Undetermined - a response to Robert Sapolsky. Part 2 - assessing the scientific evidence

In Part 1 of this series, I explored the different philosophical premises that Robert Sapolsky and I bring to the question of free will, in our respective books, Determined and Free Agents. Here, I will examine the scientific evidence that Sapolsky marshals to make his argument that all our decisions are fully determined.

Part 2

 

No, but yeah, but no – assessing the scientific evidence

 

Sapolsky presents an array of experimental evidence from studies of various kinds to support his claim that we are completely driven by all the causal factors in our past or intervening on us in the present. The word study appears 163 times in the text, in fact, and it felt a bit like being pummeled into submission at times. I’m all for providing experimental evidence to support one’s claims, but in this case, much of the supposed evidence is completely unreliable. The fields that are cited the most include social psychology, especially social “priming” experiments, candidate gene association studies, and certain kinds of neuroimaging studies. All of these suffer from very well documented methodological problems, known collectively as “questionable research practices”.

 

The problems stem from small samples, poorly defined hypotheses, excess researcher degrees of freedom (lots of ways to analyse the data), post hoc analyses, covariate mining (slicing the data in lots of ways to look for something significant somewhere), p-hacking, failure to correct for multiple tests, lack of independent replication, and the huge issue of publication bias. Collectively, these practices are empirically demonstrated to produce literatures composed almost entirely of spurious findings – apparently significant associations that really are just statistical blips. Because we only hear about the “positive” results, these bodies of literature can collectively give the impression of robustness and consistency, when in fact this results from biased reporting.  

 

Here are a few examples from the text:

 

In one highly cited study, subjects rated their opinions about various sociopolitical topics (e.g., “On a scale of 1 to 10, how much do you agree with this statement?”). And if subjects were sitting in a room with a disgusting smell (versus a neutral one), the average level of warmth both conservatives and liberals reported for gay men decreased. Sure, you think— you’d feel less warmth for anyone if you’re gagging. However, the effect was specific to gay men, with no change in warmth toward lesbians, the elderly, or African Americans. (Page 47)

 

The study is presented as solid and reliable (with the implication that it also has some relevance for real-world behavior). But you should ask if the supposedly interesting “specificity” of the result was actually an unhypothesised and spurious finding from slicing the data multiple ways, and you should also ask if it has ever been replicated. Moreover, you can be sure that no one has read the results of other similar studies that may have been done that did not produce any such “positive” finding, because they never get published.

 

The whole field of social priming has been called into question as literally the poster child for the replication crisis. Even Daniel Kahneman, who was a huge proponent of this kind of work, has more recently had to concede that it is not robust and has called on the field to face up to this fact. 

 

Here’s another example:

 

What best predicted whether a judge granted someone parole versus more jail time? How long it had been since they had eaten a meal. Appear before the judge soon after she’s had a meal, and there was roughly 65 percent chance of parole; appear a few hours after a meal, and there was close to a 0 percent chance. (Page 106).

 

This particular study is trotted out frequently, again to show how much our behavior – even on really important decisions such as this, made by people literally selected to be professional decision-makers – is driven by subconscious biological states, such as how hungry we are. This very famous example appears to actually be driven by the fact that defendants without representation, who are less likely to get parole, tend to have their cases scheduled right before lunch (because they’re quick).

 

The same unfortunate trend is evident across many other types of study cited. These include ones where people’s behavior is supposedly changed by exposure to various neural signaling molecules. For example:

 

Boost your oxytocin levels experimentally, and you’re more likely to be charitable and trusting in a competitive game. (page 54).

 

Notice first how this is presented not as a particular finding from a particular study, but simply as a fact with general predictive validity. There is a veritable cottage industry of studies involving spraying oxytocin up people’s noses and testing them on all kinds of behaviors. Again, the methods and the findings have been shown to be unreliable.

 

On the role of genetics in our behavior:

 

Consider the neu­rotransmitter serotonin— differing profiles of serotonin signaling among people [KM: due to different genetics] help explain individual differences related to mood, levels of arousal, tendency toward compulsive behavior, ruminative thoughts, and reactive aggression. (Page 72).

 

This section refers to results from so-called candidate gene association studies. Again, this methodology is no longer used because it is now well known to produce spurious findings, which have failed to replicate in much larger, much more systematic studies. The gene encoding the serotonin transporter, referenced here, is probably the most notorious example of this untrustworthy literature.

 

Finally, many neuroimaging studies are appealed to, which can seem to bolster the findings from social psychology experiments by referring to different parts of the brain “lighting up” differently under different conditions across different groups. The tortured phrasing of that sentence is intended to highlight the large number of variables and possible interactions in such studies that researchers can mine for significant findings. Here’s one illustrative example, with a typically convoluted and arbitrary set of interactions:

 

In another neuroimaging study, performance on a frontal task declined in subjects primed with pictures of spiders (versus birds); among African American subjects, the more of a history of discrimination, the more spiders activated the vmPFC and the more per­formance declined.

