Oxytocin facilitates protective responses to aversive social stimuli in men..

More in the thread from last Friday's post, in this case on how our brain biases responses to positive and negative social stimuli. In spite of the fact that oxytocin reduces reactivity of the amygdala to negative social stimuli, protective responses are enhanced by a pathway that appears to recruit the insula. From Streipens et al.:

The neuropeptide oxytocin (OXT) can enhance the impact of positive social cues but may reduce that of negative ones by inhibiting amygdala activation, although it is unclear whether the latter causes blunted emotional and mnemonic responses. In two independent double-blind placebo-controlled experiments, each involving over 70 healthy male subjects, we investigated whether OXT affects modulation of startle reactivity by aversive social stimuli as well as subsequent memory for them. Intranasal OXT potentiated acoustic startle responses to negative stimuli, without affecting behavioral valence or arousal judgments, and biased subsequent memory toward negative rather than neutral items. A functional MRI analysis of this mnemonic effect revealed that, whereas OXT inhibited amygdala responses to negative stimuli, it facilitated left insula responses for subsequently remembered items and increased functional coupling between the left amygdala, left anterior insula, and left inferior frontal gyrus. Our results therefore show that OXT can potentiate the protective and mnemonic impact of aversive social information despite reducing amygdala activity, and suggest that the insula may play a role in emotional modulation of memory.

A selective magnetic zap can alter belief formation in our brains.

Dolan and collaborators continue the thread of work I mentioned first in a post last year, on our brain's rose colored glasses, how we are more likely to remember and recall pleasant than aversive stimuli. Here they show that this suppression of bad input can be blocked:

Humans form beliefs asymmetrically; we tend to discount bad news but embrace good news. This reduced impact of unfavorable information on belief updating may have important societal implications, including the generation of financial market bubbles, ill preparedness in the face of natural disasters, and overly aggressive medical decisions. Here, we selectively improved people’s tendency to incorporate bad news into their beliefs by disrupting the function of the left (but not right) inferior frontal gyrus using transcranial magnetic stimulation, thereby eliminating the engrained “good news/bad news effect.” Our results provide an instance of how selective disruption of regional human brain function paradoxically enhances the ability to incorporate unfavorable information into beliefs of vulnerability.

Are drug effects and placebo effects additive or synergistic?

Atlas et al. make observations that suggest that drug and placebo effects are not synergistic:

Placebo treatments and opiate drugs are thought to have common effects on the opioid system and pain-related brain processes. This has created excitement about the potential for expectations to modulate drug effects themselves. If drug effects differ as a function of belief, this would challenge the assumptions underlying the standard clinical trial. We conducted two studies to directly examine the relationship between expectations and opioid analgesia. We administered the opioid agonist remifentanil to human subjects during experimental thermal pain and manipulated participants' knowledge of drug delivery using an open-hidden design. This allowed us to test drug effects, expectancy (knowledge) effects, and their interactions on pain reports and pain-related responses in the brain. Remifentanil and expectancy both reduced pain, but drug effects on pain reports and fMRI activity did not interact with expectancy. Regions associated with pain processing showed drug-induced modulation during both Open and Hidden conditions, with no differences in drug effects as a function of expectation. Instead, expectancy modulated activity in frontal cortex, with a separable time course from drug effects. These findings reveal that opiates and placebo treatments both influence clinically relevant outcomes and operate without mutual interference.

I R’ Us - a waking mashup

When I am going through the daily transition from the last bit of REM sleep to having an awake self I frequently find articles I have recently noted appear in mind in an associated cluster. Thus the title of this post, which tries to point to our delusion that each of us is a tidy "I" that is running its own show. The chunks that come together are:

1). A review by Ezenwa et al. as well as an excellent article by Michael Specter in The New Yorker ('Germs are Us') discuss the microbiome of bacteria, viruses, and fugi whose cells vastly outnumber our own and whose genes outnumber our own by least 100 times. These 'invaders' influence not only our behavior but also our physiology and resistance to disease. We are being managed by a much larger ensemble of creatures than the "I" that writes or reads these lines.

2). A piece by Paul summarizes the powerful effect that social factors and stereotypes can have on our performance. And finally,

3).Nick Bilton writes on how our social boundaries and privacy are being erased as people are watching and reporting on us on Twitter, Facebook, Foursquare, Path and an interminable list of other social networks. Our identities diffuse into the public sphere, and we don't get to choose what show we are going to be on...

