Unconditional love in the brain?

From time to time we bring you the quirky side of neuroscience here at BrainEthics. Now, we discover a funny little study in Psychiatry Research: Neuroimaging that bears the attractive title “The neural basis of unconditional love” by Mario Beauregard et al. Indeed, the study of the neural bases of preference formation, aesthetics and even love have gained much momentum since this field started just a few years ago. Fields such as neuroaesthetics and neuroeconomics seem to overlap when it comes to these studies, in which the core aim is to study the fundamental processes underlying preference formation.

In the study, Beauregard and colleagues wanted to establish the neural bases of unconditioned love. So the first tricky thing would be to define and operationalise what is meant by “unconditioned love”. IMO, such kind of love is the affectionate feelings one would call religious love, or ultimate altruism…(if such ever exists).But following the name, it does suggest a broader definition of affectionate feelings towards a person (or just any thing?) regardless of their origin, persona, deeds or misdeeds, family bonds and so forth.

Claimed amygdala deactivation during maternal love, which rather looks like collateral sulcus/entorhinal cortex... (from Bartels & Zeki 2004)

Similar studies of strong affectional feelings to other persons have been conducted recently. For example, in a study of maternal love (PDF) by Bartels and Zeki, mothers were scanned while looking at baby faces, in which sometimes their own newborn’s face was shown. The researchers found that when looking at their own babies, compared to looking at other infants, mothers demonstrated stronger activation in regions such as the ventral striatum/nucleus accumbens, ventro-anterior cungulate cortex and fusiform cortex.

In addition, and to the researchers’ surprise, they also found stronger bilateral activation of the anterior insula, a structure typically involved in aversive functions (but I will not follow the speculative account of the researchers on this activation). Deactivations were claimed to be found in regions such as the amygdala – which really is not amygdala, but rather collateral sulcus, judging from their figure (see figure on right). Isn’t is strange that prominent researchers such as Semir Zeki goes so wrong in neuroanatomy? The consequences from arguing for deactivation in the entorhinal cortex, compared to the amygdala, is dramatic. Instead of talking about emotions, one would be more prone to talk about complex visual processing. Yes, it does matter where you think your blobs are…

So what did Beauregard and colleagues do differently? First, they needed to describe the uncondition love construct, which they describe as:

(…) distinct from the empathy and compassion constructs. Empathy is commonly defined as an affective response that stems from the apprehension of another’s emotional state (e.g., sadness, happiness, pain), and which is comparable to what the other person is feeling (Eisenberg, 2000). This affective response is not unconditional and does not involve feelings of love. Compassion refers to an awareness of the suffering of another coupled with the desire to alleviate that suffering (Steffen and Masters, 2005). In contrast to compassion, unconditional love is not specifically associated with suffering.

Hm, not a particularly good definition to go hunting for neural correlates to. Nevertheless, the aim was to study the neural basis of unconditional love, something that has not been done before. So how did they do it? First, the authors had to select the subjects:

Participants were assistants in two l’Arche communities located in the Montreal area. L’Arche communities (founded by Jean Vanier in 1964) are places where those with intellectual disabilities, called core members, and those who share life with them, called assistants, live together. This special population was selected on the basis that one of the most important criteria to become an assistant is the capacity to love unconditionally. (We recruited) assistants with a very high capacity for unconditional love. We ensured that all recruited individuals understood the meaning of this form of love (based on the construct presented in Section 1) and found their work at l’Arche (community help service) very gratifying.

The hypotheses were 1) unconditional love is rewarding, and therefore it was expected to be associated with activation of the VTA and dorsal
striatal regions; and 2) since unconditional love experientially differs to a large extent from romantic love and maternal love, it was predicted that this form of love would be mediated by brain regions not involved in romantic love and maternal love. I particularly hate this second hypothesis: it’s not really a hypothesis, because ANY activation that is “different” can confirm this hypothesis. If it’s a fishing trip, let us know…

Let me try a bit of further deconstructionism of this study. In the methods section, it is described how the subjects were instructed to look at unfamiliar faces and either attempt to feel unconditioned love or think about the person’s intellectual capacity (sic.).

A blocked-design was used to examine brain activity during a passive viewing (PV) condition (control task) and an unconditional love (UL) condition (experimental task).

