John F. Kihlstrom

University of California, Berkeley

Institute for the Study of Healthcare Organizations & Transactions

Note:  This is an expanded version of a commentary on "How could conscious experiences affect brains?" by Max Velmans, and appeared in the Journal of Consciousness Studies, 9(11), 30-34. 

We’re all materialists now. Among those who retain the Cartesian categories of mind and body, even the Mysterians agree that the mind is what the brain does, even if they despair of knowing how it does it (McGinn, 1991, 1999). And for those biological naturalists who reject the Cartesian categories (Searle, 1992; Searle, 1999), consciousness is a feature of brains that have achieved a certain level of organization. The materialist consensus links psychology, William James’ (James, 1890/1980) science of mental life, with the other natural sciences, such as biology, chemistry, and physics, and for that reason it has been very seductive. However, as Velmans (Velmans, 2002) cogently points out, it does not offer a complete solution to the problem of consciousness, not least because it promotes premature closure on some problems and leaves others unaddressed. Among these unaddressed questions is whether, to what extent, and how conscious mental states -- or unconscious ones, for that matter; (Kihlstrom, 1987) -- can have a causal influence on bodily functions. If we are to take consciousness seriously, as more than epiphenomenal, then we need to show that it has causal powers: that what we think, feel, or want actually has an effect on what we do.

In the first place, adopting some form of the materialist stance would seem to lead inevitably to reductionism. If it is indeed true that the mind is what the brain does, then it stands to reason that the laws of mental life discovered by psychology can and should be reduced to the laws of biological life discovered by biology -- and, presumably, to the laws of physics. If you’re a materialist, then physics is the fundamental science, perhaps the only science, and everything else is just nonscientific "folk talk". Even those who deny they are materialism of an eliminative sort can’t help moving in this direction (Churchland, 1984; Churchland, 1986). Because folk-psychology is about mental states, while real science is about physical states, it follows that "Psychology must be grounded in the real-world findings of neuroscience" (Churchland & Churchland, 1998). As if the findings of psychological research are not grounded in the real world: Without neuroscience, apparently, the science of the mind is the science of ether, and phlogiston, and fairies.

Reductionism comes in two broad forms. Strong reductionism holds that, if the brain is the physical basis of mind, and we’re all materialists now, then we should just stop being psychologists and start being neuroscientists instead. This kind of reductionism appears underlie the attraction for psychologists of behavioral and cognitive neuroscience. But psychology had its roots in physiology as well as philosophy, at least since the time of Muller and Helmholtz, and it’s hard to see anything that neuroscience does that physiological psychology (also sometimes known as psychobiology, biopsychology, and biological psychology) did not already do, and do well. And, in fact, there are things that psychology does that cognitive neuroscience cannot do, like study emotional and motivational processes -- except insofar as these are construed as cognitive constructions. Perhaps those who call themselves "cognitive neuroscientists" mean cognition in its broadest sense, as Descartes and James did, as covering all of mental life. But if so, why do we see proposals for the establishment of affective neuroscience, an endeavor running parallel to but separate from cognitive neuroscience, dedicated to the emotional domain (Davidson, 2000; Panksepp, 1992). If affective neuroscience is here now, can a conative neuroscience be far behind, dedicated to motivation in all its aspects? And once we have separate neurosciences dedicated to each element of the trilogy of mind (Hilgard, 1980), how are we to put them together? Perhaps by becoming psychologists again.

But there is also a weak version of reductionism, which doesn’t seek to substitute neuroscience for psychology, but only asserts that psychological theories should be constrained by neurobiological knowledge. Given the materialist consensus that the brain is the physical basis of the mind, this kinder and gentler form of reductionism has had wide appeal, leading to efforts to redefine psychology as a "life science", or at least relocate it in the academic table of organization from the Division of Social Sciences to the Division of Biological Sciences. This move permits psychology to retain its status as a respectable academic discipline, and it also increases faculty salaries and graduate student stipends. The only problem is that there is no justification for it.

