Csf Russo Seminar1

State the problem precisely, and state the questions to be addressed and the perspective  epistemology I’ll introduce you to the phil debate. [if u’re not interested in phil yet, u should, because, even if u don’t think that phil is serious, at least it is funny, for instead of catastrophic ex with all sorts of disease, we use squirrels, golf players etc] We shall see that phil debate turns around the so-called squirrel example, that is supposed to trouble PT, and the solution is to distinguish 2 levels of causation Epistemology works to give a better understanding of twofold c. without any unnecessary metaph assumption. And also gives us a principle to connect the levels. Finally, and time permitting, I will discuss Eells’ account of token causality and explain why it gives a metaph answ to an epist question
the golf environment fascinated various philosophers. A first version of the squirrel ex was to show a difficulty for Suppes’ prob th., i.e. when we have improbable concequences. [mention example] modified version  problem of negative causes, and consequently, to raise the problem of the levels. [Present example] Explain the difficulty raised: at the pop lev squirrels’ kick are negative causes, at the individual lev the squirrel’s kick seems to be a positive cause. The two probability inequalities at the 2 lev. do not match … whence the trick. How can be the case that the same event – namely, “the squirrel’s kick” – be a negative and a positive causal factor? It follows, PT is in trouble, if we want to claim that the squirrel’s kick is a negative cause and that the squirrel’s kick actually caused the ball to fall in one.
Tell the solution of the squirrel example: 2 levels of causation  epis says OK 2 different causal mechanisms at the 2 levels  metaph answer to epist question, details later. We are here concerned with epistemology. So, 2 doubts: causation really operates differently at the two levels? )  metaph question I won’t deal with. do we need to postulate 2 different mechanisms?  epist question  intuitively no. We need to start afresh, and to develop a better understanding of the levels which does not postulate different mechanisms. Since we are now familiar with the golf environment, let’s continue with it.
Eells account of token causation, explain why it is a metaphysical answer (somehow unjustified) The relation to analyse is: ‘x’s being X’ at <tx, sx> caused ‘y’s being Y’ at <ty, sy> , x takes place at time and place <tx, sx> , y takes place at time and place <ty, sy> . x , y = actual instantiations or tokens of the corresponding types X and Y Main idea  probability-increase idea that is appropriate for token causation; Roughly: look at how the probability of the later event y actually evolves around the time of the earlier and later events. depiction of the evolution of the probability value of the effect y , we actually draw the trajectory of its probability. Squirrel ex  the right trajectory is supposed to show that the probability of hole-in-one, after the squirrel’s kick, increases. Hence,squirrel regained qua positive causal factor. [explain trajectory] Eells: despite the fact that the probability that the probability of a birdie will take this trajectory is quite low, in this particular token case the probability of the birdie does take this trajectory. This is, in Eells’ opinion, the most plausible way to enforce the intuition that the squirrel token-caused the birdie.
Problem: P(Y) at each t = P(y|K&W)  the causal background context and on other causal factors. OSS: To say that in principle the state of the world would allow an extremely precise calculation of the probability of the birdie does not mean that – de facto – we are able to calculate it! Second problem. to evaluate P(y) at different times along the trajectory, we have to consider *different hypothetical probability distributions* that hold respectively at tx , or at any time t between tx and ty , or at ty . OSS: of course probabilities in the single case are evaluated thanks to knowledge of the corresponding population, but: the very possibility of being able to evaluate at every time the corresponding hypothetical distributions and, the fact that if at different times we evaluate probabilities in terms of different hypothetical distributions, we miss the connection to the actual population the token under analysis belongs to
So, to the first question, epist reply: Yes, there are levels Causal conclusions drawn from stat analyses concern the pop Individual causal relations take place between individuals within the population Pop-lev  causal rel *represented* by joint prob functions Ind-lev causal rel are *realizations* of joint probability functions This provides sensible understanding of non instantiated cases or outlier observations. Ind. causal relations as realizations of joint prob functions epistemologically makes sense of the golf ball falls into the cup, despite the squirrel’s kick. (More importantly) Harry didn’t develop lung cancer, in spite of his heavy smoking. OSS:I’m not reducing causes to probabilities, I’m suggesting that to account for the levels epistemology no need to postulate different mechanism. OSS2:why is this a stat understanding? Bcz knowledge of causal rel through *correlational* data Next question: how to relate the levels?
