Talk on Evolutionary Psychology, Sunday, March 2nd

Humour is a necessary corrective at times, to the more simplistic aspects of any perspective on the world.

Hi Greg

Out of interest, are you going to be running through the same misconceptions you aired at CONvergence last year - or will you be talking about new ones?

Greg, please do post about this after the event. I'm interested in your views on the subject matter.

Dave, I'm taking a different tact, though I'm sure there is overlap. This is a freshly written talk, in the form of a debate where the first half is pro, cribbed from a teaching power point from Steven Pinker, and the second half (well, more than half) is refuting the first half.

Someone emailed me to mention that the slymepit, which apparently continues to be in love with me so they can't take their eyes off me (i.e., stalking me) is very upset because I'll be giving a presentation that promotes evolutionary psychology. Which is funny for a lot of reasons.

G: I may upload the slides to youtube, but they will be context-free since most of the talk is me talking. But I'll probably write it up in some form. Hassle me again to do that later if I don't do it soon.

http://www.youtube.com/watch?v=T07-Lnk-aIU&feature=youtu.be

That does seem a bit better than your talk last year, though there are also some red flags.

One thing you still have completely off is the Environment of Evolutionary Adaptedness.

The EEA is not the Savannah Hypothesis. It is not a particular place and time - essentially it is the hypothesised natural history of a given adaptation.

So the EEA of the arm - for example - would reach right back to the development of fish fins and encompass all pertinent changes since then.

It's nonsensical to claim that the EEA is 2 million years ago, and in the Serengeti. The EEA varies according to the trait under discussion, will usually be much older (in terms of it's first pertinence) and be no particular place.

The savannah hypothesis is that when it comes to EP the last time of pertinence to the EEA of our psychological traits is probably the late Pleistocene, with certain pointers indicating a preferred environment of a savannah shortly after the rainy season (not any particular savannah - certainly not the Serengeti as we know it).

So if we were to consider a psychological history of hunger - for example - the EEA would be there to remind us that some iteration of hunger would probably go back to the need for the most simple organisms to find sustenance and that appetites for certain foods or nourishment are tied into the appearance of such things in the environment.

Whereas the savannah hypothesis would be there to remind us that as far as the evidence suggests the last time period that would have been pertinent to the "EEA of hunger" would be 40,000 years ago.

I don't think you'll find that the mating strategies of apes are applied where known trends in human mating would be at odds with them - where human habits coincide with those of other animals some pertinence might be assumed as ripe for hypotheses, however. For example: the fact that it is the mother who bears the risks and costs of childbirth and pregnancy would be seen as lacking controversy.

Weird to see a bit on IQ - most EP is pursued under the assumption that human races are psychologically equivalent. IQ is seen as a WiP psychometric that may or may not say much of pertinence about someone's psychology. EPs critics often assume EP supports stuff like the Bell Curve and so on. On the whole it does not - regarding Psychology as pan-human.

There is no mutual exclusivity to the notion of a set of modules that are inherited and a set of modules that develop during life provided some of those modules receive and store input (as they no doubt do). For example - if you think of whatever part of your brain governs vertigo - this is likely innate (experiments on babies with no experience of cliffs nevertheless show that they avoid them) but can be moderated by later experience (eg: an adult can jump out of a plane if sure of the safety of a parachute and so on).

In theory we can be confident that some modules exist in our genes as the result of congenital problems impairing certain modules. Eg: congenital prosopagnosia results in impairment of the face recognition modules. It is interactivity between modules that is altered by experience (a person with congenital prosopagnosia may learn compensatory behaviours).

So the cultural versatility you seem to be citing in the last part of your presentation isn't evidence against modules as described by EP (and cognitive psychology in general).

I have a long section on the EEA.

The mating strategies of apes are never applied. That's my point. Evol Pych is more interested in a model based on mammals in general, and it tends to skip right down to the species level.

"There is no mutual exclusivity to the notion of a set of modules that are inherited and a set of modules that develop during life provided some of those modules receive and store input (as they no doubt do). For example – if you think of whatever part of your brain governs vertigo..."

That partly depends on what EPs want to call a module, and here is where backwards pedaling bikes may play a role. In order for the EEA to not b facile, it can't be the context for the evolution of the limbic system. Modules to be as described need to be mainly cortical structures outside of the limbic system but with connections to it, or including part of it. Sub neocortical (i.e. cortical - paleocortex) only function are not EP modules. Probably (again, matter of definition). So the innate part of what you are calling "vertigo" is not module, the control of it is, and that is experiential.

We can't be confident that modules exist in our genes at any detail because they can't. The broken brain thing, I hope will come up in questions. I usually start off with that but I'm not this time.

The tomato model isn't evidence against EP, you are right. It is my alternative hypothesis.

Great points!

You're going to be there, right?

"I have a long section on the EEA."

I am sure you do - and it's a concept well worth exploring. My worry is that last year you conflated it with the savannah hypothesis, and this seems to be what you are doing again based on the information here.

