PhDwannabe

Typically, I define it while standing some distance outside of the Medical Science forum.

OK, so I'm not in the slightest sense a physicist, but I am something of a scientist, and, well... ...no f***ing way. Right?

You're totally right to be skeptical, and you should keep carrying that skepticism to the point where you say, "BS." Something I have told students many times: one of the best ways to evaluate a claim, if you don't have direct access to the evidence that might be used to test it, is to simply ask yourself how on earth somebody could possibly know it to be true or false. This is really a great example of a claim that can't be falsified very well. If I were to tell you: "think of an imaginary face," you say OK, and then I say, "actually, you didn't just imagine that face; you saw it some time in the past." How would you possibly go about proving me wrong? What positive evidence would I possibly have with which to establish something like this? We just don't have good access to the massive evidence we'd need--I haven't had anybody following you around snapping pictures of everyone you've ever looked at. I may as well be talking about the invisible unicorns in the room. Of course we can't measure them--they're invisible, stupid.

Seemed like a good idea at the time.

Real data? Real citations? Back to the dead horse we go! Let me, Marat, charitably distill the initial claims which you made which I took some issue with: 1) After a first suicide attempt, most people don't make another. 2) The exception is schizophrenics, who'll do whatever they can to finish if an attempt is not completed or interrupted. I called both of those into question. With regard to #1, I spoke up because past history of suicidality is one of the huge predictors of present or future suicidality. As Carlborg, Winnerback, Jonnson, Jokinen, and Nordstrom (2010) note: "In most studies, a history of self-harm or suicide attempts is the strongest risk factor for suicide (Cavanagh, Carson, Sharpe, & Lawrie, 2003)" (p. 1155). You haven't really responded to #1--I'm not asking you to, because the contrary point is so excessively well-supported by the literature--but you've responded to my questions about #2. First, with personal anecdote, followed by an (admirable) admission that it was personal anecdote. So, we already know why you think what you think. Now, post hoc, you've attempted to find some literature to support your anecdote-based inference. Let's take your citation that's got some decent data in it. I don't really want to deal with this: Because it's the kind of boilerplate, nodding shop-talk dreck that acts as filler in so many scholarly articles, and frequently it doesn't have anything to do with any sort of data. There's no data in this article, by the way; it's a review. So, let's look at the newer study with some data in it. What's really astounding is that the results here (Shrivastata et al., 2010), taken grossly, don't really support your claim at all... Fully 100% of their sample reported some amount of suicidality by the end of the study--48.3% of whom actually displayed attempts. Between 5 and 10% of schizophrenia patients eventually die by suicide. Where's this heroic effort to stop them once the attempt is initiated? The authors don't mention it. In fact, initial attempts, prior to or at the onset of treatment did not predict--as you claim would suggest they would--continued or further attempts: "Because most patients experienced emerging suicidality (suicidal behavior or ideation), a prior suicide attempt was not a good predictor of suicidality during the treatment phase" (p. 635). I thought schziophrenics were the only ones for whom history of attempts was predictive! The exception to the rule! Look: most schizophrenics are probably at some time suicidal, and making suicidal gestures. Most schizophrenics are not receiving adequate care of the sort that is always there to interrupt suicidality. Most schizophrenics (although certainly at a higher rate than normals--never disputed) are not dying by their own hand. Where's that "fanatacism" at? We don't need elaborate stats to doubt your claims here--simple baserates don't square with them. Indeed, the study actually casts doubt on your proffered explanation for your anecdotal hypothesis. When attempting to "reason through" your hypothesis "logically", you suggested the following: So, positive symptoms of schizophrenia are to blame for the persistence of suicidality, because they interfere with/are not amenable to the normal process by which other people are set right by the jarring experience of a suicide attempt. Let's see what Shrivistata and colleages have to say about it: "baseline severity of symptomatology, positive and negative symptoms, and global functioning in daily life (as well as gender, age, and duration of untreated illness before first hospitalization) may not help clinicians predict suicidality in schizophrenia patients. The mean positive symptoms score was reduced by more than 65% between baseline and the end of the study" (p. 636). Positive symptoms decreased quite a bit during the study--during a time when suicidality actually increased. Their schziophrenia symptoms--remember, the ones your dataless a priori reasoning process regarded as so important?--turned out not to have the effects you'd seem to have thought. Again, the authors: "patients who improved in the psychopathologic components of their disorder were at high risk of suicide" (p. 636). Again: "The results of the present study indicate that clinical improvement is not a key element in decreasing suicide risk. On the contrary, improvement in schizophrenia symptoms may increase suicidality" (p. 637). It's not the symptoms that are doing it. Look at the tables in the article. Read the stats. Isn't it wonderful how empirical data can show us these sorts of things, rather than just having to sit around and think about how it "logically" happens, based on our own biased and limited experiences? Edit: Looks like me and the Capn were simultaneously hard at work responding to this one. Happy to make some of the same points, Capn. We'll make a psychologist out of you yet.

