Define physicalism as the thesis that the things described by physics — whatever those may turn out to be — are the only things which ‘really’ exist. Define materialism as the additional thesis that those ‘things’ happen to be the material substances described by Newtonian physics: the idea of the world as a “great machine.” Under this definition, there can hypothetically be a non–materialist physicalism, and I will describe a possible one shortly (though I will assume that idealistic interpretations of quantum physics, even if accurately representing the cutting edge picture of the world revealed by the most modern physics, should not be characterized as ‘physicalist’). But now, consider materialism. What would have to follow about the nature of consciousness, were the materialist thesis as defined here true?
First, let’s be abundantly clear as to what we mean here by “consciousness.” We are not referring merely to a person’s ability to do the kinds of things they are able to do when in a waking state as opposed to a sleeping state—the ability to react to stimuli, give verbal reports, and so forth. Rather, we are referring very specifically to phenomenal conscious experience per se: the ‘redness’ of red, the ‘painfulness’ of pain, the ‘happiness’ of happiness, and so forth, whenever any of these are consciously experienced. By phenomenal, we mean that there is a character to these experiences that simply cannot be explained—when I talk about the ‘painfulness’ of pain, you know what it is that I’m referring to; but only because you have experienced the phenomena yourself. This is simple, but it is the primary data which philosophy of mind is concerned with, and discussions in philosophy of mind routinely get bogged down in confusion over just which sense of the term “consciousness” someone is using at any given time.
Now, if materialism is true, then one thing must necessarily follow: if material events are all that really exist, then either phenomenal conscious experience must literally be a material event, or else it simply cannot exist at all—and as will soon become clear, these options aren’t actually alternatives to each other. But it is indisputably clear that conscious experience does exist. It would be meaningless to try to call it an “illusion,” because this merely leads to a regress: is that “illusion” being experienced, or not? If it is, then it really exists, and it isn’t an illusion; and if it isn’t, then it isn’t an illusion here either, as illusions have at least a certain form of ‘existence.’ Thus, it may make sense to call certain aspects of the way consciousness appears illusory, but it would make no sense to call consciousness itself an illusion: either it exists, or it doesn’t; and as is indisputably evidenced by the fact that it feels like something for you to be sitting where you are, reading this at this very moment, it incontrovertibly does. This paragraph may sound trite, but a small subset of philosophers who recognize the failure of other forms of physicalism yet remain dogmatically attached to the materialist thesis anyway call themselves “eliminative materialists” and happily deny that conscious experience really exists at all—preposterously, they are more convinced of an indirect inference they have consciously made (that is, the one from scientific observations to the real existence of ‘material substance’) than of the very existence of their conscious experience itself.
So, might trying to identify conscious experience with a material event rescue materialism? Not any more than eliminating it could, because this is in effect just what “identification” does: recall that we described the definition of consciousness we are using here by using as example the ‘redness’ of the color red, that is, the ineffable phenomenal experience per se. When we give a description of the process of this perception in strictly material terms, it comes out something like this: lightwaves vibrating at 650 nanometers strike electrical synapses wrapped inside balls of vitreous, are converted into electric impulses which excite neurons in section V4 inside a grey organ inside the skull. Then a reaction is produced: blood flow to the section of the grey organ known as the amygdala increases, and the signal from neurons in V4 travels to the nervous system, causing the body to move.
Is there a problem with this description? Obviously, it totally omits any mention of experience. Not only is there no possible way that a ‘material’ account can hint that the excited neurons in section V4 of the brain are perceived as the redness of red in particular — it can’t even hint that any experience accompanies those neurons at all. There is no hint here — and on materialist terms, no possible way to hint — that the increase of blood flow to the amygdala feels like what we know as fear; or that it feels like anything at all — or that the transfer of the signal from photoreceptor neurons to the nervous system feels like the intention to move (or anything at all), and so on. But if two things are identical, then a full description of each should reveal that identity: if it turns out that my next door neighbor Jim and the robber on fourth street happen to be the same person, then a full description of both should make this obvious. Yet there is no way in principle that experience–per–se can ever be put in ‘material’ terms, and no way in principle that any material description of anything can ever hint at whether or not there is any experience accompanying that process at all (nevermind its particular character and quality). So “identifying” conscious experience with something other than conscious experience necessarily can only ‘work’ by wholly eliminating it.
Another way of talking about identism is with the term ‘supervenience.’ But it is clear that this term introduces nothing new to the conversation thus far: it collapses into either identism or eliminativism. Consider the analogy that is usually made—one example of a ‘supervenient’ relationship in nature is in the relationship between ‘wetness,’ a property of water, and the properties of molecular H2O behavior: wetness is said to ‘supervene’ on this micromolecular activity. What does this really mean? In essence, what it actually means is that ‘wetness’ is a shorthand term we use to describe the behavior of H2O molecules when a detailed description of the latter is unnecessary (i.e., all practical everyday intents and purposes). So the disanalogy in the relationship between wetness and H2O molecules on the one hand, and conscious experience and the brain on the other is actually instructive as to why identism fails: when we understand the behavior of H2O molecules, there is nothing left about ‘wetness’ to understand! Yet there is clearly something crucial left to understand about consciousness even after we have explained the physical processes of the brain.
Furthermore, the phenomena we refer to as ‘wetness’—precisely because it is identical with the micromolecular behavior of H2O—simply follows logically from that very behavior: there is no way that something could exhibit that behavior at the microphysical behavior, and not be “wet.” But something could easily perform the physical processes of the human brain, and not be conscious. When we understand how molecules of H2O roll across each other because of their loose connections, and when we understand how another object composed of more tightly connected molecules would fall through the gaps between those loosely collected molecular rings of H2O (that is, sink), then “wetness” follows as a straightforward logical consequence and there is nothing left about it to understand. But when we understand how neurons connect and relate in material terms, however, we do not understand conscious experience; it does not follow as a straightforward logical consequence. So the relationship is not one of ‘supervenience’ and consciousness is not identical with any material substance. So, the materialist version of physicalism (as I have defined these terms) necessarily fails; it doesn’t even exit the gate to become a live option, as it could only work by either eliminating conscious experience or ‘identifying’ it with something that is not conscious experience (which amounts to eliminating it). With materialism done away with, physicalism isn’t necessarily dead. There is at least one form of physicalism which is not materialist: nonreductive emergentism. I will assume here that it is the only form of ‘physicalism’ worthy of the name and thus conclude that between eliminativism, identism, and emergentism, ‘physicalism’ is exhausted.
