Orientation
A gene does not fire until something happens to the person carrying it. Caspi and colleagues, in the study that reshaped attachment research as read by John Bowlby’s later interpreters, found that only carriers of the short allele in the serotonin transporter system became vulnerable to depression under adverse conditions: the polymorphism was a lock, not a verdict, waiting on an environmental key. Francine Shapiro makes the same point clinically, insisting that a genetic predisposition to addiction still requires a triggering life event to become a pattern, and that its presence complicates recovery without foreclosing it. Kenneth Blum treats the inheritance more literally, describing children born with polygenic vulnerability to reward deficiency syndrome and ADHD, a baseline the clinician must acknowledge rather than argue away. Gabor Mate supplies the counterweight, dismantling the “alcoholism gene” narrative that researchers themselves allowed to circulate, and arguing that adoption studies mistake prenatal environmental exposure for pure heredity. Ruth Lanius’s edited volume names the synthesis the field increasingly favors: the diathesis-stress model, in which early-life stress activates or silences genetic vulnerability rather than standing apart from it. Predisposition, on this reading, is a probability distribution, not a sentence.
