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‘Brain String Theory’, 2012. Jeremy Strain

InNeuroaesthetics is killing your soul(MUSE, March 2013), science writer Philip Ball argues that our artistic experience and understanding cannot ever be understood in terms of neurophysiological structure and function (i.e., mechanism). Ball claims that neuroscientific research on aesthetics (‘neuroaesthetics’) is wasteful, uninformative, and impossible.

Ball’s article on neuroaesthetics received two thoughtful and critical comments from Brad Foley and Dhalia Zaidel, with whom I entirely agree. In this post, I consider the thoughts that Ball expresses in this passage of the article:

“And what will a neuroaesthetic ‘explanation’ consist of anyway? Indications so far are that it may be along these lines: “Listening to music activates reward and pleasure circuits in brain regions such as the nucleus accumbens, ventral tegmental area and amygdala”. Thanks, but no, thanks. Although it is worth knowing that musical ‘chills’ are neurologically akin to the responses invoked by sex or drugs, an approach that cannot distinguish Bach from barbiturates is surely limited.

There are certain to be generalities in art and our response to it, and they can inform our artistic understanding and experience. But they will never wholly define or explain it”.

In the first paragraph of this passage, Ball objects to the alleged utility of neuroaesthetic explanations of artistic experience. By ‘utility’, I assume Ball means ‘being informative’. The sample neuroaesthetic explanation he gives is: “Listening to music activates reward and pleasure circuits in brain regions such as the nucleus accumbens, ventral tegmental area and amygdala”. Ball denies the utility of this type of explanation because it fails to inform of the actual difference, at the level of the brain, between equally pleasurable experiences as listening to Bach, taking barbiturates or having sex.

I want to make clear here two observations that are (implicitly, I think) backgrounded in Ball’s article. First, it is conceivable that stimulus-driven (external or internal) sensory experience may be subserved by an unconscious physical base with a specific neurophysiological signature. Explaining sensory experience in this direct way aims first to describe the base as a correlate of sensory experience, then ultimately to achieve a reductive neurophysiological explanation of sensory experience (Churchland, 2007; Churchland, 1989, 2002, 2011). Second, brain mechanism responses to stimuli can be correlated for a variety of reasons: (1) the mechanism is part of the cause of the stimulus-induced experience; (2) the mechanism is part of the effect of the experience; (3) the mechanism indirectly parallels the experience; (4) the mechanism is what the experience can be identified with (i.e., x = y) (Churchland, 2007; Churchland, 1989, 2002, 2011). Discovering the neurophysiological signature of aesthetic experience as a type of experience requires the identification of some neurophysiological mechanism with aesthetic experience.

Now, Ball’s sample neuroaesthetic explanation describes a correlation between listening to music and brain response, such as we typically find reported in neuroimaging studies in neuroscience using functional magnetic resonance imaging (fMRI). But, it is not clear which one of the four neuroscientific correlation types he designates in his sample. It would be ironic if the physical signature of aesthetic experience proves to be the very one Ball now denies as even being sufficiently informative. This is possible, but highly unlikely, since the signature will probably reveal a highly complex and interdependent nervous-endocrine-immune ensemble (compare Chapman et al. 2008). In any event, and to challenge Ball’s assertion to the contrary, the correlation of brain response x (e.g., concurrent activation in nucleus accumbens, ventral tegmental area, amygdala) with pleasure in music-listening is informative because x may be the one for identifying musical pleasure. Correspondingly, a brain response y hypothesized by neuroscientists that does not correlate with musical pleasure indicates that y may not be the one. It may turn out that listening to Bach and receiving fellatio do not share the same neural signature. At the end of the day, the implicit target in Ball’s article, and the hidden target of all those people who think as he, is the theoretical identification of aesthetic experience with mechanism (i.e., mind-brain identity theory). Mind-brain identity theory is a philosophy of mind. The identity theory of mind claims that states and processes of the mind are identical to states and processes of the brain (Place, 1956; Polger, 2004; Smart, 1959; van Rysewyk, 2013). If Ball and others surely wish to engage with neuroaesthetics at the intended level, they should acquire some expertise in philosophy of mind and philosophy of art.

