A mechanism of why novelty seeking individuals are more vulnerable to social defeat stress.

Duclot and Kabbaj offer an interesting result that suggests at least part of the reason for why individuals more likely to seek novelty (whether humans or mice) are also more vulnerable to social defeat stress. They do not demonstrate the stress induced increase in levels of a brain growth factor (brain derived neurotrophic factor, or BNDF), that is observed in low novelty seeking individuals. BDNF regulation after stress has been suggested as an important mediator of vulnerability and resilience. Higher BDNF levels in the hippocampus - which can be caused by classic antidepressants - promote resilience to a chronic mild stress. Here is the abstract, with technical details:

Some personality traits, including novelty seeking, are good predictors of vulnerability to stress-related mood disorders in both humans and rodents. While high-novelty-seeking rats [high responders (HRs)] are vulnerable to the induction of depressive-like symptoms by social defeat stress, low-novelty-seeking rats [low responders (LRs)] are not. Here, we show that such individual differences are critically regulated by hippocampal BDNF. While LR animals exhibited an increase in BDNF levels following social defeat, HR individuals did not. This difference in hippocampal BDNF expression promoted the vulnerability of HR and the resilience of LR rats. Indeed, preventing activation of BDNF signaling by infusing the BDNF scavenger TrkB-Fc into the dentate gyrus of the hippocampus of LR rats led to social defeat-induced social avoidance, whereas its activation in HR rats by the TrkB agonist 7,8-dihydroxyflavone promoted social approach. Along with the changes in BDNF expression following defeat, we report in LR animals a downregulation of the inactive BDNF receptor TrkB.T1, associated with an activation of CREB through Akt-mediated signaling, but not MSK1-mediated signaling. In HR animals, none of these molecules were affected by social defeat. Importantly, the BDNF upregulation involved an epigenetically controlled transcription of bdnf exon VI, associated with a coherent regulation of relevant epigenetic factors. Altogether, our data support the importance of hippocampal BDNF regulation in response to stressful events. Moreover, we identify a specific and adaptive regulation of bdnf exon VI in the hippocampus as a critical regulator of stress resilience, and strengthen the importance of epigenetic factors in mediating stress-induced adaptive and maladaptive responses in different individuals.

Positive feedback loop between social connections, positive emotions, and vagal tone.

Kok et al. suggest that positive emotions, positive social connections, and physical health reinforce one another in a positive feedback loop.They use cardiac vagal tone as an objective proxy for physical health. Indexed at rest as variability in heart rate associated with respiratory patterns, vagal tone reflects the functioning of the vagus nerve, which is the 10th cranial nerve and a core component of the parasympathetic nervous system, which regulates heart rate in response to signals of safety and interest. Low vagal tone has been linked to high inflammation, greater risk for myocardial infarction, and lower odds of survival after heart failure.

Their positive feedback loop suggestion sounds good - and is consonant with many recent studies correlating positive emotions, physical health, and longevity - but they do tend to confuse cause and correlation, and do not have appropriate control groups. A 'waiting list control group' really doesn't hack it. A control group should at least have some sort of experimenter engagement with subjects that is as similar as possible to the control group except without the exercises for self-generated positive emotions. Still, the results do show convincing correlations between vagal tone, positive emotions, and social connections in a group that receives training and practices loving kindness meditation for 61 days. Here is the abstract:

The mechanisms underlying the association between positive emotions and physical health remain a mystery. We hypothesize that an upward-spiral dynamic continually reinforces the tie between positive emotions and physical health and that this spiral is mediated by people’s perceptions of their positive social connections. We tested this overarching hypothesis in a longitudinal field experiment in which participants were randomly assigned to an intervention group that self-generated positive emotions via loving-kindness meditation or to a waiting-list control group. Participants in the intervention group increased in positive emotions relative to those in the control group, an effect moderated by baseline vagal tone, a proxy index of physical health. Increased positive emotions, in turn, produced increases in vagal tone, an effect mediated by increased perceptions of social connections. This experimental evidence identifies one mechanism—perceptions of social connections—through which positive emotions build physical health, indexed as vagal tone. Results suggest that positive emotions, positive social connections, and physical health influence one another in a self-sustaining upward-spiral dynamic.

http://pss.sagepub.com/content/24/7/1123.abstract http://pss.sagepub.com.ezproxy.library.wisc.edu/content/24/7/1123.full

Sebastian - The Maestro

Deric and 16 month old grandson Sebastian improvising.

An ancestral logic of politics?

Another evolutionary psychology speculation: If individual dispositions about modern political conflicts are partly generated by evolved mechanisms designed for evolutionarily recurrent conditions, then men with greater upper-body strength should be more likely to adopt political positions that increase their share of resources, whereas men with lesser upper-body strength should be more likely to adopt positions that relinquish resources demanded by other individuals. Peterson et al. test this speculation:

Over human evolutionary history, upper-body strength has been a major component of fighting ability. Evolutionary models of animal conflict predict that actors with greater fighting ability will more actively attempt to acquire or defend resources than less formidable contestants will. Here, we applied these models to political decision making about redistribution of income and wealth among modern humans. In studies conducted in Argentina, Denmark, and the United States, men with greater upper-body strength more strongly endorsed the self-beneficial position: Among men of lower socioeconomic status (SES), strength predicted increased support for redistribution; among men of higher SES, strength predicted increased opposition to redistribution. Because personal upper-body strength is irrelevant to payoffs from economic policies in modern mass democracies, the continuing role of strength suggests that modern political decision making is shaped by an evolved psychology designed for small-scale groups.

Pathways through which loneliness affects health.

From Jaremka et al., some technical data on how stress correlates with activation of inflammatory chemistry in our bodies - chemistry started up by our immune system as if it were responding to infections or disease:

Although evidence suggests that loneliness may increase risk for health problems, the mechanisms responsible are not well understood. Immune dysregulation is one potential pathway: Elevated proinflammatory cytokines such as interleukin-6 (IL-6) increase risk for health problems. In our first study (N = 134), lonelier healthy adults exposed to acute stress exhibited greater synthesis of tumor necrosis factor-alpha (TNF-α) and IL-6 by peripheral blood mononuclear cells (PBMCs) stimulated with lipopolysaccharide (LPS) than their less lonely counterparts. Similarly, in the second study (N = 144), lonelier posttreatment breast-cancer survivors exposed to acute stress exhibited greater synthesis of IL-6 and interleukin-1 beta (IL-1β) by LPS-stimulated PBMCs than their counterparts who felt more socially connected. However, loneliness was unrelated to TNF-α in Study 2, although the result was in the expected direction. Thus, two different populations demonstrated that lonelier participants had more stimulated cytokine production in response to stress than less lonely participants, which reflects a proinflammatory phenotype. These data provide a glimpse into the pathways through which loneliness may affect health.

How exercise calms anxiety.

In my scans of journals' tables of contents I missed this interesting piece by Schoenfeld et al., which is pointed to by a summary in the New York Times "Well" section. Running is known to stimulate the production of more dendritic spines, the primary sites of excitatory synapses, on excitatory neurons throughout the hippocampal circuitry known to be involved in emotion processing. In spite of producing more excitable nerve tissue, exercise also calms anxiety (in mice and in humans). Schoenfeld suggest that this is because another effect of exercise is to increase the levels of proteins that process the inhibitory neurotransmitter GABA in local inhibitory nerve cells. Their results suggest that running improves anxiety regulation by engaging local inhibitory mechanisms in the ventral hippocampus. (By the way, GABA is a popular dietary supplement for supposedly calming social anxiety.) Here is their more technical abstract:

Physical exercise is known to reduce anxiety. The ventral hippocampus has been linked to anxiety regulation but the effects of running on this subregion of the hippocampus have been incompletely explored. Here, we investigated the effects of cold water stress on the hippocampus of sedentary and runner mice and found that while stress increases expression of the protein products of the immediate early genes c-fos and arc in new and mature granule neurons in sedentary mice, it has no such effect in runners. We further showed that running enhances local inhibitory mechanisms in the hippocampus, including increases in stress-induced activation of hippocampal interneurons, expression of vesicular GABA transporter (vGAT), and extracellular GABA release during cold water swim stress. Finally, blocking GABAA receptors in the ventral hippocampus, but not the dorsal hippocampus, with the antagonist bicuculline, reverses the anxiolytic effect of running. Together, these results suggest that running improves anxiety regulation by engaging local inhibitory mechanisms in the ventral hippocampus.