Nonreductive emergentism admits that consciousness is a real phenomena in its own right, and contends that it is in some sense ‘produced’ by the physical processes of the brain. The first problem is already clear: how? The interaction problem — “how is it that mind and brain, conceived as categorically different types of things, interact?” — is often taken to be a conclusive argument against accepting substance dualism. But it seems that any nonreductive physicalism must necessarily put itself in precisely the same boat, unable to give any explanation of how it is brains produce minds — which is, clearly, a kind of interaction. Furthermore, a nonreductive emergent view could either proclaim consciousness an epiphenomena, or grant that conscious experience has genuine causal efficacy, and either way, there is a definitive problem. Arguably, emergent physicalism has to proclaim consciousness an epiphenomena, since its claim by definition is that consciousness is produced by physical processes. If so, the problem is that this qualifies as a modus tollens conclusively refuting emergentism, because epiphenomenalism is demonstrably, irredeemably false.
The contention of epiphenomenalism is that conscious experience has no causal efficacy of any kind. That is, the relationship of the physical processes of your brain to your conscious experiences is like the relationship of your actual body to your reflection in a mirror: your body at time slice (1) makes movement (a), which causes mirror movement (A) in the reflection. At time slice (2), your bodily movement (a) continues into movement (b), which causes mirror movement (B) in the reflection. The actual causality, on this view, is running from (a) to both (A) and (b), and then from (b) to both (B) and (c). If it appears that (A) causes (B), then this is only an illusion, and (A) certainly has no causal impact on (b). Alternatively, Thomas Huxley in the nineteenth century famously described it by stating that mental events are like “the steam whistle which signals but doesn't cause the starting of the locomotive.” Now, philosophies should not be dismissed out of hand simply because they seem unintuitive. But there is a very simple reason why epiphenomenalism is in a pathetic degree of error about the nature of consciousness: we are talking about it right now. You are reading these words, which refer to conscious experience, and you understand what they mean. If conscious experience per se were purely a byproduct of physical processes with no causal efficacy of its own, this would simply not occur, because the supposedly ‘physical’ processes producing your supposedly epiphenomenal conscious experience of thought would have no concept of conscious experience in order to be able to think about it as you are at this very moment: conscious experience would not exist in the causal order such that your physical brain could ever produce any thoughts directly about it. Yet, we demonstrably can communicate ideas about conscious experience per se through (physical) speech—and on that one consideration alone, epiphenomenalism is conclusively refuted.
So might nonreductive emergentism contain room to acknowledge the reality of causally efficacious experience? Probably not. Emergentism is a very similar notion to the idea of supervenience which we discussed and dismissed above: all the natural examples involve cases where the supposedly ‘emergent’ (or supervenient) phenomena are not truly new phenomena over and above that which they ‘emerge’ from (or supervene upon). But suppose for the sake of argument that it truly could be possible: how, then, would this option be any better than substance dualism at all?!
Not only are we left with no possible way to explain how conscious experience emerges from material substance, we are also left with an exact analogue of the interaction problem again: how does conscious experience effect those material substances? In fact, nonreductive physicalism faces an even worse version of the problem than dualism does, and it very likely faces it in a way that is—unlike for dualism—insoluble because it is simply flat out conceptually incoherent: how does conscious experience exert causal power over the very microphysical processes which it emerges from? At worst, this is equally as incoherent as supposing that the phenomena of ‘wetness’ could somehow exert causal power over the very molecules of H2O which it supervenes upon. At best, this leaves nonepiphenomenal emergentism facing the same problem which supposedly refute dualism and left physicalism as a given by default … even more severely than dualism itself. So if the interaction problem was our motivation for abandoning dualism, then it should be a far greater motivation for abandoning emergentism.
But there is a second, and largely epistemological, problem with both classes of emergentism too—take my definition of it: “consciousness is a real phenomena in its own right … that it is in some sense ‘produced’ by the physical processes of the brain….” Dualism admits that consciousness is a real phenomena. So what does the step towards emergentism do, besides add the additional premise that consciousness must be produced by physical processes in the brain? Nothing—it does nothing else at all. But how could this step be justified? What kind of observation could possibly establish once and for all that consciousness is ‘produced’ in this way (besides, perhaps, the cessation of consciousness at death?) Observing that reported states of consciousness consistently correlate with particular physical brain states could just never accomplish this in principle, since the mere observation of correlation is (again!) not proof of any particular direction of causation. So could anything possibly falsify emergentism? It seems not. There is a further, important confounding variable: we never observe others’ states of consciousness directly. Rather, we are relying on verbal reports—and those reports necessarily have to be spoken, by mouths attached to brains. Thus, relying on such verbal reports to try to determine whether consciousness can exist without the brain places us in a position like that of primitives who have discovered a television set and are attempting to determine whether the images flashing across its screen are produced by it, or whether the television is merely transmitting a signal of some sort from elsewhere: what kind of test could we possibly devise; what kind of empirical finding could possibly establish once and for all that the television is indeed producing the images individually? Observing that the images stop when a button is pressed would clearly not suffice. So even if the problems above did not conclusively refute emergentism, is there anything that could possibly warrant our belief in it?
And thus, the “physicalist” options are exhausted. Eliminativism is preposterous. Identicism is incoherent. Epiphenomenalism cannot account for the fact that we are discussing consciousness here at all. And emergentism, the most plausible option of the bunch, not only faces exactly the same problem that dualism faces—twice, and even more severely both times (on the upwards direction, we have not only the problematic question of how material processes could provide inputs into conscious experience but the further problematic question of how material processes could produce consciousness itself; in the downwards direction, we have not only the problematic question of how consciousness can influence material processes but the further problematic question of how it could influence the very same material processes which it is emerging from). Perhaps barring idealistic interpretations of quantum physics which I have excluded by definition, there are no ‘physicalist’ options left.
