An effect of maleness
An article by Alla Katsnelson in Nature (28 April; doi:10.1038/nature.2014.15106; currently free) reports on new results from Jeffrey Mogil, a well-known pain researcher at McGill. Mogil and his team have shown that olfactory exposure to males (humans, rats, cats, dogs, guinea pigs) dampens pain responses in mice. In a paper published in Nature Methods (doi:10.1038/nmeth.2935), Mogil and his team report that even a T-shirt, or the scent of chemicals from a male armpit, had the same effect. The only exception was male cage-mates of the subjects. Women, on the other hand, had no effect on pain sensitivity.
Sensitivity to pain was decreased (by about 40%), it turned out, because male scent increased stress, as indicated by increased levels of cortiosterone.
That the presence of an experimenter could alter the responses of animals to pain was long suspected. Mogil says it is
“something that people have been whispering about at meetings for years […] But no one had bothered to look at this systematically.”
Two take-home results are indicated in the article:
“It’s the kind of result a lot of people wish wouldn’t happen,” says Douglas Wahlsten, an emeritus professor of psychology at the University of Alberta, Canada who has studied how animals react to experimenters. Such effects should be taken more seriously, Wahlsten says. “I think this paper will make people more aware.”
Animal researchers, says [Joseph] Garner, will have to embrace statistical methods that compensate for a greater range of variability. “We need to think about animals as more like human subjects,” he says, “than as controllable reagents.”
It’s worth noting that in an all-male lab a systematic biasing of results by the presence of males would not be noticed (the same would hold, of course, in an all-female lab).
Perhaps the same could be said of philosophical results.
Three other articles on pain and empathy I noticed while researching the above:
- Jeffrey Mogil. “Animal models of pain: progress and challenges.” Nature Reviews Neuroscience 10.4 (2009): 283–294. (doi:10.1038/nrn2606).
- Bartal, Inbal Ben-Ami, Jean Decety, and Peggy Mason. “Empathy and pro-social behavior in rats.” Science 334.6061 (2011): 1427–1430. Reported on in Nature by Virginia Gewin. (See also Mogil 2012.) From the abstract: “To test for empathically motivated pro-social behavior in rodents, we placed a free rat in an arena with a cagemate trapped in a restrainer. After several sessions, the free rat learned to intentionally and quickly open the restrainer and free the cagemate. […] They freed cagemates even when social contact was prevented. When liberating a cagemate was pitted against chocolate contained within a second restrainer, rats opened both restrainers and typically shared the chocolate.”
- Monya Baker. “Animal models: Inside the minds of mice and men”. Nature 475, 123–128 (07 July 2011) doi:10.1038/475123a. On the use of animals in the study of mental illness. Intriguing quote:
As human genetic studies reveal gene variants with increasingly smaller impacts on disease, there is increasing demand for new behavioural tests to assess them. Results of assays are highly variable, and they may not measure the most meaningful symptoms, says Jeffrey Mogil, a neuroscientist at McGill University in Montreal, Canada. “We’ve made a lot of advances in making ever-fancier mice, but at the end of the day the question is, what’s your assay and what’s your measure and are they relevant?” he says. “The slow link in the chain, the messy link in the chain, has always been the behavioural assays.”
This summer I learned to walk. More precisely, I learned to walk normally. My gait had gotten unsteady, and I was dragging my right foot. Work with an excellent physical therapist helped straighten me out. But balance problems, tremors, and hesitations continued.
At the beginning of August I was diagnosed with Parkinson’s. I want to describe the phenomenology of my version of it, and begin thinking through its implications for the philosophy of perception and action. But first the disease itself.
▶ For a first-person account of Parkinson’s by a neurologist, see this recent article in Nature.
What Parkinson’s is
The immediate underlying problem is a deficiency of the neurotransmitter dopamine. Levels at diagnosis are typically 30% to 70% below normal. Dopamine is involved in many neural processes, not only motor activity but decision-making and the regulation of emotion. The symptoms from which Parkinson’s is diagnosed — tremor, bradykinesia, rigidity, and postural instability — will in time be accompanied by others, including loss of smell (mine, however, is rather more sensitive than less), autonomic dysfunction, troubled sleep, and dementia.
