Category: Neuroscience

  • Where is my mind? Is the materialistic model of reality incorrect?

    My belief about the nature of reality is that the only “thing” that exists is matter. That is, there is no soul, no heaven and no hell. Effects aren’t caused without an interaction with different pieces of matter, and consciousness exists within the confines of the physical head that gives rise to it.

    However, although I used to be extremely firm in this position, now I am less sure, because of one question. I don’t know how to answer this from a materialist perspective. Maybe there’s just a really simple answer that I’m missing, but I’ve spoken to many people on this and no one has given it to me. Maybe you can. So here’s the question.

    Where is the cat?

    “HAHAHA puny humans you will never find me. (Photo by Tambako the Jaguar

    I can make a picture of a cat in my head; I can close my mind and think of it. So I’m perceiving this image of a cat.

    Where is the image? Where is the cat?

    I first heard this question (well, I added the cat part myself) in a lecture on the mind/body problem, and my initial answer is that the cat is simply a 1:1 correlate of certain neurological activity in the brain. That is, if you open up my head you won’t see a picture of a cat, but you’d see something that’s the equivalent of it, sort of like the dots and dashes of Morse code are not English characters, but they are equivalents of them. From a materialistic perspective, you’d theoretically be able to interpret the activity in my brain through some technology, and recreate the image of the cat that I am picturing on a screen.

    In fact, we’re past theorising on this, as a famous experiment last year that was widely reported as “Mind Reading” in the media demonstrated. Here’s what they did:

    1) Measured brain activity as someone watched a load of YouTube videos
    2) Linked up the brain imaging data with the image on the screen, creating a sort of database whereby such-and-such brain activity relates to, say, a red object in the middle of the screen, such-and-such relates to certain shape moving to the left, and so on. I’m probably over-simplifying, but that’s the gist.
    3) Get the same person to watch a new set of YouTube videos, again while in the scanner measuring brain activity.
    4) Use the database created in step 2 to predict what the person was seeing in step 3.

    Here’s how the reconstructions compared to the original videos:

    It’s important to note that the brain may not code imagined images in the same way as those you see with your own eyes, and also that each person’s brain will likely code the image of the cat in different ways (hence the need for steps 1 and 2), but, since all of the activity of the mind is thought to have a direct neural correlate, the principle is the same.

    So when I was asked “where” my mental image of the cat is, that’s why I responded in this way — the image is located in the brain – it’s just in a different format.

    But really, I’m not satisfied with that answer. Because in my mind I can see (well maybe not see, but certainly perceive) the cat; not the equivalent neural ‘code’, but the actual cat. I know where the neural code is, but I don’t know where the cat is.

    I can’t think how the materialistic model can explain where the cat is. Doesn’t this mean then that there’s more to reality than the purely materialistic? That the materialistic model is incomplete? What am I missing?

    To use a computer analogy, the words you are reading now (hello!) are represented in a chip in a computer as a string of 0’s and 1’s. That’s like the neural code in your brain. But the actual words are represented on the screen in front of your eyes. What’s the equivalent of the screen in the case of the cat? Where is it?

    I’m actually asking this to you – do you know where the cat is? Am I making a simple mistake? Please leave a comment and help me out!

    Where is reality?

    That’s probably enough for one day, but just to take this one step further; we know that what we see is not the world. The image we see is a mental construction of the world, and psychology has identified numerous examples of how we each see the world a little differently. An obvious example is colour-blindedness. Since the brain is constructing the world we see around us, and if we assume that the neural code and the image are different things… where is reality?

    Ref:

    Nishimoto S, Vu AT, Naselaris T, Benjamini Y, Yu B, & Gallant JL (2011). Reconstructing visual experiences from brain activity evoked by natural movies. Current biology : CB, 21 (19), 1641-6 PMID: 21945275

  • Meditation is associated with changes in the physical structure of the brain

    In this post, I mentioned some interesting studies where neuroscientists put Buddhist monks into brain scanners, trying to find out what effect meditation has on the brain. They found some interesting results in terms of brain activity. If you throw neuroplasticity into the mix too, you’d expect some structural differences too. A study led by Sara Lazar looked into just that.

