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Part IV: Questions from the audience
482
MARTIN
PART
IV:
E. P.
SELIGMAN
QUESTIONS
and
FROM
JOSEPH FRANCHINA, VP1 and SU: I have a question
JAY M. WEISS
THE
AUDIENCE
for Marty. Is learned helplessness an explanatory concept or an empirical concept? That is, are we talking about a learned helplessness effect or are we talking about an explanatory concept we call learned helplessness? And if it’s an explanatory concept, what’s the operational definition of the concept? DR. SELIGMAN: I think if you make an ungenerous reading of the helplessness literature that I’ve been party to, it’s not difficult to say that I’ve been sloppy, particularly in the more publicized places, about using learned helplessness to describe a procedure, to describe an outcome, and to describe a process. I think it can be documented that in some places I’ve talked about learned helplessness as being the operation of presenting things inescapably, and, in other places, I’ve talked about it as a name for the outcome, that is, given that operation, passivity occurring. And also as the name for a process, that is, the kind of cognition that Jay thinks that should only be accepted as a last resort and may be unverified. My heart is in the third, obviously. I think it is an explanatory concept and the sloppiness occurs in the first two. As an explanatory concept, I think it predicts the following things that none of the alternatives predict. First, if learned helplessness is cognition of response-outcome independence, it should transfer widely. Second, not only does it transfer widely, but you can see antagonistic transfer. That is, if you reverse the motor requirements, but have the relevant cognition. you can see positive transfer. ‘The third general class of predictions that learned helplessness makes concerns learned irrelevance. That is, if you externalize situations which don’t involve responding, you should see the same retardation. Joe’s final question is the most difficult. What’s the operational definition of the process of learned helplessness? I’m unsympathetic with the question. Let me try to say why. I want you to consider examples of things we consider, in other sciences, good explanatory processes and ask if the processes have operational definitions. The dependent variables and the independent variables in good science do have operational definitions. My claim is that often the processes don’t have operational definitions. This, Joe, is another way of talking about the intervening variable-hypothetical construct dispute. I’m a hypothetical construct theorist. I don’t believe that explanatory concepts need be exhausted by input-output relationships; they can mean more. So, for example, consider the discovery of the perturbations of the orbit of Uranus, which led to the discovery of Neptune. Uranus wobbled and it had to be postulated, before anyone observed it, that there was something out there, with a given mass, that was causing it to wobble, that was pulling it out there. That turned out some years later to be Neptune. The wobbling of Uranus did not define Neptune, was not the operational definition of Neptune. Rather, Neptune was something out there with a mass, with a size that was unknown, with a temperature that was unknown. It was not exhausted by its operations. So, I want to claim that it is a very common move all over science not to exhaust your explanatory concepts by operational definitions. Expectations are such an example. Rods and cones before they were actually discovered are such an example. A preference function in economics is such an example, etc. UNIDENTIFIEDQUESTIONER:This is more of a comment or an observation than a question. If depression has as an underlying chemical cause in the brain, NE depletion, then I suppose it would be nice and neat to give depression to the medical people to take care of. That seems to pose serious problems with respect to behavioral manipulations of the onset and course of depression in human subjects. For example, if you change their environment or cause them to change their behavior, you can very quickly, in some cases, get rid of a depression. Or if you teach people that what you do when you become depressed is to start talking yourself down and down further, cognitively, further and further into a depression and that the way to stop that is to recognize what
Learned helplessness, physiological change and learned inactivity
483
you’re doing, stop at this point, and go do something else. In addition, we also have the problem that even NE depletion returns to normal levels within 24 or 48 h. How do we deal with the long-term chronic depression which may last for years? This is not a question. I’m just speculating. DR. WEISS: I’ll comment on that. The behaviorists are not left out at all. There is an intense interaction between the organism’s behavior and the events on the outside in terms of the physiological changes which these events produce. In other words, if you get an organism to behave in a way which you are reinforcing, or establishing contingencies to its behavior, this may indeed, affect its brain catecholamines. So, you’ve got an intimate interaction. By the way, what you’ve just said is the mistake the medical people make. I don’t mean that you were making a mistake. Rather, you were voicing the position that medical people do. Because they think they’ve got a neurochemical mediator for disorder, be it schizophrenia or depression, they immediately start to think of the disease as being endogenous and having nothing to do with behavioral inputs. It simply has to do with the fact that there is a chemical lesion up there. The fact of the matter is that behavior and the events going on in the environments, like experiencing control and non-control, can have tremendous effects on neurochemistry and tremendous effects on those neurochemical systems, which if impaired, can lead to impaired