The common thread here is the message that our lives are being run by a vast army of creatures, microscopic to human size, that we usually take to be external to our "I".

Mouse song: features similar to human and bird song.

A MindBlog reader has pointed out to me an interesting article by Arriaga et al. that notes that mice courtship ultrasonic sound has some anatomical features and limited learning abilities previously thought unique to humans and birds. Their abstract:

Humans and song-learning birds communicate acoustically using learned vocalizations. The characteristic features of this social communication behavior include vocal control by forebrain motor areas, a direct cortical projection to brainstem vocal motor neurons, and dependence on auditory feedback to develop and maintain learned vocalizations. These features have so far not been found in closely related primate and avian species that do not learn vocalizations. Male mice produce courtship ultrasonic vocalizations with acoustic features similar to songs of song-learning birds. However, it is assumed that mice lack a forebrain system for vocal modification and that their ultrasonic vocalizations are innate. Here we investigated the mouse song system and discovered that it includes a motor cortex region active during singing, that projects directly to brainstem vocal motor neurons and is necessary for keeping song more stereotyped and on pitch. We also discovered that male mice depend on auditory feedback to maintain some ultrasonic song features, and that sub-strains with differences in their songs can match each other's pitch when cross-housed under competitive social conditions. We conclude that male mice have some limited vocal modification abilities with at least some neuroanatomical features thought to be unique to humans and song-learning birds. To explain our findings, we propose a continuum hypothesis of vocal learning.

Brain correlates of switching consciousness on and off again

Kock points in Scientific American Mind to work by Långsjö et al. (open access), who image the neural core of consciousness. They performed MRI imaging of patients recovering from propofol, dexmedetomidine, or sevoflurane anesthesia. Here is their abstract, followed by a key figure from the paper:

One of the greatest challenges of modern neuroscience is to discover the neural mechanisms of consciousness and to explain how they produce the conscious state. We sought the underlying neural substrate of human consciousness by manipulating the level of consciousness in volunteers with anesthetic agents and visualizing the resultant changes in brain activity using regional cerebral blood flow imaging with positron emission tomography. Study design and methodology were chosen to dissociate the state-related changes in consciousness from the effects of the anesthetic drugs. We found the emergence of consciousness, as assessed with a motor response to a spoken command, to be associated with the activation of a core network involving subcortical and limbic regions that become functionally coupled with parts of frontal and inferior parietal cortices upon awakening from unconsciousness. The neural core of consciousness thus involves forebrain arousal acting to link motor intentions originating in posterior sensory integration regions with motor action control arising in more anterior brain regions. These findings reveal the clearest picture yet of the minimal neural correlates required for a conscious state to emerge.

Colored areas indicate the parts of the brain that first come online when patients emerge from consciousness after being anesthetized with one of two different agents. The three critical regions are the anterior cingulate cortex (a), the thalamus (b) and parts of the brain stem (c).

A new study on implicit attitudes and voting..

Following my post on implicit attitudes and voting I have received an email from a group of collaborators doing further studies on the same issue. They need to recruit undecided voters and request that I post this note including the URL of their study in MindBlog.

Gender bias is alive and well in academic science.

Handelsman and collaborators do a rather clear study on how the academy works, showing that science faculties favor male students:

Despite efforts to recruit and retain more women, a stark gender disparity persists within academic science. Abundant research has demonstrated gender bias in many demographic groups, but has yet to experimentally investigate whether science faculty exhibit a bias against female students that could contribute to the gender disparity in academic science. In a randomized double-blind study (n = 127), science faculty from research-intensive universities rated the application materials of a student—who was randomly assigned either a male or female name—for a laboratory manager position. Faculty participants rated the male applicant as significantly more competent and hireable than the (identical) female applicant. These participants also selected a higher starting salary and offered more career mentoring to the male applicant. The gender of the faculty participants did not affect responses, such that female and male faculty were equally likely to exhibit bias against the female student. Mediation analyses indicated that the female student was less likely to be hired because she was viewed as less competent. We also assessed faculty participants’ preexisting subtle bias against women using a standard instrument and found that preexisting subtle bias against women played a moderating role, such that subtle bias against women was associated with less support for the female student, but was unrelated to reactions to the male student. These results suggest that interventions addressing faculty gender bias might advance the goal of increasing the participation of women in science.