Consider, for example, the study of the amnesic syndrome, one of the core areas of cognitive neuroscientific research. The description of the famous Patient H.M. (Scoville & Milner, 1957) eventually led us to appreciate that the hippocampus and related structures played an important role in memory (Squire & Zola-Morgan, 1991), but our understanding of the function of the medial-temporal lobe memory system has changed as psychological theories of memory changed. At first, Talland (Talland, 1965), thought the deficit was primarily motivational, in line with traditional interpretations of the function of the limbic system. When Atkinson and Shiffrin (Atkinson & Shiffrin, 1968) described memory as the encoding, presented evidence supporting a multistore model of memory, amnesia was interpreted as a selective impairment in long-term rather than short-term memory, and theorists began debating whether the problem with long-term memory was one of encoding, storage, or retrieval (Warrington & Weiskrantz, 1970). When further research suggested that the difference between short- and long-term memory was actually one of "level" of processing, (Craik & Lockhart, 1972), amnesia was re-interpreted as a selective deficit in deep as opposed to shallow processing (Cermak, Butters, & Moreines, 1974). When cognitive psychologists distinguished between episodic and semantic memory (Tulving & Donaldson, 1972), and then between declarative and procedural memory (Anderson, 1976; Winograd, 1975), amnesia was successively interpreted as a selective deficit in episodic (Kinsbourne & Wood, 1975), and then as a selective deficit in declarative (Cohen & Squire, 1980); (Squire & Knowlton, 1995), memory. We now believe that amnesia reflects a selective deficit in explicit (conscious) rather than implicit (unconscious) memory (Schacter, 1987). It is possible to argue that the notion of implicit memory arose from neuroscientific, or at least neuropsychological, research on amnesic patients (Warrington & Weiskrantz, 1968), but the studies in question were behavioral studies of human performance on standard memory tasks, and the basic concept of implicit memory was well in place long before we knew the details of the medial-temporal lobe memory system.

This general picture is repeated at every turn in the history of the relations between biology and psychology is that in every instance where they have had contact, psychology has led biology. For example, the essential principles of the opponent-process theory of color vision were worked out on the basis of psychological phenomena like negative after-images, long before we had any clear idea of the anatomy and physiology involved (Hering, 1878/1964; Hurvich & Jameson, 1957; Ladd-Franklin, 1929). The existence of biological clocks was inferred from strictly behavioral evidence, long before we knew anything about the suprachiasmatic nucleus and locus coeruleus (Kleitman & Richardson, 1938?; Richter, 1922). While it is true that physiological recordings revealed unsuspected ultradian rhythms on the circadian sleep-wake cycle (Berger, 1929; Loomis, Harvey, & Hobart, 1935), the significance of these changes in the EEG was revealed only when a medical student had the idea of waking subjects up and asking what was going through their minds (Aserinsky & Kleitman, 1953). In each case, once psychologists had worked the problem out at the behavioral level, only then could neurobiologists begin to figure out how the visual systems of the brain actually work to produce color. Put another way, far from being constrained by neuroscientific research, psychologists have always told neurobiologists what to look for, and what their findings meant. Psychological theories don’t need to be biologically plausible. The need only to be true, or at least empirically supported. Then, the problem can be kicked downstairs for the neuroscientists to work out the biological mechanisms involved.

For all the recent debate about the mind-body problem, people seem to have forgotten that Descartes presented us with not one mind-body problem but two: his "substance dualism" gave us the problem of figuring out how the subjective experience of conscious awareness could arise from a brain consisting solely of neurons, synapses, and neurotransmitters, while his "interactive dualism" gave us the problem of figuring out how mental states and processes could cause changes in the physical state of the brain and the rest of the body. Of course, both problems are solved by the view that consciousness is epiphenomenal: if consciousness is nothing more than froth on waves of neural activity, then it plays no causal role in anything, and we might just as well be zombies. But if we are to take consciousness seriously, as more than epiphenomenal, then we need to show that it has causal powers: that what we think, feel, or want actually has an effect on what we do.

In all of this debate, one relevant body of evidence tends to be ignored: the so-called "psychosomatic" disorders known to psychiatry, in which a mental state, usually emotional in nature, appears to cause some bodily symptom, such as an ulcer (Graham, 1972; Weiner, 1977). In large part, I suspect that this neglect occurred because the psychosomatic disorders have long been tainted by some of the very worst sort of psychoanalytic thinking. For example, Franz Alexander (Alexander, 1950) argued that a whole host of physical diseases could have their origins in unconscious and unresolved "nuclear conflicts": anorexia nervosa was caused by envy and jealousy, peptic ulcers were caused by conflicts between infantile dependency versus ego pride and aspiration, bronchial asthma was caused by excessive unresolved dependence on one’s mother, essential hypertension was caused by chronically inhibited aggressive impulses, rheumatoid arthritis was caused by rebellion against restrictive parental influences, and so on.