Quality of early parent input predicts child vocabulary 3 years later

Here is a fascinating result from Cartmill et al.:

Children vary greatly in the number of words they know when they enter school, a major factor influencing subsequent school and workplace success. This variability is partially explained by the differential quantity of parental speech to preschoolers. However, the contexts in which young learners hear new words are also likely to vary in referential transparency; that is, in how clearly word meaning can be inferred from the immediate extralinguistic context, an aspect of input quality. To examine this aspect, we asked 218 adult participants to guess 50 parents’ words from (muted) videos of their interactions with their 14- to 18-mo-old children. We found systematic differences in how easily individual parents’ words could be identified purely from this socio-visual context. Differences in this kind of input quality correlated with the size of the children’s vocabulary 3 y later, even after controlling for differences in input quantity. Although input quantity differed as a function of socioeconomic status, input quality (as here measured) did not, suggesting that the quality of nonverbal cues to word meaning that parents offer to their children is an individual matter, widely distributed across the population of parents.

A defense of evolutionary psychology.

For those of you who follow the debate over the legitimacy of the evolutionary psychology perspective, I recommend a look at this contribution by Jerry Coyne, which features Steven Pinker responding to a critique originating from a panel at the Convergence 2013 conference (described here). whose main point was summarized by P.Z. Myers as:

Developmental plasticity is all. The fundamental premises of evo psych are false.

The response:

This paragraph disturbed me for two reasons. First, the notion that “the fundamental premises of evo psych are false” seems deeply misguided. After all, those premises boil down to this statement: some behaviors of modern humans reflect their evolutionary history. That is palpably uncontroversial, since many of our behaviors are clearly a product of evolution, including eating, avoiding dangers, and the pursuit of sex.  And since our bodies reflect their evolutionary history, often in nonadaptive ways (e.g., wisdom teeth, bad backs, the coat of hair we produce as a transitory feature in fetuses), why not our brains, which are, after all, just bits of morphology whose structure affects our behaviors?

Second, “developmental plasticity” does not stand as a dichotomous alternative to “evolved features.” Our developmental plasticity is to a large extent the product of evolution: our ability to learn language, our tendency to defer to authorities when we’re children, our learned socialization—those are all features almost certainly instilled into our brains by natural selection as a way to promote behavioral flexibility in that most flexible of mammals.

These points are followed by a list of rejoinders made by Pinker to points in the panel discussion

The obesity paradox - fat people may live longer!

Virginia Hughes writes about accumulating data on obesity and longevity that many researchers wish would just go away, after all the effort that has been put into documenting the health risks that go with obesity. At issue, for example, is a meta-analysis, lead by Katherine Flegal, of 97 studies including 2.88 million people that reported people deemed 'overweight' by international standards to be 6% less likely to die than were those of 'normal' weight over the same time period. There has been furious debate over this result because the epidemiology involved is complex, and eliminating confounding factors is difficult. However,

....many researchers accept Flegal's results and see them as just the latest report illustrating what is known as the obesity paradox. Being overweight increases a person's risk of diabetes, heart disease, cancer and many other chronic illnesses. But these studies suggest that for some people — particularly those who are middle-aged or older, or already sick — a bit of extra weight is not particularly harmful, and may even be helpful. (Being so overweight as to be classed obese, however, is almost always associated with poor health outcomes.)  Click on graphic to enlarge:

...the most contentious part of the debate is not about the science per se, but how to talk about it. Public-health experts, including Willett, have spent decades emphasizing the risks of carrying excess weight. Studies such as Flegal's are dangerous, Willett says, because they could confuse the public and doctors, and undermine public policies to curb rising obesity rates. “There is going to be some percentage of physicians who will not counsel an overweight patient because of this,” he says. Worse, he says, these findings can be hijacked by powerful special-interest groups, such as the soft-drink and food lobbies, to influence policy-makers.

But many scientists say that they are uncomfortable with the idea of hiding or dismissing data — especially findings that have been replicated in many studies — for the sake of a simpler message. “One study may not necessarily tell you the truth, but a bulk of studies saying the same thing and being consistent, that really is reinforcing,” says Samuel Klein, a physician and obesity expert at Washington University in St Louis, Missouri. “We need to follow the data just like the yellow brick road, to the truth.”

The gospel according to me...

I want to pass on a few clips from the stimulating essay by Critchley and Webster in "The Stone" forum of the New York Times:

…many citizens in rich Western democracies have merely switched one notion of God for another — abandoning their singular, omnipotent (Christian or Judaic or whatever) deity reigning over all humankind and replacing it with a weak but all-pervasive idea of spirituality tied to a personal ethic of authenticity and a liturgy of inwardness. The latter does not make the exorbitant moral demands of traditional religions, which impose bad conscience, guilt, sin, sexual inhibition and the rest.

In the gospel of authenticity, well-being has become the primary goal of human life….The stroke of genius in the ideology of authenticity is that it doesn’t really require a belief in anything, and certainly not a belief in anything that might transcend the serene and contented living of one’s authentic life and baseline well-being. In this, one can claim to be beyond dogma.

This is the phenomenon that one might call, with an appreciative nod to Nietzsche, passive nihilism….In a seemingly meaningless, inauthentic world awash in nonstop media reports of war, violence and inequality, we close our eyes and turn ourselves into islands. We may even say a little prayer to an obscure but benign Eastern goddess and feel some weak spiritual energy connecting everything as we listen to some tastefully selected ambient music. Authenticity, needing no reference to anything outside itself, is an evacuation of history. The power of now.

Work is no longer a series of obligations to be fulfilled for the sake of sustenance: it is the expression of one’s authentic self…But here’s the rub: if one believes that there is an intimate connection between one’s authentic self and glittering success at work, then the experience of failure and forced unemployment is accepted as one’s own fault…A naïve belief in authenticity eventually gives way to a deep cynicism. A conviction in personal success that must always hold failure at bay becomes a corrupt stubbornness that insists on success at any cost. Cynicism, in this mode, is not the expression of a critical stance toward authenticity but is rather the runoff of this failure of belief.

Nothing seems more American than this forced choice between cynicism and naïve belief. Or rather, as Herman Melville put it in his 1857 novel “The Confidence Man,” it seems the choice is between being a fool (having to believe what one says) or being a knave (saying things one does not believe). For Melville, who was writing on the cusp of modern capitalism, the search for authenticity is a white whale.

Order your DIY brain stimulation kit to improve your cognition?

Nature Magazine has an interesting editorial on dealing with the fact that transcranial direct-current stimulation (tDCS) kits (costing ~ $200) are likely to soon get into the hands, and onto the heads, of many more people. A few clips:

The recent surge in interest in tDCS piggybacks on an increasing number of academic studies of its potential to boost cognitive ability, which themselves build on decades-old work using electrical stimulation of the brain to treat ailments such as depression (see Nature 472, 156–159; 2011).

In an opinion piece published earlier this month, Nicholas Fitz and Peter Reiner of the National Core for Neuroethics at the University of British Columbia in Vancouver, Canada, argue that scientists and regulators can no longer ignore the amateurish meddling with tDCS (N. Fitz and P. Reiner J. Med. Ethics http://doi.org/mv8; 2013). “The challenge for the field,” they write, “is to develop policy that thoughtfully deals with the issues stemming from people using tDCS devices at home.”

Such home use of experimental laboratory kit puts neuroethicists, and journals such as Nature, in a bind. To draw attention to it could promote and accelerate its use, and so increase the risk of a mishap. To ignore it leaves the risks unexplored. The scale of at-home tDCS use is unclear at present. It might fizzle out. Or, as scientific interest in the power of electrical stimulation of the brain grows, it might appeal to more enthusiasts, just as the fascination and potential of synthetic biology has spawned a parallel DIY community known as biohackers. The scientific interest is certainly there.

Last month, researchers at the University of Oxford, UK, published a study suggesting that random electrical stimulation of the brain could improve mathematical abilities (A. Snowball et al.Curr. Biol. 23, 987–992; 2013). And there is no lack of exposure. Drawn by the ease of access and the killer copy, science journalists are queuing up to try tDCS for themselves and to write about the effects.

Fitz and Reiner are not the first to raise concerns over the DIY tDCS community. Brain researchers flagged the problem last year, as part of a discussion on the broader ethics of using non-invasive brain-stimulation (R. Cohen Kadosh et al. Curr. Biol. 22, R108–R111; 2012). The researchers even raised the prospect of the ultimate in pushy parents: those who would use the technology on their children to try to boost their cognitive function. And back in 2011, scientists working on tDCS told Nature that they were concerned for the safety of those who tried it at home.

It is easier to raise these questions than to answer them. Fitz and Reiner have some sensible suggestions, ranging from greater reporting of the possible long-term risks of tDCS to mimicking the open communication and education strategy with which the life-sciences field has started to engage biohackers. The first step is to acknowledge the issue to get a sense of how widespread the demand for home electrical self-improvement really is. The next few months will tell us more.

Want to see the metadata on yourself (like the NSA already has)??