Diagnosis typically occurs five to eight years after the conjectured onset of the disease. Before diagnosis, in the so-called “presymptomatic” phase, there may have been nonmotor symptoms, including rigidity, aversion to novelties, and depression. In my case the presymptomatic phase may have begun as early as 2005. With no doubt fallible hindsight I can recall evidence of motor problems at least two years ago.
Dopamine deficiency, once regarded as the cause of Parkinson’s, is now accounted rather as a symptom. (Progress in understanding “causally deep” diseases like Parkinson’s consists in travelling back along the chain of causes; the aim, however, is not to find ultimate causes but to find the most effective points of therapeutic intervention; manipulability is key.) It is now thought that Parkinson’s, like Alzheimer’s, includes the buildup of aggregates of proteins that eventually disable or kill the neurons that contain them. A cascade of further problems ensues. In Parkinson’s the proteins in question are “synucleins”, smallish proteins which, in aberrant forms, tend to stick together. Mitochondrial malfunctions [pdf] are also present that may both cause and be caused by the protein aggregates. As yet there is no cure for either abnormality. Consensus on the chain of causes that issues in Parkinson’s ends here.
What degrades first is the substantia nigra, the “black stuff”, responsible for production and regulation of dopamine. Like other parts of the midbrain, it is very old, and was perhaps already present in the first vertebrates, 500 million years ago. The breakdown of proteins eventually spreads to other areas associated with motor activity and with impulse control, and ultimately to the cortex. Motor symptoms improve upon the administration of levodopa (a dopamine precursor that can pass through the blood-brain barrier, made famous by Oliver Sacks’s Awakenings). But eventually its effects diminish, as the condition of the brain worsens. For nonmotor symptoms there is no established treatment. Nothing is yet known to stop or slow down the progress of the disease, although exercise, especially “forced” exercise, is thought to have some positive effect. I now own a treadmill.
▶For a recent survey on Parkinson’s diagnosis, etiology, and treatment see Nature Outlook (2010) [paylink], and Michael J. Fox’s website.
I will mention two striking perceptual effects of my symptoms. The first is that my perception of spatial relations has changed. Things a block away seem — unsurprisingly — further, no doubt because it requires more effort than it used to to walk five hundred feet. Things within fifty feet or so, on the other hand, feel closer. I say “feel” because I’m referring not to visual perception, not to how things look, but to how close they seem [paylink], and thus how threatening if they are moving toward me or I toward them. The involuntary fear of heights that Hume notes is impervious to reason has become almost overwhelming; the involuntary flinching that occurs if something large looms too quickly now kicks in sooner. Crowds have become more unnerving. Even when I am in the kitchen with only my wife I sometimes stop short three or four feet from her, though I realize even as I stop that there’s no risk of collision.
This is owing, I suspect, to my decreased mobility. It takes effort to turn, effort to bend at the waist, effort to start moving out of the way. My awareness of that — I don’t mean explicit thoughts of being immobile but the feeling of stiffness, of effortful change of posture — seems to have resulted in a recalibration of my “proximity detectors”, and that in turn to altered perceptions of the ambient space and objects within it.
A second effect has again to do with spatial perception. I notice a marked reluctance to reach down. A book on the floor feels farther away. It is as if the perception of something like Gibsonian affordances has been altered, or the locomotive field, the viscosity, of nearby space. The same applies more generally to reaching in general, especially if the thing to be reached is behind me.
A third effect, more cognitive than perceptual, and thankfully infrequent, has occurred when I find myself in a kneeling position on the floor and momentarily unable to rise. The thought that immediately comes to mind is not that I can’t stand up, but that I have forgotten how. Incapacity is refashioned into ignorance.
It would follow, if I had indeed forgotten, that I would now have to learn anew the sequence of acts by which one rises to a standing position. That is indeed what I did this summer as I worked on my gait and balance. One exercise consisted simply in this: from a standing position, lean forward until you start to fall, and (deliberately) take a single step forward to maintain your balance. I was taking several small steps, which is more likely to be ineffective.