    I’ve mentioned my thoughts on neuroscience and positive psychology previously. My key point is that, since neuroplasticity is a given these days, it’s not all that impressive to demonstrate changes in the brain as a result of consistent practice of a given activity. But that doesn’t mean it’s not an important study to do. The key questions are: what changes, how much, and does this fit in with other results and theory?

    Twenty experienced meditators (had been one at least one retreat, practice 4 hours a week on average), were compared to a matched control group (by age, sex, race, and years of education). So note here that we don’t have random assignment, but we’ve got the next best thing if we want to study experienced meditators right now.

    What happened?

    Cortical thickness was compared between the two groups. Over the whole brain, there was no difference, meaning the changes were limited to a specific area. The areas were related to somatosensory, auditory, and interoceptive processing. If you want the specific brain regions, here they are:

    • A region of the right anterior insula
    • The right middle and superior frontal sulci (Brodmann areas 9 and 10, roughly)
    • The left superior temporal gyrus (auditory cortex)
    • A small region in the central sulcus

    Also, normal age-related decreases in Brodmann areas 9/10 were seen in the control group but not the meditation group. In other words, meditation potentially helps prevent age-related deterioration in the brain!

    Of course, this is a correlation study, and when two things are measured at the same time, it’s impossible to say what is the cause and what is the effect. Maybe people with enhanced cortical thickness tend to be drawn to meditation, rather than the other way around? It’s certainly possible, but as the authors note, if that were true you might expect greater cortical thickness overall, which wasn’t found here.

    Meditation gives a double-whammy when it comes to making structural changes in the brain. Firstly, there is the control of attention during a consistent practice schedule. Secondly, the relaxed state of the body appears to facilitate cortical plasticity, at least in the auditory areas according to one study. This is comparable to the idea that sleep aids learning, study breaks aid recall, and so on.

    That the structural changes were consistent with the brain areas associated with the techniques being practised, and that these changes may stave off age-related cortical decline, is encouraging. Presumably, different types of mental exercise would have effects on the brain areas related to them, and you could devise a routine aimed at the faculties you expect you’ll most need in your old age.

    Ref:

    Lazar SW, Kerr C, Wasserman RH, Gray JR, Greve D, Treadway MT, McGarvey M, Quinn BT, Dusek JA, Benson H, Rauch SL, Moore CI, Fischl B. Meditation experience is associated with increased cortical thickness. NeuroReport, 2005; 16: 1893-1897.

  • How relevant is neuroscience to positive psychology?

    Not long ago, many scientists had the belief that after the age of about three, the brain was pretty much fixed in function. You could imprint new memories and learn new skills, but that was about it. There was an opposing belief too, that said the brain was a ‘blank slate’ upon which the various human parameters were written almost ad lib as life went on – an idea, of course, that Steven Pinker refuted in his famous book of the same name (Pinker, 2002).

    It is generally accepted that the truth is somewhere in-between. The brain appears to develop into a specific set of sub-systems, with the same ‘modules’ performing the same functions in different individuals (eg., Restak, 1994). But, these subsystems are flexible, and can be altered to some extent; brain areas can grow, connections can be made and broken, and new neurons can grow. This is a constant process; the brain is always changing; in fact, just by reading this sentence, your brain is changing. Same with this sentence. And this one. I’ll stop now.

    As you know, this is called ‘neuroplasticity’, and the $4,000,000 question is: how is this buzzword relevant to positive psychology? (1)

    Well, as fascinating as I find neuroscience to be, it’s no surprise (anymore) to find different brain areas involved in different functions, including so-called ‘positive’ functions. Accepting the above ideas (modular brain/no blank slate, neuroplasticity), it’s not a profound thing to find a brain area associated with, say, positive affect: or even large differences in that area between, say, novice meditators and Tibetan monks with 20,000 hours’ meditation practice. If there’s a massive difference on the outside, there should be one on the inside. It’s what you’d expect.

    To give another example, there are brain areas associated with motor tasks, allowing me to type this blog post (Cannonieri et al, 2007). These areas are probably very different in me than in the Tibetan monks, who have quite possibly never used a keyboard (or maybe they each take a MacBook Pro into the mountains with them; I really don’t know).

    But you wouldn’t need a brain scan to find this out. A simple typing test would do. I would be faster than the monks, and this functional difference has to have a biological correlate of some sort. It has to ‘be’ somewhere.