It would be generous to say that the evidence for propositions such as these is weak, based as it is on subjective impressions of personality in individual cases of unknown representativeness without adequate controls. Moreover, to some extent discussion of psychological causes of physical illnesses has been impeded by advances in biomedical knowledge about both "physical" and "mental" disease processes. So, for example, it is common to see such psychiatric syndromes as depression, anxiety, and schizophrenia as "real diseases" because we now think we know something about their neurobiological underpinnings in the amygdala, dopamine, the human genome, or whatever -- as if these mental illnesses were not real until they had been characterized in neurobiological terms. As another example, the discovery of the role of Helicobacter pylori in gastric ulcers (Marshall & Warren, 1984) led Steven E. Hyman, later to become the Director of the National Institute of Mental Health, to gleefully report that "Another One Bites the Dust" (Hyman, 1994), and to question "the allure of attributing… illnesses primarily to psychological factors" (p. 295). Unfortunately for the argument, it turns out that while a large proportion of ulcer patients may be infected with h. pylori, a high rate of infection is also found in people without ulcers (Nomura, Stemmermann, Chyou, Perez-Perez, & Blaser, 1994). In other words, bacterial infection may be necessary for ulcers to occur, but it is not sufficient for it to occur, as even the discoverer of H. pylori himself seems to agree (Marshall, 1995).

In fact, animal research shows a clear role for stress in the predisposing organisms to ulcers, precipitating ulcers, and sustaining ulcers once they have developed (Overmier & Murison, 1997; Overmier & Murison, 2000; Weiss, 1972). Although "stress" is in some sense a physiological construct, in terms of any event that challenges an organism’s current level of adaptation (Selye, 1956), in this research "stress" refers specifically to a mental state. Beginning in the 1960s, the cognitive revolution in learning theory led to a reinterpretation of classical conditioning in terms of the organism’s efforts to predict environmental events (Kamin, 1969; Rescorla, 1967), and of instrumental conditioning in terms of the organism’s efforts to gain control over environmental events (Maier & Seligman, 1976; Seligman & Maier, 1967). In psychology, organisms (including people) are stressed when they are exposed to unpredictable and unavoidable events, especially if these are aversive (Mineka & Kihlstrom, 1978; Seligman, Maier, & Solomon, 1971). To the extent that psychological stress is a psychological, i.e., mental, state, then, the literature on ulcers yields clear evidence of an effect of the mind on the body. We now know that stress, defined psychologically as the exposure to unpredictable and/or unavoidable aversive events, is sufficient to produce ulcers.

Another area of relevant research is on Viagra (sildenafil ciltrate), the well-known (and increasingly popular) treatment for male erectile dysfunction marketed by Pfizer. Viagra is a pill, and so we might assume that its mechanism of action is purely physiological. And for the most part, it is: according to Phizer’s package insert, sildenafil selectively inhibits phosphodiesterase type 5 (PDE5), which in turn enhances the effect of nitric oxide (NO) on the release of cyclic guanosine monophosphate (cGMP), causing muscle relaxation and vasodilation in the corpus cavernosum, and the increased bloodflow of results in tumescence and full erection erection. It’s all a matter of biochemistry, except -- as Pfizer’s package inserts and advertising clearly state, none of this occurs in the absence of sexual stimulation, which is what releases NO in the first place. This sexual stimulation may be tactile (Maytom et al., 1999), in which case we may be dealing with a simple spinal reflex, or it may be visual (Boolell, Gepi-Attee, Gingell, & Allen, 1996), in which case we are dealing with something much less reflexive, and something much closer to an intentional mental state. Unfortunately, there have been no published studies of the effects of Viagra in the absence of any kind of sexual stimulation. But the available literature suggests that, in the absence of tactile stimulation, the biochemical mechanics of Viagra begin with a conscious mental state of sexual arousal.