functioning later on. So, if anything, it really brings us, I think, very strongly into the picture, if we take a look at it from that side. The issue of chronicity of the depressions is something, I think, everyone in the field has very little hold on. The fact of the matter is we are only beginning to make the crudest approximations of what the neurochemical changes are that are involved in these behavioral deficits which we see. And I think you may fairly definitively state now that the ones we have identified are the wrong ones. They look like they have some overlap invariance with the right ones and, perhaps, are sharing much of what is taking place in those that are critical, but we really haven’t identified the correct ones as yet. Of course, we do have the advantage over other explanations of being able to get in there and measure them. We can measure brain catecholamines directly. DR. SELIGMAN:We can also measure human cognitions directly. Laughter. DR. FRANCHINA: What concerns me is how does learned helpiessness get into the test situation-the shuttle situation, for example, or into the FR-2 situation-to produce its effects? If it’s a process, what triggers it in the test situation? Remember, you’ve got a wide variety of conditions to explain-not only aversive to aversive but aversive to appetitive. DR. SELIGMAN:The question is, have I boxed myself into a corner by showing you that there is tremendous generality of learned helplessness across events? DR. FRANCHINA: I want to know what the stimulus is. DR. SELIGMAN:And the question is, “‘Well, Seligman, you think it’s a memory that sets it off. What sets the memory off? Why is it that you see learned helplessness there?” And the answer is, Joe, that I don’t know; but I think it’s an empirical question. Here are the possibilities: Being taken out of your home cage would explain all of the stimulus mediation of all of the dog and rat helplessness events. Being handled by this enormous predator-a human being-another possibility. Grid floor would explain about 80% of them. Confined space other than the home cage would explain almost all of it. Being faced with a learning task might do it. I just don’t know what it is. DR. FRANCHINA:Have you attempted to condition learned helplessness? DR. SELIGMAN:To bring it under discriminative control? Oh yes, let me say something about that, and I think it’s the kind of thing that Jay’s explanation would find quite congenial. Learned helplessness is unhappy with it, but I don’t think it’s a critical problem. In humans, .learned helplessness has been discriminatively conditioned by Carol Dweck and by others. In humans, for example, if Teacher 1 only gives you unsolvable problems and Teacher 2 always gives you solvable problems, and then
484
MARTIN E. P. SELIGMANand JAY M. WEBS
Teacher 1 starts to give you solvable problems, you can’t solve them. Even though you’ve just solved them with Teacher 2! But in animals, I don’t know of any good data which show discriminative conditioning of leaned helplessness.
MARTIN
PART
IV:
E. P.
SELIGMAN
QUESTIONS
and
FROM
JOSEPH FRANCHINA, VP1 and SU: I have a question
JAY M. WEISS
THE
AUDIENCE
for Marty. Is learned helplessness an explanatory concept or an empirical concept? That is, are we talking about a learned helplessness effect or are we talking about an explanatory concept we call learned helplessness? And if it’s an explanatory concept, what’s the operational definition of the concept? DR. SELIGMAN: I think if you make an ungenerous reading of the helplessness literature that I’ve been party to, it’s not difficult to say that I’ve been sloppy, particularly in the more publicized places, about using learned helplessness to describe a procedure, to describe an outcome, and to describe a process. I think it can be documented that in some places I’ve talked about learned helplessness as being the operation of presenting things inescapably, and, in other places, I’ve talked about it as a name for the outcome, that is, given that operation, passivity occurring. And also as the name for a process, that is, the kind of cognition that Jay thinks that should only be accepted as a last resort and may be unverified. My heart is in the third, obviously. I think it is an explanatory concept and the sloppiness occurs in the first two. As an explanatory concept, I think it predicts the following things that none of the alternatives predict. First, if learned helplessness is cognition of response-outcome independence, it should transfer widely. Second, not only does it transfer widely, but you can see antagonistic transfer. That is, if you reverse the motor requirements, but have the relevant cognition. you can see positive transfer. ‘The third general class of predictions that learned helplessness makes concerns learned irrelevance. That is, if you externalize situations which don’t involve responding, you should see the same retardation. Joe’s final question is the most difficult. What’s the operational definition of the process of learned helplessness? I’m unsympathetic with the question. Let me try to say why. I want you to consider examples of things we consider, in other sciences, good explanatory processes and ask if the processes have operational definitions. The dependent variables and the independent variables in good science do have operational definitions. My claim is that often the processes don’t have operational definitions. This, Joe, is another way of talking about the intervening variable-hypothetical construct dispute. I’m a hypothetical construct theorist. I don’t believe that explanatory concepts need be exhausted by input-output relationships; they can mean more. So, for example, consider the discovery of the perturbations of the orbit of Uranus, which led to the discovery of Neptune. Uranus wobbled and it had to be postulated, before anyone observed it, that there was something out there, with a given mass, that was causing it to wobble, that was pulling