Marat, to echo SMF's sentiments, I'm going to again respond to your "new" post--if it can be called new: ...with something I already said... We have little business sitting around and trying to reason through fundamentally empirical questions. You simply don't have the data to support your claims. You cover this by talking in circles. There's nothing wrong with logical reasoning--you can't form good hypotheses or design good studies without it, and it's as much a part of science as empiricism is (indeed, it's something that often seems sadly missing from many of my colleagues, who possess a lot of empirical acumen). But some claims simply sit further on one side or the other. This issue is substantially empirical. Continuing to try to make relatively decisive statements about it in the absence of empirical data is a waste of breath or keystrokes. You've already admitted where your inferences come from: This horse is dead. I'm done helping you beat it.

Well, there's my belly laugh for the day. Your experiential fallacy is not going to take you places with me. I have clinical experience in both inpatient and outpatient mental health environments, including experience with individuals suffering from psychotic disorders. Being a normal human, it confuses and deludes me often. Being a decent scientist, when I sense myself beginning to make large inferences from it, I wag my finger at myself in the mirror and tell myself I'm entering very dangerous territory. I try not to use too much logic in the service of what are essentially empirical questions. As much as I try not to resort to empiricism for what are essentially logical questions. Your claims are perfectly amenable to empirical investigation. They deserve more than a priori reasoning and the silly, biased pleas to personal clinical experience or judgment. Furthermore: Absolutely. All perfectly informative findings that I'm somewhat aware of already. The public's (and sadly, many professionals') predictions of both suicidality and violence/risk of harm to others from individuals with psychotic disorders is completely disproportionate to the real rates. A really important finding. Additionally, as the study you cite does an excellent job of demonstrating, empirically, factors which predict suicide among individuals with schizophrenia are not always obvious, and certainly not always what "clinical experience," or some sort of "logical" reasoning process might helpfully suggest. Great citations, SMF. Finally: Well, there is no "self-mutilation disorder," per se. Non-suicidal self-injury (NSSI) is a behavior not currently enshrined as a distinct diagnosis, but frequently found as part of larger patterns of behavior that we do classify as disorders, the really common ones being Borderline Personality Disorder, Major Depression or other mood disorders, eating disorders or Body Dysmorphic Disorder, or psychotic disorders, and to some extent, many major mental illnesses. You can also see the behavior in lower-to-moderate-functioning disorders of the autistic spectrum and various other developmental conditions, but that's kind of a different animal. I have little doubt that the people Marat is describing did indeed meet criteria for schizophrenia or a similar condition. NSSI, as well as gestures with higher degrees of suicidal intent, are certainly not unknown among those disorders--indeed, rates of them are higher within them than in the normal population. That's not really anything I'd dispute, or have disputed. The contention that schizophrenics, once they make a suicide attempt, will then do anything they can to complete it--that's something I wanted to see some data for, and have so far received nothing but one guy's report of his personal experiences. Which is worthless. Less than worthless, because it so often misleads. Look, I'll be really clear: I'm not even saying that this particular narrow claim of Marat's is impossible. I register my suspicion of it, because it seems to smack of some clinical biases people have about schizophrenics which I know that empirical findings have not borne out. I don't have any evidence against it. Since negative evidence really isn't evidence in most cases, I'm not really even making an affirmative stance to the contrary. I just think it's suspect, I want to see some real data, and in the absence of it (or worse, in the presence of only anecdote) I have no reason to accept it. If that data were out there, I'd be 1) surprised, 2) happy to accept it, and 3) happy to admit I'm surprised. I'm surprised often. It's a glorious thing to be wrong. Welcome to science, kids.