Until new habits have worn in, I must plan acts that before were performed “on the fly”, without deliberation. To get off the floor from a kneeling position if I cannot give myself a boost with my arms, I have learned to first set my left foot on the floor in front of me, and then, as I unbend my left left knee, pull up the right leg so that at the end both legs are straight and my feet are flat on the ground. I’ve described the act in Molloy- or Kafka-like detail; in such detail must I construct it. Needless to say doing things thus is slow and inefficient by comparison with the fluent, unreflected doing I was used to. The slowness associated with Parkinson’s has to do not only with the reluctance of the nervous system to respond to one’s intentions, but with the need to substitute plans for long-standing habits.
All this provides further illustration, if any is needed, for the close relation between perception and action argued for by Merleau-Ponty in the 1940s (Phénoménologie de la perception, 1945; see Jean-Luc Petit "La Spatialité originaire du corps propre", Revue de synthèse 124.1 (2003): 139–171) and more recently by Susan Hurley [pdf], Alva Noë, and others. Parkinson’s, in its early stages, has no direct effect on perception (although it may hinder visual perception by affecting the basal ganglia, which control visual saccades). What it does to perception will therefore be by way of its influence on motor control. Early-stage Parkinson’s provides a natural settingf in which to test the so-called ‘enactive hypothesis’. The more general point that loss of motor capacity provides a test has, of course, not gone unnoticed. What I would urge is a more fine-grained analysis of its effects, for example, that the space around one could feel different than before in various ways — with respect to “looming”, for example — that do not consist in its looking different, and that the feel I am trying to articulate — with respect to heights, say — seems to be an amalgam of perceptions, motor inclinations, and emotions.
I see some evidence in my experience also that for certain emotions, notably anxiety, the Jamesian theory may be true, at least in a weak form according to which certain bodily goings-on, though not perhaps necessary, suffice for it to be present. The awkward tension I often feel in my muscles, especially in the abdomen and upper torso, resembles that of anxious anticipation, and it requires concentration not to feel anxious as a result. On the other hand, if the capacity to have emotions depends in part on the capacity to express them, then one can make sense of the impassivity of Parkinson’s patients even without invoking the “dopamine hypothesis” alluded to earlier.
I am sobered by the thought that it was child’s play for my understanding to make intelligible to itself my altered dispositions in terms of more-or-less reasoned preferences. I’ve noticed that to the extent that I’ve become more impulsive (more likely to interrupt, for example), reasons come readily to mind both to explain and to excuse my behavior. The higher capacities seem to operate here in the manner of an overly accommodating servant who manages to make sense of even the most outlandish expressions of his master…
The soul of man pictured
The illustration above is from Jan Comenius’ celebrated, oft-reprinted school-book. The Orbis sensualium pictus presents, in words and in pictures, “all the fundamental things in the world and all the acts of life”. In pictures (an expensive novelty at the time) because, after all, “in Intellectu autem nihil est, nisi priùs fuerit in Sensu” (a famous Aristotelian slogan), and so one must exercise the senses, perceiving by their means the differences of things, so as to lay the foundations of wisdom and right action.
The doddering Hans effect
Another well-worn example bites the dust? You remember that famous study in which the participants, if primed with words connoting agedness, walked more slowly when leaving the lab.
A new study by the Belgian team of Stéphane Doyen, Olivier Klein, Cora-Lise Pichon, and Axel Cleeremans not only failed to replicate the effect, but also appeared to show that the effect observed in the original study was owing to the experimenters’ expectations.
Experimenters’ expectations seem to provide a favorable context to the behavioral expression of the prime. Obviously, this interpretation remains tentative, as we do not know how this process operates. However, it is likely that [experimenter-subjects] who expect their participants to walk slower behave differently than those who expect their participants to walk faster and that such behavioral cues are picked up by participants.
- The setup was one that included not only the usual subjects being primed or not with a scrambled-sentence task, but also other “experimenter-subjects” whose task it was to time the usual subjects’ passage down the hall as they left the lab. Doyen et al “were indeed able to obtain the priming effect on walking speed for both subjective and objective timings. Crucially, however, this was only possible by manipulating [experimenter-subjects’] expectations in such a way that they would expect primed participants to walk slower”.
