Submitted by godlesscapitalist (not verified) on Sun, 2006-08-13 15:31.

When an advantaged group of people calls a disadvantaged group innately less able, you must forgive the disadvantaged folks if they try to defend themselves.

First, the debate here is about the facts -- and the facts are not determined by who is advocating them, but by reality.

Second, in academia the disadvantaged are those who have the courage to speak out against biology denial. Very few people in academia have the courage to speak out when senior faculty monolithically condemn the positions of Summers, Pinker, and even Lawrence. Even those with tenure figure it's just not worth it to be attacked --- as they were in your article, which denounced the very idea of free speech as "verbal violence".

Fortunately we have the internet, the last refuge of anonymous free speech -- and we can use it to point out some important papers on sex differences on the brain. Here's just a sample of a voluminous literature:

Sexually dimorphic gene expression in mouse brain precedes gonadal differentiation.

* Dewing P,
* Shi T,
* Horvath S,
* Vilain E.

Department of Human Genetics, University of California, Los Angeles, CA 90095, USA.

The classic view of brain sexual differentiation and behavior is that gonadal steroid hormones act directly to promote sex differences in neural and behavioral development. In particular, the actions of testosterone and its metabolites induce a masculine pattern of brain development, while inhibiting feminine neural and behavioral patterns of differentiation. However, recent evidence indicates that gonadal hormones may not solely be responsible for sex differences in brain development and behavior between males and females. Here we examine an alternative hypothesis that genes, by directly inducing sexually dimorphic patterns of neural development, can influence the sexual differences between male and female brains. Using microarrays and RT-PCR, we have detected over 50 candidate genes for differential sex expression, and confirmed at least seven murine genes which show differential expression between the developing brains of male and female mice at stage 10.5 days post coitum (dpc), before any gonadal hormone influence. The identification of genes differentially expressed between male and female brains prior to gonadal formation suggests that genetic factors may have roles in influencing brain sexual differentiation.

Positron Emission Tomography with [18F]deoxyglucose was used to compare brain activation in men and women while they performed mathematical reasoning.
Right greater than left-hemisphere activation was predicted, especially in temporal lobes. Forty-four participants were selected and matched for high or average Scholastic Aptitude Test-Math scores. There were no sex differences in cortical glucose metabolic rate (GMR). However, GMR in temporal lobe regions was positively correlated with math reasoning score in men but not in women. The temporal lobes, bilaterally, are implicated in math reasoning ability for men; no specific cortical areas were related to math reasoning performance in women.

Gender and parental status affect the visual cortical response to infant facial expression.

* Proverbio AM,
* Valentina B,
* Matarazzo S,
* Del Zotto M,
* Zani A.

Department of Psychology, University of Milano-Bicocca, Viale dell'Innovazione 10, 20126 Milan, Italy; Institute of Molecular Bioimaging and Physiology, National Research Council (CNR), Segrate-Milan, Italy.

This study sought to determine the influence of gender and parental status on the brain potentials elicited by viewing infant facial expressions. We used ERP recording during a judgement task of infant happy/distressed expression to investigate if viewer gender or parental status affects the visual cortical response at various stages of perceptual processing. ERPs were recorded in 38 adults (male/female, parents/non-parents) during processing of infant facial expressions that varied in valence and intensity. All infants were unfamiliar to viewers. The lateral occipital P110 response was much larger in women than in men, regardless of facial expression, thus indicating a gender difference in early visual processing. The occipitotemporal N160 response provided the first evidence of discrimination of expressions of discomfort and distress and demonstrated a significant gender difference within the parent group, thus suggesting a strong interactive influence of genetic predisposition and parental status on the responsivity of visual brain areas. The N245 component exhibited complete coding of the intensity of facial expression, including positive expressions. At this processing stage the cerebral responses of female and male non-parents were significantly smaller than those of parents and insensitive to differences in the intensity of infant suffering. Smaller P300 amplitudes were elicited in mothers versus fathers, especially with infant expressions of suffering. No major group differences were observed in cerebral responses to happy or comfortable expressions. These findings suggest that mere familiarity with infant faces does not explain group differences.