Intrigued by two recent articles by Lapidos and Chen, I've taken myself to the MIT media program called "Immersion". "... it only works with Gmail and you have to reveal your password...but, unlike Google, or the NSA, the project also offers an instant deletion option: Remove your name, and it erases your metadata.”  I couldn't resist. I forward all of my older email accounts (University of Wisconsin, etc.) to gmail, so it gives a good picture of my email contacts.  Below I show the graphic of my modest contact network, with names deleted.  And, of course, I've now erased the data and withdrawn the access permissions.  While doing this, I was astounded to see the list of widgets (I was completely unaware of) that have access to all my google data.  I started to delete a few, but gave up after awhile.  I assume the NSA has a vastly more complete picture, which is not being deleted!   And - whistling in the dark - I hope that nothing I do could possibly be of interest to security snoops.  

How our brain cortex receives information about the world

This post is for that subset of MindBlog readers interested in details of brain wiring. Constantinople and Bruno have upset a basic dogma taught to budding neuroscientists (like myself, in the 1960s) - that (from the Science editor's summary):

...there is a “canonical microcircuit” in the neo cortex, in which information is transformed as excitation spreads serially along connections from thalamus, to cortical layer 4, then to layers 2/3, to layers 5/6, and finally to other brain regions. Each cortical layer is thought to transform sensory signals to extract behaviorally relevant information. Now, from Constantinople and Bruno...In vivo whole-cell recordings revealed that sensory stimuli activate neurons in deep cortical layers simultaneously to those in layer 4 and that a large number of thalamic neurons converge onto deep pyramidal neurons, possibly allowing sensory information to completely bypass upper layers. Temporary blockade of layer 4 revealed that synaptic input to deep cortical layers derived entirely from the thalamus and not at all from upper cortical layers. This thalamically derived synaptic input reliably drove pyramidal neurons in layer 5 to discharge action potentials in the living animal. These deep layer neurons project to numerous higher-order brain regions and could directly mediate behavior.

Here is a summary graphic from the paper:

(A) In the conventional serial model, sensory information is transformed as excitation spreads from thalamus to L4 to L2/3 to L5/6 along the densest axonal pathways (green). (B) In the bistratified model, thalamus copies sensory information to both an upper stratum (L4 and L2/3) and a lower stratum (L5/6), which differ in coding properties and downstream target

s.

Eye widening in fear - sensory and social benefits

An interesting bit from Lee et al. Their abstract:

Facial expressions may have originated from a primitive sensory regulatory function that was then co-opted and further shaped for the purposes of social utility. In the research reported here, we tested such a hypothesis by investigating the functional origins of fear expressions for both the expresser and the observer. We first found that fear-based eye widening enhanced target discrimination in the available visual periphery of the expresser by 9.4%. We then found that fear-based eye widening enhanced observers’ discrimination of expressers’ gaze direction and facilitated observers’ responses when locating eccentric targets. We present evidence that this benefit was driven by neither the perceived emotion nor attention but, rather, by an enhanced physical signal originating from greater exposure of the iris and sclera. These results highlight the coevolution of sensory and social regulatory functions of emotional expressions by showing that eye widening serves to enhance processing of important environmental events in the visual fields of both expresser and observer.

Inflammation links ageing to the brain.

Gabuzda et al. do a nice review of work by Zhang et al., that suggests that manipulation of hypothalamus regulation, and especially levels of the hormone GnRH (gonadotropin-releasing hormone) might abrogate some effects of ageing.  I want to pass on several clips from their summary:

One of the least-understood aspects of ageing is its coordinated and stereotyped progression in all organ systems. Although researchers have long suspected that the brain orchestrates systemic ageing, compelling evidence of this in mammals has been lacking. Furthermore, we have had no clear understanding of how ageing is affected by inflammation, which is a hallmark of age-related diseases such as diabetes, cardiovascular disease, arthritis and Alzheimer's disease. Zhang et al. help to make this connection by documenting the integration of inflammatory responses with systemic control of ageing by the hypothalamus — a part of the brain that controls growth, reproduction and metabolism.

FIGURE - Zhang et al. report that inflammation leads to activation of the signalling molecule NF-κB in the hypothalamus of the brain, and suggest that this contributes to the control of systemic ageing. They show that NF-κB activation in hypothalamic cells called microglia results in production of TNF-α, which, in turn, stimulates NF-κB activity in nearby neurons. This signalling results in epigenetic repression of the gene that encodes gonadotropin-releasing hormone (GnRH), leading to reduced GnRH release from the neurons, which is associated with multiple physiological changes related to ageing, including bone loss, skin atrophy, muscle weakness and memory loss. This pathway might also mediate the effects of a variety of environmental and physiological stressors.

'Inflammageing' describes the close relationship between low-grade chronic inflammation and ageing that has been linked to a wide spectrum of age-related disorders in various organs, including the brain6. Healthy ageing and longevity could relate, in part, to reduced levels of inflammation or strong protective mechanisms that guard against adverse effects of chronic inflammation. Conversely, genetic and environmental factors that promote inflammation or disrupt the mechanisms involved in reducing inflammation seem to confer increased susceptibility to 'accelerated ageing' and age-related disorders such as insulin resistance, metabolic disorders and cardiovascular disease7. Accelerated ageing typically involves multiple organ systems, although the effects in some organs might not be seen as clinical symptoms.

In addition to the classical activity of GnRH in regulating the release of sex steroids involved in development and reproduction (oestrogens and progesterone in females and androgens in males), the hormone might also mediate other functions12. Notably, Zhang et al. found that when mice were administered GnRH, it abrogated ageing effects and increased the production of new neurons in the hypothalamus and hippocampus (a part of the brain that regulates memory). By contrast, sex steroids did not have these anti-ageing effects. A decrease in gonadal sex steroids is a well-established marker of ageing, but many other hormonal changes occur as well; and some of these age-regulated hormones (such as dehydroepiandrosterone) also regulate inflammation and other immune responses. Thus, interplay between the hormonal and immune systems occurs at multiple levels.

How might hypothalamic regulation of ageing have evolved? Chronic inflammation arises from many kinds of insult, from acute infection to genomic instability. The concept that the hypothalamus can sense inflammation through immune pathways is a new one; just as the hypothalamus responds to nutrient status, its response to inflammation may enable the organism to rapidly adapt to physiological perturbations. Turning down the hypothalamic release of modulators such as GnRH to prevent reproduction and reduce growth may be evolutionarily advantageous during acute infection, injury or deprivation. Although this would have been adaptive for our shorter-lived ancestors, it may accelerate ageing in older individuals and have become apparent now that we live longer. This idea also raises the intriguing possibility that hypothalamic regulation could be therapeutically manipulated to have broad effects on the ageing process and age-related pathology.

A spiritual home for atheists.

For many of us secular humanists, agnostics, or atheists, life after our alienation from conventional religious congregations that offer prayers to an anthropomorphic god (or gods) ends up feeling a bit rye-crispy. We lose also the sense of belonging and community that was part of the experience of being in a church congregation. Thus I was struck by this article about a former Pentecostal minister who has started in Baton Rouge, LA., to offer atheist services with impassioned sermons, singing and light swaying, exhortations to service, etc., everything but God! Jerry DeWitt, who was raised as a pentecostal and served 25 years as a minister, now offers an emotional counterpoint to more academic atheist exponents like Richard Dawkins and Christopher Hitchens. While other non-deistic spiritual congregations now exist, especially in many larger urban areas ( usually with some mix or mysticism, new age rituals, or religious-scientific components) I doubt that many of them get quite as close to reproducing the gut-wrenching intensity of DeWitt’s pentecostal service minus God!

Linking brain imaging to our subjective experience - focused attention versus mind-wandering

An interesting study from Garrison et al at Yale:

Recent advances in brain imaging have improved the measure of neural processes related to perceptual, cognitive and affective functions, yet the relation between brain activity and subjective experience remains poorly characterized. In part, it is a challenge to obtain reliable accounts of participant's experience in such studies. Here we addressed this limitation by utilizing experienced meditators who are expert in introspection. We tested a novel method to link objective and subjective data, using real-time fMRI (rt-fMRI) to provide participants with feedback of their own brain activity during an ongoing task. We provided real-time feedback during a focused attention task from the posterior cingulate cortex, a hub of the default mode network shown to be activated during mind-wandering and deactivated during meditation. In a first experiment, both meditators and non-meditators reported significant correspondence between the feedback graph and their subjective experience of focused attention and mind-wandering. When instructed to volitionally decrease the feedback graph, meditators, but not non-meditators, showed significant deactivation of the posterior cingulate cortex. We were able to replicate these results in a separate group of meditators using a novel step-wise rt-fMRI discovery protocol in which participants were not provided with prior knowledge of the expected relationship between their experience and the feedback graph (i.e., focused attention versus mind-wandering). These findings support the feasibility of using rt-fMRI to link objective measures of brain activity with reports of ongoing subjective experience in cognitive neuroscience research, and demonstrate the generalization of expertise in introspective awareness to novel contexts.