Now that the options it is being compared to are clearer, let us revisit the interaction problem for substance dualism. Just how destructive is this problem for dualism by comparison? We have outlined how emergentism faces exact analogues of the interaction problem which are even more severe than those facing dualism, and summarized those in the preceeding paragraph. But on emergent physicalism, it is clear that there must be intermediate mechanisms between microphysical processes and consciousness: there is clearly something to explain about how the microphysical could ‘produce’ conscious experience. But the same is not obvious on dualism! Why is this? Because it is not clear that, on dualism, there would be any intermediate mechanism in need of explanation.
Consider: we can ask why it is that turning the ignition on a car causes the engine to start, because there is something in between the two that can be given an explanation. But it would make no sense at all to ask how pressing the gas pedal causes it to move, since this is so basic that there is nothing inbetween the two that could possibly be elaborated on. On dualism, the interaction between mind and brain is plausibly more like the relationship between pressing the gas pedal and causing it to move than it is like turning the keys and wondering why it should follow that the engine then starts. But even supposing there were intermediate mechanisms mediating the dualistic interaction, it would still follow that the burden of explaining them would not be so heavy for dualism: for, on dualism, it probably follows as a consequence that we should have no way of understanding them! To understand this point, consider a case in which a sort of dualism would hold: suppose we are all, at this very moment, plugged up into virtual reality machines.
Our memories of our outside selves have been erased, so that we assume we are identical to our virtual avatars. In this world, there is a dualism between the real self and the virtual self. From within that virtual world, we would never — in principle — be able to locate or identify our ‘real self’ (except at best perhaps by inner reflection). No matter how long we probed our virtual brains, we would never locate our actual real minds inside of them (since our real minds would not, in fact, be inside of them). And for just the same reason, it should follow that we would never — from the limited perspective we are capable of within that virtual world — know anything about whatever mechanisms intermediate between our real, and virtual, selves to conduct the interaction. Therefore, on dualism, either there are no intermediate mechanisms and thus nothing about interaction in need of explanation, or else there are intermediate mechanisms which dualism itself predicts we should have no capacity to understand. By contrast, emergent physicalism (the only kind of physicalism potentially capable of avoiding the eliminative–epiphenomenal trap) in the best case faces that problem twice as many times as dualism would have, were it truly even a serious difficulty for dualism at all.Dualism therefore remains a live option which is neither trivially nor obviously false. As the renouned materialist philosopher William Lycan, admits in Giving Dualism its Due, “the standard objections to dualism are not very convincing; if one really manages to be a dualist in the first place, one should not be much impressed by them.”
He continues, “Being a philosopher, of course I would like to think that my stance is rational, held not just instinctively and scientistically and in the mainstream but because the arguments do indeed favor materialism over dualism. But I do not think that, though I used to. My position may be rational, broadly speaking, but not because the arguments favor it … My purpose in this paper is to hold my own feet to the fire and admit that I do not proportion my belief to the evidence.” So, in conclusion: depending on whether an emergent physicalism which does not imply epiphenomenalism is possible (which in turn depends on whether it is even conceptually coherent to suppose an ‘emergent’ phenomena could have causal efficacy over the very processes it ‘emerges’ from), materialist physicalism is at worst not even a live option, and at best an even larger ‘leap of faith’ than dualism.
“Saying ‘science may someday find a way to reduce consciousness (or reference, or whatever) to physics’ is, here and now, saying that science may someday do we–know–not–what, we–know–not–how. And from the fact that those words may in the future come to have a sense we will understand, … (it does not follow that they mean anything now)….” (Putnam, 1999, p. 173).
Links for the Week (June 5–11, 2011)
• (1) South African Medical Journal Vol.98, No.10 (2008): Regarding the studies in South Africa which claimed to find that circumcision was an effective measure for HIV prevention, see the editorial ‘Rolling out male circumcision as a mass HIV/AIDS intervention seems neither justified not practicable’ (p. 781), which states the following: “Three randomized controlled trials (RCTs) from South Africa, Kenya and Uganda in 2006–2007 show a protective effect of male circumcision (MC). However, Garenne [6] has subsequently shown from observational data that there is considerable heterogeneity [inconsistency] of the effect of MC across 14 African countries. Despite the South African RCT showing a protective effect, he reports for the nine South African provinces that ‘there is no evidence that HIV transmission over the period 1994–2004 was slower in those provinces with higher levels of circumcision.’ Interestingly, in both Kenya and Uganda, where two of the RCTs were done, a protective effect of MC was observed, but a harmful effect was observed in Cameroon, Lesotho and Malawi. The other eight countries showed no significant effect of MC.”
• (2) An article on pp.762–766 addresses the issue as well, concluding that “Male non–therapeutic infant circumcision is neither medically nor ethically justified as an HIV prevention tool. … the WHO and UNAIDS appear to be basing these multi–million–dollar prevention programmes on limited and … biased information. In order to prevent … misguided decisions … a much broader review process would be called for. Such a process would involve more objective scientific opinion, and the involvement of a representative panel of African experts, such as paediatric surgeons and neonatologists.”
• (3) Likewise, see this study (“Cost-effectiveness of newborn circumcision in reducing lifetime HIV risk among U.S. males.”) in the National Institute of Health which found that circumcision “reduced the 1.87% lifetime risk of HIV among all males by about 16%.” In other words, the 1.87% risk was reduced by 0.29% to about 1.57%. Or in other words, 1000 circumcisions will only help prevent about 3 contractions of HIV ( from 19 to 16). Keep in mind that this is probably the single most touted medical benefit of male circumcision!
• (4) Quote: “Our society has become excessively commoditized. Anything that can be easily marketed is going to attract all the money and the attention, bypassing other ways of being that are harder to market but usually more effective. The people who came up with Barbie dolls made tons of money, while people who are trying to teach children how to play with each other, or parents how to interact with their children, did not. So if you were trying to make a living in child care, what would you do? I’m sure there are a lot of idealists out there who would become kindergarten teachers, day-care providers, and the like, but that’s not where the money is. The big money is in Barbie dolls. Barbie dolls are portable. They can be easily transported, traded, and sold. They are easy to price. It’s easy to assign property rights to them.