 

Again, recent work has highlighted how unreliable these kinds of studies are. In particular, studies that look across the whole brain for any kinds of differences between test groups are typically statistically “under-powered” by two to three orders of magnitude. That is, many of them have samples in the tens, when, to be reliable, they would need samples in the thousands or tens of thousands.

 

So, overall, the evidence base that Sapolsky draws on to emphasise the potency of all these supposed determinants of our behavior is, to put it bluntly, completely untrustworthy. This isn’t just my opinion. This is the opinion of researchers in these fields themselves, many of which, like human genetics, have completely overhauled the way they work to overcome the limitations of these kinds of “artisanal” studies.  

 

 

But yeah…

 

That was the “No” part. But there is a “but yeah” to follow. Even though the types of studies that Sapolsky relies on are unreliable and unconvincing, this doesn’t mean such effects don’t exist. These factors are probably not as individually potent as he suggests, but it is still absolutely true that all kinds of prior causes influence our behavior.

 

For example, the fact that we can’t identify strong associations between individual genes and individual personality traits does not undermine the very strong evidence that such traits are partly heritable. (That is, that a sizeable proportion of the variance observed in such traits across the population can be attributed to genetic variation generally). It just means the relationship between genotypes and phenotypes is highly complex.

 

The same is true for neuroimaging experiments – the failure to associate complex psychological traits with variation in structure or function of isolated brain areas does not undermine the idea that such traits are associated with some differences in the brain. Again, it’s just highly complex.

 

And while most of the social priming literature is clearly artifactual, that doesn’t mean that we are not affected in the real world by all kinds of factors in the environment, some of which we may not be aware of. 

 

All of these factors constrain (or inform) our behavior. However, if the existence of such factors is supposed to be a challenge to the idea of free will, it is only a challenge to an absolutist form. Some argue that having free will requires being absolutely free from the influence of any prior cause whatsoever. A quick scratch beneath the surface reveals how incoherent this notion is. A being that was free from all prior causes would have no reason to do anything, no evolved nature to begin with, no responsiveness to the environment, and neither future-directed goals nor memories of past experience to guide its behavior. It would just be a random-behavior-generator.

 

It would not in fact be a self with any continuity through time – and continuity through time is the very thing that defines selves. For any living organism, being a self entails doing work to constrain its component parts and processes to remain organised in the particular way that defines that individual. This is just as true at a psychological level as it is at a physical level. It is precisely our individual personalities and character traits, our memories, our ongoing projects and commitments, our habits and attitudes and policies that collectively make us who we are. Indeed, when people start acting “out of character”, it is often a sign of neurological or psychiatric illness.

 

So, we don’t have absolute freedom – we wouldn’t be ourselves if we did. What we have are degrees of freedom – some set of options available to us, informed by all these past and current factors. These influences only become a threat to a more reasonable conception of free will if they are taken to be complete determinants of what we do at any moment – if they reduce our degrees of freedom to zero. This is what Sapolsky asserts, but without evidence.

 

 

But no…

 

In discussing these various influences, stretching backwards over different timescales, Sapolsky is careful to state that each one of them is only an influence and not an absolute determinant by itself. That is good, because if any one of them (say your genetics) were determinative, it would rule out any role for any of the others (like your experiences). 

 

But he does assert, completely speculatively and without evidence, that all of them collectively do completely determine our behavior, precluding the possibility of the organism itself playing a role in settling what happens. He claims that while we don’t yet have all the details, “we already know enough” to say there is not the smallest gap left in which free will could reside. (Note that this also means no further biological causes can be admitted, since we’re full up of causes already).

 

As an aside, but perhaps an important one, the use of the words “causes” in these kinds of discussions is highly loaded and likely to lead our thinking astray. It suggests a chain of necessitating events, deterministically driving behavior. And it seems to require the mythical beast – an “uncaused cause” – to arise somewhere to break this inexorable chain. But if you replace “causes” with “influences”, you get a much more open, flexible, ecumenical picture that much better captures the real nature of what’s going on.

 

Sapolsky doesn’t do that, however. His view is that all these influences collectively determine what we do at every moment. Clearly, this goes completely against the phenomenology of our everyday experience. It seems, most of the time, that we are in fact deciding what to do, that we do have options and we do choose between them, even if that is within a constrained set of possibilities. To assert otherwise is thus truly an extraordinary claim, which should be accompanied by extraordinary evidence. In the absence of any such evidence, Sapolsky relies on a series of arguments to try and make his case. One of those arguments – the central one, in fact – is that while we can do what we intend, our intentions are not up to us.

 

In Part 3, I will examine why that argument misses its mark.