- 最后登录
- 2011-8-15
- 在线时间
- 493 小时
- 寄托币
- 901
- 声望
- 34
- 注册时间
- 2009-9-26
- 阅读权限
- 25
- 帖子
- 0
- 精华
- 0
- 积分
- 847
- UID
- 2703629

- 声望
- 34
- 寄托币
- 901
- 注册时间
- 2009-9-26
- 精华
- 0
- 帖子
- 0
|
----reading continued
With the data gathered in the video intervention, the Leiden team began to test the orchid hypothesis. Could it be, they wondered, that the children who suffer most from bad environments also profit the most from good ones? To find out, Bakermans-Kranenburg and her colleague Marinus van Ijzendoorn began to study the genetic makeup of the children in their experiment. Specifically, they focused on one particular “risk allele” associated with ADHD and externalizing behavior. (An allele is any of the variants of a gene that takes more than one form; such genes are known as polymorphisms. A risk allele, then, is simply a gene variant that increases your likelihood of developing a problem.)
Bakermans-Kranenburg and van Ijzendoorn wanted to see whether kids with a risk allele for ADHD and externalizing behaviors (a variant of a dopamine-processing gene known as DRD4) would respond as much to positive environments as to negative. [省略的用法]A third of the kids in the study had this risk allele; the other two-thirds had a version considered a “protective allele,” meaning it made them less vulnerable to bad environments. The control group[对照组,may be useful in my own essay], who did not receive the intervention, had a similar distribution.
Both the vulnerability hypothesis and the orchid hypothesis predict that in the control group the kids with a risk allele should do worse than those with a protective one. And so they did—though only slightly. Over the course of 18 months, the genetically “protected” kids reduced their externalizing scores by 11 percent, while the “at-risk” kids cut theirs by 7 percent. Both gains were modest ones that the researchers expected would come with increasing age. Although statistically significant, the difference between the two groups was probably unnoticeable otherwise.
The real test, of course, came in the group that got the intervention. How would the kids with the risk allele respond? According to the vulnerability model, they should improve less than their counterparts with the protective allele; the modest upgrade that the video intervention created in their environment wouldn’t offset their general vulnerability.
As it turned out, the toddlers with the risk allele blew right by their counterparts. They cut their externalizing scores by almost 27 percent, while the protective-allele kids cut theirs by just 12 percent (improving only slightly on the 11 percent managed by the protective-allele population in the control group). The upside effect [正面作用]in the intervention group, in other words, was far larger than the downside effect in the control group. Risk alleles, the Leiden team concluded, really can create not just risk but possibility.
Can liability really be so easily turned to gain? The pediatrician W. Thomas Boyce, who has worked with many a troubled child in more than three decades of child-development research, says the orchid hypothesis “profoundly recasts the way we think about human frailty.” He adds, “We see that when kids with this kind of vulnerability are put in the right setting, they don’t merely do better than before, they do the best—even better, that is, than their protective-allele peers. “Are there any enduring human frailties that don’t have this other, redemptive side to them?”
As I researched this story, I thought about such questions a lot, including how they pertained to my own temperament and genetic makeup. Having felt the black dog’s teeth a few times over the years, I’d considered many times having one of my own genes assayed—specifically, the serotonin-transporter gene, also called the SERT gene, or 5-HTTLPR. This gene helps regulate the processing of serotonin, a chemical messenger crucial to mood, among other things. The two shorter, less efficient versions of the gene’s three forms, known as short/short and short/long (or S/S and S/L), greatly magnify your risk of serious depression—if you hit enough rough road. The gene’s long/long form, on the other hand, appears to be protective.
In the end, I’d always backed away from having my SERT gene assayed. Who wants to know his risk of collapsing under pressure? Given my family and personal history, I figured I probably carried the short/long allele, which would make me at least moderately depression-prone. If I had it tested I might get the encouraging news that I had the long/long allele. Then again, I might find I had the dreaded, riskier short/short allele. This was something I wasn’t sure I wanted to find out.