On the other hand, trying to sell knowledge of how to interact with children is much more difficult. It’s harder to price; you have to determine whether a person actually knows about children based on their resume and experience. It’s harder to market, because knowing the basic techniques of dealing with children is not an object like a Barbie doll. Once someone else picks up this knowledge, the expert teacher has lost their exclusive possession.”
• (5) Wikileaks: More Children Imprisoned at Guantanamo than U.S. Claimed
• (6) Wikileaks: GMO conspiracy reaches highest levels of US Government: “There’s nothing they are leaving untouched: the corn, the okra, the bringe oil, white rice, the cauliflower. Once they have established the norm: that seed can be owned as their property, royalties can be collected. We will depend on them for every seed we grow of every crop we grow. If they control seed, they control food, they know it – it’s strategic. It’s more powerful than bombs. It’s more powerful than guns. This is the best way to control the populations of the world. The story starts in the White House, where Monsanto often got its way by exerting disproportionate influence over policymakers via the “revolving door”.”
• (7) An absolutely brilliant, impeccably researched and sourced essay countering the claims of the locavorist movement (which proposes that everyone should buy all and only local foods): “Green” Eggs and Ham? The Myth of Sustainable Meat and the Danger of the Local, by Vasile Stănescu (who “is a PhD candidate in the Program of Modern Thought and Literature at Stanford University and the recipient of distinguished awards and prestigious nominations for his writings on animal and environmental issues.”)
• (2) An article on pp.762–766 addresses the issue as well, concluding that “Male non–therapeutic infant circumcision is neither medically nor ethically justified as an HIV prevention tool. … the WHO and UNAIDS appear to be basing these multi–million–dollar prevention programmes on limited and … biased information. In order to prevent … misguided decisions … a much broader review process would be called for. Such a process would involve more objective scientific opinion, and the involvement of a representative panel of African experts, such as paediatric surgeons and neonatologists.”
• (3) Likewise, see this study (“Cost-effectiveness of newborn circumcision in reducing lifetime HIV risk among U.S. males.”) in the National Institute of Health which found that circumcision “reduced the 1.87% lifetime risk of HIV among all males by about 16%.” In other words, the 1.87% risk was reduced by 0.29% to about 1.57%. Or in other words, 1000 circumcisions will only help prevent about 3 contractions of HIV ( from 19 to 16). Keep in mind that this is probably the single most touted medical benefit of male circumcision!
• (4) Quote: “Our society has become excessively commoditized. Anything that can be easily marketed is going to attract all the money and the attention, bypassing other ways of being that are harder to market but usually more effective. The people who came up with Barbie dolls made tons of money, while people who are trying to teach children how to play with each other, or parents how to interact with their children, did not. So if you were trying to make a living in child care, what would you do? I’m sure there are a lot of idealists out there who would become kindergarten teachers, day-care providers, and the like, but that’s not where the money is. The big money is in Barbie dolls. Barbie dolls are portable. They can be easily transported, traded, and sold. They are easy to price. It’s easy to assign property rights to them.
On the other hand, trying to sell knowledge of how to interact with children is much more difficult. It’s harder to price; you have to determine whether a person actually knows about children based on their resume and experience. It’s harder to market, because knowing the basic techniques of dealing with children is not an object like a Barbie doll. Once someone else picks up this knowledge, the expert teacher has lost their exclusive possession.”
• (5) Wikileaks: More Children Imprisoned at Guantanamo than U.S. Claimed
• (6) Wikileaks: GMO conspiracy reaches highest levels of US Government: “There’s nothing they are leaving untouched: the corn, the okra, the bringe oil, white rice, the cauliflower. Once they have established the norm: that seed can be owned as their property, royalties can be collected. We will depend on them for every seed we grow of every crop we grow. If they control seed, they control food, they know it – it’s strategic. It’s more powerful than bombs. It’s more powerful than guns. This is the best way to control the populations of the world. The story starts in the White House, where Monsanto often got its way by exerting disproportionate influence over policymakers via the “revolving door”.”
• (7) An absolutely brilliant, impeccably researched and sourced essay countering the claims of the locavorist movement (which proposes that everyone should buy all and only local foods): “Green” Eggs and Ham? The Myth of Sustainable Meat and the Danger of the Local, by Vasile Stănescu (who “is a PhD candidate in the Program of Modern Thought and Literature at Stanford University and the recipient of distinguished awards and prestigious nominations for his writings on animal and environmental issues.”)
SSRI: Slanted Studies; Research Inadequate
We’ve all seen the commercials for antidepressants; you can hardly turn on a TV and miss them. And we’ve all heard jokes about the side effects listed off by a rushed voice while some joyful ovoid creature ironically bounces happily across the screen. But there’s something much deeper about these commercials worth criticizing which fewer people even think to notice: their presentation of the idea of a “chemical imbalance.” (For instance, take this commercial for Zoloft, and pay attention to the bit from 0:21 to 0:30 seconds.) The kind of marketing represented by these commercials has ingrained this notion into popular question so deeply that it is hardly ever questioned at all, but there is surprisingly little evidence to support the idea.
In fact, the evidence is so weak that in Ireland in 2003, GlaxoSmithKline (the maker of Paxil, Wellbutrin, and other antidepressant drugs) published a letter explaining that, in response to demands from the Irish Medical Board, they were retracting their previous advertisements claiming that Paxil “works by bringing serotonin levels back to normal.” This claim amongst others, they explained, was “not consistent with the scientific literature.” An article published in the Public Library of Science in November 8, 2005 by Jeffrey R. Lacasse and Jonathan Leo, titled ‘Serotonin and Depression: A Disconnect between the Advertisements and the Scientific Literature,’ noted this event: “The Irish equivalent of the FDA, the Irish Medical Board, recently banned GlaxoSmithKline from claiming that paroxetine corrects a chemical imbalance even in their patient information leaflets.” The authors then go on to describe correspondence with various media outlets, none of which could supply any study to support their claims when questioned on their references to the chemical imbalance hypothesis. They conclude by rightly observing the problem with this promotion: “If a patient comes into the office believing the serotonin theory and the doctor doesn't take the time to correct them, we wonder where that leaves the issue of informed consent … they might have chosen an alternative approach to their distress if they were fully informed.”
