Friday, February 12, 2010
worthwhile websites
Two worthwhile websites: torahanytime.com and innernet.org.il. The former has been filming me for more than a year and has much later versions of my shiurim than are on my website.
Fodor vs. Darwin
Modern Materialism
Atoms and the void. And yet it is all so very much indeed.
Tuesday, February 24, 2009
Darwin was wrong?
This past Wednesday witnessed a debate between Rutgers’ own Jerry Fodor and Philip Kitcher on the merits of the theory of evolution by natural selection. What was unusual about this debate, as compared to others on the same topic, was that neither participant was anti-science, anti-reason, or pro-God. However, Jerry holds the iconoclastic (for a materialist) view that “the theory of evolution by natural selection is either false or vacuous, depending on how you read it.” Them, as they say, is fightin’ words.
I don’t want to resurrect that debate here. I went to the debate not to see arguments, but to watch people yell at Jerry (Tim Maudlin memorably said “Jerry, you accuse adaptationists of committing the intentional fallacy, while you yourself commit the fallacy of saying something is false when it’s been demonstrated right in front of you!”) However, I think it’s sad that no-one gives Jerry a sympathetic ear, because he’s a smart guy and even if he’s wrong, I think it would be a big advance in human inquiry just to know exactly why he’s wrong. So I want to explain what Jerry didn’t explain in the debate, though often adverted to: the analogy that Jerry sees between Chomsky’s argument against Skinner and Jerry’s argument against Darwin.
Part I of the analogy: Chomsky vs. Skinner
Most people, I imagine, have no idea what Jerry means when he says his argument more or less is Chomsky’s argument. We all thought that Skinner was wrong because, I don’t know, natural language syntax is recursive. But that’s not what Chomsky says in his review of Verbal Behavior (at least not in the selections reprinted in the Block anthology), so it’s worth taking a look at what Jerry sees in the review.
Simplifying a little, Skinner’s theory of learning by operant conditioning is that if an animal’s behavior B in situation S is reinforced (let’s just say “rewarded” for the time being), then the animal will learn to do B in S. For example, if a rat is rewarded for bar-pressing when shown a red thing, the rat will learn to press the bar when shown a red thing.
It’s an interesting fact that every finite set of red stimuli will share (that is, the members of the set will share) infinitely many properties other than being red. For instance, suppose the rat is presented with a series of bright red triangles in the bar-pressing experiment, when we want to enforce the behavior of bar-pressing given a red stimulus. The red stimuli here are not only red, but also closed figures; triangles; bright things; isosceles triangles; Granny’s favorite shape; triangles in a cage; things in a cage; etc. In addition, some infinite subset of these properties will be locally correlated with redness. That is, it might be true, in the rat’s environment (the cage), that something is red if and only if it’s a triangle; that something is red if and only if it’s an isosceles triangle; etc. Of course, not all the properties shared by the stimuli will be locally correlated with redness: ‘thing in a cage’ is true of both the red stimulus and the white rat. But an infinite amount of correlations is correlations enough. Call this “the ubiquity of local correlation.”
Now suppose we condition the rat in the way proposed. A bright red triangle is flashed, and when the rat presses the bar, it is rewarded with a food pellet. Question: can we use Skinner’s theory of learning by operant conditioning to tell us what the rat has learned? Answer: no—the theory construed in one way is false; in another way, it’s vacuous. Let’s investigate why.
A Skinnerian might be tempted to say: the rat has learned to press the bar when presented with a red stimulus. But in saying this, we need to ask her a further question, namely: is ‘learn’ here an intensional or an extensional verb? We (philosophers) say that ‘learn’ is extensional, if it follows from ‘Rat R learned to perform action A given a stimulus that is S’ and ‘S is locally correlated with F’ that ‘Rat R learned to perform action A given a stimulus that is F.’ That is, is it equally true to say that the rat learned to press the bar when presented with a red stimulus AND learned to press the bar when presented with a triangular stimulus AND learned to press the bar when presented with a stimulus that is an isosceles triangle AND…?
Let’s suppose the behaviorist says ‘yes,’ that ‘learn’ is extensional as used in her theory. Then the theory is clearly false. In order to show that the theory is false, we need only decouple two correlated variables and try the experiment again. Suppose we train the rat as described and then present it with a dull blue circle. Since ‘closed regular geometric figure’ had been locally correlated with ‘is red’ during conditioning, the rat, we are supposing, has learned to press the bar given a stimulus that is a closed regular geometric figure. A dull blue circle is a closed regular geometric figure, so the behaviorist predicts bar-pressing behavior. Now, maybe the rat will and maybe the rat won’t press the bar. If it doesn’t, behaviorism is falsified. If it does, behaviorism is left standing. But it won’t take long for a clever graduate student to find some or other local correlation the rat isn’t sensitive to (unless the rat learned ‘press the bar given any stimulus at all’), and we would all be well-advised to just abandon behaviorism now.
Horn II of the dilemma: suppose the behaviorist says ‘no,’ that ‘learn’ is not extensional as used in her theory. That is, the behaviorist asserts that the rat has learned to press the bar given a red stimulus, but that it does not follow from this and the fact that redness is locally correlated with property P that the rat has learned to press the bar given a P-stimulus. We ask: is the theory of learning by operant conditioning capable of predicting what the rat has learned, in the non-extensional sense of ‘learn’? NB. By this question we do not mean ‘is it possible to determine what the rat has learned?’ for if the rat has indeed learned anything, of course this is possible. We want to know what the theory in question has to say about what the rat learned.
Well, again, suppose we condition the rat as described, by rewarding it for pressing a bar in the presence of a bright red triangle. Has the rat learned (in the non-extensional sense) to press the bar given a red stimulus, a bright stimulus, a triangular stimulus, or some other kind of stimulus? Notice that the theory of learning by operant conditioning does not give us any guidance. The stimuli were all of these things. The experimenter receives no helpful advice from the theory about what hypothesis to hold.
Now suppose we test some hypothesis, say, the hypothesis that the rat learned to press the bar given a red stimulus. We present the rat with a blue triangle. If the rat does not press the bar, we have some confirmation of our hypothesis; if it does press the bar, perhaps we will be led to instead propose that the rat learned to press the bar given a triangular stimulus. This is how science goes. But the question is: is Skinnerian learning theory confirmed by any of this? And the answer is: vacuously, yes. If the rat does not press the bar, the Skinnerian will say ‘look, we were right: the rat’s bar-pressing behavior was rewarded when the rat was given a red stimulus, and it learned to press the bar when given a red stimulus.’ If the rat does press the bar, the Skinnerian will say: ‘look, we were right: the rat’s bar-pressing behavior was rewarded when the rat was given a triangular stimulus, and it learned to press the bar when given a triangular stimulus.’
We can go on. After the first decoupling experiment, the experimenter will have ruled out a certain hypothesis, say, that the rat learned to press the bar when presented with a red stimulus. But there will still be infinitely many properties locally correlated with triangularity, so it will not follow that the rat learned to press the bar when presented with a triangular stimulus. Here again, Skinnerian learning theory is of no help whatsoever in constructing hypotheses about what the rat learned. It cannot predict, it can only incorporate empirical findings post-hoc into the behaviorist model.
So the theory of learning by operant conditioning (a) makes no predictions (b) does not guide researchers in formulating hypotheses about learning and (c) is trivially compatible with any outcome whatsoever. That is not how science goes.
This is how I’ve heard Fodor present Chomsky’s case against Skinner. And I think it’s a compelling case. The claim is that the theory of learning by operant condition is false, if ‘learn’ is read extensionally and trivially true if ‘learn’ is read intensionally. And I take it that no-one wants to defend Skinner at this point. So without further ado:
Part II of the analogy: Fodor vs. Darwin
[Every sentence of this section should really begin with ‘According to Fodor, as I understand him.’ Please don’t attack me for attacking Darwin; I am not attacking Darwin. I am presenting Fodor’s views, as I understand them.]
Simplifying a little, Darwin’s theory of evolution by natural selection is that if two heritable traits T and T’ are possessed by some ancestral population in some ecological environment, and T is more fit than T’, then T will increase in prevalence in the population over time, eventually moving to fixation (except in certain cases where the fitness of T depends on prevalence of T’). For example, suppose there is a population of brown bears that live in the arctic wastes. At some point a mutant white bear arises. Since coat color is heritable, and a white coat is more fit than a brown one, whiteness moves to fixation in the bear population.