Enhanced emotion regulation persists after meditation training.

Desbordes and collaborators have looked at the effects of training in both mindful attention meditation and compassion meditation in two groups of subject with no previous experience meditating enrolled in 8-week training courses in both. 12 participants from each group reacted to images of people in situations with positive, negative, or neutral emotional content during fMRI measurements made during three weeks before or at three weeks after the training sessions. From the review in The Harvard Gazette:

In the mindful attention group, the after-training brain scans showed a decrease in activation in the right amygdala in response to all images, supporting the hypothesis that meditation can improve emotional stability and response to stress. In the compassion meditation group, right amygdala activity also decreased in response to positive or neutral images. But among those who reported practicing compassion meditation most frequently outside of the training sessions, right amygdala activity tended to increase in response to negative images, all of which depicted some form of human suffering. No significant changes were seen in the control group or in the left amygdala of any study participants.

The Harm-Made Mind

Here is a fascinating bit from Daniel Wegner and his collaborators. (I cite Wegner extensively in my "I-Illusion" web-lecture in introductory lectures sections of the left had column of this web page.)

People often think that something must have a mind to be part of a moral interaction. However, the present research suggests that minds do not create morality but that morality creates minds. In four experiments, we found that observing intentional harm to an unconscious entity—a vegetative patient, a robot, or a corpse—leads to augmented attribution of mind to that entity. A fifth experiment reconciled these results with extant research on dehumanization by showing that observing the victimization of conscious entities leads to reduced attribution of mind to those entities. Taken together, these experiments suggest that the effects of victimization vary according to victims’ preexisting mental status and that people often make an intuitive cognitive error when unconscious entities are placed in harm’s way. People assume that if apparent moral harm occurs, then there must be someone there to experience that harm—a harm-made mind. These findings have implications for political policies concerning right-to-life issues.

Are you married? Did you meet on-line or off-line?

Interesting bit from Cacioppo et al.

Marital discord is costly to children, families, and communities. The advent of the Internet, social networking, and on-line dating has affected how people meet future spouses, but little is known about the prevalence or outcomes of these marriages or the demographics of those involved. We addressed these questions in a nationally representative sample of 19,131 respondents who married between 2005 and 2012. Results indicate that more than one-third of marriages in America now begin on-line. In addition, marriages that began on-line, when compared with those that began through traditional off-line venues, were slightly less likely to result in a marital break-up (separation or divorce) and were associated with slightly higher marital satisfaction among those respondents who remained married. Demographic differences were identified between respondents who met their spouse through on-line vs. traditional off-line venues, but the findings for marital break-up and marital satisfaction remained significant after statistically controlling for these differences. These data suggest that the Internet may be altering the dynamics and outcomes of marriage itself.

Brain science backlash, throwing out the baby with the bathwater.

A recent NYTimes Op-Ed piece by David Brooks' ("Beyond the Brain") references the recent book "“Brainwashed: The Seductive Appeal of Mindless Neuroscience.” a book that appropriately notes some of the limitations of zealous over interpretation of brain imaging data but also includes some facile straw man arguments. Brooks kind of loses it in his comment:

It is probably impossible to look at a map of brain activity and predict or even understand the emotions, reactions, hopes and desires of the mind...there appears to be no dispersed pattern of activation that we can look at and say, “That person is experiencing hatred."

These sentiments are simply wrong, and I thought, rather than rambling on myself, I would point interested readers to two cogent commentaries on the recent anti-brain science surge, one in The New Yorker blog posted by Gary Marcus, the other in The Neurocritic blog.

Paternal stress changes stress axis in offspring

A study from Bale and colleagues shows that stress on preadolescent and adult male mice induces an epigenetic mark in their sperm that reprogramms their offspring's hypothalamic-pituitary-adrenal (HPA) axis, the brain regions that governs responses to stress. Offspring from paternal stress groups displayed significantly blunted levels of the stress hormone corticosterone -- in humans, it's cortisol -- in response to stress. It is curious that both male and female offspring had abnormally low reactivity to stress. Perhaps this reduced physiological stress response may reflect some adaptive evolutionary benefit passed on to offspring to ensure survival in what is expected to be a more stressful environment.

Neuropsychiatric disease frequently presents with an underlying hyporeactivity or hyperreactivity of the HPA stress axis, suggesting an exceptional vulnerability of this circuitry to external perturbations. Parental lifetime exposures to environmental challenges are associated with increased offspring neuropsychiatric disease risk, and likely contribute to stress dysregulation. While maternal influences have been extensively examined, much less is known regarding the specific role of paternal factors. To investigate the potential mechanisms by which paternal stress may contribute to offspring hypothalamic–pituitary–adrenal (HPA) axis dysregulation, we exposed mice to 6 weeks of chronic stress before breeding. As epidemiological studies support variation in paternal germ cell susceptibility to reprogramming across the lifespan, male stress exposure occurred either throughout puberty or in adulthood. Remarkably, offspring of sires from both paternal stress groups displayed significantly reduced HPA stress axis responsivity. Gene set enrichment analyses in offspring stress regulating brain regions, the paraventricular nucleus (PVN) and the bed nucleus of stria terminalis, revealed global pattern changes in transcription suggestive of epigenetic reprogramming and consistent with altered offspring stress responsivity, including increased expression of glucocorticoid-responsive genes in the PVN. In examining potential epigenetic mechanisms of germ cell transmission, we found robust changes in sperm microRNA (miR) content, where nine specific miRs were significantly increased in both paternal stress groups. Overall, these results demonstrate that paternal experience across the lifespan can induce germ cell epigenetic reprogramming and impact offspring HPA stress axis regulation, and may therefore offer novel insight into factors influencing neuropsychiatric disease risk.

Paper is not dead...

Sorry to spam you, but particularly after yesterday's post about smartphone apps I thought this was hysterical.

More on smartphone brain training apps.

This post is just a quickie pointer to update the series of posts I have done on smart phone or PC apps that give your brain a workout.  It reviews several current products.  I try each new iteration for a bit,  but then fade because I am phobic about "competing" with myself or anyone else and also get concerned that my scores are not improving fast enough.  I didn't grow up in a video game playing world, and they feel too much like hard work - I like things that feel easy with the skills I have,  like learning a new piano score. 

Neuroimaging our self esteem - be happy!

There are more papers coming out on brain correlates of whatever aspect of our behaviors you care to name than anyone could possibly keep up with. I have the ‘my eyes glaze over’ experience in just scanning tables of contents of the relevant journals. Occasionally an item pops out that grabs my attention, such as this one (open access) on imaging brain correlates of self esteem. The drums continue to beat (see this book review) on how important a positive self image and an "Up" attitude are for health and longevity. Maybe someone will develop some kind of magnetic zapper that we can shoot ourselves up with whenever whenever we are feeling like a piece of …... 

Although neuroimaging studies strongly implicate the medial prefrontal cortex (ventral and dorsal), cingulate gyrus (anterior and posterior), precuneus and temporoparietal cortex in mediating self-referential processing (SRP), little is known about the neural bases mediating individual differences in valenced SRP, that is, processes intrinsic to self-esteem. This study investigated the neural correlates of experimentally engendered valenced SRP via the Visual–Verbal Self-Other Referential Processing Task in 20 women with fMRI. Participants viewed pictures of themselves or unknown other women during separate trials while covertly rehearsing ‘I am’ or ‘She is’, followed by reading valenced trait adjectives, thus variably associating the self/other with positivity/negativity. Response within dorsal and ventral medial prefrontal cortex, cingulate cortex and left temporoparietal cortex varied with individual differences in both pre-task rated self-descriptiveness of the words, as well as task-induced affective responses. Results are discussed as they relate to a social cognitive and affective neuroscience view of self-esteem.

.... stimulus presentations were blocked in terms of the conditions Reference (Self vs Other, i.e. photographs) and Valence (words), creating four trial types: self-negative (S-N), self-positive (S-P), other-negative (O-N) and other-positive (O-P). Participants were not instructed that they ‘should try to press the buttons as fast as possible’ as is often done in social cognition experiments. In contrast, participants were instructed only to press the buttons ‘so that we can assess afterwards whether you are paying attention to and completing the task’. This passive orientation was intended to focus attention towards introspection and interoception with participants reminded repeatedly of the importance of ‘paying close attention to how you are feeling throughout the different parts of the task’.