- Subjective timings (with a stopwatch) yielded errors when experimenter-subjects were told that subjects would be primed to walk faster as well as when they were told that subjects would be primed to walk slower. But objective timings yielded an effect only when the priming was for walking more slowly; no effect was observed when the priming and the experimenter--subjects’ expectations were at odds.
The authors agree that unconscious behavioral priming appears to be well established,
in line with our result it seems that these methods need to be taken as an object of research per se before using it can be considered as an established phenomenon.
It’s worth noting that Doyen et al do not report any awareness on the subjects’ part of having been cued by the experimenter-subjects, even though there was some awareness (as revealed by a forced-choice test) of the priming (not as priming, but as a salient feature of the stimulus).
- Anonymous. (2012) “Behavioral priming paradigm needs update”. Medical Xpress 18 Jan 2012.
- J. A. Bargh, M. Chen, L. Burrows. (1996) “Automaticity of social behavior: direct effects of trait construct and stereotype-activation on action”. Journal of personal & social psychology 71.2:230-44. See also Bargh and Chartrand, “The unbearable automaticity of being”, American Psychologist, 54.7 (1999) 462-479, available here.
- S. Doyen, O. Klein, C.-L. Pichon, A Cleeremans. (2012) “Behavioral priming: it's all in the mind, but whose mind?” PLoS ONE 7.1: e29081. doi:10.1371/journal.pone.0029081
On magnets and lies, and checking sources
The historian’s attitude, when attempting to establish matters of fact, toward the sources, is one of tempered but universal skepticism. The same applies to the history of the present. For example:
Don’t depend on popularizations for your knowledge of neuroscience (see the previous item in this blog for a similar issue concerning the biology of sex). A recent headline in several newspapers and online sources reads something like this: “Magnetic Pulses To The Brain Make It Impossible To Lie”. Wow! That’s exciting! And scary too…
The only problem is, it’s false. The original study, which takes two minutes to retrieve if you have access to the journal (Behavioural Brain Research, Volume 225.1 (Nov 2011) 209-214; doi:10.1016/j.bbr.2011.07.028) states its main result as follows:
In our study we found support for the general hypothesis: rTMS targeted at DLPFC changed spontaneous truth-telling/lying rate in a task with no mock-criminal, guilty knowledge, or personally relevant information processing contexts being involved. Importantly, clear hemispheric differences were found. In principle, artificial inhibition of the sustained neuronal activation-states in left DLPFC and possibly the concomitant effect on the systems intimately associated with DLPFC decreases the willingness to tell the truth (more non-truthful answers produced) and/or increases the willingness to tell lies. Conversely, inhibitory rTMS effect on right DLPFC and possibly the concomitant secondary effect on the DLPFC-associated systems increases willingness to tell truth (more truthful answers produced) and/or decreases willingness (or capability) to lie.
[Acronyms unpacked: rTMS = repetitive transcranial (from outside through the skull) magnetic stimulation; DLPFC = dorsolateral prefrontal cortex.]
The authors carefully note the limitations of their study.
- The effects of the magnetic stimulation may spread beyond the area adjacent to the coil; and so “ interpretations on causal effects of TMS exclusively through the TMS-targeted area should be taken with care”.
- The dorsolateral prefrontal cortex has many functions, and in a complicated task like “spontaneous” lying more than one may be activated: because “perceptual stimuli had to be named and two response variants chosen and reversed from time to time, the number of possible neural mechanisms that influence readiness to lie in our task and their possible interactions remain too numerous at present” to be sorted out.
- The spontaneity of the lying was limited to some unknown degree. Subjects were “instructed to name the colour correctly or just lie about it, naming the other colour that was not presented in this trial, being free to choose whether to lie or not”, but they were also told that only lying or only telling the truth would not be “good for the experiment”.
The upshot is that there is a positive correlation between spontaneous truth-telling and rTMS stimulation of the right dorsolateral prefrontal cortex; and between spontaneous lying and stimulation of the left DLPFC. That’s very interesting. But it’s far from what you would gather from the headlines and stories online.