Resilience to stress replacing happiness as fashionable research topic

Nature has published a special supplement on Stress and Relilience, a topic also of major emphasis in Richard Davidson's new book. I thought the article by Nestler on epigenetic regulation of resilience to stress was particularly interesting, especially following on this past Monday's post (look there for reminder of definitions of epigenetic changes, etc.) His research is on epigenetic differences between mice that are resilient versus susceptible to stress:

We can make susceptible mice resilient by blocking or inducing epigenetic modifications to certain genes or by altering the expression patterns of those genes to mimic the epigenetic tweaks. Likewise, epigenetic modifications and gene expression can be altered in resilient mice to make them more susceptible.

Other groups have found similar epigenetic alterations that last a lifetime. For instance, rat pups that are rarely licked and groomed by their mothers are more susceptible to stress later in life than are pups with more diligent carers. They are less adventurous than better-cared-for offspring and put up less of a fight in unpleasant situations (such as being placed in a beaker of water). Moreover, the females are less nurturing towards their own offspring. Epigenetic modifications seem to occur at several genes in the hippocampus in response to how much grooming young rats receive, and these alterations persist into adulthood.

These findings are likely to hold up in humans. For example, researchers have found that the genes identified in the rat-grooming studies were more methylated in the hippocampi of suicide victims who had experienced trauma as children than in the those of people who had died from suicide or natural causes and whose childhoods were normal. Likewise, our findings in mice given cocaine mirror epidemiological studies from the past few decades that have linked drug abuse, obesity and conditions such as multiple sclerosis, diabetes and heart disease to increased susceptibility to stress in humans.

More controversial is whether animals inherit epigenetic vulnerability to stress. According to this notion, epigenetic modifications in sperm or eggs drive aberrant patterns of gene expression in the next generation. Several groups have reported that male mice exposed to stress — by being removed from their mothers as pups or exposed to more aggressive mice as adults, for example — produce offspring that are more vulnerable to stress.

A mechanism is still elusive. Exposure to stress could somehow corrupt the male mouse's behaviour or affect some signalling molecule in his semen such that his partner alters her care for their young. Another possibility is that stress-linked epigenetic 'marks' in the sperm affect the development of offspring. No causal evidence yet links epigenetic changes in sperm to altered behaviour in offspring.

Mechanism of unconscious internal bias in our choices

What's actually happening when we make choices that do not seem to be justifiable on purely economic or logical grounds? Wimmer and Shohamy do some interesting work showing how the hippocampus can instill an unconscious bias in our valuations, whereby an object that is not highly valued on its own, increases in value when it becomes implicitly associated with a truly high-value object. As a consequence, we then end up preferring the associated object over a neutral object of equal objective value while not really knowing why. The abstract:

Every day people make new choices between alternatives that they have never directly experienced. Yet, such decisions are often made rapidly and confidently. Here, we show that the hippocampus, traditionally known for its role in building long-term declarative memories, enables the spread of value across memories, thereby guiding decisions between new choice options. Using functional brain imaging in humans, we discovered that giving people monetary rewards led to activation of a preestablished network of memories, spreading the positive value of reward to nonrewarded items stored in memory. Later, people were biased to choose these nonrewarded items. This decision bias was predicted by activity in the hippocampus, reactivation of associated memories, and connectivity between memory and reward regions in the brain. These findings explain how choices among new alternatives emerge automatically from the associative mechanisms by which the brain builds memories. Further, our findings demonstrate a previously unknown role for the hippocampus in value-based decisions.

The details of the experiment are kind of neat. I pass on two figures:

Fig. 1 The task consists of three phases: association learning, reward learning, and decision-making. (A) In the association phase, participants were exposed to a series of pairs of pictures (S1 and S2 stimuli) while performing a cover task to detect “target” upside-down pictures. S1 stimuli were either face, scene, or body part pictures; S2 stimuli were circle images. (B) In the reward phase, participants learned through classical conditioning that half of the S2 stimuli were followed by a monetary reward (S2+), whereas the other S2 stimuli were followed by a neutral outcome (no reward, S2–). S1 stimuli never appeared in this stage. (C) In the decision phase, participants were asked to decide between two stimuli (both S1 or both S2) for a possible monetary win. No feedback was provided, and all gains were awarded at the end of the experiment. Decision bias was operationalized as the tendency to choose S1+ over S1– stimuli in this phase.

Fig. 3 Reactivation of category-specific visual areas during the first half of the reward phase is related to subsequent decision bias. (A) Example participant region of interest masks (derived from the association phase) for body, face, and scene S1 stimuli. Masks were applied to S2 presentations during the reward phase. (B) S2 presentation elicits activation in visual regions responsive to associated S1 stimuli when participants later exhibit decision bias. Error bars indicate ±SEM; a.u., arbitrary units.