Note: using block designs are typically used to study differences in state (e.g. comparing neural activation during different attentional states).

Five blocks of pictures were presented during both conditions. Each block consisted of a series of four pictures. Each picture was presented during 9 s (pre-experimentation revealed that, on average, participants needed that long to feel unconditional love toward the individuals depicted in the pictures).

OK, so some of the activation differences between the UL condition and the PV condition may be due to task difficulty and reaction time, and not, as they would have wanted, the nature of the task.

Blocks were separated by periods of 30 s. Pictures depicted individuals (children and adults) with intellectual disabilities. These individuals were unfamiliar to the participants. Instructional cue words (“View”, “Unconditional love”) printed in white first appeared in the center of a black screen for 2 s. While the picture remained on the screen, participants performed the tasks specified by the prior cue. In the PV blocks, participants were instructed to simply look at the individuals depicted in the pictures. In the UL blocks, participants were instructed to self-generate a feeling of unconditional love toward the individuals depicted in the pictures.

OK, there are many assumptions here… Just to illustrate, do the following for me: close your eyes and for 20 seconds DO NOT THINK ABOUT AN ELEPHANT!!! What happens? Well, you’d probably be surprised to see that elephant does really appear in your mind even if you try to suppress it. Thought suppression studies have demonstrated this through the past many decades. So IMO, what the study might also be about is thought suppression – or comparing elephant thinking to elephant-suppression activation. IOW, I’m not sure that the viewing condition did not evoke some “unconditioned love”-suppression.

Therefore, the UL task involved both a cognitive component (self-generation) and an emotional–experiential component (feeling). Blocks were presented in alternation (PV, UL, PV, UL, etc.). At the end of each block for both experimental conditions, a four-point scale (1 = “No feeling”, 2 = “Some feeling”, 3 = “Moderate”, 4 = “Very intense”) for rating the extent to which they currently felt unconditional love was presented for 3 s.

Strangely, what the researchers found when doing the UL minus PV comparison, was stronger activation in “the middle insula, superior parietal lobule, right periaqueductal gray, right globus pallidus (medial), right caudate nucleus (dorsal head), left ventral tegmental area and left rostro-dorsal anterior cingulate cortex.” This can be seen in the figure below:

Regions showing stronger activation during "unconditional love" condition

So what are the interpretations of these results? Does it surprise you that both hypotheses were confirmed? First, that unconditioned love was related to reward structure activation was not surprising. But the researchers over-interpret the results: they claim that this is prima facie proof that unconditioned love is rewarding. But hey, the results can just as well suggest that the unconditioned love state is just a framing of how we look at faces (for example, imaging you are either told that person/face X is a wonderful person OR an evil sadistic terrorist).

Second, is it surprising that they also found “activation not found for maternal or romantic love”? Not to me: the tasks are different, the selection of subjects are different, the confounds are plenty…

And what about that strong and bilateral insula activation? Yes, it’s right that it confirms the second hypothesis…but how does the insula play a role in unconditioned love? As I noted in my previous post, it does seem to play an important role in negative emotions and aversion. Here, the authors assert:

There is increasing evidence that the insula is implicated in the representation of bodily states that colour conscious experiences (or “background feelings”) (…) it is plausible that the middle insular activation noted during the UL condition was associated with the somatic and visceral responses elicited by the presented pictures.

Uh yes, but this is typically reflected in negative emotions. So how is unconditioned love related to aversion? Or maybe one could relate the findings to a recent review that suggest a role for the insula in addiction and urges? I don’t know, if you’re into speculating, go with whatever seems to work… Basically, this handwaving interpretations is not much better than old-style phrenology or hand-reading. They may be right, but only because they make the right guesses from previous studies.

Briefly put, although we enjoy the quirky side of neuroscience, and how it can be used to explore human nature, we at BrainEthics are also sceptical at the level at which quirky science turns into flaky science.

-Thomas

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Two ways of reducing fear

Emotional reactions may come in many forms and have different causes. But one of the main responses is the fear response, which has been shown to involved the amygdala. Different nuclei of the amygdala may contribute differentially to the fear response process.

