iankirk.net

People divulge more sensitive information on sites that look less safe.

Researchers at Carnegie Mellon University have found that the appearance of website has a big effect on how honestly people answer personal questions put to them by the site. But paradoxically, it turns out we're more likely to spill our secrets on websites that appear less reputable. The way a website phrases questions also affects our willingness to disclose revealing information, the researchers found.

(author unknown)

In a bid to one-up their competition, Hyundai has announced that they will sell hydrogen fuel cell cars starting in 2012 – three years before Toyota, Honda and the rest of the competition. Seeing that renewable energy is becoming decidedly cheaper and that hydrogen fuel cell cars are more commercially viable than they were a year ago, Hyundai has said that will deliver the world’s first series production fuel cell vehicle in 2012, with 500 hydrogen vehicles rolling off the line that year and more afterwards.

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Archaeologist and anthropologist Timothy Taylor explains how a long-vanished artefact explains human evolution and led to "survival of the weakest." More » (Read on Source)Amanda Gefter

SHIFTboston is calling on architects, space-architects, scientists, engineers, urban designers, landscape designers, industrial designers, fashion designers, artists and futurists to submit their most provocative ideas for the moon.(author unknown)

I've long argued that we live in the nutritional dark ages where belief seems to trump science and evidence in the creation of nutritional public health policy and recommendations.

Moreover even in cases where science is purported to be a cornerstone (for instance Canada's Food Guide), I believe the wrong science is given too much sway.

Putting aside my concerns regarding the hijacking of Canada's Food Guide by the food industry and political interests, the Guide was built explicitly to ensure Canadians met their recommended dietary allowances of various nutrients and micronutrients and as I've noted before, the bulk of the science on the interaction of diet on chronic disease prevention centres on the consumption of different patterns of foods, not nutrients.

In an editorial that clearly nails my confirmation biases square on their heads, Drs. Dariush Mozaffarian and David Ludwig take on this madness, and they do such an amazing job discussing the issue that I'm going to reprint a pile of it for those without institutional journal access to read,"Nutritional science has advanced rapidly, and the evidence now demonstrates the major limitations of nutrient based metrics for prevention of chronic disease. The proportion of total energy from fat appears largely unrelated to risk of cardiovascular disease, cancer, diabetes, or obesity. Saturated fat—targeted by nearly all nutrition-related professional organizations and governmental agencies—has little relation to heart disease within most prevailing dietary patterns. Typical recommendations to consume at least half of total energy as carbohydrate, a nutrient for which humans have no absolute requirement, conflate foods with widely divergent physiologic effects (eg, brown rice, white bread, apples). Foods are grouped based on protein content (chicken, fish, beans, nuts) despite demonstrably different health effects. With few exceptions (eg, omega-3 fats, trans fat, salt), individual compounds in isolation have small effects on chronic diseases. Thus, little of the information found on food labels’ “nutrition facts” panels provides useful guidance for selecting healthier foods to prevent chronic disease.

In contrast with discrete nutrients, specific foods and dietary patterns substantially affect chronic disease risk, as shown by controlled trials of risk factors and prospective cohorts of disease end points. Fruits, vegetables, whole grains, and nuts are consistently associated with lower risk of disease. Fish consumption reduces risk of cardiac mortality, belying categorization with other protein sources. Conversely, processed meats, packaged and fast foods, and sugar sweetened beverages increase chronic disease risk. The effects of foods likely reflect complex, synergistic contributions from and interactions among food structure, preparation methods, fatty acid profile, carbohydrate quality (eg, glycemic index, fiber content), protein type, micronutrients, and phytochemicals. Healthy eating patterns share many characteristics, emphasizing whole or minimally processed foods and vegetable oils, with few highly processed foods or sugary beverages. Such diets are also naturally lower in salt, trans fat, saturated fat, refined carbohydrates, and added sugars; are higher in unsaturated fats, fiber, antioxidants, minerals, and phytochemicals; and are more satiating. Thus, a focus on foods increases the likelihood of consuming more healthy nutrients and fewer calories and decreasing chronic disease risk, whereas the opposite has arguably occurred through decades of nutrient-focused guidelines.