It’s an interesting fact that every finite set of whiteness phenotypes will share (that is, the members of the set will share) infinitely many phenotypic properties other than whiteness. For instance, suppose that at present 20% of the bear population possesses the whiteness phenotype (and for simplicity’s sake, suppose the bear head-count is 100 total individuals, so that 20 of them are white). The white bears will not only be white, but also bears; four-legged; the same color as snow; the same color as paper; more closely related to one another than to any non-white non-parental bear (assuming that whiteness is a dominant trait); located in some perhaps-disjoint spatio-temporal region; etc. In addition, some infinite subset of these properties will be locally correlated with the whiteness phenotype. That is, it might be true, in the bears’ environment (the arctic), that something is a white bear if and only if it’s a bear the same color as snow; that something is a white bear if and only if it’s more closely related to white bears or its parents than non-white non-parental bears; etc. Of course, not all the properties shared by the whiteness phenotype will be locally correlated with it: ‘bear’ is true both of white bears and of brown ones. But an infinite amount of correlations is correlations enough. This is another instance of the ubiquity of local correlation.
So suppose a mutant white bear arises in the population. Question: can we use Darwin’s theory of evolution by natural selection to tell us why the phenotype moves to fixation in the population? Answer [again, Fodor’s answer, not mine]: no—the theory construed in one way is false; in another way, it’s vacuous. Let’s see why one might think this is so.
An adaptationist might be tempted to say: the whiteness phenotype moved to fixation because being white increased the probability that a bear would produce viable offspring as compared to the probability that a brown bear would produce viable offspring. But in saying this, we need to ask her a further question, namely: is ‘phenotype P increases fitness relative to competing phenotypes C’ an intensional or extensional context at position P? It’s an extensional context if it follows from ‘phenotype P increases fitness relative to competing phenotypes C’ and ‘phenotype P is locally correlated with phenotype Q’ that ‘phenotype Q increases fitness relative to competing phenotypes C.’ That is, if it’s an extensional context, it should be equally true to say that the whiteness phenotype increases fitness AND the same-color-as-snow phenotype increases fitness AND the being-located-in-region-R (where R is the region containing all and only white bears) phenotype increases fitness AND...
So let’s suppose that the adaptationist does indeed say that ‘phenotype P increases fitness relative to competing phenotypes C’ is extensional at the P-position. Then the theory is clearly false. In order to show that the theory is false, we need only decouple two correlated variable and see what happens in the population. Suppose, to take a flight of fancy, that we’re super-scientists capable of making snow brown (we’re already capable of making it yellow, so this shouldn’t require too much of a technical advance). The adaptationist told us that ‘the same-color-as-snow phenotype increases fitness’ and by this she also meant that ‘the white phenotype increases fitness.’ Now we change the color of the snow to brown. Suppose the brownness phenotype now goes to fixation. It looks like we’ve falsified adaptationism, for it is not true after all that whiteness increases fitness.
[If you don’t like the example, because you’re worried we’ve changed the ecology, which is a free variable we’d been suppressing, you should realize that I could have run the example with any of the local correlates of the whiteness phenotype. For example: the phenotype of being a bear with exactly 19 other individuals of the same color. We don’t have to even intervene at all to watch adaptationism get falsified, we can just let whiteness go to fixation. And if you think I’m cheating by using extended phenotypes, talk to Dawkins.]
Horn II of the dilemma: suppose instead that the adaptationist says that ‘phenotype P increases fitness relative to competing phenotypes C’ is not extensional (is intensional) at the P-position. That is, the adaptationist asserts that the same-color-as-snow phenotype in bears in their present ecology increases fitness, but it does not follow from this and the fact that the same-color-as-snow phenotype is locally correlated with the whiteness phenotype that the whiteness phenotype increases fitness in bears in their present ecology. We ask: is the theory of evolution by natural selection capable of predicting what heritable traits increase fitness among bears in their present ecology? NB. By this question we do not mean ‘is it possible to determine what heritable traits increase fitness’ for if some traits do and others do not, of course this is possible. We want to know what the theory in question has to say about the relative fitness of bear phenotypes.
So suppose the whiteness phenotype has gone to fixation and there are now, say, 200 white bears. Did the whiteness phenotype increase the fitness (in the intensional sense) of the ancestral white bears or was it rather the same-color-as-snow phenotype, the same-color-as-paper phenotype, or any other phenotype that the white bears happen contingently to share with one another and not brown bears? Notice that the theory of evolution by natural selection does not give us any guidance. The ancestral bears (and the present bears) were all of these things. The evolutionary scientist receives no helpful advice from the theory about what hypothesis to hold (though of course the scientist has a helpful set of priors, and is likely to latch on to the correct hypothesis, without invoking Darwin’s theory).
Now suppose the field scientist actually runs some controlled tests on the population of bears in order to test the hypothesis that it was the same-color-as-snow phenotype that increased the fitness of the bears in their ecology, relative to the competing different-color-from-snow phenotype. Perhaps she isolates some of the bears in an area where the snow has been made artificially brown, along with some other conspecific brown bears taken from a different population. If the brownness phenotype goes to fixation in this new population, we will have some confirmation for our hypothesis; if whiteness goes to fixation, we may be led to instead propose that the whiteness phenotype (rather than the same-color-as-snow phenotype) increased fitness (maybe females prefer white bears or something). This is how science goes. But the question is: is Darwinian evolutionary theory confirmed by any of this? And the answer is [again, Fodor’s answer, not mine]: vacuously, yes. If brownness goes to fixation, the Darwinian will say: ‘look, we were right: the same-color-as-snow phenotype was more fit than the whiteness phenotype, and it went to fixation.’ Similarly, if whiteness goes to fixation, the Darwinian will say: ‘look, we were right: the whiteness phenotype was more fit than the same-color-as-snow phenotype, and it went to fixation.’
We can go on. After the first decoupling experiment, the experimenter will have ruled out a certain hypothesis, say, that the same-color-as-snow phenotype was not fitter than its competitors. But there will still be infinitely many properties locally correlated with the whiteness phenotype, so it will not follow that that phenotype was fitter. Here again, Darwinian evolutionary theory is of no help whatsoever in constructing hypotheses about which traits increase fitness. It cannot predict, it can only incorporate empirical findings post-hoc into the adaptationist model.
So the theory of evolution by natural selection (a) makes no predictions (b) does not guide researchers in formulating hypotheses about evolution and (c) is trivially compatible with any outcome. That is not how science goes [or so says Fodor].
This, I take it, is an intriguing argument. It has nothing to do with God. The claim is that the theory of natural selection read extensionally is false, and read intensionally is vacuously true. Nothing about the tree of life is questioned, nothing about inheritance through genes, nothing about the physical basis of all observable phenomena. The hard work of evolutionary biologists in the field is not ignored, nor is it taken to be irrelevant. Fodor is merely arguing that for biologists to attribute their scientific findings on evolution to The Law of Natural Selection is rather like contemporary computational psychologists attributing their findings to Behaviorism. The findings are still there, and still correct: they’re just neither suggested nor explained by natural selection. Or again, so says Fodor.
Conclusion
I don’t know whether Fodor’s right or not. Maybe that makes me an idiot, because maybe he’s as obviously wrong as Randy (Gallistel) and Tim say he is. So be it. But I’d like to be very clear on why Fodor is wrong, if he is. I used to think he was just arguing: there are no biological laws; explanation is subsumption under a law; therefore there are no biological explanations. And I used to think the response should be: that’s an exceedingly narrow conception of explanation. But now I take his argument to be what I presented above: it’s about whether the theory of natural selection itself has any content whatsoever. And one can’t answer that challenge by modifying what one counts as explanation. I invite civil discussion in the comments. No Godbotting, plz.
Posted by Michael Johnson at 2:34 PM
Labels: evolution, Fodor
Atoms and the void. And yet it is all so very much indeed.
Tuesday, February 24, 2009
Darwin was wrong?
This past Wednesday witnessed a debate between Rutgers’ own Jerry Fodor and Philip Kitcher on the merits of the theory of evolution by natural selection. What was unusual about this debate, as compared to others on the same topic, was that neither participant was anti-science, anti-reason, or pro-God. However, Jerry holds the iconoclastic (for a materialist) view that “the theory of evolution by natural selection is either false or vacuous, depending on how you read it.” Them, as they say, is fightin’ words.
