Top-Down Causation (Part 1): Mechanisms and Their Levels

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This post is part of my series on the work of the philosopher Carl Craver. The series looks at the nature of neuroscientific explanation. For an index, see here.

Over the next few posts, I will be looking at the following article:

Craver and Bechtel "Top-down Causation without Top-down Causes" (2007) 22 Biology and Philosophy 547.

The article deals with the problem of top-down causation. This is the idea that the higher-level, abstract properties of a mechanism can causally affect the lower-level components. If you have ever wondered whether your thoughts cause your neurons to fire, or whether your firing neurons cause you to think, then you have wondered about this problem.

The difficulty with top-down causation is that it seems ontologically spooky. Craver and Bechtel offer a qualified defence of the concept. They suggest that what is referred to as top-down causation is a real phenomenon, but that it is best explained in terms of the constitutive relations between the levels of a mechanism.

There is a lot of technical jargon being employed here. In this first post, I will try to cut through the jungle of jargon.



1. What is a Mechanism?
The first thing we need to know is: what exactly is a mechanism? This question has been exhaustively answered elsewhere on this blog. In the interests of brevity, only three properties of mechanisms are described here:

• A mechanism is a spatially and temporally organised collection of entities and activities.
• Mechanisms are affected by and have effects on "things".
• The individual entities and activities of the mechanism do not have the same effects in isolation from the mechanism.

An example might help to flesh-out these ideas. Take an MRI scanner. It maps the spatial and temporal distribution of certain molecules in the human body. So, it is a mechanism with a particular cartographic capability.

An MRI scanner is a long tubular construction consisting of three coils. The first coil generates a magnetic field, the second corrects for inhomogeneities in the magnetic field and produces fields that vary along three dimensions, and the third sends out radiofrequency pulses and records the echoes that are returned. When put together, these coils have certain effects on the hydrogen atoms in the human body. Effects that allow us to build-up a 3-d image of the tissues in the body.

On their own, the components would not have these capabilities; together, they do. Thus, we can begin to see how talk of top-down causation is so common.

2. The Levels of a Mechanism

Of course, to fully appreciate the attraction of top-down causation we need to appreciate how there can be different "levels" in a mechanism. The human eye provides a beautiful illustration of this phenomenon.

The eye is mechanism that transduces (i.e. changes) a photonic signal into a neural or electrical signal. This is the overall change that is brought about by the mechanism. The overall mechanism is itself constituted by separate mechanisms. First, there is a mechanism for collecting the light; then a mechanism for focusing the light; then a mechanism for projecting the light onto the retina; and then a mechanism in rod and cone cells for absorbing the light and converting it into a neural signal.

There is a well-known mechanistic story to be told about what happens within the rod cells as well. The absorbed photons change the conformation of rhodopsin (a protein found in rod cells). This stimulates G-proteins, which in turn set-off a biochemical cascade leading to the hyperpolarisation of the cell. If you would like to get more detail on this story, I suggest the following video (long, but worth the effort):

The eye is thus to be thought of as hierarchical nest of mechanisms. The question to ask is: what distinguishes higher levels from lower levels? The informal way of looking at it is that higher levels are spatially and temporally extended, when compared with lower levels, and that the higher levels are aggregated from the lower levels.

We can turn this into a more formal definition:

 An item (X) is at a lower level than an item (S) if and only if X is a component in the mechanism for some activity (V) of S. And X is a component in a mechanism if and only if it is one of the entities and activities organised such that S Vs.

So, G-proteins are at a lower level than rod cells, because G-proteins are part of the mechanism that allow rod cells to send neural signals. And rod cells are in turn at a lower level to the eye because they are part of the mechanism that allows the eye to transduce photons into neural signals.


That's it for Part One. In Part Two we will consider exactly why interlevel causation might be thought problematic and sketch Craver and Bechtel's solution.