The nutrient-based approach may foster dietary practices that defy common sense. Countless highly processed products are now marketed in which refined carbohydrate replaces fat, providing an aura of healthiness but without actual health benefits. School nutrition guidelines specify a minimum number of total calories but a maximum proportion of fat calories, and foods like gelatin desserts and sugar-sweetened low-fat milk have been used to achieve these nutrient targets. Based primarily on consideration of a few nutrients, a national obesity prevention program categorizes whole-milk yogurt and cheese with donuts and french fries as foods to eat occasionally; sauteed vegetables and tuna canned in vegetable oil with processed cheese spread and pretzels as foods to eat sometimes; and fresh fruits and vegetables with trimmed beef and fat-free mayonnaise as foods to eat almost anytime. Taking the nutrient approach to self serving extremes, the food industry “fortifies” highly processed foods, like refined cereals and sugar-sweetened beverages, with selected micronutrients and recharacterizes them as nutritious. These marketing ploys provide little public health benefit and could potentially produce harm.

The prevailing nutrient-focused approach has broad consequences, influencing food-labeling priorities, school lunch and low-income food assistance policies, industry and restaurant product formulations, and public perceptions of healthier vs unhealthy foods. This focus contributes to confusion, distracts from more effective strategies, and promotes marketing and consumption of processed products that nominally meet selected nutrient cut points but undermine overall dietary quality. The relatively recent focus on nutrients parallels an increasing discrepancy between theory and practice: the greater the focus on nutrients, the less healthful foods have become. As national and international organizations update dietary guidelines, nutrient targets should largely be replaced by food-based targets. Such change would facilitate translation to the public, correspond with scientific advances in chronic disease prevention, mitigate industry manipulation, and remedy widespread misperceptions about what constitutes healthful diets.

Although this approach may seem radical, it actually represents a return to more traditional, time-tested ways of eating. Healthier food-based dietary patterns have existed for generations among some populations. Modern nutritional science now provides substantial evidence for how foods and food-based patterns affect health, guiding the design of more effective approaches for the prevention of chronic disease."AMEN! yonifreedhoff@gmail.com (Yoni Freedhoff)169165823984605761190723466898231602756313668192798155847539

The government's watching you, but who's watching the government? Trevor Paglen stalks black sites and covert facilities to capture images of the things you're not supposed to see.Pete Brook

Last August, our 18-year-old cat finally succumbed to chronic kidney disease, the most common cause of death for pet cats in the US. I am trying to turn the story of Denver (the cat) into a children's book about living with the trials and tribulations of chronic disease. Since I know nothing about non-academic publishing, I attended a workshop on the topic last spring (and blogged it here). Throughout my time in Boston, the instructors all hammered home the importance of platform. Not my usual platform; in this case, platform broadly means your credentials, and not merely in the academic sense. Do you get quoted in the media? Do you blog and twitter? Do you have a professional presence on facebook?  Do you control your domain? Seems that an appearance on Oprah is the current gold standard for platform. Some of these I could answer affirmatively; others required some work on my part. I'm still trying to get 25 folks to "like" my professional facebook page so I can get the vanity URL, but things are going pretty well for platform. Increasing web visibility, among other things, has probably helped my consulting work as well. [caption id="attachment_189" align="alignleft" width="210" caption="Growing Trend!"][/caption] Turns out many faculty pursue these options in a growing online trend reported August 19 at www.timeshighereducation.co.uk: "Increasingly, academics are looking for a way to create a digital presence that is not dependent on their current place of employment and that can go beyond the stodgy faculty pages at department websites with their mugshots and lists of courses and CVs," says Larry Cebula, an associate professor of history at Eastern Washington University who has a personal interest in the topic. Robert Levers, a  website designer in Boston, recently launched a special do-it-yourself website "package for professors"for $3,000. Last October Harvard announced a free website-creation package for academics called OpenScholar. Obviously, the trend must be strong. Another advantage I see is a permanent presence online. Right now my email and website could be linked solely to my current employer. By purchasing my domain and building my own site, I have a permanent place of contact, regardless of where my career may lead. As long as I keep renewing my hosting and registration agreements, I can be found at pascalelane.net. As with all things under the sun, some academic, somewhere is studying it: One of the few scholars to have carried out research specifically on academics' websites is Mike Thelwall, professor of information science at the University of Wolverhampton. In the five years since he has been examining the issue, he says, one of the biggest trends has been the move by university marketing departments to insist on standardisation for departmental and personal home pages. He isn't surprised, therefore, to have observed an increase in the number of academics opting to operate in a separate web space outside the institution's control. But Thelwall puts his comments in context. While a scholar's home page is overall "still an important presence to have" - particularly to allow other academics to keep track of you - it is less essential than it once was, with increasingly important roles played by Facebook for personal connections and Google Scholar for the location of papers. My own university "rebranded" last year. The new web design presents a host of difficulties aside from all the broken links that occurred with the initial roll-out. The colors and logo are ugly, and the site really cannot be browsed comfortably on a mobile device. The powers-that-be now have "standard templates" that we are told to use for brochures, research posters, and even PowerPoint slides. All of the fun and creativity gets sucked out of these things (if we follow the rules). No wonder I prefer to send people to my own site where I can choose the colors and organize materials as I see fit. I worry less about personal and academic connections. I have a facebook profile visible only to friends, those who should be seeing my vacation photos. Academic colleagues can find me through professional organization directories, LinkedIn, or by using Google. I'm not exactly hiding online. I do ask myself, in these public locations, how I would feel about my patients or their relatives reading each and every post. Some editing occurs, but less than you might think. Read the entire article. It includes tips for designing a website and links to faculty sites. Soon everyone may be master owner of their domain. Good to be on the leading edge of a trend, for once. Image courtesy of PhotoXpress.

