David Dobbs explains the orchid hypothesis:
Though this hypothesis is new to modern biological psychiatry, it can be found in folk wisdom, as the University of Arizona developmental psychologist Bruce Ellis and the University of British Columbia developmental pediatrician W. Thomas Boyce pointed out last year in the journal Current Directions in Psychological Science. The Swedes, Ellis and Boyce noted in an essay titled “Biological Sensitivity to Context,” have long spoken of “dandelion” children. These dandelion children — equivalent to our “normal” or “healthy” children, with “resilient” genes — do pretty well almost anywhere, whether raised in the equivalent of a sidewalk crack or a well-tended garden. Ellis and Boyce offer that there are also “orchid” children, who will wilt if ignored or maltreated but bloom spectacularly with greenhouse care.
Bakermans-Kranenburg and her colleague Marinus van Ijzendoorn began to study the genetic makeup of the children in their experiment on problem children exhibiting “externalizing” behaviors — whining, screaming, throwing tantrums, etc.:
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. 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, 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 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.
(Hat tip to Steve Sailer, who asks, Was Genghis Khan a dandelion or an orchid?)