One vital feature of emotion and amygdala is that emotional responses can be reduced, and eventually diminish. This is one of the basic mechanisms at play when we habituate to (or even extinguish) fearful stimuli. But is is also possible to reduce fear responses through more controlled processes, what has been termed cognitive emotion regulation. Such basic cognitive mechanisms underlie the psychological treatment of, e.g., phobias. In other words, there are two ways of reducing fear responses of the amygdala: 1) through habituation/extinction and 2) through cognitive (“rational”?) processing.

However, the exact neurobiological nature of these processes have been unknown. In a recent paper in Neuron, authored by Mauricio Delgado, and including prominent emotion researchers such as Joseph LeDoux, Elisabeth Phelps, looks at precicely this relationship. Using an emotion regulation strategy, the researchers compared the brain mechanisms (using fMRI) for conditioned fear regulation and for classic extinction.

From the methods section, one can read:

Each trial began with the presentation of a word cue, presented for 2 s, which instructed the participant on the type of trial. It was followed by either a blue or yellow square that served as a conditioned stimulus (CS) and was presented for 4 s. A mild shock to the wrist served as the unconditioned stimulus (US) and was administered during the last 200 ms for six of the CS trials. During one experimental session, a specific colored square (e.g., blue) was paired with the US, thus serving as the CS+, while the other square (e.g., yellow) served as the CS−. This contingency was counterbalanced across participants. The trial concluded with a 12 s intertrial interval.

When instructed to “attend,” participants were asked to view the stimulus and attend to their natural feelings regarding which CS was presented. In these Attend trials, for example, participants might focus on the fact that they may receive a shock (if the cue was followed by a CS+) or would never receive a shock (if the cue was followed by a CS−). When instructed to “reappraise,” participants were asked to view the CS and try to imagine something in nature that was calming, prompted by the color of the CS. During these Regulation trials, for example, participants could think of an image of the ocean or a blue sky when viewing the blue square, or they could think of the sunshine or a field of daffodils when viewing the yellow square.

During both cases of fear reduction, the amygdala (red in top image) activation level went from high to low, for both What the researchers found was that during extinction learning, the ventromedial prefrontal cortex (orange in top) showed a higher activity, and this was thought to cause the observed reduction in amygdala activation. In contrast, cognitive emotion control lead to a higher activation in the dorsolateral PfC (blue in top image).

So this is a very nice demonstration of two different mechanisms of emotion regulation. However, it stills seems open to me whether the two are overlapping or very different mechanisms. One way of assuming the relationship is that the dorsolateral PfC works through the ventromedial PfC on regulating the amygdala. However, it may also be possible that the dorsolateral PfC bypasses the ventromedial PfC altogether. By comparing the activation patterns of all three structures, the findings suggested that the dorsolateral PfC works on the amygdala through the ventromedial PfC. Or, as put by the authors:

Our results support a model in which the lateral PFC regions engaged by the online manipulation of information characteristic of cognitive emotion regulation strategies (for review see Ochsner and Gross, 2005) influences amygdala function through connections to vmPFC regions that are also thought to inhibit the amygdala during extinction (Milad and Quirk, 2002). These results are consistent with the suggestion that vmPFC may play a general regulatory role in diminishing fear across a range of paradigms (e.g., [Kim et al., 2003] and Urry et al., 2006 H.L. Urry, C.M. van Reekum, T. Johnstone, N.H. Kalin, M.E. Thurow, H.S. Schaefer, C.A. Jackson, C.J. Frye, L.L. Greischar, A.L. Alexander and R.J. Davidson, Amygdala and ventromedial prefrontal cortex are inversely coupled during regulation of negative affect and predict the diurnal pattern of cortisol secretion among older adults, J. Neurosci. 26 (2006), pp. 4415–4425. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (55)[Urry et al., 2006]).

The implications of these findings may be plenty, but a few immediately comes to mind: first, the identification of the dorsolateral PfC in controlling emotions may, in general, be used as a marker for emotional regulation in different psychological states. Lie detection may be one issue, and studies of implicit racism seem to suggest the same. Another interesting consequence is in the modelling of the phylogeny and ontogeny of emotion regulation in primates. The present results may suggest that the dorsolateral PfC role in emotion regulation has occurred later in primate evolution, and that it works through a more “ancient” ventromedial PfC basic regulation of the amygdala. It may even be possible that developmental studies can show that the later maturation of the dorsolateral PfC also corresponds to the development of emotional control. Finally, this idea may also serve as a good model for studying brain injury and the consequences of emotion regulation.