    Don’t get the impression that I’m ‘against’ neuroscience – no way, far from it. I like an fMRI study as much as the next person; I just think it’s important to remain skeptical, not get too carried away too soon, and understand that a neural correlate might not be the holy grail.

    There is even some preliminary evidence that diagrams of brains (McCabe and Caster, 2006) and neurological explanations (Weisberg et al, 2008) can increase the persuasiveness of even poor arguments! So let’s not mistake inherent fascination with our own brains as having any special relevance, and judge it as a starting point, like any other correlational evidence – until there is more data to go on.

    That said, I actually think neuroscience has a lot to offer. Here is where I think combining these two fields may be useful:

    1) Validation of scale measures

    Discovering neural correlates of variables can allow the questionnaires used to measure these variables to be tested for validity – as long as the neural correlates are themselves validated against things other than the questionnaire. For example, if there are studies testing things like altruism, humour, and so on, the neural correlates of these could be compared with VIA strengths inventory, which measures character. That could be interesting. Likewise, well-being measures have been compared to left-right prefrontal asymmetry, because the left prefrontal cortex is thought to be involved in ‘positive’ emotion.

    2) Building theoretical models

    Neuropsychology can provide evidence to help to build theoretical models, from which further predictions can be made. For example, the debate around whether positive and negative affect are along the same or distinct dimensions. Some people believe they lie on one continuum, e.g., -10 (negative) to +10 (positive). Others believe they lie on two dimensions, and can be largely unrelated. One way of digging into this is to measure the biological correlates of each, which Ryff et al (2006) did and found support for the ‘distinct’ hypothesis.

    3) A two-way street?

    Maybe positive psych is good for neuroscience too. If we accept Seligman’s founding premise that psychology had been skewed onto what you might call ‘less positive’ lines of inquiry – that is, focused (understandably, following WWII) on reducing illness and disorder as opposed to cultivating character and positive traits, then the same is possibly true of neuropsychology. Combining the two fields could bring a broader understanding of the brain and behaviour, encouraging lines of research that might not have been considered otherwise.
    I’m generally always in favour of combining different avenues of research – I think it’s good to look at things through a different lens – in science and in life in general!

    NOTE:

    (1) I mean that literally. The Templeton Foundation has pumped $4,000,000 into answering that question.

    References:

    Cannonieri, G., Bonilha, L., Fernandes, P., Cendes, F.,&Li, L. (2007). Practice and perfect: Length of training and structural brain changes in experienced typists. NeuroReport: For Rapid Communication of Neuroscience Research, 18(10), 1063-1066

    McCabe, D.,&Castel, A. (2008). Seeing is believing: The effect of brain images on judgments of scientific reasoning. Cognition, 107(1), 343-352.

    Pinker, S. (2002). The Blank Slate: The Modern Denial of Human Nature, Penguin Putnam

    Restak, R. (1994). The modular brain: How new discoveries in neuroscience are answering age-old questions about memory, free will, consciousness, and personal identity. New York: Scribner’s.

    Ryff, C., Love, G., Urry, H., Muller, D., Rosenkranz, M., Friedman, E., et al. (2006). Psychological Well-Being and Ill-Being: Do They Have Distinct or Mirrored Biological Correlates?. Psychotherapy and Psychosomatics, 75(2), 85-95.

    Weisberg, D.S., Keil, F.C., Goodstein, J., Rawson, E., Gray, J. R. (2008). The Seductive Allure of Neuroscience Explanations. Journal of Cognitive Neuroscience, 20 (3), 470-477

  • Love on the brain

    Love is a topic that scientists have shied away from – perhaps in the same way as studying humour, they worry that they will take the magic out of it. But as Helen Fisher, one of the foremost researchers of love says, you can know all the ingredients of chocolate cake and it will still taste delicious.

    One of the more popular early theories was Sternberg’s triangular theory of love. This theory has immediate appeal because it points out three aspects of loving relationships that we can instantly recognise – intimacy, passion, and commitment. A relationship can have any two or all three of these, and in the theory, each combination has its own name (see this article for more on that).

    It’s a nice, tidy model. But one problem I first had with it, is that maybe it only has intuitive appeal because I recognise it in Hollywood movies, rather than in people. Is this love?

