Life History Strategy and Borderline personality disorder

[calvnandhobbs68]

Associations Between Early Life Adversity, Reproduction-Oriented Life Strategy, and Borderline Personality Disorder

This cross-sectional study examines whether the emergence of borderline personality disorder is associated with the prioritization of immediate reproductive goals over longer-term somatic maintenance goals.

jamanetwork.com

Wanted to see what others thought about this….feel like this is such a weird take on this data and pretty clearly trying to make this data (that we already know about, people with more unstable early development tend to be ya know more unstable on a population statistical level going forward) trying to make it fit a evolutionary theory.

Have to admit I’d never really heard of this even being a theory before in terms of Life History Theory being used to try to explain psychiatric conditions but I’m thinking it seems like quite the stretch.

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[clausewitz2]

With any apparently maladaptive trait/set of traits that has any degree of heritability and seems to pop up across the population at a significant rate, the question evolutionary biologists always have to ask is "how could this have possibly survived in the population in an enduring way?" We have pretty good mathematical biological models that tell us how long you can expect a trait that impacts reproductive fitness negatively to last in a population, and it isn't that long in the grand scheme of things. This suggests that any suite of behaviors that seems to be a) not vanishingly rare and b) not a total flash in the pan must either be neutral wrt reproductive fitness or offer some kind of advantage. This is an attempt to come up with a theory of how BPD could be advantageous reproductively that is interesting to the extent it invokes well-established mechanisms outside of mental health (r v. k strategies) to explain this.

Regardless of whether this theory is actually correct, this is certainly interesting work and salutary. The more we can explain human behavior in one context terms of well-understood phenomena that have been observed in other contexts or even other species, the better. Consilience suggests we are more likely to be on the right path if it is actually empirically supported.

EDIT: It is also an attempt to provide a more testable explanation of the frequently observed fact that most people who suffer significant trauma in childhood do not, in fact, develop BPD, and how some people with BPD do not report any history of identifiable childhood trauma.

 

[dl2dp2]

The effect of BPD on having children early is VERY small. I wouldn't read too much into this study. I suspect it wouldn't replicate.

If you read carefully, on raw scores, people without BPD end up having slightly more children if you test on the mean (2.14 vs. 2), and no difference if you test on the median. So you say okay the strategy to prioritize reproduction clearly didn't really work. So that's falling apart already. Then you say okay let's adjust for age, perhaps that'll yield an argument that BPD reproduces earlier, but then you get a b score of 0.06. Simplistically this gives a relative risk of ~0.94. Then they argue using mediation analysis that this mediates the early life experience causal effect on BPD. Do you see how convoluted this argument is?

They were only able to get P values because NESARC gave this very clean nice large sample size. Of course, they have some famous people on this paper and their friends were able to read a very nice story and get the paper into JAMA Psychiatry.

 

[clausewitz2]

The effect of BPD on having children early is VERY small. I wouldn't read too much into this study. I suspect it wouldn't replicate.

If you read carefully, on raw scores, people without BPD end up having slightly more children if you test on the mean (2.14 vs. 2), and no difference if you test on the median. So you say okay the strategy to prioritize reproduction clearly didn't really work. So that's falling apart already. Then you say okay let's adjust for age, perhaps that'll yield an argument that BPD reproduces earlier, but then you get a b score of 0.06. Simplistically this gives a relative risk of ~0.94. Then they argue using mediation analysis that this mediates the early life experience causal effect on BPD. Do you see how convoluted this argument is?

They were only able to get P values because NESARC gave this very clean nice large sample size. Of course, they have some famous people on this paper and their friends were able to read a very nice story and get the paper into JAMA Psychiatry.

I am not sure I agree that the idea of using mediation analysis was as post hoc as you are suggesting. It seems fairly central to their thesis. At the same time, I agree that this paper is in no way, shape, or form a slamdunk proof of this concept. It is an attempt to buttress previous work on BPD as a "fast Pace of Life syndrome that is more interesting conceptually I think than empirically or clinically.

 

[R. Matey]

Then they argue using mediation analysis that this mediates the early life experience causal effect on BPD. Do you see how convoluted this argument is?

To add, causality isn't really justified given the cross-sectional mediation design. All that has been shown in the final model is this latent variable (which looks very close to being just identified) intervenes in the lay evaluations of BPD with early life adversity as the authors chose to measure it.

 

[dl2dp2]

To add, causality isn't really justified given the cross-sectional mediation design. All that has been shown in the final model is this latent variable (which looks very close to being just identified) intervenes in the lay evaluations of BPD with early life adversity as the authors chose to measure it.

Well no, this is doable if you do the analysis correctly. This is all Judea Pearl's causal inference framework.

 

[R. Matey]

Well no, this is doable if you do the analysis correctly. This is all Judea Pearl's causal inference framework.

How is time precedence accounted for in this framework?