-Thomas

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Serotonin and value-based decision making

Can antidepressive medicine alter your decision behaviour? A recent paper in Science now demonstrates that alterations in subjects’ serotonin levels leads to significant changes in their decision making behaviour. In the study, subjects were set to play the Ultimatum Game repeatedly. Subjects had to do the task two times at two different days, and at one of the days they were administered an acute tryptophan depletion (ATD), i.e., their serotonin levels would drop for a period of time. The design was double-blind and placebo controlled.

The Ultimatum Game is an experimental economics game in which two players interact to decide how to divide a sum of money that is given to them. The first player proposes how to divide the sum between themselves, and the second player can either accept or reject this proposal. If the second player rejects, neither player receives anything. If the second player accepts, the money is split according to the proposal. The game is played only once, and anonymously, so that reciprocation is not an issue.

What the researchers found was that the ATD led subjects to reject more offers, but only unfair offers. That is, ATD did not interact with offer size per se, and there was no change in mood, fairness judgement, basic reward processing or response inhibition. So serotonin seemed to affect aversive reactions to unfair offers.

The study is a nice illustration of how we now are learning to induce alterations in preferences and decision making. Along with other studies using, e.g., oxytocin to increase trust in economic games (see also my previous post about this experiment), one may expect that increasing the serotonin level may actually make subjects less responsive to unfair offers.

This knowledge is also important to learn more about, as it poses a wide range of ethical problems. If our preferences and decisions are really influenced by these stimuli, can this be abused? It should be mentioned that many of these substances are not necessarily detected (oxytocin is odourless), so we may be influenced without our consent or knowledge. The wide applicances could include casinos, stores (e.g. for expensive cars), dating agencies and so on. If we did not accept subliminal messages in ads, how can we accept this?

-Thomas

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Brain plasticity and sexual aberrations

I’m having the pleasure of reading The brain that changes itself by Norman Doidge, as a reviewer for a potential translation here in Denmark. Brain plasticity, or neuroplasticity, has always been a hot topic, from it’s (re)birth in modern neuroscience, and all the way up until today, where researchers are still fiercely debating how plastic the brain is and how functions relate to brain structures – aka the debate of modularism. In its early days, the neuroscientific community strongly believed that the modularity of the brain was established during childhood, and that little, if any, change could occur later on. Researchers suggesting otherwise were eschewed, heavily criticized on the ground that their data/ideas did not fit into the existing model. The land did not fit onto the map, so to say. This book is dedicated to the idea of neuroplasticity.

The book introduces brain plasticity in a very vivid and close-up manner, as Doidge tells the story from the inside, through some of the biggest names in this research, including the late Paul Bach-y-Rita, Michael Merzenich, and Gerald Edelman. Not only is the book very interesting to read as a historical background, but it also takes a look behind the scenes in two ways. Doidge has talked the researchers himself, and bring their experience of how plasticity came to go from a ignored (and carreer risky business) field, to a scientifically acceptable and highly influential topic. Even today, one may claim that we do not fully comprehend or apply the insights from this research.

Doidge also does a great job in describing patient cases of brain plasticity, including:

(…) a woman born with half a brain that rewired itself to work as a whole, a woman labeled retarded who cured her deficits with brain exercises and now cures those of others, blind people learning to see, learning disorders cured, IQs raised, aging brains rejuvenated, painful phantom limbs erased, stroke patients recovering their faculties, children with cerebral palsy learning to move more gracefully, entrenched depression and anxiety disappearing, and lifelong character traits altered.

(from the book cover)

The stories from both researchers and patients are written in a most vivid and entertaining way, and the first 100 pages alone makes the book a page-turner. The book as a whole is filled with these fantastic descriptions and stories that equal great writers such as Oliver Sacks.

So how about the sex part? Yes, this is where I got a little puzzled, too. Going from the insights of neuroplasticity, Doidge turns his attention to sexual disorders and abberations. This is, of course, both a very interesting, challenging and risky choice, but it is also a topic that Doidge is intimately close to through his clinical work. In much the same manner as the description of neuroplasticity cases, we are presented to patients of Doidge (or his peers) that suffer from psychological illnesses, in particular sex related problems. Interestingly, it seems that the insights from plasticity can be applied to these disorders and problems, and Doidge does a great job in presenting and discussing these issues.