    It may be: Sternberg’s model matches up nicely with some work in neuroscience and animal behaviour. It seems that there are discrete but interrelated emotional systems common to most if not all mammals and birds, which solve the ‘problem’ of mating. These are lust, attraction, and attachment, and they correspond roughly to Sternberg’s passion, intimacy and commitment. Example behaviours are:

    • Lust / passion – craving for sexual gratification, associated with elevated levels of estrogens and androgens.
    • Attraction / intimacy – increased energy spent on the preferred mating partner, in humans this also includes ‘intrusive thinking’ about the love interest. Associated with increased dopamine and norepinephrine, and decreased serotonin.
    • Attachment / commitment – Characterised by mutual territory/resource defence, nest building, close proximity, separation anxiety. Associated with the neuropeptides oxytocin and vasopressin. (see references 1 and 2 for a review of this evidence)

    These are powerful chemicals, and the power of love should not be underestimated; in one study, evidence of romantic attraction was found in 147 of 166 societies (3). People elope together because of love, they sing songs because of love, and they kill themselves – and others – because of love. Clearly, it is more than a feeling. What is actually going in this attraction / intimacy part of Fisher/Sternberg’s models that has such a maddening effect on us?

    To find out, Helen Fisher stuck a bunch of madly-in-love people in fMRI scanners, while showing them pictures of their loved one. The results? It appears that romantic love is located primarily in the ventral tegmental area of the brain. This is part of the dopaminergic system, involved in reward, want, and craving. It’s the same area of the brain that fires up when addictive drugs are taken, particularly cocaine and the amphetamine derivatives. In other words, love is addictive – literally.

    But of course, every rose has its thorn, and love does not always end well. In another interesting study, Fisher and colleagues stuck people who had recently been dumped into an fMRI (4). Where is this experience located in the brain? The same place! But additionally, there was also activation in the nucleus accumbens, an area associated with judgements of gain and loss; the area that lights up when we’re willing to take great risks to achieve a high perceived gain – the same area involved in gambling. This is why we get people going to great lengths to get their love back – they are simultaneously focused on what they have lost and at the same time more likely to take high risks.

    So what is love? It is an addiction. It meets the criteria necessary for something to be classed as an addiction (tolerance, withdrawal, relapse). The implications of the above findings are massive – if love is associated with the above neuotransmitters, peptides and hormones, then our experience of love could be influence by anything that interferes with these chemicals – recreational drugs and anti-depressants in particular. In addition to this, the brain areas involved in love seem to suggest that, rather than being an emotion per ce, it is a goal-oriented state.

    old_couple_dancing
    (Credit: txd)

    But, at the risk of leaving on a low note, I’ll finish by mentioning a recent study by the same research team (5). So fond of sticking people into fMRI scanners, this time they scanned couples who had been married for 25+ years, and still report feeling in love with their partners. What was the brain activity in these couples? As Sternberg would predict, they showed greater activity in areas associated with long-term pair bonding in animals. But what about attraction / intimacy? Well, they found just the same activity as they did in the earlier experiments. Perhaps true love can last forever.

    PS. The titles of five love songs are hidden in this article. See if you can find them!

    Recommended Reading:

    References:

    (1) Fisher, H. (1998). Lust, attraction, and attachment in mammalian reproduction. Human Nature, 9(1), 23-52.

    (2) Fisher, H., Aron, A., Mashek, D., Li, H., & Brown, L. (2002). Defining the brain systems of lust, romantic attraction, and attachment. Archives of Sexual Behavior, 31(5), 413-419.

    (3) Jankowiak, W., & Fischer, E. (1998). A cross-cultural perspective on romantic love. Human emotions: A reader (pp. 55-62). Malden: Blackwell Publishing

    (4) Fisher,H, A Aron, G Strong, DJ Mashek, H Li, LL Brown. (2005). Motivation and emotion systems associated with romantic love following rejection: an fMRI study.

    (5) Aceveda, B., Aron, A., Fisher, H., Brown, L. L. (2008). Neural correlates of long-term pair-bonding in a sample of intensely in-love humans. Poster Session#297, Society for Neuroscience, annual meeting

  • Differential Susceptibility – Are some brains more plastic than others?

