The Extended Phenotype: The Long Reach of the Gene (Popular Science) Read Online Free PDF

something determines something? Philosophers, possibly with justification, make heavy weather of the concept of causation, but to a working biologist causation is a rather simple statistical concept. Operationally we can never demonstrate that a particular observed event C caused a particular result R, although it will often be judged highly likely. What biologists in practice usually do is to establish
statistically
that events of class R reliably follow events of class C. They need a number of paired instances of the two classes of events in order to do so: one anecdote is not enough.
    Even the observation that R events reliably tend to follow C events after a relatively fixed time interval provides only a working hypothesis that C events cause R events. The hypothesis is confirmed, within the limits of the statistical method, only if the C events are delivered by an
experimenter
ratherthan simply noted by an observer, and are still reliably followed by R events. It is not necessary that every C should be followed by an R, nor that every R should be preceded by a C (who has not had to contend with arguments such as ‘smoking cannot cause lung cancer, because I knew a non-smoker who died of it, and a heavy smoker who is still going strong at ninety’?). Statistical methods are designed to help us assess, to any specified level of probabilistic confidence, whether the results we obtain really indicate a causal relationship.
    If, then, it were true that the possession of a Y chromosome had a causal influence on, say, musical ability or fondness for knitting, what would this mean? It would mean that, in some specified population and in some specified environment, an observer in possession of information about an individual’s sex would be able to make a statistically more accurate prediction as to the person’s musical ability than an observer ignorant of the person’s sex. The emphasis is on the word ‘statistically’, and let us throw in an ‘other things being equal’ for good measure. The observer might be provided with some additional information, say on the person’s education or upbringing, which would lead him to revise, or even reverse, his prediction based on sex. If females are statistically more likely than males to enjoy knitting, this does not mean that all females enjoy knitting, nor even that a majority do.
    It is also fully compatible with the view that the reason females enjoy knitting is that society brings them up to enjoy knitting. If society systematically trains children without penises to knit and play with dolls, and trains children with penises to play with guns and toy soldiers, any resulting differences in male and female preferences are strictly speaking genetically determined differences! They are determined, through the medium of societal custom, by the fact of possession or non-possession of a penis, and that is determined (in a normal environment and in the absence of ingenious plastic surgery or hormone therapy) by sex chromosomes.
    Obviously, on this view, if we experimentally brought up a sample of boys to play with dolls and a sample of girls to play with guns, we would expect easily to reverse the normal preferences. This might be an interesting experiment to do, for the result just might turn out to be that girls
still
prefer dolls and boys still prefer guns. If so, this might tell us something about the tenacity, in the face of a
particular
environmental manipulation, of a genetic difference. But all genetic causes have to work in the context of an environment of some kind. If a genetic sex difference makes itself felt through the medium of a sex-biased education system, it is still a genetic difference. If it makes itself felt through some other medium, such that manipulations of the education system do not perturb it, it is, in principle, no more and no less a genetic difference than in the former, education-sensitive case: no doubt some other environmental manipulation could