“One Perfect Cube” by Florian Jenett is made of three synchronized clocks that form a sign every 12 hours for exactly one second. There’re actually 43200 constellations within every 12 hours.
This video is a time lapse of the work running for 24 hours.

found at CreativeApplications

The hunt of the hares is a recurring motif in the margins of medieval manuscripts, one I discussed here some time ago. For a quick refresher, the motif is just your average scene of hunters and hounds chasing rabbits with the principles reversed so that its the rabbits hunting the most dangerous game of all, etc. But this series of images from the lower margins of the British Library's MS royal 10 E IV* takes rabbit vengeance to the next level. We begin with a rabbit taking down a hunting hound with a volley of arrows:


You might think the hound is done for, but the marksmanship of the rabbit is Robinhoodian; the hound is merely wounded until he's weak enough to be captured by the rabbit and his buddies and tied up:


But the rabbits, it turns out, are not hunters at all. They're some sort of rabbit police force. Next stop for the hound is the rabbit judicial system, where he stands trial before a rabbit judge:


It's unclear if the jury was made up of hounds or hares, but the verdict is swift and certain. The hound is bound and carried in a cart to the gallows:


For you see, the sentence was death by hanging:


Poor hunting hound. Surely, society was to blame! But wait, there's one final insult. Flip the page of the manuscript and we find that some months later** the hound's grave is desecrated... by another hound!:


Bad, dog.  Bad!  But, I suppose this is merely a problem of insufficient anthropomorphizing. If the rabbits can run courts and hounds are competent to stand trial, surely hounds would know not to chew the bones of their kinsmen.

--

*The same manuscript I used for my vacation marginalia post. This thing is chock full of weirdness, so expect to see it a few more times in the coming months.
**Note the blue leaves of the weirdly shaped tree have turned orange in between.

noreply@blogger.com (Got Medieval)

There's been a lot of buzz and some scepticism about the
New brain scan to diagnose autismHere's a quick overview. Autism is believed to be a disorder of brain development. If so, it should be possible to diagnose it based on a brain scan. Unfortunately, it's not. You can't tell, from a scan, whether someone has autism or not. Not even if you're a world expert.

There are reports of various differences between autistic and non-autistic brains - a bit smaller here, a bit bigger there - but there's a lot of overlap. So at present, diagnosis of autism is purely based on symptoms.

Ecker et al, a team based at the Institute of Psychiatry in South London, made use of a mathematical technique called a Support Vector Machine (SVM) to try to spot differences that the naked eye can't. An SVM is a learning algorithm: you "teach" it to spot differences by showing it lots of examples. In this case, they showed it 20 autistic brains, and the brains of 20 healthy controls matched for age, gender, and IQ.

How does an SVM work? Imagine that there are two kinds of, say, fruit. Both are kind of round but A's are more spherical than B's. So you could draw a plot of sphere-ness, and find a line separating A and B:
An SVM is an automatic method of finding that line. How? It's complex, but fortunately you don't need to know (I don't). Of course, that's easy, but imagine that things got more tricky. As well as the variable of roundness, there's colour. Fruit B can be either spherical and dark, or non-spherical and light (maybe it's two different stages of ripeness).

An SVM could do this easily too:
Now suppose that there's 1000 different variables, and you want to find the "line" - actually a 1000-dimensional "hyperplane" (a line is 2D, a plane is 3D, anything with 4D or more is a hyper-plane) - dividing the "space" of possibilities into two.