 

[tr]

The theory is logical (and not at all novel) but it's not particularly useful to study it in a dataset of modern Western humans with access to contraceptives. Behaviors that would have conferred a reproductive advantage across human evolutionary history are now either irrelevant or have distorted effects on reproductive rates in modern technological societies.

Agree with dl2dp2 that what they found as far as reproductive rates doesn't actually support their theory; however I think this is largely irrelevant and the theory remains logical, it's just that this was just a pretty fruitless way to try to test it.

I do think there is some naive conflation of early life adversity with BPD. They are correlated but not at all interchangeable. Most people with ELA don't end up with BPD; and many people with BPD didn't have ELA. The individual's interpretation of their experiences seems to be important, and the orchid/daisy hypothesis is relevant here.

Early menarche and early sexual debut are well established to be associated with early life adversity, particularly with absent fathers. I'm not sure the BPD angle fits as neatly.

 

[calvnandhobbs68]

Appreciate all the replies, I didn't get a chance to actually circle back to elaborate until now.

I get the theory here, I feel like this is one of those situations though where there's an attempt to mash evolutionary theory and psychiatric conditions or behavioral traits together. Just in general I think in modern human history it's a real stretch to attribute almost ANY behavioral "phenotype" to some sort of selection pressure because there are so many other variables now (advanced social systems, medical systems and modern nutrition being major ones, contraception is a perfect example above) which influence reproduction or perpetuation of these traits much more rapidly than any evolutionary selection pressure.

Weird thing to me here is that they're basically trying to call borderline personality disorder a result of "increase the likelihood of expressing a reproduction-oriented life strategy, thereby increasing the risk of BPD" and "evolutionarily informed approaches suggest that BPD-related traits offer advantages, not in terms of health but in terms of biological fitness, for navigating adverse environments where the risks of dying young or living in poor health conditions are higher."

I guess my major gripe here is that this whole theory is trying to go a step further than suggesting that a certain cluster of traits or disorder is genetically influenced but that in fact EXPRESSION increases fitness somehow because it's shifting the tradeoff between somatic maintenance and reproduction and not providing basically any evidence of this...rather than just simply stopping at the "probably mediated by both genetic loading and environmental factors".

Their whole approach to the "somatic maintenance" issue within the paper also doesn't actually make sense to me and doesn't fit with the actual theory. They somehow throw BMI, metabolic syndrome and self reported "physical health functioning" all together into the "reproduction/maintenance trade off" variable.

 

[clausewitz2]

Appreciate all the replies, I didn't get a chance to actually circle back to elaborate until now.

I get the theory here, I feel like this is one of those situations though where there's an attempt to mash evolutionary theory and psychiatric conditions or behavioral traits together. Just in general I think in modern human history it's a real stretch to attribute almost ANY behavioral "phenotype" to some sort of selection pressure because there are so many other variables now (advanced social systems, medical systems and modern nutrition being major ones, contraception is a perfect example above) which influence reproduction or perpetuation of these traits much more rapidly than any evolutionary selection pressure.

Weird thing to me here is that they're basically trying to call borderline personality disorder a result of "increase the likelihood of expressing a reproduction-oriented life strategy, thereby increasing the risk of BPD" and "evolutionarily informed approaches suggest that BPD-related traits offer advantages, not in terms of health but in terms of biological fitness, for navigating adverse environments where the risks of dying young or living in poor health conditions are higher."

I guess my major gripe here is that this whole theory is trying to go a step further than suggesting that a certain cluster of traits or disorder is genetically influenced but that in fact EXPRESSION increases fitness somehow because it's shifting the tradeoff between somatic maintenance and reproduction and not providing basically any evidence of this...rather than just simply stopping at the "probably mediated by both genetic loading and environmental factors".

To the extent it is a phenotype that has a substantial genetic contribution that we believe has stuck around in the human population, there has to be some way in which it is either entirely reproductively neutral or increases reproductive fitness. Otherwise you'd expect it to be gone in not very many generations because it's sure not increasing survival. @tr 's point about the impact of modern contraceptives is a good one and certainly changes what might contribute to reproductive fitness, but I think it is probably safe to say there is a positive correlation between impulsive sexual activity and imperfect use of contraceptives. Of course, if it is not a coherent phenotype and is a mostly non-genetic epiphenomenon of other factors, this is a less compelling line of argumentation.

Their whole approach to the "somatic maintenance" issue within the paper also doesn't actually make sense to me and doesn't fit with the actual theory. They somehow throw BMI, metabolic syndrome and self reported "physical health functioning" all together into the "reproduction/maintenance trade off" variable.

The idea is that if you are less invested in pursuing strategies that would tend to maximize your life span, you make impulsively rewarding but long-run detrimental choices that would tend to contribute to higher BMI, development of metabolic syndrome, etc. Again, it does fit the theory, doesn't mean the theory fits the data better.