Young blood makes younger hearts (and brains) - also, aging resistant brains

I've previously mentioned work showing that providing young blood to an older brain can be beneficial, and now want to note work by Loffredo et al. that shows that exposure to a young circulation reverses age-related cardiac hypertrophy, which is a prominent feature of age-related diatolic heart failure. The TGFβ family member GDF11 appears to be the crucial circulating factor that declines with age; restoring GDF11 to youthful levels reverses age-related cardiac hypertrophy. 

Also, relevant to aging, I might note a longitudinal study by Pudas et al. comparing MRI data from elderly people most successful in preserving episodic memory and ability on paired association tasks with measurements on average contemporaries. The results suggest that successful cognitive aging is associated with preservation of the responsiveness of the hippocampus and prefrontal cortex.

Heart rate variability, ANS aging - a new device from "Phyode" - therapeutic agent or scam??

I want to put in this post a comment by reader "Andre" on my June 11 post ("Changes as an autonomic nervous system ages 11 years - The "Wild Divine" is a bit less wild.", along with my response.

Last week I backed a Kickstarter project from Phyode called the W/Me (http://goo.gl/en1Ea), a smartwatch that uses HRV and "ANS Age" as its primary markers for assessing the user's "mental state". I couldn't find a research precedent for using ANS aging for this purpose until your post came up in a Google search. Do you think Phyode's methodology is valid?

My response on looking at the website:

This is a very slick presentation, and looks like a potentially interesting product...If it were not for the fact that its development appears to be limited to Android products (i.e. no iPhone App)[NOTE! 10/22/13 - comment below says I'm wrong, it is for iPhone, not Android, my bad..] I would probably try it out when it is sold (There are, by the way several iPhone apps that do heart rate, HRV, etc.).....BUT, there are no pointers to basic scientific references on heart rate variability, ANS age, how it can be therapeutically altered in a beneficial way, or how his device would be used to do that. The FAQ section at the end of the web page with what look like links to such items as "What is HRV?" don't link to anything!! The Phyode "Full bio and links" doesn't yield anything significant! I would be interested in seeing something a bit more substantial from the people in the flashy video presentations (all appear to be 20-somethings, by the way). I don't want to play the complete nasty guy here, because a lot of effort went into the slick videos and description, and they look plausible, but what assures us that the fund raising "Back this project" (minimum donation $1.00) is not a scam? Does the Kickstarter cloud funding site that hosts this webpage have any quality controls or review criteria?? The "report this site to Kickstarter" link takes you to a page that requires you to join or be member of Kickstarter, and I'm not inclined to take that much time on this....

Carrying human (and mouse) babies reduces their crying and heart rate.

Esposito et al. present some really nice observations. They demonstrate for the first time that the infant calming response to maternal carrying is a coordinated set of central, motor, and cardiac regulations and is a conserved component of mammalian mother-infant interactions. You should watch the video.


-Maternal carrying reduces crying, body movement, and heart rate of infants
-In mice, a similar set of calming responses is observed during carrying
 -Mouse calming response requires proprioception and somatosensation
 -The calming responses in infants function to increase maternal carrying efficacy

Here we show a novel set of infant cooperative responses during maternal carrying. Infants under 6 months of age carried by a walking mother immediately stopped voluntary movement and crying and exhibited a rapid heart rate decrease, compared with holding by a sitting mother. Furthermore, we identified strikingly similar responses in mouse pups as defined by immobility and diminished ultrasonic vocalizations and heart rate. Using pharmacologic and genetic interventions in mouse pups, we identified the upstream and downstream neural systems regulating the calming response. Somatosensory and proprioceptive input signaling are required for induction, and parasympathetic and cerebellar functions mediate cardiac and motor output, respectively. The loss of the calming response hindered maternal rescue of the pups, suggesting a functional significance for the identified calming response.

Our memory can be selectively rewritten during its reconsolidation.

Chan and LaPaglia make an interesting observation in humans that had previously only been reported in animal studies. We can mess with an existing declarative memory of an event after that memory has been reactivated, if during its reconsolidation we are presented with changes that target and change some details of the original memory. Reactivated memories are vulnerable only to interference that specifically targets the existing memories. This work provides yet another example of how eye witness testimony of the sort used in legal proceedings can become unreliable.

During the past decade, a large body of research has shown that memory traces can become labile upon retrieval and must be restabilized. Critically, interrupting this reconsolidation process can abolish a previously stable memory. Although a large number of studies have demonstrated this reconsolidation associated amnesia in nonhuman animals, the evidence for its occurrence in humans is far less compelling, especially with regard to declarative memory. In fact, reactivating a declarative memory often makes it more robust and less susceptible to subsequent disruptions. Here we show that existing declarative memories can be selectively impaired by using a noninvasive retrieval–relearning technique. In six experiments, we show that this reconsolidation-associated amnesia can be achieved 48 h after formation of the original memory, but only if relearning occurred soon after retrieval. Furthermore, the amnesic effect persists for at least 24 h, cannot be attributed solely to source confusion and is attainable only when relearning targets specific existing memories for impairment. These results demonstrate that human declarative memory can be selectively rewritten during reconsolidation.

Antonin Scalia Does Not Believe in Molecular Biology

Thanks to my son Jon for pointing this out to me.

Private behaviors from public records...

The exposure of the PRISM surveillance system by Edward Snowden gave me a sort of "So what else is new?" reaction... I thought we knew this unfortunate stuff was happening, particularly in view of numerous academic articles in the vein of the following from Kosinski et al.:

We show that easily accessible digital records of behavior, Facebook Likes, can be used to automatically and accurately predict a range of highly sensitive personal attributes including: sexual orientation, ethnicity, religious and political views, personality traits, intelligence, happiness, use of addictive substances, parental separation, age, and gender. The analysis presented is based on a dataset of over 58,000 volunteers who provided their Facebook Likes, detailed demographic profiles, and the results of several psychometric tests. The proposed model uses dimensionality reduction for preprocessing the Likes data, which are then entered into logistic/linear regression to predict individual psychodemographic profiles from Likes. The model correctly discriminates between homosexual and heterosexual men in 88% of cases, African Americans and Caucasian Americans in 95% of cases, and between Democrat and Republican in 85% of cases. For the personality trait “Openness,” prediction accuracy is close to the test–retest accuracy of a standard personality test. We give examples of associations between attributes and Likes and discuss implications for online personalization and privacy.

Changes as an autonomic nervous system ages 11 years - The "Wild Divine" is a bit less wild.

Just after I retired from being a Univ. of Wisconsin department chair in 2001 I bought a set of finger sensors that fit on one's three middle fingers to report skin conductance and heartbeat to a PC or MAC via an A/D converter. These were part of a package with several CDs that installed a new age game on the computer that lead you through a rich environment of classical greek temples and waterfalls, attended by soothing music, that presented tasks in which you dinked with your own heart rate variability and sympathetic (arousing)/parasympathetic (calming) balance, going alternatively through periods of calm and arousal. I thought it was a hoot, and took the time to go through the "Journey to Wild Divine: passage" and "Journey to Wild Divine: Wisdom Quest."

Some of the current incarnations of these programs have moved to web browsers. Over the years a number of heavy weight new age gurus have signed on with their wares - Deepak Chopra, Dean Ornish, and Andrew Weil (Weil was in my Harvard graduating class...I'm tempted, but I won't burden you with my jaded opinion of this class of entrepreneurs, particularly Mr. Chopra.)

The main point of this post is note my experience on pulling out the finger sensors after 11 years trying the same exercises in their new presentation. What's the difference when this 71 year old tries the same manipulations of calm and arousal that the 60 year old played with with 11 years earlier? In a nutshell, I have less command over heart rate variability, which is lower, as the swings between calm and arousal have less amplitude.

And indeed, this fits with the literature on changes in the autonomic nervous system that occur on aging. If you simply do a google search for "autonomic nervous system and aging" numerous references appear that document how healthy aging is associated with lowered heart rate variability, elevated basal sympathetic nervous activity, and reduction of overall autonomic reactivity of sympathetic and parasympathetic nervous systems. Here is a very recent review, from which I pass on one figure:

Schematic of proposed features associated with the imbalance in the autonomic nervous system during aging. During aging there is a shift in the balance of the autonomic nervous system (ANS) towards the sympathetic nervous system (SNS). This may be influenced by circulating or local brain levels of angiotensin (Ang) II and leptin. The lower activity of the parasympathetic nervous system (PSNS) is proposed to result at least in part from an age-related decline in Angiotensin-(1–7). Lower Angiotensin-(1–7) and higher Ang II or leptin in the brain medulla would predispose to a decline in baroreceptor reflex sensitivity (BRS) for control of heart rate and heart rate variability (HRV), both of which are associated with aging. Moreover, impairments in BRS and HRV can contribute to target organ damage, including metabolic dysfunction, with or without an increase in blood pressure. 