My quarrel, however, is with Doidge’s theoretical position — psychoanalysis. Is it not itself strange to combine the insights from the edgy yet stringent scientific approaches of neuroplasticity with the unscientific theoretical (armchair) century old approach? Doidge does use the suggestions from Freud to interpret the psychological cases he presents. This includes the interpretation of dreams, a business receiving a lot of criticism, too. At best, I think this part of the book becomes an anachronism. The problem lies in why, at all, Doidge needs to invoke a theoretical position like psychoanalysis at all in order to understand what is going on. This is where science becomes fiction, and where the book breaks down. But not totally. If one is aware of the problems associated with psychoanalysis and science, the book is still a wonderful read.

-Thomas

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Cause and effect in brain development of paedophilia

Physorg reports about an interesting forthcoming MRI study linking paedophilia to regional changes in white matter. Analysing structural MRI using voxel-based morphometry, paedophiles were found to have significantly smaller white matter volumes in specific regions, as the abstract demonstrates:

The present investigation sought to identify which brain regions distinguish pedophilic from nonpedophilic men, using unbiased, automated analyses of the whole brain. T1-weighted magnetic resonance images (MRIs) were acquired from men who demonstrated illegal or clinically significant sexual behaviors or interests (n = 65) and from men who had histories of nonsexual offenses but no sexual offenses (n = 62). Sexual interest in children was assessed by participants’ admissions of pedophilic interest, histories of committing sexual offenses against children, and psychophysiological responses in the laboratory to erotic stimuli depicting children or adults. Automated parcellation of the MRIs revealed significant negative associations between pedophilia and white matter volumes of the temporal and parietal lobes bilaterally. Voxel-based morphometry corroborated the associations and indicated that the regions of lower white matter volumes followed, and were limited to, two major fiber bundles: the superior fronto-occipital fasciculus and the right arcuate fasciculus. No significant differences were found in grey matter or in cerebrospinal fluid (CSF). Because the superior fronto-occipital and arcuate fasciculi connect the cortical regions that respond to sexual cues, these results suggest (1) that those cortical regions operate as a network for recognizing sexually relevant stimuli and (2) that pedophilia results from a partial disconnection within that network.

Now, a few things strikes me odd in this analysis and interpretation. First of all, why is the comparison group nonsexual offenders? After all, that the crime is of a sexual nature is absolutely central to the present question, and especially that the sexual offender has been interested in children. The obvious choice would be to compare paedophilic sexual offenders to sexual offenders who had adult victims (typically a male offending a woman). Here, the act of sexual offence is similar between the two groups, while the sexual “object” is the vital difference. In the present study, any significant difference could just as well be explained by the nature of the crime as the sexual inclination of the subjects. It’s a classic case of poor control of confounding variables.

Second, I strongly dislike the over-interpretations offere in both the article and the news story. First, the authors find significant differences in the superior fronto-occipital and arcuate fasciculi, and link these regions to studies showing involvement in response to sexual stimuli. Following this, they suggest that paedophilia may occur due to a disconnection in this network. Just based on the reasons given in the previous section, these results may be interpreted just as well as brain alterations in sexual offence in general.

But more than this, if one just skims the literature on these regions (fasciculi), one can see that they have been implemented in language lateralization/function and hallucinations and delusions. So interpreting the differences as relevant to paedophilia is a long shot.

Furthermore, the physorg story suggest that this study:

challenges the commonly held belief that paedophilia is brought on by childhood trauma or abuse. This finding is the strongest evidence yet that paedophilia is instead the result of a problem in brain development.

This is a serious over-interpretation of the results. When understanding white matter (and any brain) changes during development, one should be cautious to claim that the changes observed are the mere cause of “brain development” and not experience-related phenomena. Here, we need to divide between two effects: neurogenetic and psychogenetic effects. Neurogenetic effects are, in this story, changes in the brain that are caused by biological factors. Age-related atrophy is a good example of this. The cause is the accumulation of junk within cells/neurons that eventually hinder cell division and function. Psychogenetic factors, on the other hand, are observed brain changes that are caused by behaviour, in its broadest sense. For example, if you learn to juggle, areas in the motor regions of the brain will alter their size and connectivity to a measurable extent. Likewise, London taxi drivers are known to have larger posterior hippocampi as a result of their prolonged training in navigation.