If these drugs don’t work by correcting a ‘chemical imbalance,’ how do they work? Clearly, they do ‘work’ to produce altered states of consciousness and a whole host of possible side effects. And clearly, they do inhibit the reuptake of neurotransmitters. But quite simply, we don’t have to postulate any ‘chemical imbalance’ in order to explain or understand this. A drug like marijuana can at least temporarily ‘improve’ depression as well, but we don’t have to postulate any ‘imbalance’ of THC in order to understand this either. Dr. Steven Hyman, professor of neurobiology at Harvard Medical School and head of the National Institute of Mental Health from 1996 to 2001, noted in a paper titled Initiation and Adaptation: A Paradigm for Understanding Psychotropic Drugs that antidepressants work to create a state of mind that is “both qualitatively and quantitatively different than normal.”
To be completely clear, I don’t consider this necessarily to be a bad thing at all. The issue is not that people have some moral obligation never to experience drug–altered states, but that they should not be lied to or misled. If someone finds that marijuana, antidepressants, or anything else truly does work to relieve their depression, and they can use them in a responsible way that does not negatively impact their life, then by all means they should continue to do so. Whether either drug works by ‘correcting’ something or simply by creating drug-induced states which allow them to enjoy life is, in the end, totally irrelevant.
But while it is obvious that antidepressants do ‘work’ to produce altered states of consciousness, it is actually not clear that they ‘work’ to reduce depression due to their chemical action at all. To put this more directly, it is possible that the effect that antidepressants do have on depression is actually no more than a placebo effect. At first glance, this suggestion might sound absurd: don’t these drugs have to be proven more efficient than placebo to the FDA before they can be approved for popular use at all? Unfortunately, the situation just isn’t nearly so simple.
Marcia Angell, M.D. is an American physician currently working in the Department of Social Medicine at Harvard Medical School. She is also a member of the Association of American Physicians, the Institute of Medicine of the National Academy of Sciences, the Alpha Omega Alpha National Honor Medical Society, a Master of the American College of Physicians, and the first woman ever to serve as the editor-in-chief for the New England Journal of Medicine. In an article published to the New York Times’ Review of Books in January of 2009, she spoke out: “It is simply no longer possible to believe much of the clinical research that is published, or to rely on the judgment of trusted physicians or authoritative medical guidelines. I take no pleasure in this conclusion, which I reached slowly and reluctantly over my two decades as an editor of The New England Journal of Medicine. … [Drug] company employees or their agents often design the studies, perform the analysis, write the papers, and decide whether and in what form to publish the results. Sometimes the medical faculty who serve as investigators are little more than hired hands, supplying patients and collecting data according to instructions from the company.” She goes on to note part of the answer to the previous question: “The results of all the trials (there may be many) are submitted to the FDA, and if one or two trials are positive—that is, they show effectiveness without serious risk—the drug is usually approved, even if all the other trials are negative.” That is, the FDA doesn’t actually require proof that any drug is on the whole better than placebo; it only requires one or two studies; and negative results simply don’t count, meaning it doesn’t matter how many tries it might take for a manufacturer to find those two positive outcomes.
Furthermore, the results of all of these trials do not even have to be published.
In a landmark 1998 study (Listening to Prozac but Hearing Placebo: A Meta-Analysis of Antidepressant Medication), Irving Kirsch had performed a meta-analysis incorporating all the published studies on antidepressants into one large picture. He found that a whopping 75% of antidepressants’ effect could be attributed to placebo, which was surprising enough. But susequently, he was criticized by defenders of the benefits of antidepressants for only incorporating the published studies into his analysis without knowing what information the unpublished studies might hold—and so Kirsch and colleagues proceeded to file a Freedom of Information request against the FDA in order to gain access to these trials. What he discovered from this request alone is shocking: while roughly 94% of all published trials found a benefit for the antidepressants beyond placebo, forty percent of all studies were not published, because most of them did not find a positive result. Accounting for all the trials together, only about 51% of all trials found any benefit for antidepressants beyond placebo! Marcia Angell’s article, linked above, noted this phenomena as well: “A review of seventy–four clinical trials of antidepressants, for example, found that thirty–seven of thirty–eight positive studies were published. But of the thirty–six negative studies, thirty–three were either not published or published in a form that conveyed a positive outcome. It is not unusual for a published paper to shift the focus from the drug’s intended effect to a secondary effect that seems more favorable.” Clearly, once Kirsch’s analysis accounted for all these additional unpublished studies, the result for antidepressants would be even more dismal.
In the updated, more comprehensive analysis (Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration), the placebo effect now accounted for 82% of the antidepressants’ effect . So what does this number actually mean in practical terms? The studies in question ranked depression on what is known as the Hamilton Rating Scale (or HAM–D). An example HAM-D questionnaire can be seen here. When the statistic that placebo accounted for 82% of the antidepressant effect is translated into this scale, the result is that the net benefit of taking an antidepressant over taking a placebo is only 1.8 points! As the example questionnaire shows, a total of six points on this scale relate entirely to patterns of sleep. A 1.8 point difference could thus be explained in full if either patients in the drug group begin falling asleep more easily, or if they tend to stay asleep more easily, or if they find themselves falling asleep more easily if and when they do wake up during the night. And since many trials administer benzodiazepines like Xanax—well known for their sedative and hypnotic properties—along with the antidepressant in question, even this incidental detail alone might explain the small difference between the drug and placebo groups completely.
It is also crucial to note that even placebo-controlled studies of antidepressants are not always truly “double–blind.” In RCTs (random controlled trials) today, patients are not considered legally to have given true consent unless they consent with full knowledge of both the design of the study and the possible effects and side effects of the drug; and thus, they go into the trial knowing in detail what side effects the active drug is likely to produce. Then, if they experience those side effects, they can easily infer that they have been given the real thing; and if they do not, they can infer that they are on the placebo. This means that since expectations are lessened in those experiencing no side effects and raised in those who are, the placebo effect is actually weakened for the placebo control group and enhanced for the drug group. One study, indeed (Inert placebo versus active medication: Patient blindability in clinical pharmacological trials) found that 75% of all patients were able to correctly guess whether they were in the drug or placebo group, and that virtually 100% of those experiencing side effects were able to correctly guess that they were on the active drug. In another study (Side Effects and the ‘Blindability’ of Clinical Drug Trials), even an independent evaluator was able to distinguish whether patients were taking a placebo or the active drug on the basis of reported side effects alone. It is plausible that this unblinding effect might even explain the small difference between drug and placebo groups.