Memory fading? Try some dopamine...

From Chowdhury et al. in the Journal of Neuroscience:

Activation of the hippocampus is required to encode memories for new events (or episodes). Observations from animal studies suggest that, for these memories to persist beyond four to six hours, a release of dopamine generated by strong hippocampal activation is needed. This predicts that dopaminergic enhancement should improve human episodic memory persistence also for events encoded with weak hippocampal activation. Here, using pharmacological functional MRI (fMRI) in an elderly population in which there is a loss of dopamine neurons as part of normal aging, we show this very effect. The dopamine precursor levodopa led to a dose-dependent (inverted U-shape) persistent episodic memory benefit for images of scenes when tested after six hours, independent of whether encoding-related hippocampal fMRI activity was weak or strong (U-shaped dose–response relationship). This lasting improvement even for weakly encoded events supports a role for dopamine in human episodic memory consolidation, albeit operating within a narrow dose range.

A revolution in understanding our genetics, personality, and disease.

A revolution is taking place. It challenges the basic genetic orthodoxy of the past century, changing what all of us thought we knew. This is dense material, but very important, and I would urge general readers to try to have a go at it. (Few MindBlog readers would be up for taking on the Wonkish details of Nelson et al.'s paper on 'epigenetic effects of…cytidine deaminase deficiency…etc.' - so I want to pass on edited and rearranged clips from a commentary by Mattick that shows (still Wonkish, but less so) the context and importance of this and similar studies):

Nelson et al. present intriguing evidence that challenges the fundamental tenets of genetics. It has long been assumed that the inherited contribution to phenotype is embedded in DNA sequence variations in, and interactions between, the genes endogenous to the organism, i.e., alleles derived from parents with some degree of de novo variation. This assumption underlies most genetic analysis, including the fleet of genome-wide association studies launched in recent years to identify genomic loci that influence complex human traits and diseases....the perplexing and much debated surprise has been that most genome-wide association studies have superficially failed to locate more than a small percentage of the inherited component of complex traits. This may be a result of a number of possibilities...including... intergenerational epigenetic inheritance, which is not polled by DNA sequence. However, the latter has not thus far been paid much attention or given much credence as a major factor.

Now Nelson et al. provide data suggesting that epigenetic inheritance may be far more important and pervasive than expected. (Mechanistically, epigenetic memory is embedded in DNA methylation and/or histone modifications, which are thought to be erased in germ cells, but may not be, at least completely, as some chromatin structure appears to be preserved. Some information may also be cotransmitted by RNA.) Their findings add to a growing list of studies indicating that genetic influence of ancestral variants can commonly reach through multiple generations and rival conventional inheritance in strength. These include the demonstrations, with considerable molecular and genetic detail, of epigenetic inheritance (i.e., “paramutation”) in plants, and, although still somewhat controversial, in animals.

Although the genetics are complex, Nelson et al.show in an elegant and comprehensive series of analyses that grand-maternal (but not grand-paternal) heterozygosis for a null allele of the Apobec1 cytidine deaminase gene modulates testicular germ cell tumor susceptibility and embryonic viability in male (mouse) descendants that do not carry the null allele, an effect that persists for at least three generations.

...here is now good evidence that epigenetic inheritance is RNA-mediated...as it is becoming clear that a major function of the large numbers of noncoding RNAs that are differentially expressed from the genome is to direct chromatin-modifying complexes to their sites of action. This conclusion is consistent with the recent findings of the ENCODE project, suggesting that much if not most of the human genome may be functional, and explains the informational basis of the extraordinary precision and complexity of the epigenetic superstructure of the genome in different cells required to specify developmental architecture.

The available evidence not only suggests an intimate interplay between genetic and epigenetic inheritance, but also that this interplay may involve communication between the soma and the germline. This idea contravenes the so-called Weismann barrier, sometimes referred to as Biology’s Second Law, which is based on flimsy evidence and a desire to distance Darwinian evolution from Lamarckian inheritance at the time of the Modern Evolutionary Synthesis. However, the belief that the soma and germline do not communicate is patently incorrect—as demonstrated by the multigenerational inheritance of RNAi-mediated phenotypes delivered to somatic cells in Caenorhabditis elegans.

