“Thin” and “thick” causality

Kathryn Paige Harden’s book The Genetic Lottery: Why DNA Matters for Social Equality includes a really nice primer on causality, including a distinction between “thin” and thick” versions of it. The book is about genetics, but that’s not what I’m interested in this post; more about the book here and here. Here are some excerpts of her treatment of causality:

Causes and Counterfactuals

In 1748, the Scottish philosopher David Hume offered a definition of “cause” that was actually two definitions in one:

“We may define a cause to be an object, followed by another, and where all the objects, similar to the first, are followed by objects similar to the second. Or, in other words, where, if the first object had not been, the second never had existed.”

The first half of Hume’s definition is about regularity–if you see one thing, do you always see a certain other thing? If I flick the light switch, the lights regularly, and almost without exception, come on…

Regularity accounts of causality occupied philosophers’ attention for the next two centuries, while the second half of Hume’s definition–where if the first object had not been, the second had never existed–was relatively neglected. Only in the 1970s did the philosopher David Lewis formulate a definition of cause that more closely resembled the second half of Hume’s definition. Lewis described a cause as “Something that makes a difference, and the difference it makes must be a difference from what would have happened without it.”

Lewis’s definition of a cause is all about the counterfactual–X happened, but what if X had not happened?…

[Saying that X causes Y] does not imply that researchers know the mechanism for how this works…

Each of these mechanistic stories could be decomposed into a set of sub-mechanisms, a matryoshka doll of “How?”…

But understanding mechanism is a separable set of scientific activities from those activities that establish causation…

p. 99-104

She goes on to describe a concept of “portability” that then ties into the problem of generalizability:

The portability of a cause can be limited or unknown… The developmental psychologist Urie Bronfenbrenner referred to the “bioecological” context of people’s lives. Everyone is embedded in concentric circles of context… I find Bronfenbrenner’s bioecological model to be a helpful framework for thinking about the portability of causes of human behavior: Which of these circles would have to change, and by how much, in order for the causal claim to no longer be true? Here, knowing about the mechanism also helps knowing about portability, as a good understanding of mechanism allows one to predict how cause-effect relationships will play out even in conditions that have never been observed.

p. 106-107

Finally she distinguishes between “thin” and “thick” causal explanations:

In the course of ordinary social science and medicine, we are quite comfortable calling something a cause, even when (a) we don’t understand the mechanisms by which the cause exerts its effects, (b) the cause is probabilistically but not deterministically associated with effects, and (c) the cause is of uncertain portability across time and space. “All” that is required to assert that you have identified a cause is to demonstrate evidence that the average outcome for a group of people would have been different if they had experienced X instead of Not-X…

I’m going to call this the “thin” model of causation.

We can contrast the “thin” model of causation with the type of “thick” causation we see in monogenic genetic disorders or chromosomal abnormalities. Take Down’s syndrome, for instance. Down’s syndrome is defined by a single, deterministic, portable cause… And this causal relationship operates as a “law of nature,” in the sense that we expect the trisomy-Down’s relationship to operate more or less in the same way, regardless of the social milieu into which an individual is born.

p. 108

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