The moral should be obvious. In matters of science, there is no substitute for reading the original studies. Science journalists, and for that matter popularizing philosophers, should be drawn upon cautiously. Moreover, the studies often present complexities and issues (as here) that summaries, especially of the ax-grinding sort, tend to omit.
I learned this long ago when reading studies on animal perception that were cited over and over in the philosophical literature on representation. It was clear that only a few people had read the original studies; everyone else drew on their predecessors’ summaries. When I read the original studies, I discovered not only mistakes in the summaries but also a world of fascinating work that the “poor diet of examples” in the literature had simply omitted. Insect senses in particular offered much food for thought, and I recommend it highly if you’re thinking about the origins of representation or defining sensory modalities.
Philosophers have done a better job in the last twenty years. A much broader range of scientific results is brought to bear on philosophical debate, and prejudices according to which doing so is somehow unphilosophical have waned. Experimental Philosophy even generates its own results. But it’s well worth remembering, both when doing philosophy and when judging scientific results of political import, that although a great deal of expertise is required to contribute to ongoing research, rather less is needed to acquire a basic understanding of the results of research, to understand their limitations, and to evaluate second-hand accounts.
Jeffrey Zacks, a colleague here in Psychology, and his collaborators have been studying human perception of events for the last ten years. A recent paper, in press at the Journal of cognitive neuroscience, and available at his website (pdf) argues that perceptual event boundaries occur in experience at points where prediction becomes difficult.
[…] working memory representations of the current event guide perceptual predictions about the immediate future [less than 10 sec]. These predictions are checked against what happens next in the perceptual stream; most of the time perceptual predictions about what happens next are accurate. From time to time, however, activity becomes less predictable, causing a spike in prediction errors. These spikes in prediction error are fed back to update working memory and reorient the organism to salient new features in the environment. According to this model, the increase in prediction error and consequent updating results in the subjective experience of an event boundary in perceptual experience.
The tenets of Zacks’s view are (i) that the unity of experience consists in representations actively maintained in working memory; (ii) present experience consists partly in anticipations of future experiences. Memory, insofar as it enters the stream of experience, would be on this account proleptic, forward-looking; mere recall has no place.
Aristotle says that animals don’t recollect: they don’t search their memories for information about the past (De memoria ii, 453a8, Hist. anim. 488b26; see Grote, Aristotle 476). On what grounds he said that I don’t know, but whether it was a shrewd surmise or a lucky guess he seems to have been right. Aristotle also put forward a version of what became the predominant philosophical picture of memory—that it consists in the registering of an “impression” which is subsequently to be recalled, as if the mind had a filing-card drawer or a mental museum (such as figured in Ancient and Renaissance arts memoriæ). That picture, attractive though it is, may well be fundamentally misleading. Modelling biological memory on the specifically human capacity that consists in voluntary recall of items subject to intersubjective standards of accuracy (e.g., the procedures of memorization employed by the reciters of epic poetry, to take an example Aristotle would have known) may turn out to be yet another case where intuition has led us astray.
A predominantly proleptic function for working memory, moreover, fits nicely with theories according to which perception requires activity on the part of the perceiver, so that the perception of red, for example, to use Mohan’s example (taken from Justin Broackes) is effectively the perception of a pattern of sensations that arises from the perceiver’s having regarded the red thing from several perspectives—a feat normally posssible only by moving. Event perception too may be governed, if not by activity itself, then by anticipations of activity.
On the difference of humans from animals and the difference it makes
This is a response to a post on Justin Erik Halldór Smith by the philosopher of that name, and containing comments by Abraham Stone and Frans de Waal. You might well want to read that first before reading this.
The problematic here can be found already in Spinoza and Bayle. It can be resolved into two challenges to the person who holds that there is a profound difference, in the moral sphere, between humans and animals. The first challenge is to exhibit a difference between humans and every other species of living thing that is not a mere matter of degree; the second is to show that that difference has moral significance, e.g. that on its basis we have duties toward humans that we don’t have toward animals. I’m not sure even the first challenge can be met, let alone the second.
Every time I read Spinoza I’m troubled by the lack of motivation for his claim that humans can treat animals as we please (subject to their “natural right” against us, which is nothing more than their power to resist or overcome us).