Stated in Sober’s 1986, CP entirely neglected in the philosophical literature. We need a CP bcz we might be interested in the chance of Harry’s getting lung cancer, or how likely is that it was his smoking to cause him to get cancer. OSS: These are two different issues. concerns the way priors are assigned in particular cases, while is concerned with the likelihood of hypotheses. CP deals directly with the (ii)
OSS: while the rough idea seems correct, but sober’s formulation seems imprecise, compared to what is stated before. Rough idea: S(token hypothesis) is *proportional* to the strength of the causal relation at the population level, the support of C(t1)  E(t2) is proportional to the strength of C  E . Formulation: if *strength* of C  E is m , then the *support* of C(t1)  E(t2) , given that C(t1) and E(t2) occurred, will be * m* as well. My doubt: not sure that Sober is interested in the support of the token hypothesis given that the relata occurred, as the formulation states. Rather, Sober seems interested in the support of the token hypothesis, given that at the population level the corresponding causal relation holds. So, I tried to reformulate CP in order to make it consistent with the rough idea
OSS: new notation c , e  causes and effects at the population level. m  magnitude or strength of the population level causal relation. Consider S(H|E): E  evidence, or prior knowledge when interested in the assessment of *support of individual hypotheses*. Hence E denotes the population-level causal relation, having a certain strength m . H  ind-level causal relation; in particular, H refers to the ind hypothesis under analysis. CP reformulated, says that if we know that a certain population-level causal relation has strength m , then the support of the corresponding token hypothesis, given this evidence, is *proportional* to m . The stronger the pop-lev causal rel, the higher the supp of ind-lev causal rel
Strength m The choice of the strategy to assess the causal strength not of secondary importance BUT not main worry: other possible measures of correlation as long as different strategies are coherent (= detect causal strength in same direction positive or negative) it does not matter which one is preferred. Replacement of equality better mirrors the intuition expressed in the rough idea: the higher the strength of the population level relation, the greater the support of the ind relation. OSS: different measures of correlations will give different values, so it seems odd to say that the value of S *equals* m
Fisher (1922)  likelihood = predicate of hypotheses in the light of data. So, the likelihood of a hypothesis relative to an observation indicates how well the observations support the hypothesis. Rephrased L(H|E) = likelihood that the hypothesis that c token-caused e , given that the corresponding population-level causal relation holds and has a certain strength m . Edwards (1972)  S(H|E) is def as the ln of the likelihood ratio. CP  *S*(H|E) is *proportional* to the causal *strength*, namely the stronger the population-level causal relation, the more likely the hypothesis about token-level causal relation. OSS: likelihoods allow comparison among different sets of data or of different hypotheses. Ex: support of the hypothesis that Harry got lung cancer because of his heavy smoking, given that in the population smoking is a considerable risk factor. Or, support that asbestos caused him lung cancer, given the same results at the population-level. [rapp likelihood – probability] Edwards (1972)  likelihood L(H|E) proportional to P(E|H) ; the likelihood ratio of two hypotheses on some data is the ratio of their likelihoods on the same evidence
IN SUM: Sober interprets the support S(H|E) as ln of likelihood ratio of the hypothesis relative to the available evidence. strength of pop-lev causal rel assessed by measure of correlation. Then, knowledge of pop-lev causal rel used to allocate priors in the ind case and to establish the support of the corresponding token hypothesis.  CP* allows to relate epistemologically the two levels of causation: from prior knowledge of pop we are able to assess the support of the corresponding ind-lev hypothesis.  CP* epistemologically relates pop-lev causal claims and ind-lec causal claims. OSS1: CP* not to assign the strength of the ind-lev causal relation; rather, CP* tells us what is to be expected at the ind-lev. OSS2: twofold causality is metaph parsimonious  it abstains from postulating different causal mechanisms at the two lev. OSS3: distinction btw epist - metaph of causality is fundamental  ind -lev causation clearly ontologically primitive: pop are made of individuals among which token causes and not type causes take place. BUT pop-lev causation is epistemologically primitive. –bcz- causal conclusions drawn from statistical analyses concern pop, not directly indiv in the population, to assign prob values to individuals we refer to probability values pertaining to the corresponding pop
Squirrels show: that we definitively need two levels of causation, but we do not need to postulate that causation operates differently at the two levels. Of course this does not hold only for squirrels … If we take up the epistemological perspective, we obtain a meaningful understanding of the levels: (i) metaphysically parsimonious, (ii) accounts for discrepancies at the individual and population level. CP says how we should conceive of the relation of the two levels. (i) ruled out the possibility that from knowledge of the population we can know the strength of the individual causal relation, (ii) but from this knowledge we can assess the likelihood of individual hypotheses.

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