Workouts at the brain gym.

Patricia Marx writes an engaging article in The New Yorker, "Mentally Fit," that describes her foray into various regimes for building cognitive and emotional muscle, to stave off the declines in memory and attention capacity that come with aging, and are accelerated by vascular dementia and Alzheimer's pathology.

Staving off dotage is not cheap. According to a recent report issued by SharBrains, the amount spent on brain fitness in 2012 was more than a billion dollars, and by 2020, it is estimated, that figure will exceed six billion dollars. Most of the merchandise is some kind of software (note: which have been the subject of several MindBlog posts). …. to name just a few: Cogmed, Lumosity, Brain Games, Jungle Memory, Cognifit, MindSparke, MyBrainSolution, Brain Spa, brainTivity, Brainiversity, Brain Metrix, Mind Quiz, Your Brain Coach, Brain Exercise with Dr. Kawashima, Nintendo's Brain Age, MindHabits, NeuroNation, Happyneuron. There seem to be enough products to give each of your synapses its very own person-training program.

The cost of these programs ranges from zero to $1,500. The author chose BrainHQ, a platform offered by Posit Science, a San Francisco company co-founded by respected neuroscientist Michael Merzenich. It's exercises center around making your eyes and attention more childlike and sparky, countering the decay that makes the peripheral vision of a sixty-year-old three-quarters as panoramic as that of a twenty-year-old. After training for an hour a day over six weeks, scores in an array of different exercises were higher across the board. Merznich is probably correct in stating that the observed stronger, faster, more accurate and reliable brain performance after training comes from synaptic remodeling in the brain, a change that he says can persist for a year or more, but that does slips back past the neurological position that you were at when you began the training. (Motivated readers can email me to obtain a PDF of the article.)

Loneliness promotes inflammation in our bodies

Jaremka et al provide further data on how our social status reaches down to the most intimate details of our personal chemistry, with their present study providing details of how loneliness during stress turns on our inflammatory pathways, thus putting us at greater risk for health problems. Here's the abstract:

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 the 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 the second study, 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.

Markers of our aging

I thought I would point to this interesting piece in the New York Times about the search for some simple objective assay of our biological age, as distinct from our chronological age. We all know people who seems much older or younger than their actual age. Things like skin wrinkles or blood pressure are not a very useful indicator, because they can be confounded by factors unrelated to aging. Reliable biomarkers of aging could:

...tell us a lot about our current and future health. Tracking these indexes before and after starting a new diet or exercise program, for instance, might show you whether it was actually pushing off your decline and fall. Aging-rate tests could help scientists evaluate possible anti-aging compounds in humans without prohibitively long studies.

One study of older women age 65-69 found that 13 factors correlate with healthy aging, including the eye’s ability to pick out very lightly shaded images on white backgrounds, and the number of rapid step-ups on a low platform that subjects could complete in 10 seconds. A more promising approach is finding that a number of chemical tags on our DNA - epigenetic markers, which I have mentioned in previous posts - correlate with our biological age in a way that yields a signature of aging that is not changed by disease or ethnic background.

If this continuing research pans out, aging-rate tests may someday be standard in annual physicals, and tracking the results over time would offer unprecedented insights on health risks. But such tests also may well raise fractious privacy and social equity issues.

Insurers might demand that customers take them in order to set premiums for life and health care policies. The tests may also reveal how factors like exposure to environmental toxins and the stress of job loss accelerate aging, and by how much — fodder for lawsuits.

Some of us will be relatively short-lived, fast-aging “less fortunate,” and others will be long-lived, slow-aging “more fortunates,” predicted John K. Davis, a philosophy professor at California State University, Fullerton. And age discrimination will gain an entirely new meaning.

Unconscious activation of our brains' inhibitory controls.

Hepler and Albarracin have done the interesting experiment of exposing participants in an experiment to subliminally presented inaction (calm) and action (move) words, and then ascertaining that participants were unaware of these primers. They subsequently presented the participants with a Go/No-Go task (press a button if you see an "X", don't press it if you see a "Y") and also measured the P3 component of the event-related brain potential known to index inhibitory control. The subliminally presented inaction (calm) and action (move) words increased inhibitory neural activity whereas the latter set decreased it, relative to a control set of neutral words. Here is the author's summary:

-Event-related potentials were recorded during two go/no-go task with subliminal primes

-Subliminal primes related to general concepts of action, inaction, or were controls.

