinent, where indigenous macaques can be found, they dwell in jungles, hardwood forests, savannahs, the fringes of deserts, and the rocky outcrops of the Himalayan foothills. They have made their homes happily in rural Maryland, islands off the coast of Puerto Rico, the swamps of Louisiana, the high arid plains of Texas, and the San Fernando Valley. And while many of these macaque colonies are bolstered by human intervention, they are more than capable of surviving without us.

      In the 1930s, a tour boat operator known as Colonel Tooey released a troop of rhesus macaques into the forests of Silver River State Park, Florida, in order to provide his river cruise business with a bit of exotic colour. Eighty years later, the descendants of these monkeys have become a significant part of the local ecosystem despite the repeated attempts of local farmers to wipe them out. These are not Great Apes in captivity, their environment meticulously regulated, their intergenerational survival hinging on the constant efforts of trained zoologists. These are monkeys that we’re actively trying to kill, but can’t. That’s truly impressive, because if there’s one thing human beings are good at, it’s killing our competition.

      There exists a correlation between high-reactive serotonin transporter genes and primate adaptability. Does the former cause the latter? We cannot yet definitively say. Causation is a far harder relationship to prove than correlation. Yet it remains a tantalizing hypothesis. After all, our ability to adapt to new environments has been paramount to our success as a species; without it we would all remain nestled in the cradle of civilization, our numbers culled by severely limited resources and our ingenuity stunted by an absence of necessity. And studies have shown that high reactivity is only a liability when it and the surrounding environment clash. When they harmonize, it can prove to be a tremendous advantage. Could this two-tiered reactivity be the key to the success of us and our rhesus macaque cousins? Bold, high-reactive wagers hedged with a larger population of low-risk, moderate-yield alleles? We may never know for sure, but any new parents left wringing their hands as they await the results of their child’s genotype testing can relax. An s/s 5-HTT allele is not a death sentence. In fact, under the right environmental conditions, its presence could very well be an advantage.

      The Two Faces of DRD4

      Remember our Dutch friends, Bakermans-Kranenburg and Van IJzendoorn? They designed a study examining the effects of maternal sensitivity on externalizing behaviour. Researchers videotaped mothers as they interacted with their infants, noting both how much attention the mother paid to her baby and how the baby responded to that attention. A distracted, inattentive, or easily frustrated mother received a low maternal sensitivity score, and a crying, inconsolable, aggressive child ranked higher on the scale of externalizing behaviour. Bakermans-Kranenburg and Van IJzendoorn’s theory was that the presence of the 7-repeat DRD4 allele in children would make them more likely than average to act out when raised by low-sensitivity mothers.

      The numbers agreed with them. Among children from low-sensitivity homes, those with the 7-repeat allele scored an average of 7 points higher on the Child Behavior Checklist externalizing behaviour scale than those without the 7-repeat. This is not surprising, as these children learned from an early age that, to ensure a response from their parents, they had to act out vigorously.

      The results were more dramatic still when comparing 7-repeat children from low- and high-sensitivity homes. Those with low-sensitivity mothers scored over twice as high on the externalizing behaviour scale as those whose mothers were more cognizant of and attentive to their needs. That is a big jump. However, one comparison the researchers glossed over was between 7-repeat and non-7-repeat children in high-sensitivity homes. Among these two groups, the children with the 7-repeat allele (the high-sensitive version of the gene) scored over 4 points lower than their peers without the offending allele. In other words, the children with the risky, “problem” allele were actually better behaved than those with the stable, less reactive allele. Four points is a less significant discrepancy than 7 points, and not even close to the 10-point, 100 percent markup seen between 7-repeat children in low- and high-sensitivity homes. But it’s not peanuts, either.

      The Dutch duo were not the only researchers to document this trend. Half a dozen different СКАЧАТЬ