Didn’t read the article, but at least based on the excerpts, it sounds like many of these are pretty common misunderstandings of evopsych. E.g.
(2) “Neuroscientists have been aware since the 1980s that the human brain has too much architectural complexity for it to be plausible that genes specify its wiring in detail,”
In considering the issue of a gene shortage, it is important to
distinguish between architectural modularity and developmental
modularity. As discussed in the evolutionary developmental biology literature, an aspect of the phenotype is developmentally
modular to the degree that natural selection can act on it independent
of other aspects of the phenotype (e.g., Griffiths, in press;
Riedl, 1978; Schlosser & Wagner, 2004; Wagner & Altenberg,
1996). Architectural modularity refers to the endpoints of development—the
degree to which the phenotype is “chunked” into
functional components (e.g., Sperber, 2002). A single developmentally
modular process can give rise to multiple architectural
modules. For example, the process that produces hair follicles is
presumably at least somewhat developmentally modular, yet it
produces many millions of individual architectural modules in the
form of individual hair follicles.
Does this apply to cognition? Module-like representational
structures for face recognition are probably constructed for each
face one can reliably recognize even though there are obviously no
separate genes for recognizing each one. Architecturally modular
novel tokens no more undermine developmental modularity than
do novel tokens in other domains. The human immune system
generates novel responses to parasites all the time (see, e.g.,
West-Eberhard, 2003, p. 58), yet no one seems to question whether
there are sufficient genes to explain this process. Further, as
discussed above, “high-level” modular architectures, such as the
cognitive structures underlying chess skill, are probably tokens of
module-generating developmental processes designed for other
functions. The inference that such systems “cannot be based on a
Darwinian algorithm” (Sterelny & Griffiths, 1999, p. 330) is
unlicensed. Critics of massive modularity must articulate why
novel cognitive tokens are more problematic than novel tokens
elsewhere in the phenotype.
Further, developmental processes that give rise to distinct phenotypic
structures in the brain presumably share many procedures
in common as well as many of their necessary genes (i.e., genes
that contribute causally to the development of the structure). Many
developmental processes exhibit a nested hierarchical structure:
They share common beginning points, with bifurcation or decision
points during the process as structures become differentiated from
one another and are more precisely specified (Gilbert, Opitz, &
Raff, 1996; Riedl, 1978; see especially chap. 4 of West-Eberhard,
2003). Large numbers of modules in the brain might begin from a
common starting point, and share many of the processes that build
them, the more so the earlier one looks in development. This is a
common pattern for evolved developmental systems in general
(West-Eberhard, 2003). Subsequently, regulatory processes cause
structures to diverge in their development, mediated by inputs
from the internal or external world. In fact, different environments
might cause different structures to develop by design (because of
a history of selection for that outcome) even if there is complete
overlap in the genes responsible for the development of the two
different structures. [...]
Therefore, the answer to the question “Does each module need
‘its own’ set of dedicated genes?” is no: Finding genes responsible
for building that module and only that module is unlikely. Consider
the genes “for” (in the sense of Dawkins, 1976) arms and
legs. The genes that play a causal role in building arms and in
building legs (as well as many other structures) overlap heavily.
The same logic applies to the construction of mental modules.
As another way of seeing this, if one tried to specify the number
of phenotypic details in the human body that reliably recur during
development because of a history of natural selection acting on
historically contingent developmental systems, one would certainly
find that the number is greater than 30,000, the approximate
number of genes in the human genome.6 That is, it would require
more than 30,000 parameters to specify the human phenotype in
blueprint or informational terms. If such a one-to-one mapping
were required, there probably wouldn’t be “enough genes” to build
a single cell in the human body (for a similar argument, see
Marcus, 2004).
Most of the other numbered points in the second list also seem to be based on similar misunderstandings/misrepresentations of the field.
A single developmentally modular process can give rise to multiple architectural modules.
To the extend that a single developmental modular process leads to multiple architectual modules, it’s a reasonable argument that it’s improper to analyse the evolutionary advantages of a single architectual module without knowing looking at the other achitectual modules that spring out of the same developmental modular process.
Didn’t read the article, but at least based on the excerpts, it sounds like many of these are pretty common misunderstandings of evopsych. E.g.
is quite weak, as discussed in Barrett & Kurzban 2006:
Most of the other numbered points in the second list also seem to be based on similar misunderstandings/misrepresentations of the field.
To the extend that a single developmental modular process leads to multiple architectual modules, it’s a reasonable argument that it’s improper to analyse the evolutionary advantages of a single architectual module without knowing looking at the other achitectual modules that spring out of the same developmental modular process.
That sounds like a much more reasonable criticism than the ones presented in the OP.