Giving time gives you time.

In the same vein as Monday's post, Mogilner et al. note another activity that expands our subjective sense of time:

Results of four experiments reveal a counterintuitive solution to the common problem of feeling that one does not have enough time: Give some of it away. Although the objective amount of time people have cannot be increased (there are only 24 hours in a day), this research demonstrates that people’s subjective sense of time affluence can be increased. We compared spending time on other people with wasting time, spending time on oneself, and even gaining a windfall of “free” time, and we found that spending time on others increases one’s feeling of time affluence. The impact of giving time on feelings of time affluence is driven by a boosted sense of self-efficacy. Consequently, giving time makes people more willing to commit to future engagements despite their busy schedules.

Mental time travel and our brain's default network.

Here is some interesting material from Østby et al. on the brain basis of the quality of our remembering the past or imagining the future:

A core brain network is engaged in remembering the past and envisioning the future. This network overlaps with the so-called default-mode network, the activity of which increases when demands for focused attention are low. Because of their shared brain substrates, an intriguing hypothesis is that default-mode activity, measured at rest, is related to performance in separate attention-focused recall and imagination tasks. However, we do not know how functional connectivity of the default-mode network is related to individual differences in reconstruction of the past and imagination of the future. Here, we show that functional connectivity of the default-mode network in children and adolescents is related to the quality of past remembering and marginally to future imagination. These results corroborate previous findings of a common neuronal substrate for memory and imagination and provide evidence suggesting that mental time travel is modulated by the task-independent functional architecture of the default-mode network in the developing brain. A further analysis showed that local cortical arealization also contributed to explain recall of the past and imagination of the future, underscoring the benefits of studying both functional and structural properties to understand the brain basis for complex human cognition.

Awe is good for you…

What could most of us could do to chill out and expand our subjective sense of time? Feel a sense of awe more often! Rudd et. al. do a series of experiments illustrating that it expands our perception of time, alters decision making, and enhances well-being.

In a first experiment the authors examined whether awe would alter time perception by first manipulating whether people were induced to feel awe or happiness and then having them rate self-perceived time availability. A second experiment examined whether feeling awe, relative to feeling happiness, would alter time perception (i.e., impatience) and, in turn, willingness to donate time. A third experiment tested whether awe, compared with a neutral state, would increase participants’ choice of experiential (vs. material) goods and momentary life satisfaction, two outcomes that they hypothesized would follow from awe’s ability to expand perceptions of time. In experimental versus control subjects, awe was elicited by reliving a memory, reading a brief story, or even watching a 60-s commercial (the awe-eliciting commercial depicted people in city streets and parks encountering and interacting with vast, mentally overwhelming, and seemingly realistic images, such as waterfalls, whales, and astronauts in space.)

And, here is their abstract:

When do people feel as if they are rich in time? Not often, research and daily experience suggest. However, three experiments showed that participants who felt awe, relative to other emotions, felt they had more time available (Experiments 1 and 3) and were less impatient (Experiment 2). Participants who experienced awe also were more willing to volunteer their time to help other people (Experiment 2), more strongly preferred experiences over material products (Experiment 3), and experienced greater life satisfaction (Experiment 3). Mediation analyses revealed that these changes in decision making and well-being were due to awe’s ability to alter the subjective experience of time. Experiences of awe bring people into the present moment, and being in the present moment underlies awe’s capacity to adjust time perception, influence decisions, and make life feel more satisfying than it would otherwise.

Decreased amygdala neuroplasticity linked to early-life anxious temperament.

Some interesting work from the research groups of my University of Wisconsin colleagues Ned Kalin and Richard Davidson that suggests that altered amygdala neuroplasticity may play a role the early dispositional risk to develop anxiety and depression.:

Children with anxious temperament (AT) are particularly sensitive to new social experiences and have increased risk for developing anxiety and depression. The young rhesus monkey is optimal for studying the origin of human AT because it shares with humans the genetic, neural, and phenotypic underpinnings of complex social and emotional functioning. In vivo imaging in young monkeys demonstrated that central nucleus of the amygdala (Ce) metabolism is relatively stable across development and predicts AT. Transcriptome-wide gene expression, which reflects combined genetic and environmental influences, was assessed within the Ce. Results support a maladaptive neurodevelopmental hypothesis linking decreased amygdala neuroplasticity to early-life dispositional anxiety. For example, high AT individuals had decreased mRNA expression of neurotrophic tyrosine kinase, receptor, type 3 (NTRK3). Moreover, variation in Ce NTRK3 expression was inversely correlated with Ce metabolism and other AT-substrates. These data suggest that altered amygdala neuroplasticity may play a role the early dispositional risk to develop anxiety and depression.

Biology of social adversity.

PNAS has done a special issue on the biology of adversity. I mention only a few of the articles here:

Ziol-Guest et al. show that low income, particularly in very early childhood (between the prenatal and second year of life), is associated with increases in early-adult hypertension, arthritis, and limitations on activities of daily living. Moreover, these relationships and particularly arthritis partially account for the associations between early childhood poverty and adult productivity as measured by adult work hours and earnings. The results suggest that the associations between early childhood poverty and these adult disease states may be immune-mediated.

McDade looks at studies of inflammatory processes involved in a wide range of chronic degenerative diseases in low income populations in the Philippines and lowland Ecuador that reveal now low levels of chronic inflammation, despite higher burdens of infectious disease, point to nutritional and microbial exposures in infancy as important determinants of inflammation in adulthood.