Psychologist David Antonuccio, a professor at the University of Nevada, points out another possible problem with clinical study design: many trials involve a ‘placebo wash–out’ period in which all participants are placed on a placebo for some specified period of time, so that anyone who responds positively to the placebo can then be removed from the study altogether. He says: “if you put everybody on an antidepressant and washed out everyone who responds, people would say, ‘That’s a very biased strategy against the drugs.’ Well, I believe we have a strategy here that’s biased against the placebo condition.” Another example is pointed out by Joanna Moncrieff, M.D. Senior Lecturer in Social and Community Psychiatry at the University College of London: in some trials, both the drug and placebo group are taken from groups of people who are already on the active drug prior to the trial. These individuals are then assigned either to continue using the active drug, or to be transitioned onto the placebo; so it is possible that the “control group” in some trials is actually not just on a placebo, but in a state of withdrawal—making it very easy to find that someone who is not in a state of withdrawal would rank better on measures of depression than someone who is. These are just two of many ways in which the study design of most clinical trials may be biased or corrupted, even on top of the inability to prevent unblinding, but it is not my purpose in this essay to survey every possible way that clinical studies can be corrupted.
In any case, one thing is clear: either the data sent to the FDA for the approval of these drugs was accurate, or it was not. If it was, then the conclusions of Kirsch’s meta-analysis hold, and these drugs should never have been approved. If it was not, then there was never any solid basis for concluding that these drugs are effective in the first place—and still they should never have been approved. Either we can safely conclude that these drugs have no real efficacy beyond placebo, or else we must admit that present data gives us no grounds for any conclusion at all and that efficacy has yet to be demonstrated. Certainly, many people do report and believe that antidepressants have helped them; for a long time, I was one of these people myself. The problem is that many people believe that inert placebos have helped them as well; and personal experience simply cannot determine whether a given response was placebo or due to a direct chemical effect—only rigorous statistical analysis can do so. And given the results of these studies, it is overwhelmingly likely that anyone who believes that an antidepressant has helped them would in fact have improved just as much on any inert substance.
If anything, this should be taken as good news for those who believe antidepressants have helped them: however much you believe your antidepressant has helped you, you probably in fact achieved that improvement yourself—and you should have little fear of relapse should you decide to go off of these drugs and save yourself the time, money, and risk of possible side effects (particularly over long-term use, where the possible effects of antidepressant use are still unknown) associated with continued use. However, there is one important word of caution: withdrawal symptoms in the days and sometimes weeks following going off of a medication can be severe, and these tend to be more or less dramatic in proportion to how quickly the drug was ended and how much of it was ended at once. If you decide to try going off of your antidepressant, you should taper off as slowly and gradually as possible, and try to find qualified supervision to guide you through the process. On the other hand, it is important to keep in mind that even dramatically lowered mood in the weeks following cessation of an antidepressant is not evidence of ‘relapse,’ but is overwhelmingly likely to be symptom of withdrawal which should pass quickly in time for almost everyone.
Still, there is one last important point to make before closing: if the conclusion you are beginning to draw from this is to think: “hey, if these drugs are just placebos, then I really don’t need them,” then this is perhaps not entirely accurate. In clinical trials, patients given placebos actually do improve substantially faster and more fully than patients who are given nothing at all. The benefit produced by a placebo actually is ‘real,’ and it is not all attributable to the improvement in depression that tends to happen naturally over time. Thus, if you believe that antidepressants have helped you and you are doing nothing else in particular to fight your depression, going off of them without replacing them with anything is probably not a good idea. To achieve the same level of improvement or more that antidepressants seem to have granted you, one would generally have to replace them with either an exercise regiment, or a vitamin regiment perhaps including neurotransmitter precursors and amino acids (I have personally found l–theanine, l–tyrosine, and 5–HTP beneficial), or psychotherapy, or something else. Like antidepressants, it is unlikely that any of these things is working to ‘correct’ any biochemical cause of depression on any direct physical level; but unlike antidepressants, all of these things are much cheaper, and none have any serious risk of negative side effects. In many cases they have positive side effects, as should be obvious enough in the case of exercise. In any case, the primary benefit of all of these things seems to come from mainly the mere fact of doing something while having faith in a positive outcome.
Our expectations of the future, whether positive or negative, tend to create loops of experience which feed on themselves. If we expect the future to be bleak, then we are likely to emotionally disengage, in which case this very act of disengagement tends to bring about an emotionally bleak future. Likewise, we are more likely to pay closer attention to ‘negative’ mood swings and consider them evidence of an approaching depression, thus pushing us into an even more negative mood. Yet, if we have positive expectations of the future, then this very attitude too tends to help create an emotionally engaging future—and we are more likely to focus on, and appreciate, our ‘positive’ mood swings instead. This is not to say that the experience of depression is ‘all in one’s mind’ or that it can simply be easily ‘willed away,’ however, as these psychological tendencies can take serious and difficult work to overcome. And not everyone comes preset with the same tendencies and expectations, either, meaning the job is objectively much harder for some people than others. But those who, for whatever reason, are set with a more difficult job should not be duped into believing that their depression has an actual biochemical ‘cause,’ as if dangerous and expensive drugs which aren’t even pleasurable are the only way to fight and overcome depression—even its most severe form.
In fact, the evidence is so weak that in Ireland in 2003, GlaxoSmithKline (the maker of Paxil, Wellbutrin, and other antidepressant drugs) published a letter explaining that, in response to demands from the Irish Medical Board, they were retracting their previous advertisements claiming that Paxil “works by bringing serotonin levels back to normal.” This claim amongst others, they explained, was “not consistent with the scientific literature.” An article published in the Public Library of Science in November 8, 2005 by Jeffrey R. Lacasse and Jonathan Leo, titled ‘Serotonin and Depression: A Disconnect between the Advertisements and the Scientific Literature,’ noted this event: “The Irish equivalent of the FDA, the Irish Medical Board, recently banned GlaxoSmithKline from claiming that paroxetine corrects a chemical imbalance even in their patient information leaflets.” The authors then go on to describe correspondence with various media outlets, none of which could supply any study to support their claims when questioned on their references to the chemical imbalance hypothesis. They conclude by rightly observing the problem with this promotion: “If a patient comes into the office believing the serotonin theory and the doctor doesn't take the time to correct them, we wonder where that leaves the issue of informed consent … they might have chosen an alternative approach to their distress if they were fully informed.”