Tony, no big deal. In response to: #25 was asking, among other things, for some evidence for this claim of Marat's: The claim is not that schizophrenics have a higher rate of suicide. That's patently obvious and can be accepted without evidence--I have no argument and offered no argument there. Marat's claim is that schizophrenics, apparently, once admitted to the hospital after an unsuccessful attempt, are somehow primed to then complete the act later on by whatever means necessary. This desire to die was characterized as "fanatical." I asked for some evidence for this and Marat already admitted that it comes from nothing more than a single person's individual experience (his own). It's an unsupported junk claim.

The making of scientific inferences--whether observations of, descriptions of, or predictions of behavior or relationships between variables of any kind--based off of personal experience is the antithesis of what science is about. This is exactly the sort of thinking that the scientific method is there to mitigate. It's there to protect us from our casual observations, which delude more often than they inform. Yes, the suicide rate is obviously higher among those with major mental illnesses. Schizophrenia included. What does that have to do with what you quoted from me?

What? How on earth is a spray of pellets a disadvantage at point-blank range? Most people don't attempt suicide with a gun that's twenty yards away. There are few things civilians have access to with more stopping power at point-blank or standoff ranges than a shotgun. Any weapon can miss. I see absolutely no reason why a shotgun in particular would make a miss more survivable. That doesn't stand to reason. Back up your claim. Uhhhh... a history of past attempts is widely known to be among the strongest predictors for future attempts. Do you have any data whatsoever to support this claim? Do you have any data whatsoever to support this claim?

So, I'm not an engineer, but I think this is pretty sweet, and I figure engineers might enjoy it even more than I would.

Modern, empirically supported psychotherapeutic treatments did not exist in 1952. You're not criticizing chemistry, you're criticizing alchemy. Stradi, I've been through all of this with you in other threads. I'm not taking the bait again.

All things proceed outward from their core. JUST TELL ME IF THE ORBIT IS FURTHER AWAY IN THE FUTURE.

Very likely that you're talking about Bonnet Syndrome. It's quite common for people in your mom's position. It can be terribly unfortunate when people don't realize that this isn't psychosis. Let the great Oliver Sacks explain. If your mom doesn't know about this (especially if she is, as many people are, confused and fearful because of it) have her listen to the Sacks talk; she'll be incredibly happy to hear it.

My first instinct is to begin my response like this: We'd really call it "early adulthood," since you're a few years off of the more conventional figure of about 18-25, with a longer tail on the right. And the figure hides a lot of details, since it matters a great deal whether we're talking about the onset of negative symptoms (usually first) or positive ones (the "break"). And finally, that's males you're talking about. Female onset tends to be later and bimodal. But instead of going on, (and on, and on) Marat, I'm going to shirk my self-assumed responsibility to correct the numerous errors of fact and inference which hide within your distinguished and admirable prose. You've danced so many miles away from the OP's topic, and I'm just plain-old done dancin'.

Of course it doesn't appear in its "Western form." Neither does depression. Or breakfast or dinner, for crap's sake. They don't have houses in the "Western form" over there either. But they're still houses. The stable baserate of schizophrenia across an enormous range of cultures is one of the fascinating truisms of psychiatric epidemiology. Yeah, it looks different. It'd be pretty weird if it didn't. The fact remains, about 1% of the population, here, there, everywhere, experiences symptoms that we in the West call "psychotic." They're different, but recognizable. Additionally: Nope. Nope. Although service availability and monitoring is obviously lower in rural, less developed areas, so they're more "invisible" than in urban areas. So, what about this?... Oh, I don't know; why was diabetes never "clinically identified" until the 19th century? This weird fatiguing syndrome with sweet-tasting urine was described thousands of years ago, but diabetes wasn't. Similarly, many forms of thought disorder and behavior associated with psychotic symptoms were described throughout history, but schizophrenia wasn't. Again, why are we surprised by this? Why does that make it made-up, or some cultural artifact, or some improper pathologization of a range of normal behavior? It doesn't.