If you're inclined, like Mr. Dylan Thomas, to not "go gently into that good night" you can find numerous sources (example here) on slowing these aging changes, usually by some sort of physical movement or stimulation.

Preventing Alzheimer’s associated brain cell atrophy with B vitamin treatment.

I pass this on because it seems like a very striking result. Douaud et al. find that high-dose B-vitamin treatment (folic acid 0.8 mg, vitamin B6 20 mg, vitamin B12 0.5 mg) causes a 7-fold decrease in cerebral atrophy of nerve cell areas most vulnerable to the Alzheimer's process over a 2-year period in a group of elderly subjects with increased dementia risk. (For comparison, Centrum Silver 50+ has Folic Acid 0.4 mg, Vitamin B6 3 mg, and Vitamin B12 0.025 mg.) The supplements decrease plasma levels of one of the bad players in the Alzheimer's story, homocysteine. (Homocysteine is a homologue of the amino acid cysteine,and can be recycled into methionine or converted into cysteine with the aid of B-vitamins.) Here's the abstract:

Is it possible to prevent atrophy of key brain regions related to cognitive decline and Alzheimer’s disease (AD)? One approach is to modify nongenetic risk factors, for instance by lowering elevated plasma homocysteine using B vitamins. In an initial, randomized controlled study on elderly subjects with increased dementia risk (mild cognitive impairment according to 2004 Petersen criteria), we showed that high-dose B-vitamin treatment (folic acid 0.8 mg, vitamin B6 20 mg, vitamin B12 0.5 mg) slowed shrinkage of the whole brain volume over 2 y. Here, we go further by demonstrating that B-vitamin treatment reduces, by as much as seven fold, the cerebral atrophy in those gray matter (GM) regions specifically vulnerable to the AD process, including the medial temporal lobe. In the placebo group, higher homocysteine levels at baseline are associated with faster GM atrophy, but this deleterious effect is largely prevented by B-vitamin treatment. We additionally show that the beneficial effect of B vitamins is confined to participants with high homocysteine (above the median, 11 µmol/L) and that, in these participants, a causal Bayesian network analysis indicates the following chain of events: B vitamins lower homocysteine, which directly leads to a decrease in GM atrophy, thereby slowing cognitive decline. Our results show that B-vitamin supplementation can slow the atrophy of specific brain regions that are a key component of the AD process and that are associated with cognitive decline. Further B-vitamin supplementation trials focusing on elderly subjets with high homocysteine levels are warranted to see if progression to dementia can be prevented.

Here is one figure from the paper:

B-vitamin treatment significantly reduces regional loss of gray matter. (A) Brain regions in blue demonstrate where B-vitamin treatment significantly reduces GM loss over the 2-y period. All blue areas correspond to regions of significant loss in placebo and known to be vulnerable in AD. (B) Percentage of GM loss for the 156 participants over the 2-y period, averaged across those brain regions that showed significant effect of B vitamins: placebo group (red triangles) had an average loss of 3.7% (±3.7), whereas the B-vitamin group (green circles) showed a loss of 0.5% (±2.9).

Visions of our high-tech future: Julian Assange, Jaron Lanier, et al. on Google, Siren servers and the banality of ‘Don’t Be Evil’

The book by Google's Eric Schmidt and Jared Cohen, "The New Digital Age" is a rosy scenario of our high-tech future that many have found a bit creepy and chilling. Since our techie surround will anticipate and take care of our every movement, it seems like we can just sign off and go along for the ride (turning in mental vegetables in the process? …and letting the rule of 'use it or lose it' do it's work on our poor brains?). Also, is it more than a coincidence that at roughly the same time as Schmidt's messianic book is appearing, the movie “The Internship,” a two-hour commercial for GoogleWorld masquerading as an aspirational buddy comedy, also appears in the movie theaters? (You might note this caustic review of the movie.)

Trying to set aside my bias, generated by extensive negative press comments on the behaviors of Wiki-Leaks' Julian Assange, I found his piece in the New York Times on the Schmidt and Cohen book to have some savory and choice screeds. A partial sampling:

“The New Digital Age” is, beyond anything else, an attempt by Google to position itself as America’s geopolitical visionary — the one company that can answer the question “Where should America go?” It is not surprising that a respectable cast of the world’s most famous warmongers has been trotted out to give its stamp of approval to this enticement to Western soft power. The acknowledgments give pride of place to Henry Kissinger, who along with Tony Blair and the former C.I.A. director Michael Hayden provided advance praise for the book.

…“Progress” is driven by the inexorable spread of American consumer technology over the surface of the earth. Already, every day, another million or so Google-run mobile devices are activated. Google will interpose itself, and hence the United States government, between the communications of every human being not in China (naughty China). Commodities just become more marvelous; young, urban professionals sleep, work and shop with greater ease and comfort; democracy is insidiously subverted by technologies of surveillance, and control is enthusiastically rebranded as “participation”; and our present world order of systematized domination, intimidation and oppression continues, unmentioned, unafflicted or only faintly perturbed.

This book is a balefully seminal work in which neither author has the language to see, much less to express, the titanic centralizing evil they are constructing. “What Lockheed Martin was to the 20th century,” they tell us, “technology and cybersecurity companies will be to the 21st.” Without even understanding how, they have updated and seamlessly implemented George Orwell’s prophecy. If you want a vision of the future, imagine Washington-backed Google Glasses strapped onto vacant human faces — forever. Zealots of the cult of consumer technology will find little to inspire them here, not that they ever seem to need it. But this is essential reading for anyone caught up in the struggle for the future, in view of one simple imperative: Know your enemy.

If you want to read what I think is one of the best articles I have seen so far on the unfortunate consequences of our digital universe and possible cures, check out Jaron Lanier's article "Fixing the Digital Economy." It describes the concentration of power and income in the small sliver of the population that designs and runs the massive servers (Siren servers) that analyze different sectors of our lives to minimize their risk and maximize their profits.

Even friendly, consumer-facing Siren Servers ultimately depend on spreading costs to the larger society. Siren Servers can function profitably only if people aren’t paid for the data that is used to calculate their statistical schemes.

Siren Servers drive apart our identities as consumers and workers. In some cases, causality is apparent: free music downloads are great but throw musicians out of work. Free college courses are all the fad, but tenured professorships are disappearing. Free news proliferates, but money for investigative and foreign reporting is drying up. One can easily see this trend extending to the industries of the future, like 3-D printing and renewable energy.

Lanier suggests that we need to nurture a middle class that can thrive even in a highly automated society. One approach:

Institute a universal micropayment system. Keep track of where information came from. Pay people when information that exists because they exist turns out to be valuable, no matter what kind of information is involved or whether a person intended to provide it or not. Let the price be determined by markets.

Person-to-person information markets might lead to a simpler and clearer online world. Because our information systems are designed to initially forget who provided information, services like Google and Bing must constantly scrape the global network to reconstitute the context of data. Siren Servers know who links to your data, but you don’t.

EVEN today’s titanic Siren Servers would benefit from a more monetized information economy, because it would be a healthier-growing economy. The information economy cannot exhibit the long-term growth it ought to if information coming from ordinary people is forever declared to be off the books.

Skeptics sometimes reveal hidden and unfounded wells of elitism. These surface in comments like: “Most people wouldn’t contribute very much.” But there are already empirical hints to counter such pessimism.

In networks with a central point of control, like YouTube or the Apple Store, we do see a Horatio Alger pattern in the distribution of outcomes, where there are very few viable winners and an unbounded number of hopefuls. But in more directly and thickly connected networks like Facebook, we see people typically exposed to a large number of other people, rather than just a few stars. Therefore, if Facebook users paid one another, they would see a less elite distribution of economic benefits.

Another potential benefit of monetized information is to balance the power of government. When information is free, there is no cost to gathering information about citizens. I would like the government, or anyone else, to pay each person each time that person is tracked by a camera. The government should be able to use cameras for security purposes, but in a limited, not unbounded way. Similarly, candidates should not be able to win elections by having the best Siren Servers, but that’s only a problem if the information is free. Citizens should not lose the power of the purse.

As a final note, this Douthat piece regarding the recently revealed NSA snooping on citizens mentions the fact that the problem isn’t that the Internet has been penetrated by the surveillance state; it’s that the Internet, in effect, is a surveillance state.

Penis size and male attractiveness - the most read article in The Proceedings of the National Academy!