In the second paragraph, Ball objects to the very possibility of a neuroaesthetic definition or explanation of artistic experience (“But they will never wholly define or explain it”). This is much stronger than the claim that neuroaesthetics is uninformative. According to Ball, a complete neuroaesethetics of artistic experience is impossible. My interpretation of Ball is speculative, since the reasons for his radical conclusion are not given in the article. And it is unclear exactly what he means by ‘wholly’. Presumably, by ‘wholly’, he means a complete and final neuroaesthetics of all aesthetic experience, irrespective of whether neuroaesthetists can formulate it. A significant casualty of Ball’s view is objective scientific explanation. Since Ball thinks a final scientific explanation of aesthetics is impossible, he is thereby commited to the view that there can be no final explanation of aesthetics which does not involve essential reference to personal opinions, experiences or points of view (i.e., a subjective explanation).

Ball does not explain why he thinks neuroaesthetics cannot ever explain or define aesthetics. I invite him to explain why. Otherwise, his article will come across as little more than a negative argument to the effect that the neuroaesthetic project will not succeed. In the meantime, I hope the following is helpful. As Churchland (1989, 2002, 2011) makes clear, explicit definitions and explanations of things tend to co-evolve in science, and emerge only quite late in the course of protracted scientific and philosophical investigations. Because neuroaesthetics is an extremely young subdiscipline of neuroscience (itself barely 60 years old), I think the prudent hope is for correlations of types (1), (2), (3), described above, to lead to novel hypothetical identities and more advanced experimental and philosophical investigation. Already, we know much more about aesthetic experience than even 5 years ago (Conway & Rehding, 2013). Ultimately, neuroaesthetics wants to produce fundamental scientific aesthetic identities; that is, robust correlations of type (4). Proximately, it is reasonable to set achievable aims. Still, the reality of the brain and body may yet thwart our best investigative attempts to identify artistic experience with neurophysiology.

References

Chapman, C. R., Tuckett, R. P., & Song, C. W. (2008). Pain and stress in a systems perspective: reciprocal neural, endocrine, and immune interactions. Journal of Pain 9: 122-145.

Churchland, P. M. (2007). Neurophilosophy at work. Cambridge, UK: Cambridge University Press.

Churchland, P. S. (1989). Neurophilosophy: Toward a unified science of the mind-brain. Cambridge, Mass.: The MIT Press.

Churchland, P. S. (2002). Brain-wise: Studies in neurophilosophy. Cambridge, Mass.: The MIT Press.

Churchland, P. S. (2011). Braintrust: What neuroscience tells us about morality. Princeton: Princeton University Press.

Conway, B. R., & Rehding, A. (2013). Neuroaesthetics and the Trouble with Beauty. PLoS Biol 11(3): e1001504. doi:10.1371/journal.pbio.1001504.

Place, U. T. (1956). Is Consciousness a Brain Process? British Journal of Psychology, 47: 44-50.

Polger, T. W. (2004). Natural minds. Cambridge, Mass.: The MIT Press.

Smart, J. J. C. (1959).  Sensations and Brain Processes. Philosophical Review, 68: 141-156.

van Rysewyk, S. (2013). Pain is Mechanism. Unpublished PhD Thesis. University of Tasmania.

Martijn D. Steenwijk’s video was a winner in the category of Best Video Illustration of the Brain in the 2012 Brain Art Competition 2012, run by The Neuro Bureau.

Martijn’s description of ‘The Brain at Rest’ video:

“By visualizing both diffusion tensor and resting-state functional MR data, this movie illustrates different concepts of image processing, connectivity and activity in a real human brain at rest. Background music was composed by assigning a musical instrument to the ten strongest functional patterns in the brain. The intensities of these patterns vary over time while the person is at rest in the scanner – these are “spontaneous” brain fluctuations that receive much attention in fMRI research now. By linking the intensity of each pattern to the pitch of its respective instrument a melody is generated, thereby making brain activity audible. The first part of the movie illustrates the source of the melody by showing functional patterns and their varying strengths. The second part shows the major fiber bundles which were obtained by running deterministic tractography from atlas seeds. In the third part, the seeds were replaced by spherical objects ‘running’ around the cortical surface. The last part combines structural connectivity with functional connectivity. Here, functional connectivity is visualized using volume rendering of the voxelwise functional correlation matrix. Together with its structural counterpart, this last part illustrates that structural and functional connectivity are quite different”.

Introduction

According to an influential neuroscientific theory, gender identity is encoded in the brain during intrauterine development. The brain is thought to develop in the male ‘direction’ through a surge of testosterone on nerve cells; in the female ‘direction’ this surge is absent (e.g., Savic et al. 2011; Swab, 2007). Call this the ‘standard view of gender identity’. The standard view of gender identity offers a plausible explanation of transsexualism. Since sexual differentiation of the brain occurs in the second half of pregnancy, and sexual differentiation of the sexual organs occurs in months 1-2 of pregnancy, transsexuality may occur. The relative masculinzation of the brain at birth may not reflect the relative masculinization of the genitals (e.g., Bao & Swab, 2011; Savic et al. 2011; Veale et al. 2010). According to the standard view, transsexualism is entirely dependent on, and thereby reduces to, specific neurophysiological changes that occur during intrauterine growth in two interconnected organ types (i.e., brain and genitals).

The reductive nature of the standard view of gender identity is compatible with  mind-brain identity theory in philosophy of mind and consciousness. Mind-brain identity theory claims that mental states are identical to brain states. Concerning gender identity, mind-brain identity theory claims that a person’s gender identity is identical to neurophysiological mechanism. A strong and profound implication of this view is that a person’s indubitable sense of being a woman or a man is nothing more than the operations of neurophysiology encoded during intrauterine growth. Mind-brain identity theory contrasts with philosophies of mind which propose that minds are dependent but still somehow ‘more than’ the body on which they depend.

Brain-Sex Theory of Transsexualism and Mind-Brain Identity

According to the strong version of ‘brain-sex’ theory of transsexualism,  transsexualism is nothing more than (one and the same as) a specific neuranatomical (i.e., structural) intersex type, in which one or more sexually dimorphic brain areas are incompatible with bological sex. The theory therefore assumes that the relationship between transsexualism and neurophysiology is one of identity. Gender identity reduces to neurophysiology. Thus, there is a specific neuroanatomical type for female gender identity in male-to-female (MTF) transsexuals, and a specific neuroanatomical type for male gender identity in female-to-male (FTM) transsexuals. The most compelling neuroscientific evidence in support of an identity view of transsexualism comes from Kruijver et al. (2000) and Zhou et al. (1995).

Neuroscientific Evidence for Brain-Sex Theory of Transsexualism

Zhou et al. (1995)

Zhou et al. (1995) observed that a group of neurons in the hypothalamus, the central subdivision of the bed nucleus of the stria terminalis (BSTc), was sexually dimorphic in humans. Zhou et al. found that the average volume of the BSTc in postmortem males was roughly 44% larger than in females. However, in 6 male-to-female (MTF) transsexuals who had feminizing hormone treatment, the average volume of the BSTc was within the typical female range. The authors found that the 6 transsexuals they investigated varied in their sexual orientations and inferred that there was no relationship between BSTc size and the sexual orientation of transsexuals. I assume that this assertion implies that transsexual sexual orientation and BSTc size are not type identical; that is, they are not the same type. Finally, further postmortem investigations conducted in a small number of nontranssexual patients with abnormal hormone levels, led Zhou et al. to reason that the small volume of the BSTc in MTF transsexuals cannot be explained by adult sex hormone levels” (p. 70). Thus, there appears to be a relationship of identity between transsexualism and small BSTc volume. They are one and the same.

Kruijver et al. (2000)

Kruijver et al. (2000) conducted a follow-up study in which they investigated the number of neurons in the BSTc rather than its volume. The authors examined tissue from the same 6 MTF transsexuals studied by Zhou et al. (1995). They also studied nerve tissue from one female-to-male (FTM) transsexual and from an 84-yr-old man who “had very strong cross-gender identity feelings but was never . . . sex-reassigned or treated . . . with estrogens” (p. 2039). The authors found that BSTc neuron number was even more sexually dimorphic than BSTc volume; namely, the average BSTc neuron number in males was 71% higher than in females. Once again, the 6 MTF transsexuals showed a sex-reversed identity pattern, with an average BSTc neuron number in the female range. BSTc neuron number was also in the female range in the untreated gender dysphoric male and was in the male range in the FtM transsexual. Again, the putative sexual orientation of the MTF transsexuals appeared to make no difference. In contrast to the claims of the standard view of gender identity, data from the few nontranssexual patients with abnormal hormone levels led Kruijver et al. (2000) to conclude that “hormonal changes in adulthood did not show any clear relationship with the BSTc . . . neuron number” (p. 2039).

Neuroscientific Objections to Brain-Sex Theory of Transsexualism

Chung et al. (2002)

Brain-sex theory of transsexualism faces several neuroscientific challenges. Chung et al. (2002) found that significant sexual dimorphism in BSTc size and neuron number does not develop in humans until adulthood. However, most MTF transsexuals self-report that their feelings of gender dysphoria began in early childhood (e.g., Lawrence, 2003). Since MTF transsexuals have not yet become sexually dimorphic by the time cross-gender feelings have become obvious, it is unlikely that BSTc volume and neuron number can be a neuroanatomical signature identifiable with gender identity. However, Chung et al. (2002) speculate that foetal or neonatal hormone levels could influence gender identity and could also produce changes in BSTc synaptic density, neuronal activity, or neurochemicals that may not affect BSTc volume or neuron number immediately, but may do so during adulthood. I am not aware of any evidence in support of this hypothesis. In any event, mind-brain identity theory can agree with Chung’s et al. (2002) speculation. Mind-brain identity theory is neutral on whether ‘brain characteristics’ will be macro or micro, or both, or what their specific developmental effects will be. Gender identity might be a state of the entire brain, synapses, or multiple, interacting physiological systems. Macro/microreductionism is optional, not required. Finally, Chung et al. (2002) speculate that inconsistency between an individual’s gender identity and biological sex might likely affect adult BSTc size and neuron number by some yet unknown mechanism or mechanisms. Given that neuroscience is in a very early stage of understanding gender identity, the implication that more time is needed to understand transsexualism appears prudent.

Joel (2011)

Joel (2011) challenges an implicit assumption in the standard view of gender identity; namely, human brains are one of two types –  ‘male’ or ‘female’ – and that the differences between these two types subserve subtype differences between men and women in gender identity and transsexualism. According to Joel (2011), this assumption is true only if there is robust correspondence (i.e., high statistical correlation) between the ‘male’/’female’ type of all of the brain characteristics in a single brain. It turns out there isn’t. As Joel points out, concerning most documented sex brain differences, there is overlap between the distributions of the two sexes (e.g., Juraska, 1991; Koscik et al. 2009). Neuroanatomical data also reveal that sex interacts with other factors during the intrauterine period and throughout life to determine brain structure (e.g., prenatal exposure to psychoactive drugs, early handling, rearing conditions, maternal separation, acute and chronic postnatal stress). Human brains therefore are a dynamic heterogeneous mosaic of ‘male’ and ‘female’ brain characteristics that cannot be type identified on a simple continuum between a ‘male type brain’ and a ‘female type brain’ (Joel, 2011). Thus, brains are not type sexed, but type intersexed; sexually multi-morphic rather than dimorphic.

Joel’s theory is compatible with brain-sex theory of transsexualism since both theories claim that transsexualism is intersexual, but incompatible because it denies what brain-sex theory asserts; namely, in transsexualism, one or more sexually dimorphic brain areas are incompatible with bological sex. Thus, Joel’s view rejects the stronger claim that gender is type identical with the sexually dimorphic brain. Accordingly, we cannot predict the specific properties of ‘male/female’ brain characteristics of an individual based on her/his sex. However, Joel’s view implies the weaker consequence that, on average, we can predict that females will have more brain characteristics with the ‘female’ type than with the ‘male’ type (vice versa for FTM transsexuals), and males will have more brain characteristics with the ‘male’ type than with the ‘female’ type (vice versa for MTF transsexuals). Whether two individuals are similar or not is dependent on the similarity in the details of their brain mosaic; not on the quantity of ‘male’ and ‘female’ characteristics. This means that two similar individuals share characteristics of the same ‘brain mosiac’ type – they have the same type. Brains of the same type must possess the characteristics and properties typical of the type, but that does not imply that they all be exactly similar to one another. This implication is compatible with mind-brain identity theory.