I don’t want to resurrect that debate here. I went to the debate not to see arguments, but to watch people yell at Jerry (Tim Maudlin memorably said “Jerry, you accuse adaptationists of committing the intentional fallacy, while you yourself commit the fallacy of saying something is false when it’s been demonstrated right in front of you!”) However, I think it’s sad that no-one gives Jerry a sympathetic ear, because he’s a smart guy and even if he’s wrong, I think it would be a big advance in human inquiry just to know exactly why he’s wrong. So I want to explain what Jerry didn’t explain in the debate, though often adverted to: the analogy that Jerry sees between Chomsky’s argument against Skinner and Jerry’s argument against Darwin.
Part I of the analogy: Chomsky vs. Skinner
Most people, I imagine, have no idea what Jerry means when he says his argument more or less is Chomsky’s argument. We all thought that Skinner was wrong because, I don’t know, natural language syntax is recursive. But that’s not what Chomsky says in his review of Verbal Behavior (at least not in the selections reprinted in the Block anthology), so it’s worth taking a look at what Jerry sees in the review.
Simplifying a little, Skinner’s theory of learning by operant conditioning is that if an animal’s behavior B in situation S is reinforced (let’s just say “rewarded” for the time being), then the animal will learn to do B in S. For example, if a rat is rewarded for bar-pressing when shown a red thing, the rat will learn to press the bar when shown a red thing.
It’s an interesting fact that every finite set of red stimuli will share (that is, the members of the set will share) infinitely many properties other than being red. For instance, suppose the rat is presented with a series of bright red triangles in the bar-pressing experiment, when we want to enforce the behavior of bar-pressing given a red stimulus. The red stimuli here are not only red, but also closed figures; triangles; bright things; isosceles triangles; Granny’s favorite shape; triangles in a cage; things in a cage; etc. In addition, some infinite subset of these properties will be locally correlated with redness. That is, it might be true, in the rat’s environment (the cage), that something is red if and only if it’s a triangle; that something is red if and only if it’s an isosceles triangle; etc. Of course, not all the properties shared by the stimuli will be locally correlated with redness: ‘thing in a cage’ is true of both the red stimulus and the white rat. But an infinite amount of correlations is correlations enough. Call this “the ubiquity of local correlation.”
Now suppose we condition the rat in the way proposed. A bright red triangle is flashed, and when the rat presses the bar, it is rewarded with a food pellet. Question: can we use Skinner’s theory of learning by operant conditioning to tell us what the rat has learned? Answer: no—the theory construed in one way is false; in another way, it’s vacuous. Let’s investigate why.
A Skinnerian might be tempted to say: the rat has learned to press the bar when presented with a red stimulus. But in saying this, we need to ask her a further question, namely: is ‘learn’ here an intensional or an extensional verb? We (philosophers) say that ‘learn’ is extensional, if it follows from ‘Rat R learned to perform action A given a stimulus that is S’ and ‘S is locally correlated with F’ that ‘Rat R learned to perform action A given a stimulus that is F.’ That is, is it equally true to say that the rat learned to press the bar when presented with a red stimulus AND learned to press the bar when presented with a triangular stimulus AND learned to press the bar when presented with a stimulus that is an isosceles triangle AND…?
Let’s suppose the behaviorist says ‘yes,’ that ‘learn’ is extensional as used in her theory. Then the theory is clearly false. In order to show that the theory is false, we need only decouple two correlated variables and try the experiment again. Suppose we train the rat as described and then present it with a dull blue circle. Since ‘closed regular geometric figure’ had been locally correlated with ‘is red’ during conditioning, the rat, we are supposing, has learned to press the bar given a stimulus that is a closed regular geometric figure. A dull blue circle is a closed regular geometric figure, so the behaviorist predicts bar-pressing behavior. Now, maybe the rat will and maybe the rat won’t press the bar. If it doesn’t, behaviorism is falsified. If it does, behaviorism is left standing. But it won’t take long for a clever graduate student to find some or other local correlation the rat isn’t sensitive to (unless the rat learned ‘press the bar given any stimulus at all’), and we would all be well-advised to just abandon behaviorism now.
Horn II of the dilemma: suppose the behaviorist says ‘no,’ that ‘learn’ is not extensional as used in her theory. That is, the behaviorist asserts that the rat has learned to press the bar given a red stimulus, but that it does not follow from this and the fact that redness is locally correlated with property P that the rat has learned to press the bar given a P-stimulus. We ask: is the theory of learning by operant conditioning capable of predicting what the rat has learned, in the non-extensional sense of ‘learn’? NB. By this question we do not mean ‘is it possible to determine what the rat has learned?’ for if the rat has indeed learned anything, of course this is possible. We want to know what the theory in question has to say about what the rat learned.
Well, again, suppose we condition the rat as described, by rewarding it for pressing a bar in the presence of a bright red triangle. Has the rat learned (in the non-extensional sense) to press the bar given a red stimulus, a bright stimulus, a triangular stimulus, or some other kind of stimulus? Notice that the theory of learning by operant conditioning does not give us any guidance. The stimuli were all of these things. The experimenter receives no helpful advice from the theory about what hypothesis to hold.
Now suppose we test some hypothesis, say, the hypothesis that the rat learned to press the bar given a red stimulus. We present the rat with a blue triangle. If the rat does not press the bar, we have some confirmation of our hypothesis; if it does press the bar, perhaps we will be led to instead propose that the rat learned to press the bar given a triangular stimulus. This is how science goes. But the question is: is Skinnerian learning theory confirmed by any of this? And the answer is: vacuously, yes. If the rat does not press the bar, the Skinnerian will say ‘look, we were right: the rat’s bar-pressing behavior was rewarded when the rat was given a red stimulus, and it learned to press the bar when given a red stimulus.’ If the rat does press the bar, the Skinnerian will say: ‘look, we were right: the rat’s bar-pressing behavior was rewarded when the rat was given a triangular stimulus, and it learned to press the bar when given a triangular stimulus.’
We can go on. After the first decoupling experiment, the experimenter will have ruled out a certain hypothesis, say, that the rat learned to press the bar when presented with a red stimulus. But there will still be infinitely many properties locally correlated with triangularity, so it will not follow that the rat learned to press the bar when presented with a triangular stimulus. Here again, Skinnerian learning theory is of no help whatsoever in constructing hypotheses about what the rat learned. It cannot predict, it can only incorporate empirical findings post-hoc into the behaviorist model.
So the theory of learning by operant conditioning (a) makes no predictions (b) does not guide researchers in formulating hypotheses about learning and (c) is trivially compatible with any outcome whatsoever. That is not how science goes.
This is how I’ve heard Fodor present Chomsky’s case against Skinner. And I think it’s a compelling case. The claim is that the theory of learning by operant condition is false, if ‘learn’ is read extensionally and trivially true if ‘learn’ is read intensionally. And I take it that no-one wants to defend Skinner at this point. So without further ado:
Part II of the analogy: Fodor vs. Darwin
[Every sentence of this section should really begin with ‘According to Fodor, as I understand him.’ Please don’t attack me for attacking Darwin; I am not attacking Darwin. I am presenting Fodor’s views, as I understand them.]
Simplifying a little, Darwin’s theory of evolution by natural selection is that if two heritable traits T and T’ are possessed by some ancestral population in some ecological environment, and T is more fit than T’, then T will increase in prevalence in the population over time, eventually moving to fixation (except in certain cases where the fitness of T depends on prevalence of T’). For example, suppose there is a population of brown bears that live in the arctic wastes. At some point a mutant white bear arises. Since coat color is heritable, and a white coat is more fit than a brown one, whiteness moves to fixation in the bear population.
It’s an interesting fact that every finite set of whiteness phenotypes will share (that is, the members of the set will share) infinitely many phenotypic properties other than whiteness. For instance, suppose that at present 20% of the bear population possesses the whiteness phenotype (and for simplicity’s sake, suppose the bear head-count is 100 total individuals, so that 20 of them are white). The white bears will not only be white, but also bears; four-legged; the same color as snow; the same color as paper; more closely related to one another than to any non-white non-parental bear (assuming that whiteness is a dominant trait); located in some perhaps-disjoint spatio-temporal region; etc. In addition, some infinite subset of these properties will be locally correlated with the whiteness phenotype. That is, it might be true, in the bears’ environment (the arctic), that something is a white bear if and only if it’s a bear the same color as snow; that something is a white bear if and only if it’s more closely related to white bears or its parents than non-white non-parental bears; etc. Of course, not all the properties shared by the whiteness phenotype will be locally correlated with it: ‘bear’ is true both of white bears and of brown ones. But an infinite amount of correlations is correlations enough. This is another instance of the ubiquity of local correlation.