On the EP Journal blog Rob Kurzban did say he had twice tried explaining the difference between the EEA and savannah hypothesis to you - and you did say you had taken some of his criticism on board. I'm just wary that you may not have based on the wording of your slide ("adaptations arise in a particular environment" and "How long is EEA and where is it [...] 2 mya. Serengeti").

Unless your talk takes issue with your slides then you are giving people a bad education on the matter - because 2 mya and the Serengeti has almost nothing to do with the EEA. In fact it doesn't even have much to do with the savannah hypothesis (which would be no particular savannah, and could relate to times as recent as 40,000 years ago).

"The mating strategies of apes are never applied. That’s my point. Evol Pych is more interested in a model based on mammals in general, and it tends to skip right down to the species level."

I'm just not sure I understand you - as far as I see it human propensities in behaviour are paramount. Cross-species studies are mainly performed to see if the behaviour in question is somewhat pertinent to other species. In this regard chimp behaviour would be seen as more pertinent than that of hyenas but there would be a greater body of work that that contrasts to.

Something like Theory of Mind, for example, is demonstrable in apes, less so in old world monkeys, and barely evident in lemurs. This is thought to be pertinent, but only in consideration of everything else thought to be known about Theory of Mind.

"That partly depends on what EPs want to call a module, and here is where backwards pedaling bikes may play a role. In order for the EEA to not b facile, it can’t be the context for the evolution of the limbic system. Modules to be as described need to be mainly cortical structures outside of the limbic system but with connections to it, or including part of it. Sub neocortical (i.e. cortical – paleocortex) only function are not EP modules. Probably (again, matter of definition). So the innate part of what you are calling “vertigo” is not module, the control of it is, and that is experiential."

I don't think backpedalling need take place - since from it's earliest assertion the theory of modules has been concerned with brain function primarily, brain architecture secondarily (if that). You seem to insist that it be about brain matter and genes first and foremost - they are obvious implications of modules - but they are not the modules themselves.

This is a mistake regarding modules that Rob Kurzban tried to clear up with you last year. They are not conceived of as part of the brain - they are functional circuits - behavioural propensities.

This was something that rendered a lot of the Convergence panel talk irrelevant. For example Indre gave a long talk about the modularity of the brain without any apparent indication that she realised the modularity of cog psy (which is pretty much the modularity of EP) isn't the same as modularity of structure. PZ said EPs claimed the amygdala was a module - which is simply not true.

A module would be something like "our propensity to crave sugar" or "our fear of snakes" - the architecture of such things may not be known, may even vary person to person.

So modules do not need to be cortical structures. They just need to be behavioural propensities. Where they "live" in the brain? In some cases we have some clues but for the most part they are interactions between various structures in the brain - not any one place. They amygdala - for example - may play a part in a great number of mental modules.

"You’re going to be there, right?"

I'm a student of psychology living in a small Northern Irish town - so not likely I'm afraid. Will you be making a transcript or recording of the talk available?

"My worry is that last year you conflated it with the savannah hypothesis, and this seems to be what you are doing again based on the information here."

Thank you for your concern! That's not conflation, its pointing out a major problem with EP.

I think you are imagining a lot of things in my talk that aren't there. Such is the danger of putting up slides that only really go with the talk, but as I say in the comments, this is mainly for people who have seen the talk and want to refresh. Keep in mind that this talk is showing two contrasting sides, so that would cause some confustion.

Yes, "modules" only need to be behavioral things, but not "propensities," I think. As I understand how that term might be used, it implies a more general learning mechanism that is different from EP.

As I said, yes, the limbic structures would likely be linked, maybe always (since limbic structures are generally highly interconnected) with anything having to do with behavior.

"Thank you for your concern! That’s not conflation, its pointing out a major problem with EP."

But it isn't a problem for EP because EP doesn't conflate the two. In the past you have conflated the two and the wording of your slides indicates the same conflation.

Now if I am wrong about that and your talk explains the differences - fine, cool, no need to worry. Hopefully your talk will include stuff like "the EEA is the natural history of a presumed innate behaviour, is as old as the behaviour and pertinent to a number of different places and times. The savannah hypothesis refers to the notion that the last time of particular pertinence to the EEA is >40,000 years ago in Central Africa".

I mean, that would be a vulgar sort of summary, but it's not too misleading.

"Yes, “modules” only need to be behavioral things, but not “propensities,” I think."

"Module" and "behavioural propensity" are effectively synonymous in cog psy. EP might add a caveat that the propensity has assumed adaptive value for the purposes of generating hypotheses.

EP specifically states that modules are fine tuned to address specific issues. Propensities, I would say, are more like aspects of temperament that shape, constrain, or potentiate general learning processes. I think the explicit stated difference for EP compared to Cog Psy is that difference.

I'm not too happy with the last part of my last answer - it's a hard thing to summarise. A module might be better thought of as the smallest functional part of a behavioural propensity.

The main point would be that they are not thought of as discrete architectural components in cog psy/EP.

"Propensities, I would say, are more like aspects of temperament that shape, constrain, or potentiate general learning processes."

Those aren't factors which are exclusive to non-modular models.

In your opinion apparently, and my opinion, true.

And, on a related topic: http://scienceblogs.com/gregladen/2014/03/07/is-human-behavior-genetic-…