Hmm, never thought (micro)blogging would be such an interesting experience… turns out it’s an excellent way to be exposed to different views and opinions. Last week, I posted an unpublished manuscript and dataset in which we attempted to make people behave more prosocially after priming them with eyes, an effect which has been originally published by Haley and Fessler in 2005, and conceptually replicated by Bates, Nettleson and Roberts in 2006.

I did not set out to directly replicate this effect, and to test its existence. Rather, I was interested in putting my theories on conscious versus unconscious perception to the test. In several papers, but most importantly Jolij and Lamme, 2005 we found that people can respond to unconsciously processed visual information (‘blindsight’), but only do so when they are in ‘guessing mode’. I proposed that this may the result of ‘repression’ of unconscious information.

What does this have to do with priming? Well, here I explain why I think sometimes we do, and sometimes we do not find blindsight. The idea is that unconscious information processing is great, but may be inaccurate. Since our behavior is so easily influenced by all kinds of external stimuli (yes, I was a firm believer in ‘social’ priming!), you don’t want any inaccurate information influencing you, and therefore the cognitive system represses the inaccurate information it gets from the unconscious visual pathway (most of the time).

To test that idea, we came up with the experiment I posted last week. We took a ‘social’ priming effect, and manipulated prime visibility by masking the primes. Our prediction was that priming would not work for masked primes. And that came out! Sadly, the priming effect was also absent for the visible primes. After running several studies, totaling almost 400 participants, I gave up. I simply could not find any reliable evidence for the effect I was looking for, not with tokens, not with study credits, not with money,  not with questionnaires. Now, all this was in 2008-2010.

After an inspiring talk by Zoltan Dienes about half a year ago (see here) I went through my archives to see if there might be anything there I could analyse with his methods and found this dataset back. I ran a Bayes factor analysis, and found that the Bayes factors were informative, and yielded substantial evidence for the null hypothesis of no effect. In other words: in the presented dataset it’s not just a null-effect, it’s actually 5.26 times more likely there is no effect of eye primes in this context than that there is. Given that there apparently was information in the data, despite a fairly low N (although nicely in line with your average priming experiment), we decided to give it a try and publish it.

Admittedly, with today’s knowledge, I tried to capitalize somewhat on the debate on social priming, and it turns out one sentence in particular was found somewhat offensive by some:

The lack of a firm theoretical background, problems with statistical power, potentially flawed methodology [6, 7], the exposure of several high-profile studies as fraudulent [8, 9], but most importantly, repeated failures to directly replicate several effects [10-13] has led to strong skepticism towards the notion of social priming.

In all fairness, I do think this statement is accurate. There is skepticism towards ‘social’ priming, and the reason for that is that quite some direct replications have failed, and that QRPs and fraud have been uncovered in others. Most importantly, though, we have yet to see a solid explanation as to why we sometimes do, and sometimes do not get these effects.

But the problem is: what is ‘social priming’ in the first place?

On the ISCON Facebook page, Jeff Sherman once mentioned that all priming (both ‘cognitive’ and ‘social’) is priming, because it’s all about priming behavior. Norbert Schwarz jokingly defined ‘social priming’ as ‘priming cognitive psychologists cannot replicate’.

Now, both of  these statements are obvious oversimplifications. One of the problems plaguing the ongoing debate on priming is the lack of a clear taxonomy of what comprises different kinds of priming, and indeed, I myself have been guilty of not properly defining what I mean with ‘social priming’ in the manuscript I posted last week.

So, let me give you my 2c  on the matter. I agree with Jeff Sherman to most extent. Priming is the modification of processing of subsequent stimuli and behavior by a given prime stimulus. Period. What distinguishes ‘cognitive’ from ‘social’ priming in my understanding (which, arguably, may be totally wrong) is mainly the length and complexity of the processing chain between prime and behavior. In what we call ‘cognitive’ priming, the chain is short. The archetypical ‘social priming’ study typically relies on a long chain of events between prime and behavior.

In most priming effects I typically employ in the lab, it’s about visuomotor transformations. In a task in which participants have to respond to the direction of an (target) arrow, presenting another (prime) arrow in the same direction, responses to the target will be faster, even if the prime is masked. This can be quite easily explained in terms of decision thresholds, or biasing processing of visual input. Several studies have shown direct communication between visual and motor areas in such tasks, and modulation of baseline motor activity by primes – in other words, as long as there is some direct visuomotor transformation, we can actually map the effect of our primes on brain activity in real time. I can pinpoint and measure the different subprocesses (perceptual encoding in the visual cortex between 80 ms and 100 ms, plus a second stage around 200-300 ms, decision making in the parietal cortex, starting around 100 ms, and  motor preparation in the motor areas, from 200 ms after stimulus onset, etc.) and study these independently. In other words: I know what’s going on.