I finally had to pass this on.... When I check out the table of contents for new issues of the Proceedings of the National Academy of Science, the right hand column of the page lists most read and most cited articles. For weeks I've been noting that the most read article is "Penis size interacts with body shape and height to influence male attractiveness." I've been trying to avoid it, assuming another evolutionary psychology fairy tale...but, I did have a look. To not deprive MindBlog readers of this gem, I pass on the abstract and one illustration:

Compelling evidence from many animal taxa indicates that male genitalia are often under postcopulatory sexual selection for characteristics that increase a male’s relative fertilization success. There could, however, also be direct precopulatory female mate choice based on male genital traits. Before clothing, the nonretractable human penis would have been conspicuous to potential mates. This observation has generated suggestions that human penis size partly evolved because of female choice. Here we show, based upon female assessment of digitally projected life-size, computer-generated images, that penis size interacts with body shape and height to determine male sexual attractiveness. Positive linear selection was detected for penis size, but the marginal increase in attractiveness eventually declined with greater penis size (i.e., quadratic selection). Penis size had a stronger effect on attractiveness in taller men than in shorter men. There was a similar increase in the positive effect of penis size on attractiveness with a more masculine body shape (i.e., greater shoulder-to-hip ratio). Surprisingly, larger penis size and greater height had almost equivalent positive effects on male attractiveness. Our results support the hypothesis that female mate choice could have driven the evolution of larger penises in humans. More broadly, our results show that precopulatory sexual selection can play a role in the evolution of genital traits.

Figures representing the most extreme height, shoulder-to-hip ratio, and penis size (±2 SD) (Right and Left) in comparison with the average (Center figure) trait values.

We can learn new information during sleep.

Arzi et al. have devised a nice demonstration of how we can learn new information during our sleep. They paired pleasant and unpleasant odors with different tones during sleep, and measured the subjects’ sniffs to tones alone when they were awake. Tones associated with pleasant smells produced stronger sniffs, and tones associated with disgusting smells produced weaker sniffs, despite the subjects’ lack of awareness of the learning process. 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.

Childhood self-control predicts health, wealth, and public safety

An international collaboration between researchers at universities in the US, UK, Canada, and New Zealand has generated this study, which speaks for itself (The participants are members of the Dunedin Multidisciplinary Health and Development Study, which tracks the development of 1,037 individuals born in 1972–1973 in Dunedin, New Zealand.) :

Policy-makers are considering large-scale programs aimed at self-control to improve citizens’ health and wealth and reduce crime. Experimental and economic studies suggest such programs could reap benefits. Yet, is self-control important for the health, wealth, and public safety of the population? Following a cohort of 1,000 children from birth to the age of 32 y, we show that childhood self-control predicts physical health, substance dependence, personal finances, and criminal offending outcomes, following a gradient of self-control. Effects of children's self-control could be disentangled from their intelligence and social class as well as from mistakes they made as adolescents. In another cohort of 500 sibling-pairs, the sibling with lower self-control had poorer outcomes, despite shared family background. Interventions addressing self-control might reduce a panoply of societal costs, save taxpayers money, and promote prosperity.

Self-control gradient. Children with low self-control had poorer health (A), more wealth problems (B), more single-parent child rearing (C), and more criminal convictions (D) than those with high self-control.

MindBlog starts up some summer music - a Poulenc Valse

Calling it summer music is being optimistic... it is still very chilly in Madison. I'm starting to select some pieces for an early fall musical at my Twin Valley home in Middleton, WI. This Poulenc valse is fun and bouncy, and gives me an excuse to relearn the techie side of mixing good quality audio with video.

The chemistry of protecting our brains by fasting.

Actually, I'm making a big assumption in the post title... namely that the results obtained by Gräff et al. in mice would extrapolate to similar finding in the human brain. In several animal models, a reduced consumption of calories seems to protect against cognitive deficits such as memory loss, in addition to acting on many different cell types and tissues to slow down aging. They found that caloric restriction effectively delays the onset of neurodegeneration and preserves structural and functional synaptic plasticity as well as memory capacities. Fasting activates the expression and activity of the nicotinamide adenine dinucleotide (NAD)–dependent protein deacetylase SIRT1, a known promoter of neuronal life span. (A deacetylase is an enzyme that cleaves acetate groups - think acetic acid or vinegar - from their attachment to proteins.) Surprisingly, this effect of reduced consumption of calories is mimicked by a small-molecule SIRT1-activating compound. (Just in case you were curious, the compound is SRT3657 [tertα-butyl 4-((2-(2-(6-(2-(tert-butoxycarbonyl(methyl)amino)ethylamino)-2-butylpyrimidine-4- carboxamido)phenyl)thiazolo[5,4-b]pyridin-6-yl)methoxy)piperidine-1-carboxylate])!! Mice treated with this substance recapitulated the beneficial effects of caloric restriction against neurodegeneration-associated pathologies. If this mechanism also applies to humans, SIRT1 may represent an appealing pharmacological target against neurodegeneration. Here is the abstract:

Caloric restriction (CR) is a dietary regimen known to promote lifespan by slowing down the occurrence of age-dependent diseases. The greatest risk factor for neurodegeneration in the brain is age, from which follows that CR might also attenuate the progressive loss of neurons that is often associated with impaired cognitive capacities. In this study, we used a transgenic mouse model that allows for a temporally and spatially controlled onset of neurodegeneration to test the potentially beneficial effects of CR. We found that in this model, CR significantly delayed the onset of neurodegeneration and synaptic loss and dysfunction, and thereby preserved cognitive capacities. Mechanistically, CR induced the expression of the known lifespan-regulating protein SIRT1, prompting us to test whether a pharmacological activation of SIRT1 might recapitulate CR. We found that oral administration of a SIRT1-activating compound essentially replicated the beneficial effects of CR. Thus, SIRT1-activating compounds might provide a pharmacological alternative to the regimen of CR against neurodegeneration and its associated ailments.

Long-term improvement of brain function and cognition with brain stimulation and cognitive training.

A group of collaborators from the University of Oxford and Innsbruck Medical University have published an observation that simple transcranial random noise stimulation (TRNS) of the bilateral (both sides of the brain) dorsolateral prefrontal cortex (DLPFC) applied during cognitive training over five days causes improvement in learning and performance of complex arithmetic tasks (both calculation and drill leaning) that still persist on testing 6 months later. This correlates with long lasting oxygenated blood flow changes measured by near-infrared spectroscopy that suggests more efficient neurovascular coupling within the left DLPFC. Here is their complete abstract:

Noninvasive brain stimulation has shown considerable promise for enhancing cognitive functions by the long-term manipulation of neuroplasticity. However, the observation of such improvements has been focused at the behavioral level, and enhancements largely restricted to the performance of basic tasks. Here, we investigate whether transcranial random noise stimulation (TRNS) can improve learning and subsequent performance on complex arithmetic tasks. TRNS of the bilateral dorsolateral prefrontal cortex (DLPFC), a key area in arithmetic , was uniquely coupled with near-infrared spectroscopy (NIRS) to measure online hemodynamic responses within the prefrontal cortex. Five consecutive days of TRNS-accompanied cognitive training enhanced the speed of both calculation- and memory-recall-based arithmetic learning. These behavioral improvements were associated with defined hemodynamic responses consistent with more efficient neurovascular coupling within the left DLPFC. Testing 6 months after training revealed long-lasting behavioral and physiological modifications in the stimulated group relative to sham controls for trained and nontrained calculation material. These results demonstrate that, depending on the learning regime, TRNS can induce long-term enhancement of cognitive and brain functions. Such findings have significant implications for basic and translational neuroscience, highlighting TRNS as a viable approach to enhancing learning and high-level cognition by the long-term modulation of neuroplasticity.

For those of you who might well ask "How exactly is TRNS done?" here is a clip from their experimental procedures section. The photograph suggests a rather imposing device!:

Subjects received TRNS while performing the learning task each day. Two electrodes (5 cm × 5 cm) were positioned over areas of scalp corresponding to the DLPFC (F3 and F4, identified in accordance with the international 10-20 EEG procedure; see the figure). Electrodes were encased in saline-soaked synthetic sponges to improve contact with the scalp and avoid skin irritation. Stimulation was delivered by a DC-Stimulator-Plus device (DC-Stimulator-Plus, neuroConn). Noise in the high-frequency band (100–600Hz) was chosen as it elicits greater neural excitation than lower frequency stimulation. For the TRNS group, current was administered for 20 min, with 15 s increasing and decreasing ramps at the beginning and end, respectively, of each session of stimulation. In the sham group current was applied for 30 s after upward ramping and then terminated.

When more support is less....

Finkel and Fitzsimons, whose work I mentioned in a post several years ago, do a review of studies showing that the children of parents who generously finance and regulate in detail their education ("helicopter parenting') make worse grades and feel less satisfied with their lives.

It seems that certain forms of help can dilute recipients’ sense of accountability for their own success. The college student might think: If Mom and Dad are always around to solve my problems, why spend three straight nights in the library during finals rather than hanging out with my friends?

