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An important question about moral progress is what causes it. One of the most popular proposed mechanisms is moral reasoning: moral progress often happens because lots of people reason their way to improved moral beliefs. Authors who defend moral reasoning as a cause of moral progress have relied on two broad lines of argument: the general and the specific line. The general line presents evidence that moral reasoning is in general a powerful mechanism of moral belief change, while the specific line tries to establish that moral reasoning can explain specific historical examples of moral progress. In this paper, we examine these lines in detail, using Kumar and Campbell's (2022, A Better Ape: The Evolution of the Moral Mind and How It Made Us Human. Oxford University Press) model of rational moral progress to sharpen our focus. For each line, we explain the empirical assumptions it makes; we then argue that the available evidence supports none of these assumptions. We conclude that at this point, we have no idea if moral reasoning causes moral progress. [ABSTRACT FROM AUTHOR]

Greene's influential dual-process model of moral cognition (mDPM) proposes that when people engage in Type 2 processing, they tend to make consequentialist moral judgments. One important source of empirical support for this claim comes from studies that ask participants to make moral judgments while experimentally manipulating Type 2 processing. This paper presents a meta-analysis of the published psychological literature on the effect of four standard cognitive-processing manipulations (cognitive load; ego depletion; induction; time restriction) onmoral judgments about sacrificialmoral dilemmas [n = 44; k = 68; total N = 14, 003; M(N) = 194.5]. The overall pooled effect was in the direction predicted by themDPM, but did not reach statistical significance. Restricting the dataset to effect sizes from (high-conflict) personal sacrificial dilemmas (a type of sacrificial dilemma that is often argued to be best suited for tests of the mDPM) also did not yield a significant pooled effect. The same was true for ameta-analysis of the subset of studies that allowed for analysis using the process dissociation approach [n = 8; k = 12; total N = 2, 577; M(N) = 214.8]. I argue that these results undermine one important line of evidence for themDPM and discuss a series of potential objections against this conclusion. [ABSTRACT FROM AUTHOR]