Thus, if RNA editing can alter hardwired genetic information in a context-dependent manner, and thereby alter epigenetic memory, it is feasible that not only allelic but also environmental history may shape phenotype, and provide a far more plastic and dynamic inheritance platform than envisaged by the genetic orthodoxy of the past century. Morever...RNA, more than DNA, may be the computational engine of the evolution and ontogeny of developmentally complex and cognitively advanced organisms

Learning new information during sleep.

Arzi et al. do an ingenious experiment to show that we can do associative learning during our sleep. We can associate a sound with a pleasant or unpleasant odor and react, both while still asleep and after waking, with a deeper or shallower breath. This does not, however, represent the kind of 'sleep learning' long sought by students who unsuccessfully try to remember scientific or literary facts needed for an exam by playing a tape softly during sleep. Here is the abstract:

During sleep, humans can strengthen previously acquired memories, but whether they can acquire entirely new information remains unknown. The nonverbal nature of the olfactory sniff response, in which pleasant odors drive stronger sniffs and unpleasant odors drive weaker sniffs, allowed us to test learning in humans during sleep. Using partial-reinforcement trace conditioning, we paired pleasant and unpleasant odors with different tones during sleep and then measured the sniff response to tones alone during the same nights' sleep and during ensuing wake. We found that sleeping subjects learned novel associations between tones and odors such that they then sniffed in response to tones alone. Moreover, these newly learned tone-induced sniffs differed according to the odor pleasantness that was previously associated with the tone during sleep. This acquired behavior persisted throughout the night and into ensuing wake, without later awareness of the learning process. Thus, humans learned new information during sleep.

The Neurochemistry of Storytelling.

Having in the previous post just made an ill-tempered dump on one kind of popularization, I decide to be inconsistent and now pass on this nice piece with a little less pizazz from the Brain Pickings Newsletter, on how storytelling can engage our brain neurochemistry associated with stress and empathy. It is a very effective and touching piece, and I recommend that you watch the video below:

Brain Showbiz...

Put me down as a curmudgeonly old fart, but I'm not getting a 'gee whiz' response to a recent promotional email asking for publicity on a rhythm and the brain project. It's cute, the graphics are kewl, but the science is out to lunch - it seems to me more like publicity seeking and self promotion masquerading as brain science.

Conscious awareness not required for our placebo or nocebo responses.

Interesting observations from Jensen et al. They first condition a placebo (beneficial) or nocebo (adverse) reponse to a thermal pain stimulus, and then find subliminal (non-conscious) presentation of the conditioning cues elicits the same responses. Their abstract:

The dominant theories of human placebo effects rely on a notion that consciously perceptible cues, such as verbal information or distinct stimuli in classical conditioning, provide signals that activate placebo effects. However, growing evidence suggest that behavior can be triggered by stimuli presented outside of conscious awareness. Here, we performed two experiments in which the responses to thermal pain stimuli were assessed. The first experiment assessed whether a conditioning paradigm, using clearly visible cues for high and low pain, could induce placebo and nocebo responses. The second experiment, in a separate group of subjects, assessed whether conditioned placebo and nocebo responses could be triggered in response to nonconscious (masked) exposures to the same cues. A total of 40 healthy volunteers (24 female, mean age 23 y) were investigated in a laboratory setting. Participants rated each pain stimulus on a numeric response scale, ranging from 0 = no pain to 100 = worst imaginable pain. Significant placebo and nocebo effects were found in both experiment 1 (using clearly visible stimuli) and experiment 2 (using nonconscious stimuli), indicating that the mechanisms responsible for placebo and nocebo effects can operate without conscious awareness of the triggering cues. This is a unique experimental verification of the influence of nonconscious conditioned stimuli on placebo/nocebo effects and the results challenge the exclusive role of awareness and conscious cognitions in placebo responses.

Clever crows! Now shown to reason about hidden causes.

Behavioral studies on New Caledonian crows, especially over the past twenty years, continue to yield amazing results. (A video I first posted for my Biology of Mind course over ten years ago showing some of this earlier work has received 125,000 viewings!). Taylor et al. now demonstrate reasoning about hidden causes:

The ability to make inferences about hidden causal mechanisms underpins scientific and religious thought. It also facilitates the understanding of social interactions and the production of sophisticated tool-using behaviors. However, although animals can reason about the outcomes of accidental interventions, only humans have been shown to make inferences about hidden causal mechanisms. Here, we show that tool-making New Caledonian crows react differently to an observable event when it is caused by a hidden causal agent. Eight crows watched two series of events in which a stick moved. In the first set of events, the crows observed a human enter a hide, a stick move, and the human then leave the hide. In the second, the stick moved without a human entering or exiting the hide. The crows inspected the hide and abandoned probing with a tool for food more often after the second, unexplained series of events. This difference shows that the crows can reason about a hidden causal agent. Comparative studies with the methodology outlined here could aid in elucidating the selective pressures that led to the evolution of this cognitive ability.