But as I looked into the orchid hypothesis and began to think in terms of plasticity rather than risk, I decided maybe I did want to find out. So I called a researcher I know in New York who does depression research involving the serotonin-transporter gene. The next day, FedEx left a package on my front porch containing a specimen cup. I spat into it, examined what I’d produced, and spat again. Then I screwed the cap tight, slid the vial into its little shipping tube, and put it back on the porch. An hour later, the FedEx guy took it away.
Of all the evidence supporting the orchid-gene hypothesis, perhaps the most compelling comes from [of all … the most compelling ….]the work of Stephen Suomi, a rhesus-monkey researcher who heads a sprawling complex of labs and monkey habitats in the Maryland countryside—the National Institutes of Health’s Laboratory of Comparative Ethology. For 41 years, first at the University of Wisconsin and then, beginning in 1983, in the Maryland lab the NIH built specifically for him, Suomi has been studying the roots of temperament and behavior in rhesus monkeys—which share about 95 percent of our DNA, a number exceeded only in apes. Rhesus monkeys differ from humans in obvious and fundamental ways. But their close resemblance to us in crucial social and genetic respects reveals much about the roots of our own behavior—and has helped give rise to the orchid hypothesis.
Suomi learned his trade as a student and protégé of, and then a direct successor to, Harry Harlow, one of the 20th century’s most influential and problematic behavioral scientists. When Harlow started his work, in the 1930s, the study of childhood development was dominated by a ruthlessly mechanistic behavioralism. The movement’s leading figure in the United States, John Watson, considered mother love “a dangerous instrument.” He urged parents to leave crying babies alone; to never hold them to give pleasure or comfort; and to kiss them only occasionally, on the forehead. Mothers were important less for their affection than as conditioners of behavior.
With a series of ingenious but sometimes disturbingly cruel experiments on monkeys, Harlow broke with this cool behavioralism. His most famous experiment showed that baby rhesus monkeys, raised alone or with same-age peers, preferred a foodless but fuzzy terrycloth surrogate “mother” over a wire-mesh version that freely dispensed meals. He showed that these infants desperately wanted to bond, and that depriving them of physical, emotional, and social attachment could create a near-paralyzing dysfunction. In the 1950s this work provided critical evidence for the emerging theory of infant attachment: a theory that, with its emphasis on rich, warm parent-child bonds and happy early experiences, still dominates child-development theory (and parenting books) today.
In the years since Suomi took over Harlow’s Wisconsin lab as a 28-year-old wunderkind, he has both broadened and sharpened the inquiry Harlow started. New tools now let Suomi examine not just his monkeys’ temperaments but also the physiological and genetic underpinnings of their behavior. His lab’s naturalistic environment allows him to focus not just on mother-child interactions but also on the family and social environments that shape and respond to the monkeys’ behavior. “Life in a rhesus-monkey colony is very, very complicated,” Suomi says. The monkeys must learn to navigate a social system that is highly nuanced and hierarchical. “Those who can manage this, do well,” Suomi told me. “Those who don’t, don’t.”
Rhesus monkeys typically mature at about four or five years and live to about 20 in the wild. Their development parallels our own at a fairly neat 1-to-4 ratio: a 1-year-old monkey is much like a 4-year-old human being, a 4-year-old monkey is like a 16-year-old human being, and so on. A mother typically gives birth annually, starting at around age 4. Though the monkeys copulate all year, the females’ fertility seasons are only a couple of months long. Since they tend to occur together, a troop usually produces crops of babies that have same-age peers.
For the first month, the mother keeps the baby attached to her or within arm’s reach. At about two weeks, the baby starts to explore, at first within only a few feet of its mother. These forays grow in frequency, duration, and distance over the next six to seven months, but rarely do the babies pass out of the mother’s sight line or earshot. If the young monkey gets frightened, it scampers back to the mother. Often she’ll see trouble coming and pull the infant close.