This is a substantial mischaracterization of Jaynes' hypothesis, as laid out in his Origin of Consciousness. Your summary of it, in general terms, is on-point: in short, he posits that ancient people (pre-1200ish BCE) were very differently cognitively organized, such that their moment-to-moment experience was dissimilar from modern conscious self-awareness (to the extent that they more or less lacked it) and in many ways similar to that of modern schizophrenics (a split, "bicameral" mind that converses with itself). He does not make any substantial claim, based on that similarity, that schizophrenia is 1) a normal state or within a range of normal states, a la "cognitive diversity" 2) not a disease. Neither of those claims are important to his overall thesis, a fact which he lays out quite nicely. Many theorists have attempted to make these points. Jaynes isn't one of them.

If you're really asking me if I've seen such a thing, actually, outside of One Flew Over the Cuckoo's Nest--admittedly a favorite movie--no, I havent. I have seen, however, plenty of individuals with reasonably well-controlled psychotic symptoms walking around with mildly troublesome side effects, who in general gave the appearance of having gotten a few less hours of sleep last night than they'd have liked to. Their imaginations and creativity were all quite intact; an old friend of mine is quite heavily medicated for a psychotic disorder, and makes some of the most beautiful art I've ever seen. I'm not saying that the image you create no longer exists. I'm saying that 1) it used to be far more common, and 2) it's far from the current norm. Are there troublesome, even terrible, side effects to these drugs? For crap's sake, absolutely. They're bad enough for some people that they're not worth what they give you. But you're putting me in the unadmirable position of having to defend psychiatry's relatively crude tools by painting such a ridiculous, unwarranted picture of them. The image you're calling to mind there is of a person whose dosage does not sound terribly well-managed. Or, who is taking an older neuroleptic drug, as opposed to the now-widely used atypical antipsychotics, which have a far lower rate of extrapyramidal side effects. Again, not that they're not pernicious in themselves--every kid I've ever seen on olanzapine, for instance, packed on about forty pounds in a couple of months. Is that a problem? Hell yes. So am I talking about what a great idea these drugs are? Far from it. But they're not the mythical monster you're claiming they are, either. And your plea to the most marginal case you can think of--the zombie-like horror so wonderfully portrayed in the aforementioned movie--does very little to support your extreme and uncareful claims, that: I can give you ten reasons why I generally can't stand psychiatry, and why its interventions are so unimpressive. But what you're saying about how "most of its medications" work is just far from reality. There is an enormous range of mechanisms by which psychiatric medications do their work. We're talking about antidepressants, anxiolytics, antipsychotics and mood stabilizers, psychostimulants. Many of them enhance certain forms of activity, at the neurological--and often at the cognitive and behavioral--level. Their effects on individuals, whether assessed by self-report or more formal instruments, hardly constitute a "global suppression." Good neurocognitive tests can actually pick apart fairly well the very specific processes that are being suppressed or, in some cases, enhanced. Bottom line: psychiatric drugs (in my humble and moderately informed opinion) sort of suck. But don't caricature them: No, you can't. Lay off the melodrama. Honestly, the truth is disappointing enough without it.

All three symptoms described (depending on how he means one of them) are sympathetic nervous responses: Goosebumps are sympathetic. Pupillary dilation is sympathetic. A "thickening" of saliva sounds as if salivary volume decreases, which happens in sympathetic activation. As opposed to the increased salivation which would occur in parasympathetic evaluation, which tends to thin out saliva. He could be using "thicken," of course, to just mean "more of it" as opposed to the more conventional meaning of consistency. In that case, we're 2 sympathetic, 1 parasympathetic. Also, although you're right that these can be triggered by pleasant sensations (though incorrect about what side of the autonomic nervous system they're on), that's not the whole truth. Sympathetic and parasympathetic activation doesn't cut neatly along lines of subjective experiences of pain or pleasure. There's neither a lot of sensitivity or specificity there. A rabid dog running towards you or a piece of pornography will both dilate the pupils (sympathetic). The smell of a pie baking or a noxious irritant will both make you salivate (parasympathetic). Piloerection (sympathetic) might result from a sensuous tickle, or mortal fear. In short, we can't really explain the symptoms by simply saying they're part of "activation" of one side of the ANS. Particularly given that you got the system wrong, this: ...is not correct. Although it's problematic, for reasons described above, even if you'd have gotten it right.