So in the case of paedophilia, observed changes in the brain cannot be said to support a brain-based (neurogenetic) interpretation, and to challenge psychogenetic causes. Rather, it has been suggested that many paedophiles have been subject to similar maltreatment when young. At the least, just because the brain shows a difference, one cannot conclude anything beyond this about causation.

As neuroscience enters the domain of social sciences, it holds the promise to both enlighten and naturalize these age-old discussions. However, the use of mere reporting and tailored interpretations are far from sufficient, and may even lead us astray in the goal to achieve a better understanding of these, and related, phenomena.

-Thomas

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A cure for hooliganism?

Can we rid ourselves of the meaningless violence and aggression seen in society today? A news story in Nature News this week shows that aggressiveness may be treated with a serotonin-acting ligand. At least in rats, but nevertheless the study holds the promise for human treatment as well. Serotonin levels are known to be associated with aggression. The lower the serotonin level, the more aggression. So what dd the present study find?

The team engendered violent characteristics by introducing feeble intruder rats that were bound to lose battles, each day for two or three weeks. After repeated victories over other rats, the test animals began to behave in a more pathologically violent manner, fighting all-comers more brutally — including weak females and senseless males which presented no threat to them.

Then the researchers looked at levels of the neurotransmitter serotonin in the rats’ brains. Although brain levels of serotonin don’t change in rats as a result of normal, ‘appropriate’ acts of aggression, the team found that these levels did sink in his pathologically aggressive rats.

So this is more or less a replication and strengthening of previous research, only this model seems to have additional advantages. But the big news came when the team tried to manipulate the serotonin levels in the rats. Here, they found that…

(…) they could alter the aggressive behaviour of their rats by manipulating the serotonin system. They gave the rats S-15535, a compound that binds exclusively to a neuron ‘autoreceptor’ that acts to dampen the serotonin system. This autoreceptor is called 5-HT1a. Binding to it seems to bring serotonin levels in the rats back to normal. When even very low doses of S-15535 were used to bind to the receptors, de Boer found that both the serotonin and the violence of the pathologically aggressive rats returned to normal levels.

Better still, the drug did not seem to affect other behaviour, and did not seem to be generally sedative. So the study suggests that (pathological) aggression might be controlled better using a serotonin-acting drug. The study described in the Nature News was headed by Sietse de Boer from the University of Groenigen. There’s also a story about de Boer study from this year’s SfN conference (I couldn’t make it there, duh), and a ScienceDaily article nicely relates this to other studies.

Of course, the ethical questions are unanswered still. Indeed, if we are able to synthesize these drugs, and they work, who should have them? Should they be forced upon a subject? And let’s make it even more edgy: should it be taken by people (men) going to football matches, and could one convict a hooligan to take a pill before attending a game? Is this the cure for domestic violence, bar fights, hooliganism?

-Thomas

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The evolution of animal personality

It should come as no surprise to you that after a prolonged hibernation, the BrainEthics team is heading back to the web-surface to present the novelties and oddities of cognitive neuroscience. And let’s start again with some fresh news from Nature, which besides featuring a nice focus section on the Drosophila, also has a nice article on (non-human) animal personality. Max Wolf et al. writes that personality has been shown in a number of other animal species. For pet owners such as myself, this is hardly any surprise (I can read that the cotons we have here are” playful, affectionate, intelligent breed. It loves people and as a result can have separation anxiety”. Indeed! But with the two we have, there are differences that are not only slight, but what I would say differences in temperament, or maybe even personality.

So what is new with the Nature article? Three things:

1. it is a scientific acknowledgement of animal minds and personality
2. it holds promise of the operationalization of personality
3. it provides a model to explain the existence of human personality

As a matter of fact, I can see a whole new research field coming to existence through this very article (although the earliest findings already came in the 60’s). Through the study of animal personality, it may be possible to break down the good ol’ paradigms that have solely focused on humans.

The central theme in the Wolf paper is why personalities did evolve in the first place. The researchers ask the question:

First, why do different personality types stably coexist? Second, why is behaviour not more flexible but correlated across contexts and through time? And third, why are the same types of traits correlated in very different taxa?