So suppose a mutant white bear arises in the population. Question: can we use Darwin’s theory of evolution by natural selection to tell us why the phenotype moves to fixation in the population? Answer [again, Fodor’s answer, not mine]: no—the theory construed in one way is false; in another way, it’s vacuous. Let’s see why one might think this is so.
An adaptationist might be tempted to say: the whiteness phenotype moved to fixation because being white increased the probability that a bear would produce viable offspring as compared to the probability that a brown bear would produce viable offspring. But in saying this, we need to ask her a further question, namely: is ‘phenotype P increases fitness relative to competing phenotypes C’ an intensional or extensional context at position P? It’s an extensional context if it follows from ‘phenotype P increases fitness relative to competing phenotypes C’ and ‘phenotype P is locally correlated with phenotype Q’ that ‘phenotype Q increases fitness relative to competing phenotypes C.’ That is, if it’s an extensional context, it should be equally true to say that the whiteness phenotype increases fitness AND the same-color-as-snow phenotype increases fitness AND the being-located-in-region-R (where R is the region containing all and only white bears) phenotype increases fitness AND...
So let’s suppose that the adaptationist does indeed say that ‘phenotype P increases fitness relative to competing phenotypes C’ is extensional at the P-position. Then the theory is clearly false. In order to show that the theory is false, we need only decouple two correlated variable and see what happens in the population. Suppose, to take a flight of fancy, that we’re super-scientists capable of making snow brown (we’re already capable of making it yellow, so this shouldn’t require too much of a technical advance). The adaptationist told us that ‘the same-color-as-snow phenotype increases fitness’ and by this she also meant that ‘the white phenotype increases fitness.’ Now we change the color of the snow to brown. Suppose the brownness phenotype now goes to fixation. It looks like we’ve falsified adaptationism, for it is not true after all that whiteness increases fitness.
[If you don’t like the example, because you’re worried we’ve changed the ecology, which is a free variable we’d been suppressing, you should realize that I could have run the example with any of the local correlates of the whiteness phenotype. For example: the phenotype of being a bear with exactly 19 other individuals of the same color. We don’t have to even intervene at all to watch adaptationism get falsified, we can just let whiteness go to fixation. And if you think I’m cheating by using extended phenotypes, talk to Dawkins.]
Horn II of the dilemma: suppose instead that the adaptationist says that ‘phenotype P increases fitness relative to competing phenotypes C’ is not extensional (is intensional) at the P-position. That is, the adaptationist asserts that the same-color-as-snow phenotype in bears in their present ecology increases fitness, but it does not follow from this and the fact that the same-color-as-snow phenotype is locally correlated with the whiteness phenotype that the whiteness phenotype increases fitness in bears in their present ecology. We ask: is the theory of evolution by natural selection capable of predicting what heritable traits increase fitness among bears in their present ecology? NB. By this question we do not mean ‘is it possible to determine what heritable traits increase fitness’ for if some traits do and others do not, of course this is possible. We want to know what the theory in question has to say about the relative fitness of bear phenotypes.
So suppose the whiteness phenotype has gone to fixation and there are now, say, 200 white bears. Did the whiteness phenotype increase the fitness (in the intensional sense) of the ancestral white bears or was it rather the same-color-as-snow phenotype, the same-color-as-paper phenotype, or any other phenotype that the white bears happen contingently to share with one another and not brown bears? Notice that the theory of evolution by natural selection does not give us any guidance. The ancestral bears (and the present bears) were all of these things. The evolutionary scientist receives no helpful advice from the theory about what hypothesis to hold (though of course the scientist has a helpful set of priors, and is likely to latch on to the correct hypothesis, without invoking Darwin’s theory).
Now suppose the field scientist actually runs some controlled tests on the population of bears in order to test the hypothesis that it was the same-color-as-snow phenotype that increased the fitness of the bears in their ecology, relative to the competing different-color-from-snow phenotype. Perhaps she isolates some of the bears in an area where the snow has been made artificially brown, along with some other conspecific brown bears taken from a different population. If the brownness phenotype goes to fixation in this new population, we will have some confirmation for our hypothesis; if whiteness goes to fixation, we may be led to instead propose that the whiteness phenotype (rather than the same-color-as-snow phenotype) increased fitness (maybe females prefer white bears or something). This is how science goes. But the question is: is Darwinian evolutionary theory confirmed by any of this? And the answer is [again, Fodor’s answer, not mine]: vacuously, yes. If brownness goes to fixation, the Darwinian will say: ‘look, we were right: the same-color-as-snow phenotype was more fit than the whiteness phenotype, and it went to fixation.’ Similarly, if whiteness goes to fixation, the Darwinian will say: ‘look, we were right: the whiteness phenotype was more fit than the same-color-as-snow phenotype, and it went to fixation.’
We can go on. After the first decoupling experiment, the experimenter will have ruled out a certain hypothesis, say, that the same-color-as-snow phenotype was not fitter than its competitors. But there will still be infinitely many properties locally correlated with the whiteness phenotype, so it will not follow that that phenotype was fitter. Here again, Darwinian evolutionary theory is of no help whatsoever in constructing hypotheses about which traits increase fitness. It cannot predict, it can only incorporate empirical findings post-hoc into the adaptationist model.
So the theory of evolution by natural selection (a) makes no predictions (b) does not guide researchers in formulating hypotheses about evolution and (c) is trivially compatible with any outcome. That is not how science goes [or so says Fodor].
This, I take it, is an intriguing argument. It has nothing to do with God. The claim is that the theory of natural selection read extensionally is false, and read intensionally is vacuously true. Nothing about the tree of life is questioned, nothing about inheritance through genes, nothing about the physical basis of all observable phenomena. The hard work of evolutionary biologists in the field is not ignored, nor is it taken to be irrelevant. Fodor is merely arguing that for biologists to attribute their scientific findings on evolution to The Law of Natural Selection is rather like contemporary computational psychologists attributing their findings to Behaviorism. The findings are still there, and still correct: they’re just neither suggested nor explained by natural selection. Or again, so says Fodor.
Conclusion
I don’t know whether Fodor’s right or not. Maybe that makes me an idiot, because maybe he’s as obviously wrong as Randy (Gallistel) and Tim say he is. So be it. But I’d like to be very clear on why Fodor is wrong, if he is. I used to think he was just arguing: there are no biological laws; explanation is subsumption under a law; therefore there are no biological explanations. And I used to think the response should be: that’s an exceedingly narrow conception of explanation. But now I take his argument to be what I presented above: it’s about whether the theory of natural selection itself has any content whatsoever. And one can’t answer that challenge by modifying what one counts as explanation. I invite civil discussion in the comments. No Godbotting, plz.
Posted by Michael Johnson at 2:34 PM
Labels: evolution, Fodor
Hitler y"sh on Jewish uniqueness
Contributed by a friend:
after your email i went and read Hitlers Mein Kaumf, in the chapter "Nation and Race"(http://www.hitler.org/writings/Mein_Kampf/mkv1ch11.html) the writing and acknowledgment of Jews by Hitler is similar almost at times word for word with Torah Jewish ideology. example
"...Here, of course, we encounter the objection of the modern pacifist, as truly Jewish in its effrontery as it is stupid! 'Man's role is to overcome Nature!.....'" from nation and race
everyday our rabbis and Torah teaches us to overcome nature
".....The mightiest counterpart to the Aryan is represented by the Jew. In hardly any people in the world is the instinct of self-preservation developed more strongly than in the so-called 'chosen.' Of this, the mere fact of the survival of this race may be considered the best proof. Where is the people which in the last two thousand years has been exposed to so slight changes of inner disposition, character, etc., as the Jewish people? What people, finally, has gone through greater upheavals than this one-and nevertheless issued from the mightiest catastrophes of mankind unchanged? What an infinitely tough will to live and preserve the species speaks from these facts ....."
you in your podcast at 24.00minute say we don't belong here and our survival is a miracle. Torah jews believe it as divine providence and he believes it as self preservation. He views this survival as evil i view it as g-ds love for me and humanity.