For a human that's impossible, but not for an SVM. This is essentially what Ecker et al did. Each dimension of their "space" was the amount of grey matter at a particular point in the brain. So, they were training the SVM to distinguish between autistic brains and non-autistic brains, based on their shape, but in a much more complex way than a human could.

Did it work? Surprisingly well. Here's the end result (the multi-dimensional space has been helpfully compressed into 2D by the SVM):
It wasn't perfect, but the best approach, based on the cortical thickness in the left hemisphere, managed 90% accuracy, which is pretty awesome. Focussing on the headline 90% result is cherry-picking a bit, because using other variables, like cortical curvature, wasn't as good, but even the worst ones managed 70-85%, much better than chance (50%). Importantly, they also tried the system on 20 adults with ADHD, and it classified them as non-autistic. This shows that it's not just measuring "normality".

*

Now the question everyone's asking: is this going to be used for diagnosis in the real world any time soon? The first thing to remember is that this is a scientific paper, and this result is first and foremost of research interest: it provides clues towards the biology, and ultimately the causes, of autism.

But let's suppose you're a clinician and you have someone who you suspect may have autism, but you're not sure. They're a tricky one, a borderline case. You use this system on their brain and it says they are autistic. Should that factor into your decision? It depends. The fact is that rather than an either-or result, the SVM returns a distance from the hyperplane for each brain. You can see this clearly in the plot above.

In my opinion, if you have a borderline case, and the machine says he's borderline, then that's not much help, and it doesn't matter if he's just over the line, or not quite over it. You already knew he was borderline.

But if the machine says that he's deep into the autism space, then I think that is something. It tells you that his brain is very typical of people with autism. Interestingly, Ecker et al found that distance from the hyperplane correlated with symptom severity for "social" and "communication" symptoms (though not "repetitive behaviours"). That's a pretty cool result because the SVM wasn't trained to do that, it was trained to decide on an either-or basis.

What needs to happen next? As it stands, this system only works for adults: it would fail for children or teenagers, because their brains are a very different size and shape. Exactly the same SVM approach could be used in younger age groups, though, so long as the patients and the controls were the same age.

We also need to make sure that the SVM can tell the difference between autism and other conditions; Ecker et al showed that it could distinguish autism from ADHD, but that's only one comparison and it might not be the hardest one: I would want to see it tested against things like epilepsy, mental retardation, and dyslexia as well.

Overall though, this is very exciting work, and certainly a cut above most "Brain Scans To Diagnose Mental Illness" studies that make it into the headlines.

Full Discloser: I know some of the researchers involved in this work.

Links: The same team had a paper out a few months back, using a slightly less sophisticated SVM approach, which managed 80% accuracy. I wrote about another application of SVMs previously: How To Read Minds. This study has been blogged about at The New Republic and Dormivigilia.

Ecker C, Marquand A, Mourão-Miranda J, Johnston P, Daly EM, Brammer MJ, Maltezos S, Murphy CM, Robertson D, Williams SC, & Murphy DG (2010). Describing the brain in autism in five dimensions--magnetic resonance imaging-assisted diagnosis of autism spectrum disorder using a multiparameter classification approach. Journal of Neuroscience, 30 (32), 10612-23 PMID: 20702694

Researchers from the University of Calgary have cultivated neurons on silicon microchips for the first time. They used neurons isolated from mollusc Lymnaea, also known as the great pond snail, and cultured them for 2 to 4 hours over apertures on the chips forming so-called gigaseals. The microchip allows for high quality signal recording of individual neurons cultured directly on the chip's surface. So far they have used it to monitor individual neurons only, but the technique theoretically allows for simultaneous monitoring of multiple individual neurons engaged in synaptic connectivity. This will lead to a better understanding of neuronal communication and synaptic plasticity.

“This technical breakthrough means we can track subtle changes in brain activity at the level of ion channels and synaptic potentials, which are also the most suitable target sites for drug development in neurodegenerative diseases and neuropsychological disorders,” says Syed, professor and head of the Department of Cell Biology and Anatomy, member of the Hotchkiss Brain Institute and advisor to the Vice President Research on Biomedical Engineering Initiative of the U of C.

In addition, the chips are automated, making them much easier to use than the traditional patch-clamp techniques used for neuronal studies. The findings are published online in this month's Biomedical Devices.

Press release: Neurochip technology developed by Canadian team

Article abstract: High-fidelity patch-clamp recordings from neurons cultured on a polymer microchip...