    Ever heard of the idea that for some illnesses and disorders to develop, you need to have an inherited risk factor plus environmental stress? It’s known commonly as the diathesis-stress model (diathesis basically means predisposition), and it’s a common explanation for a large range of phenomena, from schizophrenia to serial murder. Both diathesis and stress need to be present for the illness to arise.

    This has been the prevailing view for some time, but a few researchers, such as Jay Belsky and Michael Pluess of Birkbeck university, are now making a slightly different case. They don’t say that the diathesis-stress model is incorrect, rather, that it is incomplete.

    They have noted multiple instances in the existing research base in which the diathesis side of the model – for example the function of genes, or phenotypic characteristics – would be better explained as what they call ‘plasticity factors’, as opposed to ‘vulnerability factors’.

    Is the diathesis-stress model incomplete?

    Let’s look at the current viewpoint in a little more detail. Typically, certain people are thought to possess particular gene variants which make them more likely to develop a psychological condition, for example depression, when a certain conditions occur in their life. So, someone with a different allele (different versions of the same gene are known as ‘alleles’) could go through the same experiences, and not come out the other side depressed.

    The new point of view would say that rather than having a risk for certain illnesses, these people may actually have a brain that is more responsive to the environment generally. If they did not go through a stressful period, but instead a supportive, nurturing one, they would be more likely to develop beneficial psychological characteristics – and again, people who had different versions of the gene could go through the same experiences and not come out the other side as well off.

    This model is called ‘differential susceptibility’; people differ in their susceptibility to environmental influence. The implication is that some brains are more plastic than others, and are therefore more susceptible to both positive and negative effects of supportive and unsupportive environments.

    Vulnerability or Plasticity?

    Over the years a number of studies on temperament in children have been published which appeared to supported the diathesis-stress model. They generally show that differences in parenting style predict differences in self-control, externalising problems, and other aspects of difficult temperament. But the limitation of these studies is that they did not test for whether these same children would be more likely to receive benefits from different parenting styles. In other words, these studies were not designed to tell the difference between vulnerability and plasticity – only to detect vulnerability.

    temperament
    Chill out…

    A number of other studies, however, have been designed in a way that gets around this problem, and many have supported the idea of general plasticity. To give an example, one study found that teenage boys with difficult temperament were the least likely to externalise problems after 6 months with sensitive, non-controlling mothers; but they were also the most likely to externalise problems after 6 months with insensitive, controlling mothers. Furthering the support for the theory, this pattern was not found in the teenagers who did not have a difficult temperament. (2)

    Another study, this time with an experimental design, looked at mothers who were thought to be at risk of developing insecure children due to their own difficulties. These mothers were given an intervention in the form of a video feedback exercise, which successfully improved their parenting skills. Was the intervention successful in building a more secure attachment style from the infants? Yes it was, but only for those who had a high level of negative reactivity prior to the intervention. (3)

    Genetic Markers of Differential Susceptibility

    differential_susceptibility

    We’ve looked at a few studies which might demonstrate the effects of differential susceptibility in the ‘real world’. There is also some evidence looking into the effects of genes, and again Belsky and Pluess (1) argue that because previous research had been led by the diathesis-stress model, findings which might support differential susceptibility have tended to go overlooked.

    If anything I’ve said up to now has been familiar to you, you might have heard of the 5-HTTLPR gene. It has had attention in the media and popular books (eg., The How of Happiness) for being the ‘depression gene’, in that people who have a specific variant of this gene, the so called ‘short allele’, are more susceptible to depression.

    A number of studies have supported this finding, but there have been some results which suggest the pattern may not be so clear as yet. One study found, as predicted, that young adults with two short alleles had the most severe symptoms of depression when they had experienced problematic childhoods. However, when short allele children had experienced a supportive childhood, they actually showed the fewest symptoms of depression later in life. (4)

    A warm and fuzzy conclusion?

    Although the recent evidence for individual differences in plasticity is quite compelling, the authors are very tentative and cautious in their papers, which I suppose is necessary when you’re proposing something new. You don’t want to scare anyone off. So they are keen to point out that the evidence is not quite solid as yet, and there is more work to be done.