If these drugs don’t work by correcting a ‘chemical imbalance,’ how do they work? Clearly, they do ‘work’ to produce altered states of consciousness and a whole host of possible side effects. And clearly, they do inhibit the reuptake of neurotransmitters. But quite simply, we don’t have to postulate any ‘chemical imbalance’ in order to explain or understand this. A drug like marijuana can at least temporarily ‘improve’ depression as well, but we don’t have to postulate any ‘imbalance’ of THC in order to understand this either. Dr. Steven Hyman, professor of neurobiology at Harvard Medical School and head of the National Institute of Mental Health from 1996 to 2001, noted in a paper titled Initiation and Adaptation: A Paradigm for Understanding Psychotropic Drugs that antidepressants work to create a state of mind that is “both qualitatively and quantitatively different than normal.”
To be completely clear, I don’t consider this necessarily to be a bad thing at all. The issue is not that people have some moral obligation never to experience drug–altered states, but that they should not be lied to or misled. If someone finds that marijuana, antidepressants, or anything else truly does work to relieve their depression, and they can use them in a responsible way that does not negatively impact their life, then by all means they should continue to do so. Whether either drug works by ‘correcting’ something or simply by creating drug-induced states which allow them to enjoy life is, in the end, totally irrelevant.
But while it is obvious that antidepressants do ‘work’ to produce altered states of consciousness, it is actually not clear that they ‘work’ to reduce depression due to their chemical action at all. To put this more directly, it is possible that the effect that antidepressants do have on depression is actually no more than a placebo effect. At first glance, this suggestion might sound absurd: don’t these drugs have to be proven more efficient than placebo to the FDA before they can be approved for popular use at all? Unfortunately, the situation just isn’t nearly so simple.
Marcia Angell, M.D. is an American physician currently working in the Department of Social Medicine at Harvard Medical School. She is also a member of the Association of American Physicians, the Institute of Medicine of the National Academy of Sciences, the Alpha Omega Alpha National Honor Medical Society, a Master of the American College of Physicians, and the first woman ever to serve as the editor-in-chief for the New England Journal of Medicine. In an article published to the New York Times’ Review of Books in January of 2009, she spoke out: “It is simply no longer possible to believe much of the clinical research that is published, or to rely on the judgment of trusted physicians or authoritative medical guidelines. I take no pleasure in this conclusion, which I reached slowly and reluctantly over my two decades as an editor of The New England Journal of Medicine. … [Drug] company employees or their agents often design the studies, perform the analysis, write the papers, and decide whether and in what form to publish the results. Sometimes the medical faculty who serve as investigators are little more than hired hands, supplying patients and collecting data according to instructions from the company.” She goes on to note part of the answer to the previous question: “The results of all the trials (there may be many) are submitted to the FDA, and if one or two trials are positive—that is, they show effectiveness without serious risk—the drug is usually approved, even if all the other trials are negative.” That is, the FDA doesn’t actually require proof that any drug is on the whole better than placebo; it only requires one or two studies; and negative results simply don’t count, meaning it doesn’t matter how many tries it might take for a manufacturer to find those two positive outcomes.
Furthermore, the results of all of these trials do not even have to be published.
In a landmark 1998 study (Listening to Prozac but Hearing Placebo: A Meta-Analysis of Antidepressant Medication), Irving Kirsch had performed a meta-analysis incorporating all the published studies on antidepressants into one large picture. He found that a whopping 75% of antidepressants’ effect could be attributed to placebo, which was surprising enough. But susequently, he was criticized by defenders of the benefits of antidepressants for only incorporating the published studies into his analysis without knowing what information the unpublished studies might hold—and so Kirsch and colleagues proceeded to file a Freedom of Information request against the FDA in order to gain access to these trials. What he discovered from this request alone is shocking: while roughly 94% of all published trials found a benefit for the antidepressants beyond placebo, forty percent of all studies were not published, because most of them did not find a positive result. Accounting for all the trials together, only about 51% of all trials found any benefit for antidepressants beyond placebo! Marcia Angell’s article, linked above, noted this phenomena as well: “A review of seventy–four clinical trials of antidepressants, for example, found that thirty–seven of thirty–eight positive studies were published. But of the thirty–six negative studies, thirty–three were either not published or published in a form that conveyed a positive outcome. It is not unusual for a published paper to shift the focus from the drug’s intended effect to a secondary effect that seems more favorable.” Clearly, once Kirsch’s analysis accounted for all these additional unpublished studies, the result for antidepressants would be even more dismal.
In the updated, more comprehensive analysis (Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration), the placebo effect now accounted for 82% of the antidepressants’ effect . So what does this number actually mean in practical terms? The studies in question ranked depression on what is known as the Hamilton Rating Scale (or HAM–D). An example HAM-D questionnaire can be seen here. When the statistic that placebo accounted for 82% of the antidepressant effect is translated into this scale, the result is that the net benefit of taking an antidepressant over taking a placebo is only 1.8 points! As the example questionnaire shows, a total of six points on this scale relate entirely to patterns of sleep. A 1.8 point difference could thus be explained in full if either patients in the drug group begin falling asleep more easily, or if they tend to stay asleep more easily, or if they find themselves falling asleep more easily if and when they do wake up during the night. And since many trials administer benzodiazepines like Xanax—well known for their sedative and hypnotic properties—along with the antidepressant in question, even this incidental detail alone might explain the small difference between the drug and placebo groups completely.
