No god, and no "god gene", either
John Quiggin is picking on those poor evolutionary psychologists, as represented by Kristof's laughable opinion piece on the "God Gene". Quiggin hits on the usual deficits of EP: the evidence-free just-so stories, the unrealistic time-scales, the reduction of the complex to the simple, the superficial and endlessly flexible definitions of the phenomena they are addressing, etc. I agree completely with him, these are flaws in the evolutionary psychology research program. I have another gripe to add to the list, my main reason I reject evolutionary psychology and that whole line of tripe about genes "for" various things.
It's nothing but modern molecular preformationism. Palmistry for the genome. We've been fighting against this simplistic notion of the whole of the organism prefigured in a plan or in toto in the embryo since Socrates, and it keeps coming back. We've moved from imagining a little homunculus lurking in the sperm to one hiding in the genome. It's just not there. You can't point to a spot on a chromosome and say, "there's the little guy's finger!", nor can you point to a spot and say, "there's his fondness for football!".
Kristof, for instance, points to a particular gene as the source of piety. Piffle. Here's his shining locus of sacredness, VMAT2:
The vesicular monoamine transporter acts to accumulate cytosolic monoamines into synaptic vesicles, using the proton gradient maintained across the synaptic vesicular membrane. Its proper function is essential to the correct activity of the monoaminergic systems that have been implicated in several human neuropsychiatric disorders. The transporter is a site of action of important drugs, including reserpine and tetrabenazine. Liu et al. (1992) and Erickson et al. (1992) investigated cDNAs encoding the synaptic vesicular monoamine transporter in rat brain. Using sequences from rat brain SVMT, Surratt et al. (1993) identified the human homolog. Human SVMT shares 92% amino acid identity with the rat sequence, but displays one less consensus site for asparagine N-linked glycosylation and one more consensus site for phosphorylation by protein kinase C. By Southern blotting analysis of human/rodent hybrid cell lines and fluorescence in situ hybridization, Surratt et al. (1993) mapped the human SVMT gene to 10q25. They also demonstrated a TaqI polymorphism that may prove useful in assessing the gene's involvement in neuropsychiatric disorders involving monoaminergic brain systems. Peter et al. (1993) likewise assigned the brain synaptic vesicle amine transporter gene to 10q25 using a panel of mouse/human hybrids and in situ hybridization.
It's a pump. A teeny-tiny pump responsible for packaging a neurotransmitter for export during brain activity. Yes, it's important, and it may even be active and necessary during higher order processing, like religious thought. But one thing it isn't is a "god gene."
The whole genome is like that. Browse VMAT2's neighborhood, for instance, and you won't find "philoprogenetiveness," "benevolence," and "chastity" marked out on the long arm of chromosome 10. This is what you see:
|10q25||SLC18A2, VAT2, SVMT||Solute carrier family 18 (vesicular monoamine), member 2|
|10q25-q26||ACADSB||Acyl-Coenzyme A dehydrogenase, short/branched chain|
|10q25-q26||PRDX3, AOP1||Peroxiredoxin 3 (antioxidant protein 1)|
|10q25-qter||MKI67||Proliferation-related Ki-67 antigen|
|10q25.1||NEURL||Neuralized, Drosophila, homolog-like|
|10q25.1-q25.2||CASP7, MCH3||Caspase 7, apoptosis-related cysteine protease|
|10q25.1-q25.2||FACL5, ACS5||Fatty acid CoA ligase, long-chain 5|
|10q25.2-q26||DPYSL4, CRMP3, ULIP4||Dihydropyrimidinase-like 4|
|10q25.2-q26.3||HMX2||Homeo box (H6 family) 2|
|10q25.2-q26.3||UROS||Uroporphyrinogen III synthase|
|10q25.3||PGAM1||Phosphoglycerate mutase A, nonmuscle form|
|10q25.3||TCF7L2, TCF4||Transcription factor 7-like 2|
|10q25.3||XPNPEP1, SAMP, XPNPEPL||X-prolyl aminopeptidase P1|
|10q25.3-q26||GPR10||G protein-coupled receptor-10|
It's like browsing through a Mouser electronics catalog—lots and lots of parts and pieces, but thin on the interesting bits about how you put them together to create a useful apparatus. That information is all buried in the regulatory sequences that surround each gene, in the affinities for transcription factors for particular sequences of DNA, in the molecular interactions between proteins, in the pattern of environmental input to embryo and adult, and in the whole unmapped history of the organism. VMAT2 isn't the answer, it's one among many parameters. And I think it's damaging to our understanding of real biology when we have facile scryers like Kristof and Hamer and Pinker coming along and telling us silly stories rather than focusing our attention on the real and fascinating complexity of the process…although it's probably good for their careers. There'll always be a market for easy explanations, even if they are wrong.
For those readers whose eyes glaze over at biology, here's a simpler analogy. Imagine you want to format a paragraph in Microsoft Word, and the helpful tech guy comes over, pops the top on your computer, and tells you that that yellow wire over in the corner is responsible for paragraph formatting. Would you believe him? Has he helped you solve your problem? Has he even touched on your software issues? Would you even believe him if he yanked out the wire and MS Word instantly crashed? That's how I feel about evolutionary psychology: it's a field asking the wrong questions, using the wrong methods, propagating misleading myths, and doing more harm than good.