However, when I am priming people with eyes to make them behave more prosocially, I do not. I can come up with a decent chain of events, though. From fMRI studies, we know that eyes are processed in dedicated areas of the visual system, and we know that prosocial behavior (in particular in ultimatum and dictator games) is mediated by the right dorsolateral prefrontal cortex from several fMRI and TMS studies. I can well imagine a modulation of the DLPFC by eye cues, only this has not been shown (yet). And maybe it will not be, because there is no such thing – I don’t know. At least, it can be tested.

For embodiment-type priming effects, it differs. There are pretty well-understood effects: take for example the SNARC-effect: if you have to respond to a number, you’re faster responding with your left hand than your right hand when the number is small, but vice versa when the number is large. This is a quite robust effect, attributed to the automatic activation of a ‘mental number line’. We typically order numbers from left to right: 1, 2, 3, 4, etc. In other words, magnitude of a number has a direct relation with spatial cognition. Indeed there is pretty good converging evidence from fMRI and TMS studies that a fronto-parietal spatial cognition network plays a critical role in number magnitude processing.

Interestingly, there is also evidence these spatial cognition networks underlie perception of social distances. This allows me to do a very specific prediction: if you prime someone with the concept ‘close’, and subsequently ask for this judgment about his social distance to someone, this should result in ‘closer’ judgments then when you prime someone with the concept ‘far away’. I am aware that Williams and Bargh did this in 2008, and indeed found this effect, but unfortunately they used a pretty poor priming strategy, and not surprisingly Pashler et al (2012) failed to replicate the effect. What’s needed as a prime is ideally a distance judgment task in 3D (so how far an object is from you) that really draws on spatial processing, rather than drawing two dots that are either close to each other or separated.

Now, the longer the association chain becomes, the more ‘line noise’ there may be, and the less credible effects become at first sight. Take for example the pee-study by Tuk et al. (this one) claims that a full bladder leads to increased impulse control, allegedly because having a full bladder requires the ‘inhibitory’ parts of the brain to prevent you from peeing, which at the same time inhibits making impulsive decisions. A bit far-fetched, but ok. I can see this work. Your brain gets somatosensory feedback from the sphincter muscle of your bladder, but you need to put in effort to hold in your wee, which allegedly activated the cognitive control circuits of your brain. This does not automatically imply that all behavior is subsequently inhibited of course. Sadly, the authors have missed out on a great opportunity to test their explanation (their study 3 is hardly convincing for their argument): why not do a task that measures response inhibition, in a ‘full bladder’ and ’empty bladder’ condition, within-subject, of course?

It’s quite easy, really. You can do an anti-saccade task (in which participants have to suppress the urge to make an eye movement to a suddenly appearing target). If the authors are correct, one should expect better performance in the bladder-full than in the bladder-empty condition. N=30 to 40, with at least 200 – 300 trials per participant should do the trick. An experiment like this can be run in about a week.

Now,  where things get quite dubious for me as a cognition researcher is the authors’ claim that priming participants with words that have to do with urination produce similar effects on behavioral inhibition. The chain of necessary events here is very long. First, it assumes that reading a word related to peeing (such as toilet, watering, etc.) activates a semantic network related to urination. Ok. There’s evidence for that. Point granted. Second, that semantic activation somehow results in a greater awareness of an urge to pee. Maybe. If you draw attention to a bodily function, participants will be more aware of it. This increased awareness leads to an actual increased urge to pee. Good, they actually tested that, and found an effect. Subsequently, this leads to increased inhibitory control (not tested), which leads to less impulsive behavior.

Notwithstanding my doubts, combining this type of priming with an anti-saccade task may be used to prove or disprove their hypothesis. Again, if seeing the word ‘urine’ activates inhibitory systems, we would expect an improvement on anti-saccade performance after priming participants with pee.

To cut a long story short, what I miss in a lot of priming research is a justification of all the individual assumptions that are made in order to explain the priming effect observed. If we can actually be more specific about these assumptions, and test them, we might actually get somewhere.

So, why not work together and figure out what’s really going on? If anyone is interested in the distance, or pee-studies, let me know, or if you know of a priming manipulation which I could use in stead of eye priming for the study that kicked this off, please get in touch!