it out there. That turned out some years later to be Neptune. The wobbling of Uranus did not define Neptune, was not the operational definition of Neptune. Rather, Neptune was something out there with a mass, with a size that was unknown, with a temperature that was unknown. It was not exhausted by its operations. So, I want to claim that it is a very common move all over science not to exhaust your explanatory concepts by operational definitions. Expectations are such an example. Rods and cones before they were actually discovered are such an example. A preference function in economics is such an example, etc. UNIDENTIFIEDQUESTIONER:This is more of a comment or an observation than a question. If depression has as an underlying chemical cause in the brain, NE depletion, then I suppose it would be nice and neat to give depression to the medical people to take care of. That seems to pose serious problems with respect to behavioral manipulations of the onset and course of depression in human subjects. For example, if you change their environment or cause them to change their behavior, you can very quickly, in some cases, get rid of a depression. Or if you teach people that what you do when you become depressed is to start talking yourself down and down further, cognitively, further and further into a depression and that the way to stop that is to recognize what
Learned helplessness, physiological change and learned inactivity
483
you’re doing, stop at this point, and go do something else. In addition, we also have the problem that even NE depletion returns to normal levels within 24 or 48 h. How do we deal with the long-term chronic depression which may last for years? This is not a question. I’m just speculating. DR. WEISS: I’ll comment on that. The behaviorists are not left out at all. There is an intense interaction between the organism’s behavior and the events on the outside in terms of the physiological changes which these events produce. In other words, if you get an organism to behave in a way which you are reinforcing, or establishing contingencies to its behavior, this may indeed, affect its brain catecholamines. So, you’ve got an intimate interaction. By the way, what you’ve just said is the mistake the medical people make. I don’t mean that you were making a mistake. Rather, you were voicing the position that medical people do. Because they think they’ve got a neurochemical mediator for disorder, be it schizophrenia or depression, they immediately start to think of the disease as being endogenous and having nothing to do with behavioral inputs. It simply has to do with the fact that there is a chemical lesion up there. The fact of the matter is that behavior and the events going on in the environments, like experiencing control and non-control, can have tremendous effects on neurochemistry and tremendous effects on those neurochemical systems, which if impaired, can lead to impaired functioning later on. So, if anything, it really brings us, I think, very strongly into the picture, if we take a look at it from that side. The issue of chronicity of the depressions is something, I think, everyone in the field has very little hold on. The fact of the matter is we are only beginning to make the crudest approximations of what the neurochemical changes are that are involved in these behavioral deficits which we see. And I think you may fairly definitively state now that the ones we have identified are the wrong ones. They look like they have some overlap invariance with the right ones and, perhaps, are sharing much of what is taking place in those that are critical, but we really haven’t identified the correct ones as yet. Of course, we do have the advantage over other explanations of being able to get in there and measure them. We can measure brain catecholamines directly. DR. SELIGMAN:We can also measure human cognitions directly. Laughter. DR. FRANCHINA: What concerns me is how does learned helpiessness get into the test situation-the shuttle situation, for example, or into the FR-2 situation-to produce its effects? If it’s a process, what triggers it in the test situation? Remember, you’ve got a wide variety of conditions to explain-not only aversive to aversive but aversive to appetitive. DR. SELIGMAN:The question is, have I boxed myself into a corner by showing you that there is tremendous generality of learned helplessness across events? DR. FRANCHINA: I want to know what the stimulus is. DR. SELIGMAN:And the question is, “‘Well, Seligman, you think it’s a memory that sets it off. What sets the memory off? Why is it that you see learned helplessness there?” And the answer is, Joe, that I don’t know; but I think it’s an empirical question. Here are the possibilities: Being taken out of your home cage would explain all of the stimulus mediation of all of the dog and rat helplessness events. Being handled by this enormous predator-a human being-another possibility. Grid floor would explain about 80% of them. Confined space other than the home cage would explain almost all of it. Being faced with a learning task might do it. I just don’t know what it is. DR. FRANCHINA:Have you attempted to condition learned helplessness? DR. SELIGMAN:To bring it under discriminative control? Oh yes, let me say something about that, and I think it’s the kind of thing that Jay’s explanation would find quite congenial. Learned helplessness is unhappy with it, but I don’t think it’s a critical problem. In humans, .learned helplessness has been discriminatively conditioned by Carol Dweck and by others. In humans, for example, if Teacher 1 only gives you unsolvable problems and Teacher 2 always gives you solvable problems, and then
484
MARTIN E. P. SELIGMANand JAY M. WEBS
Teacher 1 starts to give you solvable problems, you can’t solve them. Even though you’ve just solved them with Teacher 2! But in animals, I don’t know of any good data which show discriminative conditioning of leaned helplessness.