Dara Birnbaum, MTV Artbreak, 1987

Got a short attention span? If so, be sure to put aside Wednesday evening for Electronic Arts Intermix's Summer Screening "Short Shorts." Drawing from EAI's massive archive of video art, all the works in the screening are under 2 minutes long - meaning that forty-five works will be shown during the entire duration of this forty-five minute screening. Blink or you'll miss it, seriously. "Short Shorts" includes work by Dan Asher, Beth B, Phyllis Baldino, Michael Bell-Smith, Dara Birnbaum, Cheryl Donegan, VALIE EXPORT, Forcefield, Matthew Geller, Gran Fury, Gary Hill, Ken Jacobs, Tom Kalin, Kalup Linzy, George Maciunas, Charlotte Moorman, Shana Moulton, Yoko Ono, Dennis Oppenheim, Nam June Paik, Martha Rosler, Paul Sharits, Stuart Sherman, Shelly Silver, Michael Smith, Leslie Thornton, Steina and Woody Vasulka, Lawrence Weiner and Bruce and Norman Yonemoto. Event begins at 6:30 at EAI in Chelsea.

Ceci Moss

Players of the online game Foldit have beaten dedicated software and human experts in working out the shape that will be adopted by novel proteins

(author unknown)0080998893582403715106955930984792814136131522643271010038771741689922565067343602147826371056247226

Thousands of Foldit players who outperformed the best known computer program designed for the task are credited in a new journal article. (Read on Source)JOHN MARKOFF

The digital offspring of researchers at Michigan State University "live" in a computer and replicate using strings of computer code instead of DNA. An article in New Scientist reports that they might even eventually evolve to become artificially intelligent life forms. ...(author unknown)

There’s an interesting new paper in Biological Psychiatry on the genetic variations underlying human personality. The study relied on a standard inventory of temperaments – novelty-seeking, harm avoidance, reward dependence and persistence – as measured in 5,117 Australian adults. What did the scientists find? Mostly nothing. The vast genetic search came up empty:

Participants’ scores on Harm Avoidance, Novelty Seeking, Reward Dependence, and Persistence were tested for association with 1,252,387 genetic markers. We also performed gene-based association tests and biological pathway analyses. No genetic variants that significantly contribute to personality variation were identified, while our sample provides over 90% power to detect variants that explain only 1% of the trait variance. This indicates that individual common genetic variants of this size or greater do not contribute to personality trait variation, which has important implications regarding the genetic architecture of personality and the evolutionary mechanisms by which heritable variation is maintained.

There has been a longstanding debate among psychologists about the proper way to measure and define human personality. On the one hand, there are plenty of researchers and clinicians who endorse tests like the Myers-Briggs Type Indicator (MBTI), which seeks to categorize people based on a series of supposedly innate personality dichotomies. (You’ve probably taken this test, and been given a summary in capital letters that describes your tendencies towards extraversion, intuition, judgement, etc.) On the other hand, there’s a camp of scientists which argues that these vague categories are mostly meaningless, and that asking people a few dozen multiple choice questions is a terrible way to summarize the soul. Walter Mischel (who I wrote about here, in the New Yorker) is one of these scientists. In 1958, while a young researcher at Harvard, he was asked to develop a survey course on “personality assessment.” Mischel quickly concluded that, while prevailing theories held personality traits to be broadly consistent – a shy person was always shy – the available data didn’t back this up. In fact, Mischel soon concluded that human personality, at least as it was then conceived, couldn’t be reliably assessed at all. A few years later, he was hired as a consultant on a personality assessment initiated by the Peace Corps. Early Peace Corps volunteers had sparked several embarrassing international incidents—one mailed a postcard on which she expressed disgust at the sanitary habits of her host country—so the Kennedy Administration wanted a screening process to eliminate people unsuited for foreign assignments. Volunteers were tested for standard personality traits, and Mischel compared the results with ratings of how well the volunteers performed in the field. He found no correlation; the time-consuming tests predicted nothing. At this point, Mischel realized that the problem wasn’t the tests—it was their premise. Psychologists had spent decades searching for traits that exist independently of circumstance, but what if personality can’t be separated from context?