When the monkey is about eight months old—a rhesus preschooler—its mother’s mating time arrives. Anticipating another child, the mother allows the youngster to spend more and more time with its cousins, with older siblings in the maternal line, and with occasional visitors from other families or troops. The youngster’s family group, friends, and allies still provide protection when necessary.
A maturing female will stay with this group all her life. A male, however, will leave—often under pressure from the females as he gets rowdier and rougher—when he’s 4 or 5, or roughly the equivalent of a 16-to-20-year-old person. At first he’ll join an all-male gang that lives more or less separately. After a few months to a year, he’ll leave the gang and try to charm, push, or sidle his way into a new family or troop. If he succeeds, he becomes one of several adult males to serve as mate, companion, and muscle for the several females. But only about half the males make it that far. Their transition period exposes them to attacks from other young males, attacks from rival gangs, attacks from new troop members if they play their cards wrong, and predation during any time they lack a gang’s or troop’s protection. Many die in the transition.
Very early in his work, Suomi identified two types of monkeys that had trouble managing these relations. One type, which Suomi calls a “depressed” or “neurotic” monkey, accounted for about 20 percent of each generation. These monkeys are slow to leave their mothers’ sides when young. As adults they remain tentative, withdrawn, and anxious. They form fewer bonds and alliances than other monkeys do.
The other type, generally male, is what Suomi calls a “bully”: an unusually and indiscriminately aggressive monkey. These monkeys accounted for 5 to 10 percent of each generation. “Rhesus monkeys are fairly aggressive in general, even when young,” Suomi says, “and their play involves a lot of rough-and-tumble. But usually no one gets hurt—except with these guys. They do stupid things most other monkeys know not to. They repeatedly confront dominant monkeys. They get between moms and their kids. They don’t know how to calibrate their aggression, and they don’t know how to read signs they should back off. Their conflicts tend to always escalate.” These bullies also score poorly in tests of monkey self-control. For instance, in a “cocktail hour” test that Suomi sometimes uses, monkeys get unrestricted access to a neutral-tasting alcoholic drink for an hour. Most monkeys have three or four drinks and then stop. The bullies, Suomi says, “drink until they drop.”
The neurotics and the bullies meet quite different fates. The neurotics mature late but do okay. The females become jumpy mothers, but how their children turn out depends on the environment in which the mothers raise them. If it’s secure, they become more or less normal; if it’s insecure, they become jumpy too. The males, meanwhile, stay within their mothers’ family circles an unusually long time—up to eight years. They’re allowed to do so because they don’t make trouble. And their longer stay lets them acquire enough social savvy and diplomatic deference so that when they leave, they usually work their way into new troops more successfully than do males who break away younger. They don’t get to mate as prolifically as more confident, more assertive males do; they seldom rise high in their new troops; and their low status can put them at risk in conflicts. But they’re less likely to die trying to get in the door. They usually survive and pass on their genes.
The bullies fare much worse. Even as babies and youths, they seldom make friends. And by the time they’re 2 or 3, their extreme aggression leads the troop’s females to simply run them out, by group force if necessary. Then the male gangs reject them, as do other troops. Isolated, most of them die before reaching adulthood. Few mate.
Suomi saw early on that each of these monkey types tended to come from a particular type of mother. Bullies came from harsh, censorious mothers who restrained their children from socializing. Anxious monkeys came from anxious, withdrawn, distracted mothers. The heritages were pretty clear-cut. But how much of these different personality types passed through genes, and how much derived from the manner in which the monkeys were raised?
To find out, Suomi split the variables. He took nervous infants of nervous mothers—babies who in standardized newborn testing were already jumpy themselves—and gave them to especially nurturing “supermoms.” These babies turned out very close to normal. Meanwhile, Dario Maestripieri of the University of Chicago took secure, high-scoring infants from secure, nurturing mothers and had them raised by abusive mothers. This setting produced nervous monkeys.
The lesson seemed clear. Genes played a role—but environment [played an equally important ]one. |
|