They reference their previous work (see MindBlog link above) showing that this effect generalizes to many 'helping' situations.

Women who thought about how their spouse was helpful with their health and fitness goals became less motivated to work hard to pursue those goals: relative to the control group, these women planned to spend one-third less time in the coming week pursuing their health and fitness goals.

....the problem: how can we help our children (and our spouses, friends and co-workers) achieve their goals without undermining their sense of personal accountability and motivation to achieve them?...The answer, research suggests, is that our help has to be responsive to the recipient’s circumstances: it must balance their need for support with their need for competence. We should restrain our urge to help unless the recipient truly needs it, and even then, we should calibrate it to complement rather than substitute for the recipient’s efforts.

(I like to think that this would be a good description of how I ran my research laboratory, training graduate and post-doctoral students, for 30 years.) A final clip:

...providing help is most effective under a few conditions: when the recipient clearly needs it, when our help complements rather than replaces the recipient’s own efforts, and when it makes recipients feel that we’re comfortable having them depend on us.

So yes, by all means, parents, help your children. But don’t let your action replace their action. Support, don’t substitute. Your children will be more likely to achieve their goals — and, who knows, you might even find some time to get your own social life back on track.

Giant, Glowing Plastic Brain on Wheels

Even though I'm usually a curmudgeon about brain hype,  Obama's Brain initiative, etc., I have to admire the enthusiasm and persistence of CUNY college senior Tyler Alterman, who as his senior thesis project, is trying to get a cognitive science lab on wheels on the road. He hopes that the mobile lab, dubbed The Think Tank, will help close the gender and race gap in STEM skills (science, technology, engineering and math), that are the key to good jobs, through hands-on psych and neuroscience learning at schools and museums.   He has raised $32,000 from crowd funding, and hopes to raise the final $20,000 needed to put the mobile lab on the streets, in part through a public gala on June 18 at the Macaulay Honor College of CUNY.

How we work: 'brain waves' versus modern phrenology

Alexander et al. have analyzed data from magnetoencephalogram (MEG), electroencephalogram (EEG) and electrocorticogram (ECoG), focusing on globally synchronous fields in within-trial evoked brain activity. They quantified several signal components and compared topographies of activation across large-scale cortex. They found the topography of evoked responses was primarily a function of within-trial phase, and within-trial phase topography could be modeled as traveling waves. Traveling waves explained more signal than the trial-averaged phase topography. Here is a edited clip of explanation from Alexander:

The brain can be studied on various scales,..."You have the neurons, the circuits between the neurons, the Brodmann areas – brain areas that correspond to a certain function – and the entire cortex. Traditionally, scientists looked at local activity when studying brain activity, for example, activity in the Brodmann areas. To do this, you take EEG's (electroencephalograms) to measure the brain’s electrical activity while a subject performs a task and then you try to trace that activity back to one or more brain areas."

..."We are examining the activity in the cerebral cortex as a whole. The brain is a non-stop, always-active system. When we perceive something, the information does not end up in a specific part of our brain. Rather, it is added to the brain's existing activity. If we measure the electrochemical activity of the whole cortex, we find wave-like patterns. This shows that brain activity is not local but rather that activity constantly moves from one part of the brain to another. The local activity in the Brodmann areas only appears when you average over many such waves.”

Each activity wave in the cerebral cortex is unique. "When someone repeats the same action, such as drumming their fingers, the motor centre in the brain is stimulated. But with each individual action, you still get a different wave across the cortex as a whole. Perhaps the person was more engaged in the action the first time than he was the second time, or perhaps he had something else on his mind or had a different intention for the action. The direction of the waves is also meaningful. It is already clear, for example, that activity waves related to orienting move differently in children – more prominently from back to front – than in adults. With further research, we hope to unravel what these different wave trajectories mean."

Video: A wave of brain activity measured by the magnetic field it generates externally to the head. The left view of the head is shown on the left side of the image and the right view of the head on the right side of the image. This wave takes about 100 milliseconds to traverse the entire surface of the brain. The travelling wave originates on the lower-left of the head and travels to the lower front-right of the head. Most of the magnetic field shown in this video is generated by brain activity close to the surface of the cortex. The times displayed at the bottom are relative to the subject pressing a button at time zero. The colour scale shows the peak of the wave as hot colours and the trough of the wave as dark colours.

Training our ability to make decisions on uncertain outcomes.

When making decisions, we often retrieve a limited set of items from memory. These retrieved items provide evidence for competing options. For example, a dark cloud may elicit memories of heavy rains, leading one to pack an umbrella instead of sunglasses. Likewise, when viewing an X-ray, a radiologist may retrieve memories of similar X-rays from other patients. Whether or not these other patients have a tumor may provide evidence for or against the presence of a tumor in the current patient. Giguèrea and Love do an interesting study showing how people's ability to make accurate predictions of probabilistic outcomes can be improved if they are trained on an idealized version of a the distribution. They say it in their abstract as clearly as I can:

Some decisions, such as predicting the winner of a baseball game, are challenging in part because outcomes are probabilistic. When making such decisions, one view is that humans stochastically and selectively retrieve a small set of relevant memories that provides evidence for competing options. We show that optimal performance at test is impossible when retrieving information in this fashion, no matter how extensive training is, because limited retrieval introduces noise into the decision process that cannot be overcome. One implication is that people should be more accurate in predicting future events when trained on idealized rather than on the actual distributions of items. In other words, we predict the best way to convey information to people is to present it in a distorted, idealized form. Idealization of training distributions is predicted to reduce the harmful noise induced by immutable bottlenecks in people’s memory retrieval processes. In contrast, machine learning systems that selectively weight (i.e., retrieve) all training examples at test should not benefit from idealization. These conjectures are strongly supported by several studies and supporting analyses. Unlike machine systems, people’s test performance on a target distribution is higher when they are trained on an idealized version of the distribution rather than on the actual target distribution. Optimal machine classifiers modified to selectively and stochastically sample from memory match the pattern of human performance. These results suggest firm limits on human rationality and have broad implications for how to train humans tasked with important classification decisions, such as radiologists, baggage screeners, intelligence analysts, and gamblers.

Here are some clips from their text:

For probabilistic problems, such as determining whether a tumor is cancerous, whether it will rain, or whether a passenger is a security threat, selectively sampling memory at the time of decision makes it impossible for the learner to overcome uncertainty in the training domain. From a signal-detection perspective, selective sampling from memory results in noisy and inconsistent placement of the criterion across decision trials. Even with a perfect memory for all past experiences, a learner who selectively samples from memory will perform suboptimally on ambiguous category structures

Figure (A) Categories A (red curve) and B (green curve) are probabilistic, overlapping distributions. After experiencing many training items (denoted by the red A and green B letters), an optimal classifier places the decision criterion (dotted line) to maximize accuracy, and will classify all new test items to left of the criterion as A and all items to the right of the criterion as B. (B) Thus, the optimal classifier will always judge item S8 to be an A. In contrast, a model that stochastically and nonexhaustively samples similar items from memory may retrieve the three circled items and classify S8 as a B, which is not the most likely category. This sampling model will never achieve optimal performance when trained on ambiguous category structures. (C) Idealizing the category structures during training such that all items to the left of the criterion are labeled as A and to the right as B (underlined items are idealized) leads to optimal performance for both the optimal classifier and the selective sampling model.

Renewing our brain's ability to make decisions.

Our dopamine neurons, which enable enable our brains to make better choices, based on outcomes, gradually die off as part of the normal aging process.  Chowdhury and colleagues have now found that increasing dopamine levels in the brain of healthy older participants increased the rate with which they learned from rewarding outcomes and changed activity in the striatum, a brain region that supports learning from rewards. To relate brain activity and behavior, they utilized fMRI, diffusion tensor imaging, reinforcement learning tasks, and computational models of behavior. Their data might suggest that some variant of the dopamine therapy used for Parkinson's disease patient, might help older people make decisions. Here is their more technical abstract:

Senescence affects the ability to utilize information about the likelihood of rewards for optimal decision-making. Using functional magnetic resonance imaging in humans, we found that healthy older adults had an abnormal signature of expected value, resulting in an incomplete reward prediction error (RPE) signal in the nucleus accumbens, a brain region that receives rich input projections from substantia nigra/ventral tegmental area (SN/VTA) dopaminergic neurons. Structural connectivity between SN/VTA and striatum, measured by diffusion tensor imaging, was tightly coupled to inter-individual differences in the expression of this expected reward value signal. The dopamine precursor levodopa (L-DOPA) increased the task-based learning rate and task performance in some older adults to the level of young adults. This drug effect was linked to restoration of a canonical neural RPE. Our results identify a neurochemical signature underlying abnormal reward processing in older adults and indicate that this can be modulated by L-DOPA.