Jensen and genetic amplification

a devil, a born devil on whose nature nurture can never stick — The Tempest Act IV, Scene I

Prior, I posted about genetic amplification versus gene-environment correlation models (it’s a somewhat muddled post that I haven’t got around to revisiting). Jensen’s theory of intelligence is a good example of the former:

Each individual comes into the world possessing all of the de facto and potential behavioral variance that exists in any large population in the world. This latent matrix consists entirely of the genetic and extra genetic material composing the still developing organism, i.e., the individual human being. Included in this developmental process are the roots of the behavior that becomes recognized as psychometrc intelligence, specifically the g factor. Information gained through sensory contact with the environment is processed and brought to bear on further sensorimotor exploration of the surrounding environmental stimulation. The rate and asymptote of mentaldevelopment are conditioned by genetic factors which account for an estimated 70 to 80% of the total population variance in psychometric g.

The chief agency for this development is the degree of the individual’s sensory contact with the environment, which in turn depends on the individual’s neural oscillation rate, OsR. The more advantaged individuals in this respect are those with higher OsR rates, as it governs the over-all rate of environmental influence. These predictions are borne out in several chronometric and psychometric experiments (Jensen, 2006, Chapters. 6 & 9). The well-established correlations between digit span memory, RT, and IQ fall under the same causal rubric.

Compare this with the models Tucker-Drob and Harden (2011) discuss.

By the genetic amplification model, differences in the capacity to process sensory information lead to differences in the amount of information processed, which leads to differences in the amount of further sensory information that can be contacted and processed and so on. By the gene-environment model, differences in disposition or slight initial differences lead to compounding environmental re-enforcements. There’s a subtle — or not so — but important difference. Imagine two students: one bright and one dull. By the former model, the bight student is bright because he was able to process information quicker (he’s bright, not dull), which led to him being given more information. By the latter model the bright student is bright because he had a propensity for seeking out information or because an initial advantage (e.g. he was a little more inquisitive) led to a cycle of him being given more information; by this latter model, if the dull student is just pushed in the right direction or given compensatory attention, he’ll shine like a LED bulb. The genetic amplification versus gene-environment correlation debate is effectively another nature-nurture debate; it’s just taking place within the behavior genetic framework. Of course, the sociopolitical implications are a little different this time as someone over at gene expression discussed a while ago:

This is where a pure social constructionist and someone who acknowledges the salience of gene-environment interaction [note: this should be correlations; g x e interactions are not the same as g-correlations] part ways. To a social constructionist once the social system is transformed it can perpetuate itself, just like the previous social system did. Remediation is necessary only to flip the system into another equilibrium (that is, nature does not load the die in any particular direction). On the other hand, if you accept gene-environment interaction, the genetic variation remains, the correlations are simply being dampened by social factors. If those incentives toward equalization and homogenization were removed, then the active correlations at least might start to work their way back into the equation. For example, if “problem” students were not proactively targeted, nurtured, cajoled and guided, they would be more likely to follow a different path than the students for whom schoolwork came naturally. This would likely result in the reemergence of passive and evocative correlations in the next generation. Soon enough all the gene-environment correlations would be salient once more. If you attempt to emphasize gene-environment correlation to explain great phenotypic variation, you must also acknowledge that it is likely that societal remediation or dampening of such correlations must be perpetuated indefintely.

Nature and a one time radical social re-engineering doesn’t sound so bad, does it?

References

Jensen, 2011. The theory of intelligence and its measurement

Tucker-Drob and Harden 2011, Intellectual Interest Mediates Gene-by-SES Interaction on Adolescent Academic Achievement

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