I'm on the whole unimpressed with psychiatry's current slate of interventions, but I'd never call it "unintelligent." But it's pretty crude, yeah. That's not really at all how they typically work, and that's not really at all why it's crude.

Genecks, since you haven't yet clarified, I'll make my best guess as to what you're getting at here: If the implication here is that the engineers and decisionmakers at Tepco are engaging in groupthink--and hence, need a bunch of outsiders to come give them fresh ideas--I don't think that's warranted. Groupthink is really widely misunderstood. It's not "the way groups think." It's what sometimes happens in particular groups with particular characteristics. Typically, the groups have extremely high cohesion and are motivated to maintain this cohesion; in so doing, they often "overminimize" conflict between members, to the extent that disagreement gets tamped down quite a bit. Often, the groups are homogenous in values, and hierarchically led. To some extent, they're isolated from outside opinion and may be excessively motivated to produce decisions. Bottom line, you can't casually observe a group from the outside and readily identify whether they're under the sway of these factors, though we like to assume that every corporate board or team we don't happen to like is under groupthink's power. Organizations can and do use social psychological principles to adjust group structure to avoid groupthink--there were broad and deep movements to do so in the science and engineering world particularly after several commentaries on the Challenger disaster identified a lot of potential groupthink processes. Not saying these groups don't have their problems. I'm just saying that yelling "groupthink" is an easy and difficult-to-justify potshot. </psychology-speak> You can now return to your regularly scheduled engineering discussion.

I'll summarize a lot of findings for you really quickly, Voltman: To put it in the conventional psychological language of the moment, you're talking about two sorts of variables. Typically, social network size is associated with positive health and developmental outcomes. Social network connectedness is associated with those same outcomes. Both of them are independently important. Also, they're distinct variables in their own right--in other words, there are more options besides "lots of acquaintances" and "few good friends." The patterns of these variables in the population don't really produce the sort of head-to-head matchup you propose, so it's difficult to examine that kind of head-to-head matchup empirically. In fact, in both children and adults, they tend to be positively, not negatively correlated--people with very good friends (which we might think of as network connectedness) have somewhat wider social networks. That's a lot of social and behavioral science in a very small nutshell; hope it makes sense.

Can you die of a broken heart? Well, several people are touching on my answer already, but hopefully I'll flesh it out a bit more and add something to the discussion: Depends on exactly how proximal of a cause we're talking about here. Medical examiners frequently list more than one cause of death because a chain of factors is frequently identifiable behind many mortality states. Many of the common ones are relatively distal--for instance, in this sense we might say that nobody really "dies of cancer," you die because eventually, you get pneumonia and your lungs fill up with fluid, or you stop eating, use up all of your electrolytes, and your heart stops beating. (If you want to be a little droll about it, I once heard a doctor say that there's basically one cause of death: cerebral hypoxia.) So, can a person die of a broken heart? Sure. As much as they can die of this thing called "cancer." Like cancer, a broken heart can kill with varying degrees of proximity to the mortality itself. In the most distal sense, we might imagine drinking yourself into lethal liver failure after your wife leaves you. There are a lot of mediators between the broken heart and death there. Psychoneuroimmunology has a lot to tell us about how chronic stressors do nasty things to the immune system, and can make all sorts of infections and other dangers more likely. Most proximally, however, what you're probably looking for is stress-induced cardiomyopathy. The burst of catecholemines from an emotionally (or sometimes physically, or as is often the case, both) stressful trigger sets of a cascade of changes in the heart muscle sometimes leading to failure. Often, of course, this event gains its lethality from its superimposition on pre-existing morbidity, but you can say the exact same thing of a plain old, garden-variety heart attack. So, should we call it a "contributing factor?" What is a broken heart's status, exactly, as a "cause?" There are questions like this spread all over medicine and psychology. It's something of a philosophical issue; something statistics can't really fully inform us on. Statistics have a maddening and persistent tendency to come out as numbers, and not nice terms like "contributing factor." I hope that doesn't upset you too much. Or, if it does, I hope you've got a good cardiologist.

Nope.