Kids as little scientists - early academics can be misguided

A review article by Gopnik offers an interesting perspective:

New theoretical ideas and empirical research show that very young children’s learning and thinking are strikingly similar to much learning and thinking in science. Preschoolers test hypotheses against data and make causal inferences; they learn from statistics and informal experimentation, and from watching and listening to others. The mathematical framework of probabilistic models and Bayesian inference can describe this learning in precise ways. These discoveries have implications for early childhood education and policy. In particular, they suggest both that early childhood experience is extremely important and that the trend toward more structured and academic early childhood programs is misguided.

Opps! Sex does decrease human male lifespan.

Animal studies have suggested that castration increases lifespan in males, and now Korean researchers have examined genealogy records and lifespan of 81 Korean eunuchs to find that their average lifespan is ~14-19 years longer than that of non-castrated men of similar class. (I doubt this finding will lead to an uptick in voluntary male castrations, the trade off of minus fifteen years for what our male sex hormones make possible doesn’t seem so bad...) The abstract:

Although many studies have shown that there are trade-offs between longevity and reproduction, whether such trade-offs exist in humans has been a matter of debate. In many species, including humans, males live shorter than females, which could be due to the action of male sex hormones. Castration, which removes the source of male sex hormones, prolongs male lifespan in many animals, but this issue has been debated in humans. To examine the effects of castration on longevity, we analyzed the lifespan of historical Korean eunuchs. Korean eunuchs preserved their lineage by adopting castrated boys. We studied the genealogy records of Korean eunuchs and determined the lifespan of 81 eunuchs. The average lifespan of eunuchs was 70.0 ± 1.76 years, which was 14.4–19.1 years longer than the lifespan of non-castrated men of similar socio-economic status. Our study supports the idea that male sex hormones decrease the lifespan of men.

Followup on evolutionary psychology as ' just so stories'

A comment on my Sept. 28 post has passed on a number of excellent response to the book review I was noting in that post. I was remiss (lazy) in not taking to task one absurd contention of the reviewer, namely that "you don’t have to know about the evolution of an organ in order to understand it." (a third of my Biology of Mind Book argued the contrary.) After Jabr notes in his Scientific American comments several examples of how understanding the evolution of different brain areas has enhanced understanding and medical practice, he gives this nice analogy:

Studying the brain and mind in ignorance of its vast evolutionary tale does not make sense. It would be equivalent to an archaeologist discovering the remains of an enormous tapestry, slicing out a particular figure from the cloth and claiming that he could learn everything he needs to know by examining that figure in isolation. Even if the archaeologist described the figure in exquisite detail, taking it apart thread by thread and sewing it back together, he would remain willfully oblivious of the whole story. In the same way, disregarding the human brain’s history limits psychology and neuroscience to a paltry understanding of our brains and minds.

The comment also points to Kurzban and Gottschall as offering further commentary.

Also, let me note this comment on the Sept 28 post by Jim Birch:

I'm a little surprised by the animosity directed at evolutionary psychology. For me, it has provided revolutionary insights and understanding. In particular, the general notion that in biology, energy is not wasted, it is utilized adaptively. Under evolution, "adaptive" is not local in time and space but statistically selected over a period and range of the species' evolution.

This gives, or actually requires, a new way of interpreting any human behaviour: as statistically adaptive. And in doing so, it blasts away the incoherent mass of narrative explanations that have been conventionally applied. Our "craziest" tendencies like dying on Everest or blowing life savings on poker machines are no longer down to Freudian death wishes or moral failings (etc) but can be seen as adaptive behaviours operating badly, or even just out of context.

Of course, no one was around in the Pleistocene recording behaviours and survival rates so there's a need for speculation, modelling and indirect evidence. It is this that opens the field up to "just-so stories" charge. There is also the potential for use of selective evidence - to simplistically support preferred moral positions, eg, tooth-and-claw v. cooperative vision of "human nature". However, this is not a problem that is peculiar to evolutionary psychology, it's a perenial problem for science, especially new fields. No doubt the situation will improve as things develop and there's a lot of baby in the bathwater of evolutionary psychology.