Basically, the authors’ model starts by assuming that an individual can either reproduce now, but having acquired low-quality resources, or delay reproduction by one year, having acquired high-quality resources. For example, an individual that becomes sexually mature at a young age will have to balance the benefit of early reproduction against the cost of reproducing at a smaller size. Individuals that postpone reproduction must be able to survive to realize their reproductive expectations, and should therefore be generally risk-averse, whereas the opposite is true for those planning to reproduce early. So stable individual differences in risk-taking behaviours can evolve and be maintained when there is a trade-off between early versus late reproduction.

I won’t go more into details now, except point you to the ongoing discussion in Nature about this article (here and here). It’s certainly also going to get non-biologically personality theorists out of their armchairs, too. I look forward to keep an eye on this debate as it rolls out.

– Thomas

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Radio interviews in Denmark

And while we’re in the talk of media coverage, I should mention to those who understand Danish that the Danish Broadcast Company, or DR, has a documentary series on their primary radio channels, P1. The series is called “Hjernerejsen” (loosely translated to “The brain travel”) and it covers topics such as emotions and bonding, brain maturation, transhumanism and neuroethics.In the program called “the soul is in the brain”, I starred in an interview about the new ideas that neuroscience brings to our traditional thoughts about personality and self. My co-interviewees were Jesper Mogensen and Albert Gjedde, both well-renowned neuroscientists both within and outside Scandinavia.

In a coming topic on the senses (tomorrow, April 19.), I speak about how neuroscience can be used in marketing, aka neuromarketing.

The series can be found here, and DR does a nice podcast: http://podcast.dr.dk/p1/rssfeed/tema_torsdag.xml (copy and paste into your preferred podcasting program)

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Want the job? Pass our OCD scan first, please

Is it possible to identify a psychiatric disorder using a structural brain scan? According to a team of researchers from Europe and Australia this can indeed be the case. In a recently published study in NeuroImage, researchers Carles Soriano-Mas et al. demonstrate that structural brain scans can identify subjects suffering from obsessive-compulsive disorder (OCD) with a 93.1% classification accuracy (for a whole-brain comparison). In addition, individual variance in OCD symptom severity was correlated with the measured neural differences. In other words, the more you suffer from OCD the more you are likely to stick out in the analysis as an oddball, compared to a healthy norm.

Here is an image showing the structural differences between OCD patiens (n=72) and healthy controls (n=72):

In the image, the heat scale indicates regions where OCD patients differ significantly from controls at the whole brain level. Interestingly, when the researchers focused on the most intense regions the predictive value of the brain scans dropped to 76.6% accuracy. This means that a whole-brain approach is the optimal for determining whether a subject is suffering from OCD.

The study clearly demonstrates that neuroscience is moving in the direction of single-subject analysis, and the application of advanced analysis methods to determine whether a given individual is structurally (or functionally) within the normal range. If the means are there, when will we see them being used — and misused? After all, if a brain scan has the close to 100% accuracy of telling whether a person is suffering from OCD, why not use it in the clinic right away? Or better, why not expect applicants to an important company position take such a scan? After all, if you suffer from OCD, you are less likely to be able to be in such a position, right? And while we’re at it, why not try for a similar approach for depression, anxiety, stress and introversion?

Are we right in being sceptical towards the application of such measures of psychic health? Methodological problems aside, should such a measure provide a robust assessment tool, why should we not use it? After all, psychological testing is really aimed at uncovering who people are. Apply for a top position and you are likely to be submitted to psychological and cognitive profiling. If scanners provide a better accuracy, would it not be preferable to use this method? Since society has decided to allow psychological and IQ testing, such measures should really be just another improved method. As a consequence, we should not be surprised to see them being used pretty soon — if they are not already in the stores.

The solutions are far from clear in the muddy waters following the blazing trail of neuroscience. As neuroscientific methods move along and create new opportunities, new problems arise, too. What is important is to bring these issues up front in the media and other forums of such debate. Neuroethics is as important as ever.

– Thomas

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Better lie detectors?

Is it really so that fMRI can enhance lie detection? This entirely depends upon your method of analysis, the experimental setup, and especially controlling for factors that influence the scanning results. Let’s take them one at a time

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