"It seems to be hard to get the female nature and the hard-driving brain working in synch. So lots of their energy gets spent in various war-with-myself campaigns." 
 
EW: 
You addressed his hypothesis with a single anecdote (his guess). If you weren't trying to say something about his hypothesis why would anyone care that you had no war with yourself?

"Interesting link on gene expression evolution being a stochastic process. I wonder if many regulatory processes simultaneously undergoing change through random mutations and filtered by selection could produce a stochastic process?" 
 
Ah, now we're talking... This reminds me of a fascinating, but apparently largely unknown paper by J.H. Gillespie on 'genetic draft'. The implication being that strong, sustained selection throughout the geome could potentially create a clock-like and stochastic signature: 
 
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T39-42696YM-3&_coverDate=12%2F30%2F2000&_alid=298874273&_rdoc=1&_fmt=&_orig=search&_qd=1&_cdi=4941&_sort=d&view=c&_acct=C000022659&_version=1&_urlVersion=0&_userid=501045&md5=4a37c88ec68fe88749b8baac5389946b

http://www.journals.uchicago.edu/AJHG/journal/issues/v77n1/42172/42172.html 
 
wrt to population differences, they find: 
 
African-descent populations have higher average CRP levels than do European-descent populations (Wener et al. 2000), although there is broad overlap in the range of levels across ethnic groups. Self-reported ethnicity in the United States is also associated with differences in morbidity and mortality from CVD and metabolic diseases, for a variety of medical, social, behavioral, and economic reasons (Watkins 2004). Thus, the genetic portion of the interethnic variance appeared to be attributable to frequency differences at three CRP SNPs (790, 1440, and 2667), in which the allele associated with lower CRP levels (790A, 1440C, and 2667C) was more frequent in EAs than in AAs. These results confirm recent observations that metabolic factors such as obesity account for a large portion of the variation in CRP levels associated with race/ethnicity (Albert et al. 2004; Anand et al. 2004) and suggest that the majority of the remaining variation in CRP levels associated with race/ethnicity in young adults is accounted for by genetic variants within the CRP locus.

Ok, I accept these " very subtle differences", but I do not agree with: 
 
" ...they will be very hard to identify against the background noise." 
 
Very subtle differences like a single nucleotide polymorphism explain behavioural differences between humans: 
 
"The temperamental predisposition of the subjects had a significant correlation with brain activity in the C/C group." 
 
http://www.jneurosci.org/cgi/content/abstract/25/27/6460 
 
" Geneticists identify 'master switch' that causes female flies to behave like males" 
 
http://hum-molgen.org/NewsGen/06-2005/msg44.html 
 
This is about complex gene-regulatory pathways: 
 
http://genomebiology.com/2005/6/7/r62/abstract 
 
An example of molecular switch for behavioral abnormalities : 
 
http://www.pnas.org/cgi/content/abstract/98/20/11042 
 
A good question for all us: How do you harmonize this  
 
"recent work has found no evidence of DRAMATIC gene expression differences between, say, human and chimp" 
 
with this: 
 
"Eighty percent of proteins are different between humans and chimpanzees" ? :-o

damn you to hell old school!

sequence changes 
 
well, there are different types. ie; repeats increasing dosage.