Hitler was evil was the opposite of what good is,
Rabbi this world truly does have good and evil, Hitler and his view of the same situation is evil and ours is good, but the interesting thing this theme happens over again and again example Mark Twain who also observes the situation and sees it as good.
after your email i went and read Hitlers Mein Kaumf, in the chapter "Nation and Race"(http://www.hitler.org/writings/Mein_Kampf/mkv1ch11.html) the writing and acknowledgment of Jews by Hitler is similar almost at times word for word with Torah Jewish ideology. example
"...Here, of course, we encounter the objection of the modern pacifist, as truly Jewish in its effrontery as it is stupid! 'Man's role is to overcome Nature!.....'" from nation and race
everyday our rabbis and Torah teaches us to overcome nature
".....The mightiest counterpart to the Aryan is represented by the Jew. In hardly any people in the world is the instinct of self-preservation developed more strongly than in the so-called 'chosen.' Of this, the mere fact of the survival of this race may be considered the best proof. Where is the people which in the last two thousand years has been exposed to so slight changes of inner disposition, character, etc., as the Jewish people? What people, finally, has gone through greater upheavals than this one-and nevertheless issued from the mightiest catastrophes of mankind unchanged? What an infinitely tough will to live and preserve the species speaks from these facts ....."
you in your podcast at 24.00minute say we don't belong here and our survival is a miracle. Torah jews believe it as divine providence and he believes it as self preservation. He views this survival as evil i view it as g-ds love for me and humanity.
Hitler was evil was the opposite of what good is,
Rabbi this world truly does have good and evil, Hitler and his view of the same situation is evil and ours is good, but the interesting thing this theme happens over again and again example Mark Twain who also observes the situation and sees it as good.
Wednesday, February 10, 2010
Fodor and Palmarini's critique of Darwin
What Darwin Got Wrong by Jerry Fodor and Massimo Piattelli Palmarini Darwin is under fire again, but Mary Midgley feels that his ideas have been misrepresented
Mary Midgley The Guardian, Saturday 6 February 2010
What Darwin Got Wrong by Jerry Fodor and Massimo Piattelli Palmarini 178pp, Profile, £20
Charles Darwin complained quite crossly in his autobiography that, despite many denials, people still kept saying he thought natural selection was the sole cause of evolutionary development. "Great is the force of misrepresentation," he grumbled. Had he known that, a century later, his alleged followers would be promoting that very doctrine as central to his teaching, and extending it into the wilder reaches of psychology and physics, he might have got even crosser. Darwin's objection was surely not just that he could see other possible causes. He saw that the doctrine itself did not make sense. No filter, however powerful, can be the only cause of what flows out of it. Questions about what comes into that filter have to be just as important. The proposed solution bears no proportion to the size of the problem.
Since his time, biologists have discovered a huge amount that is really interesting and important about internal factors in organisms that affect reproduction. This powerful little book uses that material to challenge sharply the whole neo-Darwinist orthodoxy – the assumption that, essentially, all evolution is due to mutation and selection. Its authors do not, of course, deny that this kind of classical natural selection happens. But they argue strongly that there is now no reason to privilege it over a crowd of other possible causes. Not only are most mutations known to be destructive but the material of inheritance itself has turned out to be far more complex, and to provide a much wider repertoire of untapped possibilities, than used to be thought. To an impressive extent, organisms provide the materials for changes in their own future. As the authors put it, "Before any phenotype can be, so to speak, 'offered' to selection by the environment, a host of internal constraints have to be satisfied." Epigenetic effects, resulting from different expressions of the same genes, can make a huge difference. And genes themselves are now known not to be independent, bean-like items connected to particular transmitted traits, but aspects of a most intricate process, sensitive to all sorts of internal factors, so that in many ways the same genes can result in a different creature. Recent work in "evodevo" – evolutionary developmental biology – shows how paths of development can themselves change and can change the resulting organism. And again, forces such as "molecular drive", which rearrange the genes, can also have that effect.
Besides this – perhaps even more interestingly – the laws of physics and chemistry themselves take a hand in the developmental process. Matter itself behaves in characteristic ways which are distinctly non-random. Many natural patterns, such as the arrangement of buds on a stem, accord with the series of Fibonacci numbers, and Fibonacci spirals are also observed in spiral nebulae. There are, moreover, no flying pigs, on account of the way in which bones arrange themselves. I am pleased to see that Fodor and Piattelli Palmarini introduce these facts in a chapter headed "The Return of the Laws of Form" and connect them with the names of D'Arcy Thompson, Conrad Waddington and Ilya Prigogine. Though they don't actually mention Goethe, that reference still rightly picks up an important, genuinely scientific strand of investigation which was for some time oddly eclipsed by neo-Darwinist fascination with the drama of randomness and the illusory seductions of simplicity.
This book is, of course, fighting stuff, sure to be contested by those at whom it is aimed. On the face of things, however, it strikes an outsider as an overdue and valuable onslaught on neo-Darwinist simplicities. (The one thing I would complain of is the title, which is perhaps too personal. This isn't just a point about Darwin; it's a point about the nature of life.) As the authors note, the traditional story has been defended by extending it – by widening the notion of natural selection to include some of these internal processes. But they think – surely rightly – that this device merely adds epicycles which kill the doctrine by diluting it. The long process of repeated trials and errors which has always been claimed as a central feature of natural selection cannot be incorporated in this way.
If we now ask what will take its place, their answer is that this question does not arise. There is not – and does not have to be – any single, central mechanism of evolution. There are many such mechanisms, which all need to be investigated on their own terms. If one finds this kind of position reasonable, the interesting next question is, what has made it so hard to accept? What has kept this kind of dogmatic "Darwinism" – largely independent of its founder – afloat for so long, given that much of the material given here is by no means new?
The explanation for this might be the seductive myth that underlies it. That myth had its roots in Victorian social Darwinism but today it flows largely from two books – Jacques Monod's Chance and Necessity (1971) and Richard Dawkins's The Selfish Gene (1976). Both these books, of course, contain lots of good and necessary biological facts. But what made them bestsellers was chiefly the sensational underlying picture of human life supplied by their rhetoric and especially their metaphors. This drama showed heroic, isolated individuals contending, like space warriors, alone against an alien and meaningless cosmos. It established the books as a kind of bible of individualism, most congenial to the Reaganite and Thatcherite ethos of the 80s. Monod first showed humans in Existentialist style as aliens – "gypsies" in a foreign world – and, by expanding the role of chance in evolution, concluded that our life was essentially a "casino". Dawkins added personal drama by describing a population of genes which – quite unlike the real ones inside us – operate as totally independent agents and can do as they please. It is no great surprise that these images caught on, nor that they can now persist whether or not the doctrines linked to them turn out to be scientific.
Mary Midgley The Guardian, Saturday 6 February 2010
What Darwin Got Wrong by Jerry Fodor and Massimo Piattelli Palmarini 178pp, Profile, £20
Charles Darwin complained quite crossly in his autobiography that, despite many denials, people still kept saying he thought natural selection was the sole cause of evolutionary development. "Great is the force of misrepresentation," he grumbled. Had he known that, a century later, his alleged followers would be promoting that very doctrine as central to his teaching, and extending it into the wilder reaches of psychology and physics, he might have got even crosser. Darwin's objection was surely not just that he could see other possible causes. He saw that the doctrine itself did not make sense. No filter, however powerful, can be the only cause of what flows out of it. Questions about what comes into that filter have to be just as important. The proposed solution bears no proportion to the size of the problem.
Since his time, biologists have discovered a huge amount that is really interesting and important about internal factors in organisms that affect reproduction. This powerful little book uses that material to challenge sharply the whole neo-Darwinist orthodoxy – the assumption that, essentially, all evolution is due to mutation and selection. Its authors do not, of course, deny that this kind of classical natural selection happens. But they argue strongly that there is now no reason to privilege it over a crowd of other possible causes. Not only are most mutations known to be destructive but the material of inheritance itself has turned out to be far more complex, and to provide a much wider repertoire of untapped possibilities, than used to be thought. To an impressive extent, organisms provide the materials for changes in their own future. As the authors put it, "Before any phenotype can be, so to speak, 'offered' to selection by the environment, a host of internal constraints have to be satisfied." Epigenetic effects, resulting from different expressions of the same genes, can make a huge difference. And genes themselves are now known not to be independent, bean-like items connected to particular transmitted traits, but aspects of a most intricate process, sensitive to all sorts of internal factors, so that in many ways the same genes can result in a different creature. Recent work in "evodevo" – evolutionary developmental biology – shows how paths of development can themselves change and can change the resulting organism. And again, forces such as "molecular drive", which rearrange the genes, can also have that effect.