Gender differences in the neural correlates of response inhibition during a stop signal task.

* Li CS,
* Huang C,
* Constable RT,
* Sinha R.

Department of Psychiatry, Yale University, New Haven, CT 06519, USA.

We used functional magnetic resonance imaging to examine gender differences in the neural correlates of response inhibition during a stop signal task. The task has a frequent "go" signal to set up a pre-potent response tendency and a less frequent "stop" signal for subjects to withhold their response. A contrast in brain activation was made between successful and failed inhibitions for individual subjects. We compared 20 men and 20 women matched in age and years of education and in stop signal performance, with stop success rate, post-error slowing and task-related frustration ratings as covariates. The results showed greater activation in men, compared to women, in a wide array of cortical and subcortical areas, including the globus pallidus and motor thalamus during stop signal inhibition. In contrast, no brain regions demonstrated greater activation in women, even at a lower statistical threshold. Moreover, while men activated the medial superior frontal and anterior cingulate cortices, women activated the caudate tail to mediate response inhibition. These results extended gender differences in regional brain activation to response inhibition during a cognitive motor task. Men activated the motor circuitry while women appeared to involve visual association or habit learning during stop signal performance.

Gender differences in neurological disease: role of estrogens and cytokines.

* Czlonkowska A,
* Ciesielska A,
* Gromadzka G,
* Kurkowska-Jastrzebska I.

Institute of Psychiatry and Neurology, Second Department of Neurology, Warsaw, Poland. czlonkow@ipin.edu.pl

Increasing evidence suggests that inflammatory response may be a critical component of different brain pathologies. However, the role played by this reaction is not fully understood. The present findings suggest that neuroinflammtory mediators such as cytokines may be involved in a number of key steps in the pathological cascade of events leading to neuronal injury. This hypothesis is strongly supported by experimental and clinical observations indicating that inhibition of the inflammatory reaction correlates with less neuronal damage. Estrogens are thought to play a role in the sex difference observed in many neurological diseases with inflammatory components including stroke, Alzheimer's and Parkinson's diseases, multiple sclerosis, or amyotrophic lateral sclerosis. Clinical and experimental studies have established estrogen as a neuroprotective hormone in these diseases. However, the exact mechanisms involved in the neuroprotective effects of estrogens are still unclear. It is possible that the beneficial effects of these hormones may be dependent on their inhibitory activity on the inflammatory reaction associated with the above-mentioned brain pathologies. Here, we review the current clinical and experimental evidence with respect to the inflammation-modulating effects of estrogens as one potential explanatory factor for sexual dimorzphism in the prevalence of numerous neurological diseases.

Blueprints for behavior: genetic specification of neural circuitry for innate behaviors.

* Manoli DS,
* Meissner GW,
* Baker BS.

Medical Scientist Training Program, Neurosciences Program and Department of Biological Sciences, Stanford University, Stanford, CA 94305-5020, USA.

Innate behaviors offer a unique opportunity to use genetic analysis to dissect and characterize the neural substrates of complex behavioral programs. Courtship in Drosophila involves a complex series of stereotyped behaviors that include numerous exchanges of multimodal sensory information over time. As we will discuss in this review, recent work has demonstrated that male-specific expression of Fruitless transcription factors (Fru(M) proteins) is necessary and sufficient to confer the potential for male courtship behaviors. Fru(M) factors program neurons of the male central and peripheral nervous systems whose function is dedicated to sexual behaviors. This circuitry seems to integrate sensory information to define behavioral states and regulate conserved neural elements for sex-specific behavioral output. The principles that govern the circuitry specified by Fru(M) expression might also operate in subcortical networks that govern innate behaviors in mammals.

So, to recap: we know that sex differences impact mammalian brains well before puberty. We know that in humans, they predict all kinds of neurological differences, from responses to the presence of a baby to differences in motor circuitry. We know that in other metazoans we have manipulated the genetic determinants of sexual behavior. And we know that sex differences predict differences in spatial reasoning, differences which manifest themselves in MRI scans, differences known to *impact mathematical ability*.

It is this kind of evidence which was not addressed in your article in Nature.


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