His account of the difference is that it is a matter of complexity; but complexity is a matter of degree; it is, moreover, not easily seen to be of moral significance, and certainly not to the degree required for the contrast Spinoza draws. I think Abe is on the right track when he says that the main motivation for making the possession of reason an all-or-nothing affair is to build as high a wall as possible between us and the rest of the living world; and if even so vernunftgetrunkenen a philosopher as Spinoza gets swept away by prejudice, then clearly something powerful lies behind it.
The best one can do on Spinoza’s behalf, I think, is to take it that in the Part 4 conception of morality the only basis other than power for rights (or rather for justice) is the Hobbesian state, which requires the capacity to understand and enter into contracts. Only humans, it would seem, have this capacity, and so only humans fall within the scope of justice. It’s still not easy to see how this squares with the physiological notions of Part 2, but at least the criterion is not arbitrary, and not a matter simply of our having more power. (As for the good of Part 5, the eternal love of God, that would seem to be accessible to every individual to the limit of its capacities for adequate knowledge.)
Taking this into the present, the evidence now favors the claim that intelligence is a matter of degree—except for the matter of language use. But here two additional issues would need to be addressed: whether the capacity to use language is an indissoluble, all-or-nothing capacity and whether the appearance of a discontinuity between us and the rest of the animal kingdom isn’t perhaps an artifact of the extinction of other hominids intermediate in capacity between us and surviving primates. If there are stages or degrees in language-acquisition, some of which are already present in extant species, and a full spectrum of which would have been instantiated in our hominid relatives, then in order to make “the” capacity to use language decisive you would have to explain why the precise version of it possessed by humans, or rather why the difference between that version and the others, should have moral significance. I myself don’t see much hope of that.
I think the point about our comprehension of one another as human is well taken (JS: “The only reason why we don't have any problem attributing intelligence to other human minds is that we need to suppose their existence on practical grounds”). I would add that humans who are not prepossessed by the thought that there is some deep metaphysical divide between us and the rest of the living world, though they of course distinguish themselves from other species, often regard animals as having minds. The “theory of mind” is not restricted to humans. We model them as childlike, as dependent, in part because in human society they are dependent, in part because like children they don’t have all the capacities or knowledge of adult humans. Nevertheless domestic animals, the ones we live with for years, and whom we get to know as individuals, have a sort of moral standing; and if that is thought to be some sort of invention, then I need to have shown to me the grounds upon which our attribution of moral standing to each other is not.
A New Year’s Eve post by Matt Yglesias describes quite well the mental dynamics of giving up the habit. It’s not all sweetness and light—not even if you want to quit and succeed in quitting.
There are, I suppose, people who come to hate smoking when they give it up. I don’t. I do dislike the taste of it in my mouth now. That is my primary device to turn away the urge when it comes. But I don’t think that smoking is evil. It harms the body: that much is certain. For that reason I prefer having quit to the alternative.
Smoking also makes you more or less completely a slave. The means, often time-consuming, sometimes self-abasing, by which dedicated smokers overcome the inconveniences put in their way testify to that. As do the rationalizations for continuing to smoke. Which is not to say that there isn’t some merit to the thought that disapproval of smoking is part of an increasingly repressive culture, one in which perceived risk provides a pretext for greater surveillance and control.
Women are from Venus, men are from Venus
You may have heard about the new study that purports to show that women are less happy than men. Fortunately, Language Log has developed a vaccine that will immunize you against the stupidity issuing from, among other venues, the New York Times. Meanwhile, Deborah Cameron argues in the Guardian that with respect to their use of language, men and women aren’t all that different (see also her new book, The myth of Mars and Venus, from which the Guardian piece is an extract; find it at Best Book Buys, isbn.nu, Powells, ABE).
The brain apparently has a “checklist”—a means of recording that some sequence of actions is finished (see MIT Neuroscientists Describe Brain's ‘Checklist’, Science Daily 8 Sep 2003, on work by Ann M. Graybiel and Naotaka Fujii). A malfunctioning checklist might lead to obsessive-compulsive behavior. Kevin Burton, Feedblog.