Besides this – perhaps even more interestingly – the laws of physics and chemistry themselves take a hand in the developmental process. Matter itself behaves in characteristic ways which are distinctly non-random. Many natural patterns, such as the arrangement of buds on a stem, accord with the series of Fibonacci numbers, and Fibonacci spirals are also observed in spiral nebulae. There are, moreover, no flying pigs, on account of the way in which bones arrange themselves. I am pleased to see that Fodor and Piattelli Palmarini introduce these facts in a chapter headed "The Return of the Laws of Form" and connect them with the names of D'Arcy Thompson, Conrad Waddington and Ilya Prigogine. Though they don't actually mention Goethe, that reference still rightly picks up an important, genuinely scientific strand of investigation which was for some time oddly eclipsed by neo-Darwinist fascination with the drama of randomness and the illusory seductions of simplicity.
This book is, of course, fighting stuff, sure to be contested by those at whom it is aimed. On the face of things, however, it strikes an outsider as an overdue and valuable onslaught on neo-Darwinist simplicities. (The one thing I would complain of is the title, which is perhaps too personal. This isn't just a point about Darwin; it's a point about the nature of life.) As the authors note, the traditional story has been defended by extending it – by widening the notion of natural selection to include some of these internal processes. But they think – surely rightly – that this device merely adds epicycles which kill the doctrine by diluting it. The long process of repeated trials and errors which has always been claimed as a central feature of natural selection cannot be incorporated in this way.
If we now ask what will take its place, their answer is that this question does not arise. There is not – and does not have to be – any single, central mechanism of evolution. There are many such mechanisms, which all need to be investigated on their own terms. If one finds this kind of position reasonable, the interesting next question is, what has made it so hard to accept? What has kept this kind of dogmatic "Darwinism" – largely independent of its founder – afloat for so long, given that much of the material given here is by no means new?
The explanation for this might be the seductive myth that underlies it. That myth had its roots in Victorian social Darwinism but today it flows largely from two books – Jacques Monod's Chance and Necessity (1971) and Richard Dawkins's The Selfish Gene (1976). Both these books, of course, contain lots of good and necessary biological facts. But what made them bestsellers was chiefly the sensational underlying picture of human life supplied by their rhetoric and especially their metaphors. This drama showed heroic, isolated individuals contending, like space warriors, alone against an alien and meaningless cosmos. It established the books as a kind of bible of individualism, most congenial to the Reaganite and Thatcherite ethos of the 80s. Monod first showed humans in Existentialist style as aliens – "gypsies" in a foreign world – and, by expanding the role of chance in evolution, concluded that our life was essentially a "casino". Dawkins added personal drama by describing a population of genes which – quite unlike the real ones inside us – operate as totally independent agents and can do as they please. It is no great surprise that these images caught on, nor that they can now persist whether or not the doctrines linked to them turn out to be scientific.
Monday, February 8, 2010
New book by Rabbi Dr. Tatz
Highly recommended - a new book by Rabbi Dr. Akiva Tatz, to be published by Targum:
Dangerous Disease and Dangerous Therapy in Jewish Medical Ethics
CONTENTS / 11
Contents
Introduction 19
PART ONE:
HALACHA – PRINCIPLES AND LAWS
Principles 23
Differences between Jewish and Modern Secular Approaches 23
Definition of Principles 23
Quality of Life 24
Cost 24
Best Possible Treatment 27
Halachic Methodology 27
Dispute and Opinion 30
Risk 30
The Primary Value of Life 32
Statistics 37
Unknown Benefit, Unknown Harm 37
Standard of Care 39
Clinical Logic 40
Preparation and Education 40
Clinical Case 1: Benefit or Harm? 42
Approach to Risk in Halacha 45
Minimal Risk 45
Moderate Risk 48
High Risk 51
Risk to Caregivers 54
Doubtful Danger 58
Risk in Military Situations 59
Clinical Case 2: Risk to Caregivers 60
/ DANGEROUS DISEASE & DANGEROUS 12 S THERAPY
Danger to Life and Lifesaving Interventions 61
Lifesaving Interventions with Low Risk 61
Lifesaving Interventions, Low Risk but Painful or Mutilating 62
Lifesaving Interventions that Add Immediate Risk 63
Danger to Life in Halacha: Specific Causes 63
Obligation to Incur Cost to Save Life 65
Incurring Costs or Damages to Others to Save Life 67
Obligation to Incur Discomfort or Minor Illness to Save Life 68
Endangering Others in the Course of Saving Life 68
Clinical Case 3: Incurring Cost to a Third Party to Save Life 69
Pain Relief and Functional Improvement 71
Pain Relief and Palliation in Life Threatening Conditions 71
Pain Relief and Palliation in non-Life Threatening Conditions 71
Functional Improvement 72
Danger to a Limb, Organ or Faculty 73
Incurring Cost to Save a Limb 74
Risking or Sacrificing an Organ or Limb 75
Endangering or Sacrificing a Limb to Save Life 75
Endangering a Limb to Save Function of that Limb 76
Sacrificing a Limb or Organ to Save another Limb or Organ 76
Saving Life - Risking and Donating Organs/Limbs 77
Risking an Organ or Limb to Save Another’s Life 77
Donating or Sacrificing an Organ or Limb to Save Another’s Life 77
Organ Donation with No (or Minimal) Danger to Life 77
Regenerating Organ 77
Non-regenerating Organ 78
Saving Life – Risking Life for Others 81
Organ Donation with Danger to Life 81
Regenerating Organ 81
Non-regenerating Organ 82
Non-sentient and Minor Donors 85
Risking Life for Another’s Benefit (not to save life) 87
CONTENTS / 13
Interventions in Pregnancy 89
Undertaking Risk to Become Pregnant 89
Prevention of Pregnancy to Avoid Risk 90
Screening and Diagnostic Investigations in Pregnancy 91
Invasive Testing 91
Non-invasive Testing 91
Obligation to Save a Fetus and Appropriate Interventions 92
Cesarian Section Against Mother’s Wishes 92
Fetal Reduction 93
Operating on a Fetus in Utero 94
Clinical Case 4: Obstetrical Risk 95
Clinical Case 5: Delaying Chemotherapy to Preserve Pregnancy 98
Approach to Dangerous and Terminal Illness 101
Dangerous Illness 101
Terminal Illness 101
Terminal Illness – chayei sha’a (“temporary life”) 102
Withholding and Withdrawing Therapy 103
Withholding Treatment in chayei sha’a Situations 105
Unconscious Patients 109
Minors and Mentally Incompetent Patients 110
Neonates and Infants with Short Life Expectancy 110
Analgesia in Dangerously or Terminally Ill Patients 112
Withholding Fluids, Nutrition and other Basic Needs 114
Withholding Ventilation, Dialysis, Cardiac Pacing 117
Risky Treatment in chayei sha’a Situations 118
Limits of Risk 122
Terminal Life, Therapy Safe but Efficacy Doubtful 123
Risking Terminal Life to Prolong Terminal Life 124
Intercurrent and Secondary Problems in Terminal Illness 125
Acute Intermittent Threats to Life 125
Chronic Disease with Acute Life-threatening Exacerbations 125
Extreme Old Age 126
Risking Long Term Life for Longer Term Life 126
Prolonging Long Term Life with Severe Suffering 127
Terminal Illness – goses (end-stage terminal illness) 127
Clinical Case 6: Withdrawing and Withholding Therapy 130
Clinical Case 7: Dangerous (but not Certainly Terminal) Illness 131
/ DANGEROUS DISEASE & DANGEROUS 14 S THERAPY
Clinical Case 8: Risky Procedure in chayei sha’a 131
Clinical Case 9: Risky Procedure in chayei olam 132
Clinical Case 10: Serious Disease, Risky Procedure 133
Clinical Case 11: Neonate with Abnormalities & Poor Prognosis 133
Clinical Case 12: Futile and non-Futile Treatment 134
Definition and Timing of Death 135
The Circulatory Death Debate 139