And so Mischel began a longstanding research program that sought to deconstruct the myth of personality. One of his classic studies documented the aggressive behavior of children in a variety of situations at a summer camp in New Hampshire. Most psychologists assumed that aggression was a stable trait, but Mischel found that children’s responses depended on the details of the interaction. The same child might consistently lash out when teased by a peer, but readily submit to adult punishment. Another might react badly to a warning from a counsellor, but play well with his bunkmates. Aggression was best assessed in terms of what Mischel called “if-then patterns.” If a certain child was teased by a peer, then he would be aggressive.

This led Mischel to construct a new metaphor for human personality. While modern psychology still clung to a model of personality rooted in the humors of the ancient Greeks – we were born with a certain amount of choleric temperament and that was it – Mischel proposed a model of personality called interactionism. One of his favorite metaphors for interactionism concerns a car making a screeching noise. How does a mechanic solve the problem? He begins by trying to identify the specific conditions that trigger the noise. Is there a screech when the car is accelerating, or when it’s shifting gears, or turning at slow speeds? Unless the mechanic can give the screech a context, he’ll never find the broken part. Mischel wanted psychologists to think like mechanics, and look at people’s responses under particular conditions.

And this might be why the Australian study came up empty: We’re trying to find the genes for personality constructs that don’t exist. It’s not that people don’t have personalities, or that these personalities can’t be measured – it’s that we aren’t the same person in every situation, which is what all these “tests” implicitly assume. It turns out that Shakespeare had it right all along. Just look at Hamlet – the Danish prince wouldn’t fit neatly into the categories of Myers-Briggs. He’s brooding and melancholy in one scene, and then violent and impulsive in the next. But this doesn’t seem strange to the audience. Instead, the inconsistency of Hamlet seems all too human.

Via The Neurocritic, who adds many more interesting thoughts.

CREDIT: RYAN SNOOK (from Holden, 2008).


The latest search for genetic variants that underlie differences in personality traits has drawn a blank (Verweij et al., 2010). The researchers conducted a genome-wide association study using personality ratings from Cloninger's temperament scales in a population of 5,117 Australian individuals:
Participants' scores on Harm Avoidance, Novelty Seeking, Reward Dependence, and Persistence were tested for association with 1,252,387 genetic markers. We also performed gene-based association tests and biological pathway analyses. No genetic variants that significantly contribute to personality variation were identified, while our sample provides over 90% power to detect variants that explain only 1% of the trait variance. This indicates that individual common genetic variants of this size or greater do not contribute to personality trait variation, which has important implications regarding the genetic architecture of personality and the evolutionary mechanisms by which heritable variation is maintained.But it's still fun and popular for some science writers to assert that personality traits are "hard wired" into our brains, like there's really A Brain Circuit for Bungee Jumping? [thanks for the exciting new info, ScienceNOW.] In reality, some of the major early findings in personality genetics, such as an association between Novelty Seeking and the Dopamine D4 Receptor gene (Benjamin et al., 1996; Ebstein et al., 1996), have failed to replicate (Gelernter et al., 1997; Paterson et al. 1999; Strobel et al., 2002). Fortunately, others writers have pointed out the increasingly obvious difficulties of this endeavor, as did Constance Holden in Parsing the Genetics of Behavior:For some of us, it's satisfying to attribute social awkwardness to anxiety genes or to think that the driver who cuts off other cars as he zips across lanes is pumped up by the "warrior" gene. Was it a bad dopamine receptor gene that made author Ernest Hemingway prone to depression? Can variations in a vasopressin receptor gene--a key to monogamy in voles--help explain adulterous behavior?

But as scientists are discovering, nailing down the genes that underlie our unique personalities has proven exceedingly difficult. That genes strongly influence how we act is beyond question. Several decades of twin, family, and adoption studies have demonstrated that roughly half of the variation in most behavioral traits can be chalked up to genetics. But identifying the causal chain in single-gene disorders such as Huntington's disease is child's play compared with the challenges of tracking genes contributing to, say, verbal fluency, outgoingness, or spiritual leanings. In fact, says Wendy Johnson, a psychologist at the University of Edinburgh, U.K., understanding genetic mechanisms for personality traits "is one of the biggest mysteries facing the behavioral sciences."

Nonetheless, unscrupulous businesses like My Gene Profile (which offers the "Inborn Talent Genetic Test" for the low low price of $1,397) have capitalized on the public's desire for simple explanations. Now you can find out whether your child has the Split Personality Gene! The Propensity for Teenage Romance Gene! The Self Detoxifying Gene!