-Inaction/action primes strengthened/weakened inhibitory control mechanisms (ICMs).

-The primes had never been consciously associated with task responses or goals.

-This is the first demonstration that ICMs can operate completely unconsciously.

Although robust evidence indicates that action initiation can occur unconsciously and unintentionally, the literature on action inhibition suggests that inhibition requires both conscious thought and intentionality. In prior research demonstrating automatic inhibition in response to unconsciously processed stimuli, the unconscious stimuli had previously been consciously associated with an inhibitory response within the context of the experiment, and participants had consciously formed a goal to activate inhibition processes when presented with the stimuli (because task instructions required participants to engage in inhibition when the stimuli occurred). Therefore, prior work suggests that some amount of conscious thought and intentionality are required for inhibitory control. In the present research, we recorded event-related potentials during two go/no-go experiments in which participants were subliminally primed with general action/inaction concepts that had never been consciously associated with task-specific responses. We provide the first demonstration that inhibitory control processes can be modulated completely unconsciously and unintentionally.

Why does time speed up for older people?

I've come across two recent articles recently on how our experience of time is our own invention - "mind time" - that can be faster or slower than clock or calendar time. I find myself incredulous at how fast time seems to pass now compared with my recollection of when I was a 30 or 40-something and felt large periods of leisure in the midst of what was a much more complex (and productive) life than my current retired life (at 71 years of age). In general older people are more likely than younger to report that the last decade has passed quickly. The Friedman piece has a great quote from William James, who argued that the apparent speed of time's passage was a result of adult's experiencing fewer memorable events:

“Each passing year converts some of this experience into automatic routine which we hardly note at all, the days and the weeks smooth themselves out in recollection to contentless units, and the years grow hollow and collapse.”

From Friedman:

Why, then, do older people look back at long stretches of their lives and feel it’s a race to the finish? Here’s a possible answer: think about what it’s like when you learn something for the first time — for example how, when you are young, you learn to ride a bike or navigate your way home from school. It takes time to learn new tasks and to encode them in your memory. And when you are learning about the world for the first time, you are forming a fairly steady stream of new memories of events, places and people.

When, as an adult, you look back at your childhood experiences, they appear to unfold in slow motion probably because the sheer number of them gives you the impression that they must have taken forever to acquire… Most adults do not explore and learn about the world the way they did when they were young; adult life lacks the constant discovery and endless novelty of childhood.

Studies have shown that the greater the cognitive demands of a task, the longer its duration is perceived to be…Is it possible that learning new things might slow down our internal sense of time?…It’s simple: if you want time to slow down, become a student again. Learn something that requires sustained effort; do something novel…Take a new route to work; vacation at an unknown spot. And take your sweet time about it.

The second piece, by Maria Popova article points to Hammond's recent book "Time Warped: Unlocking the Mysteries of Time Perception" and offers a synopsis through multiple quotes, including descriptions of how fear slows down subjective time.

…when people with arachnophobia were asked to look at spiders — the very object of their intense fear — for 45 seconds and they overestimated the elapsed time. The same pattern was observed in novice skydivers, who estimated the duration of their peers’ falls as short, whereas their own, from the same altitude, were deemed longer.

...and the Holiday Paradox

…the contradictory feeling that a good holiday whizzes by, yet feels long when you look back.” (An “American translation” might term it the Vacation Paradox.) Her explanation of its underlying mechanisms is reminiscent of legendary psychologist Daniel Kahneman’s theory of the clash between the “experiencing self” and the “remembering self”….We constantly use both prospective and retrospective estimation to gauge time’s passing. Usually they are in equilibrium, but notable experiences disturb that equilibrium, sometimes dramatically. This is also the reason we never get used to it, and never will. We will continue to perceive time in two ways and continue to be struck by its strangeness every time we go on holiday.

...the difference in the number of novel experiences at different ages:

…we are most likely to vividly remember experiences we had between the ages of 15 and 25. What the social sciences might simply call “nostalgia” psychologists have termed the “reminiscence bump”…The key to the reminiscence bump is novelty. The reason we remember our youth so well is that it is a period where we have more new experiences than in our thirties or forties. It’s a time for firsts — first sexual relationships, first jobs, first travel without parents, first experience of living away from home, the first time we get much real choice over the way we spend our days. Novelty has such a strong impact on memory that even within the bump we remember more from the start of each new experience.

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.