Time of Death 142
Resuscitation 143
Time of Death in Failed Resuscitation Attempt 145
When is Resuscitation Obligatory? 145
Adequate Duration of Resuscitation Attempt 145
Advance Directives and “Do Not Resuscitate” (DNR) Orders 146
“Do Not Hospitalize” and “Allow Natural Death” Orders 148
Clinical Case 13: “DNR” and “Do Not Treat” Confusion 150
Euthanasia, Suicide and Assisted Suicide 153
Euthanasia 153
Suicide and Assisted Suicide 154
Coercion and Consent 155
Principles of Coercion and Consent in Halacha 156
Treatment Obligatory 156
Treatment Forbidden 158
Treatment Discretionary 158
Treatment Against Patient’s Wishes – Summary of Principles 159
Obligation to Disclose Risk 160
Danger to Life 160
Serious Illness Without Danger to Life 161
Where Therapy May Result in Significant Harm 162
Clinical Case 14: Treatment without Consent 163
Clinical Case 15: Treating a Child Against Parents’ Wishes 164
Clinical Case 16: No Consent and Against Parents’ Wishes 165
Clinical Case 17: Obliging One Person to Save Another 168
Clinical Case 18: Unreasonable Refusal of Therapy 169
CONTENTS / 15
Triage 171
Triage in the Acute Setting 173
Proximity 173
Relatives 174
Definite vs Doubtful Danger 175
Many vs Few 175
Saving Many with Possible Harm to Few 175
Many Doubtful vs Few Certain 175
Where Treatment has Already Begun 177
Healthy vs Ill 178
Salvageable vs non-Salvageable Patients 178
One Salvageable vs Two non-Salvageable Patients 180
First Come, First Served 181
Men or Women First 181
Age 182
Marital Status 182
Military Triage 183
Conflict with Secular Protocols 184
Clinical Case 19: Triage: Many vs Few and Definite vs Doubtful 185
Clinical Case 20: Disaster Scene Triage 185
Destroying Life to Save Life 189
Sacrificing One to Save Many 189
Fetal Reduction 190
Abortion 190
Conjoined Twins 190
Killing a goses, treifa or chayei sha’a to save a chayei olam 190
Clinical Case 21: Triage; Killing One to Save Another 191
Cosmetic Surgery 197
Manipulating the Natural 197
Injury 198
Male Cross-dressing 198
Tattooing 199
Risk 200
Valid Indications for Cosmetic Procedures 201
/ DANGEROUS DISEASE & DANGEROUS 16 S THERAPY
Experimental Therapy and Research 203
Experimental and non-Established Therapies 203
Research and Clinical Trials 204
Screening and Prevention 207
Screening 207
Prevention 209
Risks 209
Clinical Case 22: Prophylactic Surgery 211
PART TWO:
LIFE AND DEATH ISSUES IN JEWISH MEDICAL
ETHICS AND THE MODERN WORLD
Comparison of Torah and Secular Principles 218
The Four Principles 218
Autonomy 219
Competence 222
Non-maleficence 224
Withholding vs Withdrawing Treatment 227
Ordinary vs Extraordinary Treatment 227
Feeding & Artificial Feeding vs Life-sustaining Technologies 227
Intended Effects vs Foreseen but Unintended Effects 228
Futility 229
Beneficence 231
Justice 232
Veracity 232
Privacy 233
Confidentiality 233
Moral Dilemmas 234
Torah and Secular Law 235
CONTENTS / 17
Euthanasia, Assisted Suicide and Withholding
Therapy in Current Thought and Practice
237
Euthanasia and Assisted Suicide – Changing
Attitudes and Practices in Recent Times
241
It’s Over, Debbie 241
Diane 247
Mind Reading 253
The Medicalization of Death 263
Kevorkian and the Suicide Machine 263
Anatomy of a Disaster: Hurricane Katrina –
A Medical Ethical Nightmare
271
Murder or Mercy? Hurricane Katrina and Euthanasia 271
Materialism and Medical Ethics 279
Not a Doctor’s Decision 279
Afterword 289
Hope and Therapy; Medical Treason; A New Ideal;
Moments of Eternity
289
Appendices
I. How a Rabbi Decides an Issue in Medical Halacha 299
II. Modern Historical Overview of Euthanasia and Assisted
Suicide in Western Countries
307
III. Monetary Cost of Saving Life 315
IV. Risky Professions 317
V. Transport Modes – Comparative Risks 321
VI. Selection Criteria for Renal Dialysis and Transplantation 323
/ DANGEROUS DISEASE & DANGEROUS 18 S THERAPY
Clinical Cases
Clinical Cases 329
Bibliography and Sources
Sources and Responsa 341
English Bibliography 349
Glossary 351
Dangerous Disease and Dangerous Therapy in Jewish Medical Ethics
CONTENTS / 11
Contents
Introduction 19
PART ONE:
HALACHA – PRINCIPLES AND LAWS
Principles 23
Differences between Jewish and Modern Secular Approaches 23
Definition of Principles 23
Quality of Life 24
Cost 24
Best Possible Treatment 27
Halachic Methodology 27
Dispute and Opinion 30
Risk 30
The Primary Value of Life 32
Statistics 37
Unknown Benefit, Unknown Harm 37
Standard of Care 39
Clinical Logic 40
Preparation and Education 40
Clinical Case 1: Benefit or Harm? 42
Approach to Risk in Halacha 45
Minimal Risk 45
Moderate Risk 48
High Risk 51
Risk to Caregivers 54
Doubtful Danger 58
Risk in Military Situations 59
Clinical Case 2: Risk to Caregivers 60
/ DANGEROUS DISEASE & DANGEROUS 12 S THERAPY
Danger to Life and Lifesaving Interventions 61
Lifesaving Interventions with Low Risk 61
Lifesaving Interventions, Low Risk but Painful or Mutilating 62
Lifesaving Interventions that Add Immediate Risk 63
Danger to Life in Halacha: Specific Causes 63
Obligation to Incur Cost to Save Life 65
Incurring Costs or Damages to Others to Save Life 67
Obligation to Incur Discomfort or Minor Illness to Save Life 68
Endangering Others in the Course of Saving Life 68
Clinical Case 3: Incurring Cost to a Third Party to Save Life 69
Pain Relief and Functional Improvement 71
Pain Relief and Palliation in Life Threatening Conditions 71
Pain Relief and Palliation in non-Life Threatening Conditions 71
Functional Improvement 72
Danger to a Limb, Organ or Faculty 73
Incurring Cost to Save a Limb 74
Risking or Sacrificing an Organ or Limb 75
Endangering or Sacrificing a Limb to Save Life 75
Endangering a Limb to Save Function of that Limb 76
Sacrificing a Limb or Organ to Save another Limb or Organ 76
Saving Life - Risking and Donating Organs/Limbs 77
Risking an Organ or Limb to Save Another’s Life 77
Donating or Sacrificing an Organ or Limb to Save Another’s Life 77
Organ Donation with No (or Minimal) Danger to Life 77
Regenerating Organ 77
Non-regenerating Organ 78
Saving Life – Risking Life for Others 81
Organ Donation with Danger to Life 81
Regenerating Organ 81
Non-regenerating Organ 82
Non-sentient and Minor Donors 85
Risking Life for Another’s Benefit (not to save life) 87
CONTENTS / 13
Interventions in Pregnancy 89
Undertaking Risk to Become Pregnant 89
Prevention of Pregnancy to Avoid Risk 90
Screening and Diagnostic Investigations in Pregnancy 91
Invasive Testing 91
Non-invasive Testing 91
Obligation to Save a Fetus and Appropriate Interventions 92
Cesarian Section Against Mother’s Wishes 92
Fetal Reduction 93
Operating on a Fetus in Utero 94
Clinical Case 4: Obstetrical Risk 95
Clinical Case 5: Delaying Chemotherapy to Preserve Pregnancy 98
Approach to Dangerous and Terminal Illness 101
Dangerous Illness 101
Terminal Illness 101
Terminal Illness – chayei sha’a (“temporary life”) 102
Withholding and Withdrawing Therapy 103
Withholding Treatment in chayei sha’a Situations 105
Unconscious Patients 109
Minors and Mentally Incompetent Patients 110
Neonates and Infants with Short Life Expectancy 110
Analgesia in Dangerously or Terminally Ill Patients 112
Withholding Fluids, Nutrition and other Basic Needs 114
Withholding Ventilation, Dialysis, Cardiac Pacing 117
Risky Treatment in chayei sha’a Situations 118
Limits of Risk 122
Terminal Life, Therapy Safe but Efficacy Doubtful 123
Risking Terminal Life to Prolong Terminal Life 124
Intercurrent and Secondary Problems in Terminal Illness 125
Acute Intermittent Threats to Life 125
Chronic Disease with Acute Life-threatening Exacerbations 125
Extreme Old Age 126
Risking Long Term Life for Longer Term Life 126
Prolonging Long Term Life with Severe Suffering 127
Terminal Illness – goses (end-stage terminal illness) 127
Clinical Case 6: Withdrawing and Withholding Therapy 130
Clinical Case 7: Dangerous (but not Certainly Terminal) Illness 131
/ DANGEROUS DISEASE & DANGEROUS 14 S THERAPY
Clinical Case 8: Risky Procedure in chayei sha’a 131
Clinical Case 9: Risky Procedure in chayei olam 132
Clinical Case 10: Serious Disease, Risky Procedure 133