Returning to the current study, the authors cast a genome-wide net to find genetic variants related to the four dimensions of temperament identified by Cloninger in his Temperament and Character Inventory (TCI), a 240 item self-report questionnaire. As described by Verweij et al., (2010):
Novelty Seeking reflects the tendency to respond strongly to novelty and cues for reward as well as relief from punishment, and is thought to play a role in the activation or initiation of behaviours. Harm Avoidance reflects the tendency to respond strongly to aversive stimuli, which leads to learned inhibition of behaviour, and is thought to play a role in the inhibition or ceasing of behaviours. Reward Dependence reflects the tendency to react strongly to rewards and to maintain behaviours previously associated with reward or relief of punishment, and is thought to play a role in the maintenance or continuation of behaviour. Persistence reflects the tendency to persevere despite frustration and fatigue.The participants completed a short form of Cloninger's (1986) original Tridimensional Personality Questionnaire (TPQ).1 The fourth dimension of temperament -- Persistence -- was constructed using a small subset of the Reward Dependence questions. The 1986 version of Cloninger's biosocial theory of personality associated Novelty Seeking with low dopamine activity, Harm Avoidance with high serotonin activity, and Reward Dependence with low noradrenaline activity. These were thought to be independent and heritable aspects of personality that influence responses to reward, punishment, and novelty. The TPQ was later revised to include Persistence and also three character dimensions (Self-Directedness, Cooperativeness, and Self-Transcendence) to form the basis of the TCI (Cloninger et al., 1993).

Cloninger's theory of personality is not without its critics. In 2008, Farmer and Goldberg challenged the psychometric validity of the TCI in a target article and in a wonderfully titled reply to Cloninger. A trenchant quote from the latter (Farmer & Goldberg, 2008) is below:
Overall, several core theoretical assumptions and predictions associated with the psychobiological model and TCI-R assessment are either non-falsifiable, in conflict with each other, or not supported by empirical evidence. So the question arises, are we dealing with a flawed set of personality constructs to begin with? No matter. The scales are widely used, so we'll go on.

For genotyping, single nucleotide polymorphisms (SNPs) across the entire genome were tested for association with each of the four traits. The Illumina and Affymetrix platforms were used. [Those technical and statistical methods are beyond the scope of this blog, so I will leave it to someone else to describe and critique the genotyping aspects of the paper.] Stated succinctly, the results showed that:
No SNPs reached genome wide significance (α = 7.2*10-8) and the SNP with the lowest p-value for each personality scale explains less than 0.5% of the total variance.None of the previously identified candidate genes (e.g., serotonin receptor gene, D4 receptor gene) were close to showing a significant relationship with any trait, nor were any of the SNPs with the lowest p value for each trait "in or close to a gene of known relevant function." The authors conclude that "common genetic variants do not contribute substantively to variation in personality." How can this be the case, when 30-60% of the variance in personality should be explained by genetics?
This raises the question of "missing heritability"... Missing heritability has been observed to a large extent in almost all complex traits. Proposed explanations focus on: many variants of very small effect that are yet to be found; rare variants that are poorly detected by available genotyping arrays that focus on variants present in at least 5% of the population; structural variants poorly captured by existing arrays, such as copy number variations; and low power to detect epistasis (interaction between genes). Newer technologies (e.g. whole genome sequencing) and novel statistical approaches combined with larger samples and meta-analyses will contribute to our understanding of the genetic architecture of complex traits.

So don't rush out and spend $1,397 on the Inborn Talent Genetic Test just yet...

Footnote

1 Note that the participants did not complete the full TCI. Did that make a difference? Perhaps not, since two previous GWAS failed to find anything for Eysenck's Neuroticism scale or for the Big Five personality traits.

References

Benjamin J, Li L, Patterson C, Greenberg BD, Murphy DL, Hamer DH. (1996). Population and familial association between the D4 dopamine receptor gene and measures of Novelty Seeking. Nat Genet. 12:81-4.

Cloninger CR. (1986). A unified biosocial theory of personality and its role in the development of anxiety states. Psychiatr Dev. 4:167-226.

Cloninger CR, Svrakic DM, Przybeck TR. (1993). A psychobiological model of temperament and character. Arch Gen Psychiatry 50:975-90.

Ebstein RP, Novick O, Umansky R, Priel B, Osher Y, Blaine D, Bennett ER, Nemanov L, Katz M, Belmaker RH. (1996). Dopamine D4 receptor (D4DR) exon III polymorphism associated with the human personality trait of Novelty Seeking. Nat Genet. 12:78-80.

