Free Savage Spawn by Jonathan Kellerman Page B

science research. But what looks like incontrovertible science often turns out to be no more than supposition and guesswork overlaid with a veneer of quantitative data. Just as is true of its softer cousin, “hard” science is profoundly vulnerable to the value judgments and prejudices of its all-too-fallible practitioners. The same methodological problems that often scrape the blush from the first fruits of social science data can apply equally to biological studies. Cautions such as our old friend
Correlation ain’t necessarily causation
are just as valid.
    Nevertheless, nearly five decades of research on the biological aspects of psychopathy and criminality have produced some provocative data that deserve to be addressed.
    And though we must examine biological data critically, we needn’t be scared off by some brave-new-world threat of genetic determinism, because while some biological phenomena are genetically based,
many others are not.
    In fact, the distinction between genetics and biology is a prime example of the correlation/causation caveat appropriately applied: Simply because something manifests itself on a cellular, hormonal, or biochemical level does not mean its
origins
are based in inborn cellular, hormonal, or biochemical processes.
    Put simply, biology modifies environment, but environment also modifies biology.
    Consider the example of identical (monozygotic) twins—pairs of siblings endowed with identical DNA. Most identical twins resemble each other strongly, yet individual sets of twins differ greatly in their degree of identicality. Some are almost completely identical, while others display significant physical and behavioral differences. Most important,
no identical twins are absolute carbon copies of each other.
    I am personally familiar with identical twins, young women, one of whom is two inches taller than her sister. Height is to a great extent determined by genes, but even here the causal pathway is clearly not 100 percent genetic.
    What nongenetic (but biological) factors might have played a role in the two-inch discrepancy? Perhaps as fetuses these women underwent specific intrauterine experiences that affected their respective heights, with one twin lucking into a superior position within the womb—a literal upper hand—that provided her with the lion’s share of placental nutrition and movement, simultaneously restricting her sibling’s snacks and aerobic exercise. Or maybe postnatal experiences, such as illness and injury, intervened.
    We needn’t limit ourselves to twins when searching for examples of the discontinuity between biological and genetic causality. Average heights and weights of Japanese citizens and those of other developing nations increased significantly following World War II, due to changes in nutrition.
    With regard to children, a variety of prenatal insults that have nothing to do with chromosomes can strongly affect growth and subsequent development. Youngsters exposed to maternal malnutrition and injury, as well as to alcohol, tobacco, and other toxins, are more likely to evince brain damage, birth defects, learning problems—and antisocial behavior—than are nonpoisoned controls. The same goes for birth complications, prematurity, and postnatal damage, such as poisoning by lead chips in old paint, head trauma, infections, and recurrent fevers.
    Several studies of child and adult murderers indicate high rates of brain damage as measured by learning disabilities, attention deficit, school problems, EEG (brain wave) measurement, and low IQ, but whether or not any of these deficits is genetic is unclear (9–13, 46). In some cases, such as documented episodes of cranial injury, they certainly are not. And given strong evidence that many psychopaths and criminals are more likely to be abused, it’s not much of a stretch to connect early maltreatment, such as kicks to the head, to environmentally caused brain