Clinical Case 11: Neonate with Abnormalities & Poor Prognosis 133
Clinical Case 12: Futile and non-Futile Treatment 134
Definition and Timing of Death 135
The Circulatory Death Debate 139
Time of Death 142
Resuscitation 143
Time of Death in Failed Resuscitation Attempt 145
When is Resuscitation Obligatory? 145
Adequate Duration of Resuscitation Attempt 145
Advance Directives and “Do Not Resuscitate” (DNR) Orders 146
“Do Not Hospitalize” and “Allow Natural Death” Orders 148
Clinical Case 13: “DNR” and “Do Not Treat” Confusion 150
Euthanasia, Suicide and Assisted Suicide 153
Euthanasia 153
Suicide and Assisted Suicide 154
Coercion and Consent 155
Principles of Coercion and Consent in Halacha 156
Treatment Obligatory 156
Treatment Forbidden 158
Treatment Discretionary 158
Treatment Against Patient’s Wishes – Summary of Principles 159
Obligation to Disclose Risk 160
Danger to Life 160
Serious Illness Without Danger to Life 161
Where Therapy May Result in Significant Harm 162
Clinical Case 14: Treatment without Consent 163
Clinical Case 15: Treating a Child Against Parents’ Wishes 164
Clinical Case 16: No Consent and Against Parents’ Wishes 165
Clinical Case 17: Obliging One Person to Save Another 168
Clinical Case 18: Unreasonable Refusal of Therapy 169
CONTENTS / 15
Triage 171
Triage in the Acute Setting 173
Proximity 173
Relatives 174
Definite vs Doubtful Danger 175
Many vs Few 175
Saving Many with Possible Harm to Few 175
Many Doubtful vs Few Certain 175
Where Treatment has Already Begun 177
Healthy vs Ill 178
Salvageable vs non-Salvageable Patients 178
One Salvageable vs Two non-Salvageable Patients 180
First Come, First Served 181
Men or Women First 181
Age 182
Marital Status 182
Military Triage 183
Conflict with Secular Protocols 184
Clinical Case 19: Triage: Many vs Few and Definite vs Doubtful 185
Clinical Case 20: Disaster Scene Triage 185
Destroying Life to Save Life 189
Sacrificing One to Save Many 189
Fetal Reduction 190
Abortion 190
Conjoined Twins 190
Killing a goses, treifa or chayei sha’a to save a chayei olam 190
Clinical Case 21: Triage; Killing One to Save Another 191
Cosmetic Surgery 197
Manipulating the Natural 197
Injury 198
Male Cross-dressing 198
Tattooing 199
Risk 200
Valid Indications for Cosmetic Procedures 201
/ DANGEROUS DISEASE & DANGEROUS 16 S THERAPY
Experimental Therapy and Research 203
Experimental and non-Established Therapies 203
Research and Clinical Trials 204
Screening and Prevention 207
Screening 207
Prevention 209
Risks 209
Clinical Case 22: Prophylactic Surgery 211
PART TWO:
LIFE AND DEATH ISSUES IN JEWISH MEDICAL
ETHICS AND THE MODERN WORLD
Comparison of Torah and Secular Principles 218
The Four Principles 218
Autonomy 219
Competence 222
Non-maleficence 224
Withholding vs Withdrawing Treatment 227
Ordinary vs Extraordinary Treatment 227
Feeding & Artificial Feeding vs Life-sustaining Technologies 227
Intended Effects vs Foreseen but Unintended Effects 228
Futility 229
Beneficence 231
Justice 232
Veracity 232
Privacy 233
Confidentiality 233
Moral Dilemmas 234
Torah and Secular Law 235
CONTENTS / 17
Euthanasia, Assisted Suicide and Withholding
Therapy in Current Thought and Practice
237
Euthanasia and Assisted Suicide – Changing
Attitudes and Practices in Recent Times
241
It’s Over, Debbie 241
Diane 247
Mind Reading 253
The Medicalization of Death 263
Kevorkian and the Suicide Machine 263
Anatomy of a Disaster: Hurricane Katrina –
A Medical Ethical Nightmare
271
Murder or Mercy? Hurricane Katrina and Euthanasia 271
Materialism and Medical Ethics 279
Not a Doctor’s Decision 279
Afterword 289
Hope and Therapy; Medical Treason; A New Ideal;
Moments of Eternity
289
Appendices
I. How a Rabbi Decides an Issue in Medical Halacha 299
II. Modern Historical Overview of Euthanasia and Assisted
Suicide in Western Countries
307
III. Monetary Cost of Saving Life 315
IV. Risky Professions 317
V. Transport Modes – Comparative Risks 321
VI. Selection Criteria for Renal Dialysis and Transplantation 323
/ DANGEROUS DISEASE & DANGEROUS 18 S THERAPY
Clinical Cases
Clinical Cases 329
Bibliography and Sources
Sources and Responsa 341
English Bibliography 349
Glossary 351
Tuesday, February 2, 2010
natural law during creation
Guide of the Perplexed I:67:
It is possible that the word va-yanah is derived either from yanah, a
verb of the class pe-yod, or nahoh, a verb of the class lamed-he,
and has this meaning :" he established" or" he governed" the
Universe in accordance with the properties it possessed on the
seventh day" : that is to say, while on each of the six days events took place contrary to the natural laws now in operation
throughout the Universe, on the seventh day the Universe was
merely upheld and left in the condition in which it continues to
exist.
Guide II:30:
The following point now claims our attention. The account of the
six days of creation contains, in reference to the creation of man,
the statement :" Male and female created he them" (i. 27), and
concludes with the words:" Thus the heavens and the earth were
finished, and all the host of them" (ii. 1), and yet the portion
which follows describes the creation of Eve from Adam, the tree
of life, and the tree of knowledge, the history of the serpent and
the events connected therewith, and all this as having taken place
after Adam had been placed in the Garden of Eden. All our Sages
agree that this took place on the sixth day, and that nothing new
was created after the close of the six days. None of the things mentioned above is therefore impossible, because the laws of
Nature were then not yet permanently fixed.
In the light of the Rambam’s statements above, the following [supplied by Rabbi Moshe Meiselman] is very interesting:
In 1939, Paul Dirac wrote, “At the beginning of time, the laws of Nature were probably very different from what they are now. Thus, we should consider the laws of nature as continually changing within the epoch, instead of holding uniformly throughout space-time.”[1]
[1] Dirac, Paul “The relationship between mathematics and physics” Proceedings of the Royal Society (Edinburgh) 59 122-129.
It is possible that the word va-yanah is derived either from yanah, a
verb of the class pe-yod, or nahoh, a verb of the class lamed-he,
and has this meaning :" he established" or" he governed" the
Universe in accordance with the properties it possessed on the
seventh day" : that is to say, while on each of the six days events took place contrary to the natural laws now in operation
throughout the Universe, on the seventh day the Universe was
merely upheld and left in the condition in which it continues to
exist.
Guide II:30:
The following point now claims our attention. The account of the
six days of creation contains, in reference to the creation of man,
the statement :" Male and female created he them" (i. 27), and
concludes with the words:" Thus the heavens and the earth were
finished, and all the host of them" (ii. 1), and yet the portion
which follows describes the creation of Eve from Adam, the tree
of life, and the tree of knowledge, the history of the serpent and
the events connected therewith, and all this as having taken place
after Adam had been placed in the Garden of Eden. All our Sages
agree that this took place on the sixth day, and that nothing new
was created after the close of the six days. None of the things mentioned above is therefore impossible, because the laws of
Nature were then not yet permanently fixed.
In the light of the Rambam’s statements above, the following [supplied by Rabbi Moshe Meiselman] is very interesting:
In 1939, Paul Dirac wrote, “At the beginning of time, the laws of Nature were probably very different from what they are now. Thus, we should consider the laws of nature as continually changing within the epoch, instead of holding uniformly throughout space-time.”[1]
[1] Dirac, Paul “The relationship between mathematics and physics” Proceedings of the Royal Society (Edinburgh) 59 122-129.
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