    This line of work is only beginning, and there are many unknowns. Much the same as in priming research, the evidence of the effect is running a little ahead of the understanding of the mechanisms involved, and researchers are unclear on whether differential susceptibility stems mostly from ‘nature’ or ‘nurture’, or on the breadth of the phenomena that it applies to. Having said that, the idea that that the people most susceptible to negative symptoms and experiences might be the people most susceptible to positive symptoms and experiences, is quite a cheerful thought.

    References:

    (1) Belsky, J., & Pluess, M. (2009). Beyond diathesis stress: Differential susceptibility to environmental influences. Psychological Bulletin, 135(6), 885-908

    (2) van Aken, C., Junger, M., Verhoeven, M., van Aken, M., & Dekovi?, M. (2007). The interactive effects of temperament and maternal parenting on toddlers’ externalizing behaviours. Infant and Child Development, 16(5), 553-572.

    (3) Klein Velderman, M., Bakermans-Kranenburg, M., Juffer, F., & van IJzendoorn, M. (2006). Effects of attachment-based interventions on maternal sensitivity and infant attachment: Differential susceptibility of highly reactive infants. Journal of Family Psychology, 20(2), 266-274.

    (4) Taylor, S., Way, B., Welch, W., Hilmert, C., Lehman, B., & Eisenberger, N. (2006). Early Family Environment, Current Adversity, the Serotonin Transporter Promoter Polymorphism, and Depressive Symptomatology. Biological Psychiatry, 60(7), 671-676.

  • The Buddhist Brain

    What happens to the brain if you spend 44,000 hours in focused meditation?

    This is a question Richard Davidson and his neuroscience team asked. To answer it, they took experienced Tibetan monks to their lab at the University of Wisconsin, and took various scans of their brains. Is the Buddhist brain fundamentally different than the average?

    Types of meditation

    Buddhism includes various types of meditation, which can be grouped into three main categories: focused attention, where the aim is to focus on one object or sensation, to the exclusion of everything else; open monitoring, where the aim is to increase awareness of all perceptions, without focusing on anything in particular; and compassion meditation, where the goal is to produce an overwhelming and unconditional mental state of kindness to all things. These all have different effects on the Buddhist brain, as we’ll see.

    Buddhist Brain
    Obligatory meditation image. (Johan Stigwall)

    Focused Attention

    As would be expected, focused attention meditation increases activation in the brain areas implicated in the control and regulation of attention, such as the prefrontal cortex. The activation is higher in meditators with more experience, up to a point of about 19,000 hours practice. After 44,000 practice, there is an initial increase in activation, followed by a return to baseline.  This means that after extensive training, it takes little effort for the attention to be controlled.

    There are also differences in another brain area – the amygdala. This is an older part of the brain involved in emotion. Expert meditators have less amygdala activation than novices in response to emotional sounds. While sat in the MRI, novice and expert meditators were bombarded with distracting, emotionally provoking noises, such as a baby crying.  Novices react to it, but while experts do hear the sound, they don’t react to it. They are less emotionally reactive to external events, and can hold their concentration in situations where in anyone else, the amygdala would be firing up so strongly that they would be powerless to resist its goal of redirecting their attention.

    Open Monitoring

    The overall effect of open monitoring is that the meditator is able to attend to all the stimuli coming at them, without getting ‘stuck’ on anything. They can just sit back and watch it all, or engage and disengage their attention as they please.

    When under an EEG scan, the meditators were able to increase the gamma-band oscillations in their brain; these are usually quite weak, and difficult to detect. Gamma bands are important in attention and perception, but also in the transmission and integration of information across the brain. It is thought that this type of activity helps to integrate distributed neural processes into more ordered functions. There was also a change in the gamma bands when the monks weren’t meditating; showing that the ‘default’ setting had been altered.

    Compassion Meditation

    This type of meditation involves deliberately generating a state of unconditional compassion and kindness towards all beings, that saturates the whole mind. This is said to create more spontaneous acts of altruism in the meditator.

    This was studied through fMRI scans. After thousands of hours of compassion meditation, the expert meditators were able to increase their empathic response to other peoples’ social signals. The brain area involved (the insula) is thicker in expert meditators than novices, and there was also greater activation in the areas associated with reading others’ mental states. In other words, by systematically creating a concern for others, the meditators are better able to process the emotions of others.

    These have been quite revolutionary findings in neuroscience, showing that things like attention can be trained and develop, where previously they had been thought to be relatively fixed.

    Recommended Reading: