UC Berkeley psychologist Tania Lombrozo has responded to the Annual Edge Question for 2014, ‘What scientific idea is ready for retirement?’, with a piece entitled ‘The Mind is Just the Brain’, in which she argues for the rejection (‘retirement’) of mind-brain identity theory.
Using a baking analogy to illustrate her case against reductionism, she writes:
But a theory of baking wouldn’t be very useful if it were formulated in terms of molecules and atoms. As bakers, we want to understand the relationship between—for example—mixing and texture, not between kinetic energy and protein hydration. The relationships between the variables we can tweak and the outcomes that we care about happen to be mediated by chemistry and physics, but it would be a mistake to adopt “cake reductionism” and replace the study of baking with the study of physical and chemical interactions among cake components.
But if you are interested in the project of explaining, predicting, and controlling the quality of your baked goods, then you’ll need something like a baking theory to work with.
Rejecting the mind in an effort to achieve scientific legitimacy—a trend we’ve seen with both behaviorism and some popular manifestations of neuroscience—is unnecessary and unresponsive to the aims of scientific psychology.
In these passages, Lombrozo makes a common anti-reductionistic mistake of thinking that mind-brain identity makes mental experiences somehow unreal or even disappear. Her reasoning implies that a correct explanation of mental phenomena cannot involve scientific reduction of mental phenomenon to neurobiological mechanism. This misunderstanding trades on a peculiar view of reduction, where it is expected that in neuroscience, mind-brain identities eliminate mental experiences. I think this expectation is incorrect.
Temperature was ontologically reduced to mean molecular kinetic energy, but no person expects that temperature therefore ceased to be real or became scientifically disrespectable or redundant. Visible light was ontologically reduced to electromagnetic radiation, but light did not disappear. Instead, scientists understand more about the real nature of light than they did before 1873. Light is real, no doubt; and so is temperature. Some expectations about the nature of temperature and light did change, and scientific progress does occasionally require rethinking what was believed about phenomenon. In certain instances, previously respectable states and substances sometimes did prove to be unreal. The caloric theory of heat did not survive rigorous experimental testing; caloric fluid thus proved to be unreal. A successful mind-brain identity of mental phenomenon such as pain means only that there is an explanation of pain. It is a reduction. Scientific explanations of phenomenon do not typically make them disappear [1,2,3].
It is critical to clear-up a further common misconception about mind-brain identity theory. This is the misconception that mind-brain identity theory is equivalent to reductionism. The truth is that whereas identity theory is compatible with a wide range of reductionistic philosophies, it is not equivalent to all of them. Here are some illustrative examples :
1) Identity theory is reductionistic in the sense that it denies minds are ontologically independent of brains and uniquely self-guaranteeing, in line with functionalist and realization (physicalist) philosophies of mind. But functionalism and realization physicalism are not equivalent to the identity theory, so identity theory is not uniquely reductionist in the sense of (1).
2) Identity theory is reductionistic in the minimal sense that it claims, in line with functionalist and realization (physicalist) philosophies, that mind is ‘nothing over and above’ the brain, but since identity theory and functionalist and realization philosophies are not equivalent, identity theory is not equivalent to reductionism. A philosopher could be a reductionist without being an identity theorist.
3) Identity theory is not reductionistic in the sense that it asserts ‘micro-reductionism’. Mental phenomena might be identified with innate genetic or molecular mechanisms (John Bickle), but this is optional, not required. The core metaphysical commitment of identity theory is that mental states are numerically identical to brain states. Nothing is expected in this core claim about the precise mechanistic nature of brain states, which is a scientific question, anyway.
4) Identity theory is not reductionistic in the sense that it asserts that (e.g.) psychology reduces to neuroscience, cognitive neuroscience reduces to molecular neuroscience, or philosophy of mind reduces to quantum mechanics. One can assert identity theory without asserting epistemic reductionism.
Positively, I entirely agree with Lombrozo when she says:
But if we want to know—for instance—how to influence minds to achieve particular behaviors, it would be a mistake to look for explanations solely at the level of the brain.
Understanding the mind isn’t the same as understanding the brain.
Understanding the mind requires first-person descriptions of mental states and experiences, and third-person scientific descriptions of associated brain states, and a method to integrate them, such as the experiential-phenomenological method . So, Lombrozo is right: ‘Understanding the mind isn’t the same as understanding the brain.’ More precisely, I argue that her correct thesis implies that the subject matter of psychology is brain mechanism as related to mental phenomena. For example, the subject of pain science is brain mechanism as related to pain phenomena (e.g., acute pain, chronic pain, fetal pain, empathy for pain, dreamed pain, near-death pain, and so on). Pain research aims to discover the brain mechanisms subserving conscious pain experiences accessible only through introspection, which means that pain research is entirely reliant on the first-person point of view and on using first-person investigative methods. This necessarily includes introspection together with third-person methods (e.g., neuroimaging). Since pain research aims to know which experience types are generated by which brain mechanism, researchers must naturally know when specific pain experiences occur and what their personal qualities are.
The history of scientific pain research shows that introspection has been extensively used. For example, pain psychophysics typically uses subject pain verbal-report or non-verbal behavior (e.g., facial expressions) to infer the presence of pain. That is, pain psychophysics is committed to subject introspection. It is also important to remember that the validity of pain-related neuroimaging was established by the correlation of brain images with self-report of pain . Pain psychophysics, like psychology, preserves an epistemological dualism in its subject matter while rejecting metaphysical dualism.
How then is mind-brain identity theory positioned relative to the indispensability of introspection in mind science? Personal introspection is a direct way of coming to know about personal experiences and their qualities. It is epistemological. Still, despite appearances to the contrary, what introspection reveals to us may be utterly mechanistic. It may be that what scientists study through third-person methods is numerically identical with what is personally experienced through introspection, that is, brain mechanisms of the appropriate type. There is only one type of activity in question: the brain mechanism with all and only physical properties. Thus, mind-brain identity theory is preserved in the study of the mind.
 Churchland PM (2007). Neurophilosophy at work. Cambridge, UK: Cambridge University Press.
 Churchland PS (1989). Neurophilosophy: Toward a unified science of the mind-brain. Cambridge, Mass.: The MIT Press.
 van Rysewyk S (2013). Pain is Mechanism. PhD Dissertation, University of Tasmania.
 Polger TW (2009). Identity Theories. Philosophy Compass, 4(5), 822-834.
 Price DD, Aydede M (2006). The Experimental Use of Introspection in the Scientific Study of Pain and its Integration with Third-Person Methodologies: The Experiential-Phenomenological Approach. In M Aydede (ed.), Pain: New Essays on Its Nature and the Methodology of Its Study, pp. 243-275. Cambridge, Mass.: MIT Press.
 Coghill RC, McHaffie JG, Yen YF (2003). Neural correlates of interindividual differences in the subjective experience of pain. Proceedings of the National Academy of Science USA, 100, 8538-8542.
William’s reasoning for the title of his excellent article – that dualism inspired by radical skepticism can mystify and confound experimental results – conveys a truth often neglected in a majority of philosophy of mind and consciousness; namely, skepticism is an organ of doubt, but please don’t forget what we already know. Doubt is useful in philosophy; but radical doubt is self-consuming.
Here, I briefly respond to Robinson, Staud and Price6 concerning what constitutes the ‘neural signature’ of pain (p. 325), note a logical mistake in their article, and highlight a reason why explaining pain is difficult. It is probable that conscious pain may be subserved by an unconscious physical base with a specific neurophysiological signature. Explaining pain in this direct way aims first to describe the base as a correlate of pain, then ultimately to achieve a reductive neurophysiological explanation of pain. Multiple evidential lines demonstrate that the neurophysiological base of pain need not be limited to one physical location, as Robinson, Staud and Price rightly note (p. 325). Since the hypothetical pain base is probably distributed, and therefore is more akin to the immune system than the liver, it is mistaken to expect that if it is not confined to a single neural region, or a single pattern of functional interaction, then there cannot be a physical signature of pain, as Robinson, Staud and Price appear to think (p. 325). Instead of a region-based view of the hypothetical pain base, it may be more accurate to think of it as a distributed mechanism.5, 8
The mechanism of pain could involve any number of neurophysiological systems (nervous, endocrine, immune), or reciprocal interactions between them, or any number of neurophysiological levels (pathway, network, single cell, molecular), or reciprocal interactions between them.1, 7, 8 The probability of a distributed mechanism, combined with the open-ended probability concerning the systems and level at which the mechanism exists, explains why current hypotheses and theories of pain in the literature, including those made in the article by Robinson, Staud and Price, are relatively unconstrained. However, the absence of constraints is not indicative of the likely truth of Cartesian dualism, the futility of searching for neurophysiological pain correlates, or the unreliability of verbal pain self-report. Rather, it indicates that pain science has much to do.
Neurophysiological mechanism and pain experiences can be correlated for a variety of reasons: the mechanism is part of the cause of pain; the mechanism is part of the effect of pain; the mechanism indirectly parallels pain; the mechanism is what pain can be identified with.2, 8 Discovering the neurophysiological signature of pain requires the identification of some neurophysiological mechanism with pain. The correlation of mechanism x with pain is informative because x may be the one for identifying pain. Correspondingly, mechanism y that does not correlate with pain indicates that y may not be the one. If there is a pain mechanism with a neurophysiological signature identifiable with pain experiences, the scientific and clinical benefits could be huge. Thus, investigating pain directly is worth a try.
Now, it is quite possible that a scientist may be looking at an instance of the pain signature without comprehending that it is an instance. This will occur if the physical base of pain does not possess an identifying property that is obvious to naïve researchers, but is comprehensible only through the availability of a more complete general theory of brain function.2, 3, 4, 8 The limitations in explaining pain are not simply technological. After all, how would a person know, independently of Antoine Lavoisier’s studies on oxygen, that metabolizing, burning and rusting are identical with the same mechanism, but that lightning and sunlight are not? Thus, Robinson, Staud and Price are right in asserting that it is misconceived to replace pain ratings with neuroimaging data, especially at this early stage of pain investigations.
Chapman CR, Tuckett RP, & Song CW: Pain and stress in a systems perspective: reciprocal neural, endocrine, and immune interactions. J Pain 9: 122-145, 2008.
Churchland PS: A neurophilosophical slant on consciousness research. Progress in brain research 149: 285-293, 2005.
Frith CD, Perry R, Lumer E: The neural correlates of conscious experience: an experimental framework. Trends in Cognitive Science 3: 105-114, 1999.
Northoff, G: Philosophy of the brain: The brain problem (Vol. 52). Amsterdam, John Benjamins Publishing Company, 2004.
Northoff, G: Region-Based Approach versus Mechanism-Based Approach to the Brain. Neuropsychoanalysis: An Interdisciplinary Journal for Psychoanalysis and the Neurosciences 12: 167-170, 2010.
Robinson ME, Staud R, & Price DD: Pain Measurement and Brain Activity: Will Neuroimages Replace Pain Ratings? J Pain 14: 323-327, 2013.
Tracey I, Mantyh PW: The Cerebral Signature for Pain Perception and Its Modulation. Neuron 55: 377-391, 2007.
van Rysewyk S: Pain is Mechanism. PhD Thesis, University of Tasmania, 2013.
‘Proof of Heaven: A Neurosurgeon’s Journey into the Afterlife‘ (2012), by neurosurgeon Eben Alexander, presents a narration and interpretation of the near-death experience (NDE) of its author. Alexander developed bacterial meningitis, and was hospitalized. During hospitalization, he became deeply comatose, a condition which lasted seven days. Alexander was fortunate to come out of his coma state and retain full wakeful consciousness. Following wakefulness, Alexander reported remarkably clear visions, sensations and thoughts he claims to have had during his near-death coma. In his book, Alexander interprets this NDE as proof that life follows death, death is not the end, there exists an extremely pleasant and serene afterlife, and that consciousness is independent of the cortical brain. It is the last claim of Alexander’s that I will consider in this post. Specifically, is consciousness independent of cortex?
According to Alexander, his coma-induced NDE occured when his cerebral cortex was ‘completely shut down’, ‘inactivated’, and ‘totally offline’. In the article he wrote for Newsweek, Alexander writes that the absence of cortical activity in his brain was ‘clear from the severity and duration of my meningitis, and from the global cortical involvement documented by CT scans and neurological examinations.’ The problem with Alexander’s view of coma is that it is not supported by evidence. First, ‘global’ (complete) cortical ‘shut down’ does not result in coma, as Alexander believes. Complete cortical ‘shut down’ is fatal, and results in brain death (e.g., Cavanna et al. 2010; Charland-Verville et al. 2012; Laureys et al. 2004a; Laureys et al. 2004b). Second, ‘flat’ EEG recordings concurrent with high alpha cortical brain activity are frequently observed in comatose patients; this event is termed ‘event-related desynchronization’. There is a vast and well-established scientific literature on this topic (e.g., Pfurtscheller & Aranibar, 1979; Pfurtscheller, 1992; Pfurtscheller et al. 1999). Thus, coma does not require complete cortical deactivation.
Alexdander’s claim that NDEs require complete cortical shut down carries the implication that fully (wakeful) sensory consciousness must involve only cortex. Alexander’s argument is in line with a trend in consciousness studies research to investigate cortical regions, pathways, and activity guided by the slogan ‘seeking the neural correlates of consciousness.’ Clinical studies of cortical lesions have motivated this approach, largely due to robust correlations such as fusiform lesions leading to prosopagnosia, or ventral stream lesions leading to the visual inability to percieve shapes. The convenience of neuroimaging cortical activity with MEG, EEG, PET and fMRI has likely also played a part in the focus on cortex.
However, viewing (wakeful) sensory consciousness as purely cortical neglects essential subcortical-cortical behavioural aspects (e.g., Churchland, 2002; Damasio, 1999; Guillery & Sherman, 2002; Llinas, 2001; van Rysewyk, 2013). Put very simply (and briefly), a basic function of mammalian and non-mammalian nervous systems is to enable and regulate movements necessary to evolutionary goals such as feeding and reproducing. Peripheral axons that carry sensory information have collateral branches that project both to subcortical motor structures (primarily, thalamus) and cortical motor structures (primary motor cortex, M1). According to Guillery and Sherman (2002), all peripheral sensory input communicates information about ongoing instructions to such subcortical-cortical motor stuctures, which implies that a sensory signal can become a prediction about what movement will happen next. Thus, as an organism learns the effects of a specific movement, it learns about what in the world will likely occur next (planning), and thus what it might do following that event (deciding, acting). Temporality emerges as central to the nature of consciousness. In order to keep the body alive, nervous systems face numerous complex challenges in learning, continuous effective prediction, attention to different sensorimotor events, and calling up stored (timing) information. Neuroanatomical loops between thalamocortico structures are a plausible physical substrate involved in (identical to?) the temporal and causal aspects of the world, and of one’s own body (e.g., Damasio, 1999; Guillery & Sherman, 2002; Llinas, 2001). This leads to the empirical prediction that in a near-death event, normal functioning of thalamocortico loops is compromised.
Cavanna, A. E., Cavanna, S. L., Servo, S., & Monaco, F. (2010). The neural correlates of impaired consciousness in coma and unresponsive states. Discovery medicine, 9(48), 431.
Charland-Verville, V., Habbal, D., Laureys, S., & Gosseries, O. (2012). Coma and related disorders. Swiss archives of neurology and psychiatry, 163(8): 265-72.
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.
Damasio, A. R. (1999). The Feeling of What Happens. New York: Harcourt Brace.
Guillery, R. W., & Sherman, S. M. (2002). The thalamus as a monitor of motor outputs. Philos. Trans. R Soc. Lond. B Biol. Sci., 357: 1809-1821.
Laureys, S., Owen, A. M., & Schiff, N. D. (2004a). Brain function in coma, vegetative state, and related disorders. The Lancet Neurology, 3(9), 537-546.
Laureys, S., Perrin, F., Faymonville, M. E., Schnakers, C., Boly, M., Bartsch, V., Majerus, S., Moonen, G., & Maquet, P. (2004b). Cerebral processing in the minimally conscious state. Neurology, 63(5), 916-918.
Llinas, R. R. (2001). I of the Vortex: From Neurons to Self. Cambridge, Mass.: MIT Press.
Pfurtscheller, G., & Aranibar, A. (1979). Evaluation of event-related desynchronization (ERD) preceding and following voluntary self-paced movement. Electroencephalography and clinical neurophysiology, 46(2), 138-146.
Pfurtscheller, G. (1992). Event-related synchronization (ERS): an electrophysiological correlate of cortical areas at rest. Electroencephalography and clinical neurophysiology, 83(1), 62-69.
Pfurtscheller, G., & Lopes da Silva, F. H. (1999). Event-related EEG/MEG synchronization and desynchronization: basic principles. Clinical neurophysiology, 110(11), 1842-1857.
van Rysewyk, S. (2013). Pain is Mechanism. Unpublished PhD Thesis. University of Tasmania.
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.
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.