Hostinar et al. look at associations between early life adversity and executive function in children adopted internationally from orphanages, providing evidence that early life adversity is associated with significant reductions in executive function performance on a developmentally sensitive battery of laboratory executive fundtion tasks that measure cognitive flexibility, working memory, and inhibitory control.

Empathy represses analytic thought, and vice versa.

Jack et al. have performed a study (online in accepted articles in the journal Neuroimage) observing brain activity in subjects while they were engaged in social versus physical analytical contexts. When the network of neurons that allows us to empathize becomes more active, it suppresses the network used for analysis. When the analytic network is more active, ability to empathize with the human effects of our actions is repressed. Here is their abstract (a bit klutzy, but does the job), and two useful summary figures from the paper.

Two lines of evidence indicate that there exists a reciprocal inhibitory relationship between opposed brain networks. First, most attention-demanding cognitive tasks activate a stereotypical set of brain areas, known as the task-positive network and simultaneously deactivate a different set of brain regions, commonly referred to as the task negative or default mode network. Second, functional connectivity analyses show that these same opposed networks are anti-correlated in the resting state. We hypothesize that these reciprocally inhibitory effects reflect two incompatible cognitive modes, each of which is directed towards understanding the external world. Thus, engaging one mode activates one set of regions and suppresses activity in the other. We test this hypothesis by identifying two types of problem-solving task which, on the basis of prior work, have been consistently associated with the task positive and task negative regions: tasks requiring social cognition, i.e., reasoning about the mental states of other persons, and tasks requiring physical cognition, i.e., reasoning about the causal/mechanical properties of inanimate objects. Social and mechanical reasoning tasks were presented to neurologically normal participants during fMRI. Each task type was presented using both text and video clips. Regardless of presentation modality, we observed clear evidence of reciprocal suppression: social tasks deactivated regions associated with mechanical reasoning and mechanical tasks deactivated regions associated with social reasoning. These findings are not explained by self-referential processes, task engagement, mental simulation, mental time travel or external vs. internal attention, all factors previously hypothesized to explain default mode network activity. Analyses of resting state data revealed a close match between the regions our tasks identified as reciprocally inhibitory and regions of maximal anti-correlation in the resting state. These results indicate the reciprocal inhibition is not attributable to constraints inherent in the tasks, but is neural in origin. Hence, there is a physiological constraint on our ability to simultaneously engage two distinct cognitive modes. Further work is needed to more precisely characterize these opposing cognitive domains.

 

Physiological benefits of leadership - Importance of a sense of control

An edited paste-up from Sapolsky's brief review pointing to work of Sherman et al. showing that leaders feeling a sense of control have lower stress levels.

Studies on primates have shown complex relationships between social dominance, physiology, and health among primates...basal cortisol levels in nonhuman primates do not so much reflect social rank as the meaning of social rank in a particular species and social group. Similar studies in humans have been challenging, because humans belong to multiple hierarchies (for example, one can have both a low position in a corporation and also be a respected church leader), and typically the one in which they rank highest is valued most. Sherman et al. have studied a population of governmental and military leaders (with equal numbers of men and women) who had been sent to an executive training program. Subjects came from a range of midlevel ranks (e.g., officers up to the rank of colonel in the army); had been in leadership positions for an average of more than 3 y; and were presumably well-regarded, given their selection by their organization for this honor. As the key findings, compared with age, sex, and ethnicity-matched nonleader controls, and after controlling for lifestyle health factors (e.g., diet, level of exercise), leaders had substantially lower resting cortisol levels and lower levels of self-reported anxiety. Thus, within this example of hierarchical stratification, high rank carries physiological and psychological advantages.

Here is the Sherman et al. abstract:

As leaders ascend to more powerful positions in their groups, they face ever-increasing demands. As a result, there is a common perception that leaders have higher stress levels than nonleaders. However, if leaders also experience a heightened sense of control—a psychological factor known to have powerful stress-buffering effects—leadership should be associated with reduced stress levels. Using unique samples of real leaders, including military officers and government officials, we found that, compared with nonleaders, leaders had lower levels of the stress hormone cortisol and lower reports of anxiety (study 1). In study 2, leaders holding more powerful positions exhibited lower cortisol levels and less anxiety than leaders holding less powerful positions, a relationship explained significantly by their greater sense of control. Altogether, these findings reveal a clear relationship between leadership and stress, with leadership level being inversely related to stress.

Further notes from Sapolsky's review:

...although both low-cortisol and low-anxiety levels correlated with leadership, neither was correlated with the other. This supports a literature that links anxiety more closely to elevated activity of the other main branch of the stress response (i.e., the sympathetic nervous system and epinephrine secretion) than to elevated cortisol secretion...The study reported additional, subtle findings. One concerned a critical mediating psychological variable in the leaders. An extensive literature shows that for the same external stressor, subjects feel less subjectively stressed, activate less of a stress response, and are less at risk for a stress-related disease if they feel a sense of control.

Both having a greater total number of subordinates and greater levels of authority were associated with a greater sense of personal control, as well as with lower levels of cortisol and anxiety; this certainly makes intuitive sense. However, having a greater number of subordinates to manage directly was not associated with those salutary psychological and physiological end points. This lends support to the stereotypical bellyaching of the office manager who says, “It’s not so much that I’m the boss of X number of people; it’s more like I have X number of bosses.”

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.