(prepared 14 June 2009 by John Jacob Lyons)
The ‘Baldwin Effect’ has been defined as an adaptive trait change in an organism – that occurs as a result of its interaction with its environment- becoming gradually assimilated into its developmental genetic/ epigenetic repertoire. My ‘genetic priming’ hypothesis seeks to clarify the process involved in the Baldwin Effect and to correct several points in the definition above that relate to the effect of this process.
The process consists of an inter-generational positive feedback loop between the adaptive trait and the positively and causally correlated subset of the genome that tends to support the trait. This is described in greater detail in my article in the ‘Evolving Ideas’ blog. As stated there, selective pressure will result in the manifestation of the trait earlier and earlier in the development of the organism.
However, the adaptive trait will never be “ – assimilated into its developmental genetic/ epigenetic repertoire.” What will happen is that selective pressure will result in the allele-configuration of the relevant subset of genes ‘trying’ to change in order to optimize the support given to the trait. In doing so, it may well be in competition with other adaptive traits ‘trying’ to optimize the subset to support them. This will obviously result in sub-optimization for any particular individual trait. The ultimate result will be that the genome will have been, within the aforementioned constraint, primed to support the manifestation of the original adaptive trait. An example will make some of these points clear.
It is well known that, over the human EEA, post-weaning lactose tolerance developed in temperate regions in which cattle were farmed. In this case, the adaptive trait was milk consumption (Vitamin D enables absorption of calcium; particularly adaptive in temperate regions) and the correlated subset of the genome was that involved in controlling lactose tolerance. The positive feedback explained above has resulted, in these regions, in the ubiquitous priming of the human genome toward post-weaning lactose tolerance and not in a genetically assimilated tendency to consume milk! There has been no assimilation of the adaptive behaviour; only genetic priming of the associated subset of the genome.
I suggest that, subject also to many relevant cultural evolutionary factors of course, humans have been genetically primed for language, religiosity, morality and love/ attachment/ empathy in a similar way.
Evolving Ideas 
To the extent that selection is effective we might expect a large number of traits to be aptations – as opposed to adaptations I agree. But I would strengthen the negative side of the argument – I think selection is inefficient for many reasons two of which you hint at: 1. antagonistic epistasis (or perhaps you mean divergent selection), 2. higher-level dynamics – to these we might add: 3. small population size/small selection coefficient (linked concepts), 4. spatial structure with interbreeding. I think that many aspects of human behaviour may be best thought of as (often composite) byproducts also – so that thinking of these often complex suites of characters as adaptations per se is incorrect, but optimising the genome for them may also be unlikely given their complexity and the complexity of the situation in general.
On a semantic note, it strikes me that this argument bears some relation to the “genes for” discussion in Dawkins’ Selfish Gene. Very few relevant traits, beyond polypeptide sequences, can be said to be directly encoded by any gene or combination of genes. Interactionism is a given so I would say that priming is rather a way of describing selection that is sensitive to this fact.