References

Bao, A. M., & Swaab, D. F. (2011). Sexual differentiation of the human brain: relation to gender identity, sexual orientation and neuropsychiatric disorders. Frontiers in neuroendocrinology, 32(2), 214-226.

Chung, W. C., De Vries, G. J., & Swaab, D. F. (2002). Sexual differentiation of the bed nucleus of the stria terminalis in humans may extend into adulthood. Journal of Neuroscience, 22, 1027-1033.

Hines M. (2004). Brain Gender. Oxford: Oxford University Press.

Koscik, T., O’Leary, D., Moser, D. J., Andreasen, N. C., & Nopoulos, P. (2009). Sex differences in parietal lobe morphology: relationship to mental rotation performance. Brain Cognition, 69, 451–459.

Kruijver, F. P., Zhou, J. N., Pool, C. W., Hofman, M. A., Gooren, L. J., & Swaab, D. F. (2000). Male-to-female transsexuals have female neuron numbers in a limbic nucleus. Journal of Clinical Endocrinology and Metabolism, 85, 2034-2041.

Joel, D. (2011). Male or female? Brains are intersex. Frontiers in integrative neuroscience, 5, 57.

Juraska J. M. (1991). Sex differences in “cognitive” regions of the rat brain. Psychoneuroendocrinology 16, 105–109. doi: 10.1016/0306-4530(91)90073-3.

Lawrence, A. A. (2003). Factors associated with satisfaction or regret following male-to-female sex reassignment surgery. Archives of Sexual Behavior, 32, 299-315.

Savic, I., Garcia-Falgueras, A., & Swaab, D. F. (2010). 4 Sexual differentiation of the human brain in relation to gender identity and sexual orientation. Progress in Brain Research, 186, 41-65.

Swaab, D. F. (2007). Sexual differentiation of the brain and behavior. Best Practice & Research Clinical Endocrinology & Metabolism, 21(3), 431-444.

Veale, J. F., Clarke, D. E., & Lomax, T. C. (2010). Biological and psychosocial correlates of adult gender-variant identities: a review. Personality and Individual Differences, 48(4), 357-366.

Zhou, J. N., Hofman, M. A., Gooren, L. J., & Swaab, D. F. (1995). A sex difference in the human brain and its relation to transsexuality. Nature, 378, 68-70.

Is gender identity – the sense of being a man or a woman – a perception identical with the nonconscious physical brain or the conscious non-physical soul? Since people who identify as transsexual verbally self-report strong feelings of being the opposite sex and a feeling that their sexual characteristics are not constitutive of their actual gender, they are a powerful case in explaining the nature of gender identity and phenomenal consciousness.

It is possible that a person’s sense of gender identity may be subserved by an
nonconscious physical base with a specific neurophysiological or neural ‘signature’. Explaining gender identity in this direct way aims first to describe the base as a correlate of gender identity, then ultimately to achieve a reductive neurophysiological explanation of gender identity.

Neurophysiological mechanism and transexual experiences can be correlated for a variety of reasons: the mechanism is part of the cause of transexualism; the mechanism is part of the effect of transsexualism; the mechanism indirectly parallels transsexualism; the mechanism is what transsexualism can be identified with. Discovering the neurophysiological signature of transsexualism requires the identification of some neurophysiological mechanism with transsexualism. The correlation of mechanism x with transsexualism is informative because x may be the one for identifying transsexualism. Correspondingly, mechanism y that does not correlate with transsexualism indicates that y may not be the one. If there is a mechanism of transsexualism with a neurophysiological signature identifiable with transsexual experiences, the scientific and clinical benefits could be huge. Thus, investigating transsexualism directly is worth a try.

There is support for theoretical identification of gender identity with neurophysiological mechanism. According to the most influential theory, during the intrauterine period, two mechanical operations may occur: (1) in the female ‘direction’, there is no surge of testosterone on nerve cells; (2) in the male ‘direction’, there is a surge of testosterone on nerve cells. Since sexual differentiation of the brain occurs in the second half of pregnancy, and sexual differentiation of the sexual organs occurs in months 1-2 of pregnancy, transsexuality may result. Thus, the relative masculinzation of the brain at birth may not reflect the relative masculinization of the genitals (e.g., Berenbaum & Beltz, 2011; Savic et al. 2011; Veale et al. 2010).