It is also crucial to note that even placebo-controlled studies of antidepressants are not always truly “double–blind.” In RCTs (random controlled trials) today, patients are not considered legally to have given true consent unless they consent with full knowledge of both the design of the study and the possible effects and side effects of the drug; and thus, they go into the trial knowing in detail what side effects the active drug is likely to produce. Then, if they experience those side effects, they can easily infer that they have been given the real thing; and if they do not, they can infer that they are on the placebo. This means that since expectations are lessened in those experiencing no side effects and raised in those who are, the placebo effect is actually weakened for the placebo control group and enhanced for the drug group. One study, indeed (Inert placebo versus active medication: Patient blindability in clinical pharmacological trials) found that 75% of all patients were able to correctly guess whether they were in the drug or placebo group, and that virtually 100% of those experiencing side effects were able to correctly guess that they were on the active drug. In another study (Side Effects and the ‘Blindability’ of Clinical Drug Trials), even an independent evaluator was able to distinguish whether patients were taking a placebo or the active drug on the basis of reported side effects alone. It is plausible that this unblinding effect might even explain the small difference between drug and placebo groups.
Psychologist David Antonuccio, a professor at the University of Nevada, points out another possible problem with clinical study design: many trials involve a ‘placebo wash–out’ period in which all participants are placed on a placebo for some specified period of time, so that anyone who responds positively to the placebo can then be removed from the study altogether. He says: “if you put everybody on an antidepressant and washed out everyone who responds, people would say, ‘That’s a very biased strategy against the drugs.’ Well, I believe we have a strategy here that’s biased against the placebo condition.” Another example is pointed out by Joanna Moncrieff, M.D. Senior Lecturer in Social and Community Psychiatry at the University College of London: in some trials, both the drug and placebo group are taken from groups of people who are already on the active drug prior to the trial. These individuals are then assigned either to continue using the active drug, or to be transitioned onto the placebo; so it is possible that the “control group” in some trials is actually not just on a placebo, but in a state of withdrawal—making it very easy to find that someone who is not in a state of withdrawal would rank better on measures of depression than someone who is. These are just two of many ways in which the study design of most clinical trials may be biased or corrupted, even on top of the inability to prevent unblinding, but it is not my purpose in this essay to survey every possible way that clinical studies can be corrupted.
In any case, one thing is clear: either the data sent to the FDA for the approval of these drugs was accurate, or it was not. If it was, then the conclusions of Kirsch’s meta-analysis hold, and these drugs should never have been approved. If it was not, then there was never any solid basis for concluding that these drugs are effective in the first place—and still they should never have been approved. Either we can safely conclude that these drugs have no real efficacy beyond placebo, or else we must admit that present data gives us no grounds for any conclusion at all and that efficacy has yet to be demonstrated. Certainly, many people do report and believe that antidepressants have helped them; for a long time, I was one of these people myself. The problem is that many people believe that inert placebos have helped them as well; and personal experience simply cannot determine whether a given response was placebo or due to a direct chemical effect—only rigorous statistical analysis can do so. And given the results of these studies, it is overwhelmingly likely that anyone who believes that an antidepressant has helped them would in fact have improved just as much on any inert substance.
If anything, this should be taken as good news for those who believe antidepressants have helped them: however much you believe your antidepressant has helped you, you probably in fact achieved that improvement yourself—and you should have little fear of relapse should you decide to go off of these drugs and save yourself the time, money, and risk of possible side effects (particularly over long-term use, where the possible effects of antidepressant use are still unknown) associated with continued use. However, there is one important word of caution: withdrawal symptoms in the days and sometimes weeks following going off of a medication can be severe, and these tend to be more or less dramatic in proportion to how quickly the drug was ended and how much of it was ended at once. If you decide to try going off of your antidepressant, you should taper off as slowly and gradually as possible, and try to find qualified supervision to guide you through the process. On the other hand, it is important to keep in mind that even dramatically lowered mood in the weeks following cessation of an antidepressant is not evidence of ‘relapse,’ but is overwhelmingly likely to be symptom of withdrawal which should pass quickly in time for almost everyone.
Still, there is one last important point to make before closing: if the conclusion you are beginning to draw from this is to think: “hey, if these drugs are just placebos, then I really don’t need them,” then this is perhaps not entirely accurate. In clinical trials, patients given placebos actually do improve substantially faster and more fully than patients who are given nothing at all. The benefit produced by a placebo actually is ‘real,’ and it is not all attributable to the improvement in depression that tends to happen naturally over time. Thus, if you believe that antidepressants have helped you and you are doing nothing else in particular to fight your depression, going off of them without replacing them with anything is probably not a good idea. To achieve the same level of improvement or more that antidepressants seem to have granted you, one would generally have to replace them with either an exercise regiment, or a vitamin regiment perhaps including neurotransmitter precursors and amino acids (I have personally found l–theanine, l–tyrosine, and 5–HTP beneficial), or psychotherapy, or something else. Like antidepressants, it is unlikely that any of these things is working to ‘correct’ any biochemical cause of depression on any direct physical level; but unlike antidepressants, all of these things are much cheaper, and none have any serious risk of negative side effects. In many cases they have positive side effects, as should be obvious enough in the case of exercise. In any case, the primary benefit of all of these things seems to come from mainly the mere fact of doing something while having faith in a positive outcome.
Our expectations of the future, whether positive or negative, tend to create loops of experience which feed on themselves. If we expect the future to be bleak, then we are likely to emotionally disengage, in which case this very act of disengagement tends to bring about an emotionally bleak future. Likewise, we are more likely to pay closer attention to ‘negative’ mood swings and consider them evidence of an approaching depression, thus pushing us into an even more negative mood. Yet, if we have positive expectations of the future, then this very attitude too tends to help create an emotionally engaging future—and we are more likely to focus on, and appreciate, our ‘positive’ mood swings instead. This is not to say that the experience of depression is ‘all in one’s mind’ or that it can simply be easily ‘willed away,’ however, as these psychological tendencies can take serious and difficult work to overcome. And not everyone comes preset with the same tendencies and expectations, either, meaning the job is objectively much harder for some people than others. But those who, for whatever reason, are set with a more difficult job should not be duped into believing that their depression has an actual biochemical ‘cause,’ as if dangerous and expensive drugs which aren’t even pleasurable are the only way to fight and overcome depression—even its most severe form.
Subscribe to:
Posts (Atom)