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An end to the blogging hiatus at last! I hope to entertain you with the fascinating story on how female wasps got rid of their men and sex in return for bacterial endosymbionts..

Despite the obvious benefits of pleasure and procreation, sex has other advantages. The genetic material of both parents gets mixed in new and unforeseen ways (like a genetic wheel of fortune) whenever a sperm and egg cell fuse. The near ubiquity of sex in the animal world should be enough proof that sex is a good way to increase the genetic variance in the population for these species.

Yet asexual species (parthenogenic species, as biologists call them) pop up every now and then during evolution. One of the most fascinating examples I recently came across is that of the parasitic wasp, Trichogramma, which is often used as biological pest control. While some of these wasp populations exclusively consist of females, this state of asexuality is not some funky route of evolution, it is induced by bacteria!

A Trichogramma wasp parasitizing on the eggs of another insect.

The mood killer in question is a particular species of Wolbachia. These bacteria inhabit the cytoplasm of their host cells. Since sperm cells don’t have any cytoplasm, male wasps are a dead end as far as Wolbachia is concerned. The only way it can be transmitted from generation to generation is via the egg cells (which do have cytoplasm) that develop into female wasps. Normally, unfertilized haploid egg cells develop into male wasps whereas the fertilized egg cells become diploid and develop into female wasps. The Wolbachia messes with mitosis in such a way that every unfertilized egg is diploid, so that only females are born.

In some populations of Trichogramma, the Wolbachia infection rate has reached 100% and males are no longer born. There’s hope for the poor wasp guys though: by treating the wasps with antibiotics, the Wolbachia die out and new male wasps can be born. These male wasps are completely normal: they can inseminate female wasps and their sperm is viable. However, the females from these previously infected populations do not use the sperm to fertilize the eggs. They have become completely dependent on their symbiont for their reproduction.

Without male wasps around to admire her, The Wasp eventually married Ant Man.

This loss of female and retention of male sexual function is fascinating. If all things were equal, both male and female genes necessary for sexual reproduction would erode away at the same rate. Since the males are sexually viable while the females are not, something else must be happening. Stouthamer and colleagues provide an interesting explanation in a recent paper published in BMC Evolutionary Biology. By modelling infection rates, wasp mating and mutation rates they found that a ‘functionaly virginity mutation’ affecting the fertilization rate in females is likely responsible for fixing asexuality in the female population.

The basic gist is that in the initial phase of infection, males will have higher mating rates because there are females aplenty and less males being born. In uninfected females, alleles that reduce fertilization rates (less fertilization, more males!) are being selected for. The uninfected females will produce fewer uninfected daughters and more males that carry the same ‘virginity mutation’. A ratchet is now in place that leads to the fixation of both the infection and the virginity mutation:

Only those females that are not yet homozygous for the mutation will mate and part of their offspring will become homozygous for the mutation. Consequently the class of females that is homozygous for the mutant allele and infected will grow relative to the class of females that is not yet homozygous and infected.

The number of uninfected females capable of normal fertilization dwindles – spelling the end for men and sex. Poor guys. Seriously though, trading in sex for a bacterial endosymbiont.. Where’s the fun in that?

Stouthamer R, Russell JE, Vavre F, & Nunney L (2010). Intragenomic conflict in populations infected by Parthenogenesis Inducing Wolbachia ends with irreversible loss of sexual reproduction. BMC evolutionary biology, 10 (1) PMID: 20667099

I have experienced a simple version of web monitoring myself: since simply checking out some office chairs at some obscure shopping website, almost every website I visit (including my own blog) is plastered with multiple Google Ads of that specific shop. After several weeks, the office chair issue is long vanished, but the ads still persist. Where can I opt out please?

What They Know [wsj.com] is an interactive graph by the Wall Street Journal, illustrating the degree to which the 50 most popular websites exposes visitors to monitoring (think cookies, beacons, Flash cookies and the like, which together reveal large parts of your past browsing patterns).

Each red slice at the top represents a unique website, like msn.com or photobucket.com. Each website tends to send hundreds of tracker files to third-party websites, such as Google, AOL, Yahoo, or Microsoft. Figure out yourself why Google (26 trackers) seems like an angel next to privacy-grabbing websites such as merriam-webster.com (131 trackers) or careerbuilder.com (118 trackers).

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Google Ventures and CIA's investment arm fund Recorded Future, a start-up that monitors Web and connects dots between people, places, events, Wired says. (Read on Source)Elinor Mills