The experiences of unpredictability and uncontrollability are mental states in the strict sense: they are beliefs that the world, or some important aspect of it, is unpredictable, uncontrollable, or both. And sexual arousal is also a mental state -- a state of sexual desire. Accordingly, they possess intentionality, or "aboutness" (Searle, 1983, 1992). But they are not particularly specific beliefs like John believes it is raining or John wants a pizza. Is there evidence for the psychosomatic role of more specific beliefs about more specific things? One relevant body of research concerns the placebo effect in medicine, where a therapeutic change occurs by virtue of the patient’s belief that he or she is receiving an effective treatment -- and, perhaps, his or her doctor’s belief that he or she is administering one (Harrington, 1997; Shapiro & Shapiro, 1997). Placebo effects have been called the "jewel in the crown" of "mind-body" medicine, and as such make biologically oriented physicians very nervous -- which may be one reason that there are occasional attempts to demonstrate that they don’t exist (Hrobjartsson & Gotzsche, 2001), or to argue that they only affect subjective, mental symptoms such as depression and pain, in which case they don’t really count as examples of psychosomatic interaction (Spiro, 1986). But there is some reason to believe that placebos can have genuine effects on objectively observed bodily functioning, as measured by dopamine release in Parkinson’s disease (de la Fuente et al., 2001), improved knee function in osteoarthritis (Bradley et al., 2002), and changes in brain function in depressed patients (Leuchter, Cook, Witte, Morgan, & Abrams, 2002). In these cases, at least, we have more than an effect of one belief -- that one has received an effective treatment -- on another belief -- that one is depressed or in pain. We have a genuine effect of a belief on the body.

Placebo effects are usually defined as nonspecific in nature, but some research indicates that they can be very specific indeed. In the domain of pain, for example, two placebos yield more relief than one, and placebo injections more than placebo pills (Evans, 1974). More recently, it has been shown that placebos administered to relief pain in one part of the body have no effect on pain in another part of the body. Perhaps most dramatically, an analysis by Evans revealed that placebo efficiency was a constant function of the active drug to which placebo was compared (Evans, 1974): placebo aspirin is 54% as effective as aspirin, placebo Darvon is 56% as effective as Darvon, and placebo morphine is 56% as effective as morphine. Evans’ findings have been questioned in some quarters (McQuay, Carroll, & Moore, 1995), but the later studies varied significantly in design from the ones Evans reviewed. Although it remains to be seen whether Evans’ findings generalize to objective as well as subjective endpoints, it appears that the effectiveness of a placebo depends on what drug the patients believe they are taking.

Turning to the effects of belief on objectively measurable physical outcomes, there are a number of studies showing the psychosomatic effects of both hypnotic and nonhypnotic suggestion (Bowers, 1977; Bowers & Kelly, 1979). In one classic study, 11 of 13 patients who were sensitive to a form of contact dermatitis similar to poison ivy showed a diminished skin reaction when exposed to the plant when the believed the leaf was harmless, and 12 of 13 showed signs of dermatitis when exposed to a harmless plant, which they believed was poisonous (Ikemi & Nakagawa, 1962). Similar results were obtained in more recent symptom-provocation studies of asthma (Luparello, Lyons, Bleecker, & McFadden, 1968) and of food allergies (Jewett, Fein, & Greenberg, 1990). Another series of carefully designed studies showed that subjects who received verbal suggestions showed improved the regression of warts, compared to those who received either a placebo or no treatment (Spanos, Stenstrom, & Johnson, 1988; Spanos, Williams, & Gwynn, 1990). In one particularly provocative study, asthmatic patients were administered either a bronchoconstrictor or a bronchodilator. Patients who received the bronchoconstrictor correctly identified as such showed greater airway response than those to whom the drug was identified as a dilator; and similarly, those who received the bronchodilator correctly identified as such showed increased greater response than those for whom it was identified as a constrictor (Luparello, Leist, & Lourie, 1970).

More research on psychosomatic interactions is clearly in order, once the medical community starts taking them seriously again. Still, the evidence available so far clearly indicate that people’s conscious beliefs can play a powerful role in creating and modifying their bodily states. Consciousness is not just an effect of bodily activity, and it is not merely epiphenomenal froth on the wave of neural connections. Consciousness also has causal efficacy, by virtue of its effects on bodily states, and one of the pleasures of dualism is that it reminds us that mind matters. Velmans is right to draw attention to this literature, and to take it seriously. I think he is also right that we will never solve the mind-body problem so long as we focus our attention on the mysterious leap between body and mind, and ignore the equally mysterious link between mind and body.

Longer version of commentary on Velmans, M., "How Could Conscious Experiences Affect Brains?", written for the Journal of Consciousness Studies, 2002. Preparation of this paper supported by Grant #MH-35856 from the National Institute of Mental Health.

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