One line of neuroscientific support for a neuroanatomical signature of gender identity derives from studies on whether gray matter volumes in (heterosexual) male-to female (MTF) transexuals before cross-sex hormonal treatment are correlated with people who share their biological sex (i.e., men), or people who share their gender identity (i.e., women). Luders et al. (2009) analyzed MRI data of 24 male-to-female (MTF) transsexuals and found that regional gray matter variation in MTF transsexuals correlates with the pattern found in men than in women. Luders et al. (2012) found thicker cortices in MTF transsexuals, both within regions of the left hemisphere (i.e., frontal and orbito-frontal cortex, central sulcus, perisylvian regions, paracentral gyrus) and right hemisphere (i.e., pre-/post-central gyrus, parietal cortex, temporal cortex, precuneus, fusiform, lingual, and orbito-frontal gyrus) than age-matched control males.

In contrast, Rametti et al. (2011) found that the white matter microstructure pattern in MTF transsexuals is halfway between the pattern of examined male and female controls. These differences may indicate that some fasciculi do not complete the masculinization mechanical operation in MTF transsexuals during foetal brain development. This implies that the social environment is co-constitutive of gender identity. Clearly, more research is needed to answer this question.

Another line of neuroscientific research has focused on intrinsic brain activity (i.e., brain resting-state) to investigate correlations between the spontaneous brain connectivity of transexuals and control groups. Santarnecchi et al. (2012) used both seed-voxel and atlas-based region-of-interest (ROI) approaches and found that brain regions sensitive to gender dimorphism (e.g., left lingual gyrus, precuneus) revealed robust correlations between the female-to-male (FTM) subject and female control group with regard to control males, with comparable extension and location of functional connectivity maps. ROI analysis supported this result, demonstrating an increased pattern of differences between the FTM subject and males and the FTM subject and females. No statistically significant difference was found between seed-voxel results in the FTM subject and females. This study supports the hypothesis that untreated FTM transgender shows a functional connectivity profile comparable to female control subjects.

Taken together, these findings provide evidence that transsexualism is correlated with a specific physical signature, in terms of neuroanatomy and brain connectivity, which supports the claim of mind-brain identity theory that neurophysiological mechanism is constitutive of gender identity. Thus, the most reasonable explanation of transsexualism and gender identity is that it is entirely physical in nature.

References

Berenbaum, S. A., & Beltz, A. M. (2011). Sexual differentiation of human behavior: Effects of prenatal and pubertal organizational hormones. Frontiers in Neuroendocrinology, 32(2), 183-200.

Luders, E., Sánchez, F. J., Gaser, C., Toga, A. W., Narr, K. L., Hamilton, L. S., & Vilain, E. (2009). Regional gray matter variation in male-to-female transsexualism. Neuroimage, 46(4), 904-907.

Luders, E., Sánchez, F. J., Tosun, D., Shattuck, D. W., Gaser, C., Vilain, E., & Toga, A. W. (2012). Increased Cortical Thickness in Male-to-Female Transsexualism. Journal of Behavioral and Brain Science, 2, 357-362.

Rametti, G., Carrillo, B., Gómez-Gil, E., Junque, C., Segovia, S., Gomez, Á., & Guillamon, A. (2011). White matter microstructure in female to male transsexuals before cross-sex hormonal treatment. A diffusion tensor imaging study. Journal of psychiatric research, 45(2), 199-204.

Santarnecchi, E., Vatti, G., Déttore, D., & Rossi, A. (2012). Intrinsic Cerebral Connectivity Analysis in an Untreated Female-to-Male Transsexual Subject: A First Attempt Using Resting-State fMRI. Neuroendocrinology, 96(3), 188-193.

Savic, I., Garcia-Falgueras, A., & Swaab, D. F. (2010). 4 Sexual differentiation of the human brain in relation to gender identity and sexual orientation. Progress in Brain Research, 186, 41-65.

Veale, J. F., Clarke, D. E., & Lomax, T. C. (2010). Biological and psychosocial correlates of adult gender-variant identities: a review. Personality and Individual Differences, 48(4), 357-366.

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