The Rubin causal model (RCM), also known as the Neyman–Rubin causal model, is an approach to the statistical analysis of cause and effect based on the framework of potential outcomes, named after Donald Rubin. The name "Rubin causal model" was coined by Paul W. Holland. The potential outcomes framework was first proposed by Jerzy Neyman in his 1923 Master's thesis, though he discussed it only in the context of completely randomized experiments. Rubin extended it into a general framework for thinking about causation in both observational and experimental studies.
Introduction The Rubin causal model is based on the idea of potential outcomes. For example, a person would have a particular income at age 40 if they had attended college, whereas they would have a different income at age 40 if they had not attended college. To measure the causal effect of going to college for this person, we need to compare the outcome for the same individual in both alternative futures. Since it is impossible to see both potential outcomes at once, one of the potential outcomes is always missing. This dilemma is the "fundamental problem of causal inference." Because of the fundamental problem of causal inference, unit-level causal effects cannot be directly observed. However, randomized experiments allow for the estimation of population-level causal effects. A randomized experiment assigns people randomly to treatments: college or no college. Because of this random assignment, the groups are (on average) equivalent, and the difference in income at age 40 can be attributed to the college assignment since that was the only difference between the groups. An estimate of the average causal effect (also referred to as the average treatment effect or ATE) can then be obtained by computing the difference in means between the treated (college-attending) and control (not-college-attending) samples. In many circumstances, however, randomized experiments are not possible due to ethical or practical concerns. In such scenarios there is a non-random assignment mechanism. This is the case for the example of college attendance: people are not randomly assigned to attend college. Rather, people may choose to attend college based on their financial situation, parents' education, and so on. Many statistical methods have been developed for causal inference, such as propensity score matching. These methods attempt to correct for the assignment mechanism by finding control units similar to treatment units.
An extended example Rubin defines a causal effect:
Intuitively, the causal effect of one treatment, E, over another, C, for a particular unit and an interval of time from t 1 {\displaystyle t_{1}} to t 2 {\displaystyle t_{2}} is the difference between what would have happened at time t 2 {\displaystyle t_{2}} if the unit had been exposed to E initiated at t 1 {\displaystyle t_{1}} and what would have happened at t 2 {\displaystyle t_{2}} if the unit had been exposed to C initiated at t 1 {\displaystyle t_{1}} : 'If an hour ago I had taken two aspirins instead of just a glass of water, my headache would now be gone,' or 'because an hour ago I took two aspirins instead of just a glass of water, my headache is now gone.' Our definition of the causal effect of the E versus C treatment will reflect this intuitive meaning."
According to the RCM, the causal effect of your taking or not taking aspirin one hour ago is the difference between how your head would have felt in case 1 (taking the aspirin) and case 2 (not taking the aspirin). If your headache would remain without aspirin but disappear if you took aspirin, then the causal effect of taking aspirin is headache relief. In most circumstances, we are interested in comparing two futures, one generally termed "treatment" and the other "control". These labels are somewhat arbitrary.
Potential outcomes Suppose that Joe is participating in an FDA test for a new hypertension drug. An all-knowing observer would know the outcomes for Joe under both treatment (the new drug) and control (either no treatment or the current standard treatment). The causal effect, or treatment effect, is the difference between these two potential outcomes.
Y t ( u ) {\displaystyle Y_{t}(u)} is Joe's blood pressure if he takes the new pill. In general, this notation expresses the potential outcome which results from a treatment, t, on a unit, u. Similarly, Y c ( u ) {\displaystyle Y_{c}(u)} is the effect of a different treatment, c or control, on a unit, u. In this case, Y c ( u ) {\displaystyle Y_{c}(u)} is Joe's blood pressure if he doesn't take the pill. Y t ( u ) − Y c ( u ) {\displaystyle Y_{t}(u)-Y_{c}(u)} is the causal effect of taking the new drug. From this table we only know the causal effect on Joe. Everyone else in the study might have an increase in blood pressure if they take the pill. However, regardless of what the causal effect is for the other subjects, the causal effect for Joe is lower blood pressure, relative to what his blood pressure would have been if he had not taken the pill. Consider a larger sample of patients:
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