Eating Disorders Information (EDI)

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A Quantum Psychopathological Account of Anorexia Nervosa

Posted by a.marlow on May 1, 2013 at 7:25 PM Comments comments (0)

To those regular readers who have noticed a sizeable reduction in output recently, I apologise. However, there is good reason: I have spent the last few months working on a research paper recently published in the academic journal Neuroquantology entitled "A Quantum Pyschopathological Account of Anorexia Nervosa", which is free to read online or download as a pdf if you click on the link.he basic thesis takes recent theoretical work on the potential link between quantum physics and the brain, and applies it to the specific case of anorexia nervosa. I invite you to give it a critical read-through and share your thoughts with me. I hope you find it interesting and helpful.

This last weekend, I was in Palermo, Sicily, delivering a talk based on this article to an assembled multidisciplinary crowd of psychologists, physicists and others who had assembled for a two day conference on the topic of "Quantum Paradigms of Psychopathology". I shan't bore you with details, except to say that current research into the role of neuronal microtubules as a possible site of quantum computation within the brain is flying ahead apace, with particularly interesting evidence submitted regarding the way in which certain microtubular structures closely resemble certain plant structures used in photosynthesis that are now known to exhibit effects best explicable by quantum mechanics. If these developments bear fruit, then the account of the unconscious quantum logic that I present in the Neuroquantology article linked above might represent a valid and crucial step forward in understanding the neuronal basis of anorexia nervosa.

Recovery from Anorexia includes development of neural coping mechanisms for negative emotional reactions to bodies

Posted by a.marlow on January 18, 2013 at 6:35 PM Comments comments (0)

How do recovered anorexics emotionally react to negative images of the body? Does recovery involve dampening one’s emotional reaction to them, or simply finding other ways of coping?

A recent study by Pruis et al in the International Journal of Eating Disorders has found that women who have recovered from eating disorders retain a greater emotional reaction to negative images of bodies as opposed to neutral or positive images as compared with a control group, and from this they conclude that recovery from anorexia nervosa does not include a dampening of one’s emotional responses to negative body images, but merely the development of mental coping mechanisms that prevent these emotional responses from disturbing cognition.

The researchers specifically looked at three parts of the brain, and found unexpected results from a fourth. Their intention was initially focused on the amygdala, which is related to one's initial fearful and/or emotional response to stimuli; a subregion of the fusiform that particularly responds to bodies; and the lateral prefrontal cortex, which is supposed to regulate emotions.

While they found no difference between the recovered anorexics and the control group in terms of how their lateral prefrontal cortexes reacted to a working memory task, they did find increased activity in the recovered anorexics' amygdalas and fusiforms and, unexpectedly, a suppression of activity in their medial prefrontal cortexes.

The increased activity in the amygdala and fusiform is seen as evidence of a greater emotional response by the recovered anorexics' to the stimulus of a negative body image. This could be taken as a 'scar' left behind by the anorexia, an indication that these particular women were predisposed to get anorexia, or perhaps evidence that their recovery is not quite complete on a psychological level.

An increase in activity of the lateral prefrontal cortex was hypothesised as the means by which the recovered anorexics' emotional responses to negative body images could be mediated. However, there was no difference between the activity here in the recovere anorexic group and the control group. This in itself is a result, given that those still ill with anorexia show reduced activity in the lateral prefrontal cortex; however, it was not the result the researchers were looking for.

What they found instead was asuppression of the medial prefrontal cortex, which was hypothesised to be involved in the control of self-referential emotional responses in order to allow other cognitive processes to continue. 

The practical results of such research for therapists are as follows: recovery from anorexia does not necessarily involve salvation from one's initial negative emotional response upon seeing a negatively rated body image, but it does involve the learning of coping mechanisms to prevent these emotional responses from blocking other cognitive processes, these perhaps being expressed in the increase to normal levels of activity in the lateral prefrontal cortex and in the suppression of activity in the medial prefrontal cortex. 



Pruis, T. A., Keel, P. K., & Janowsky, J.S., 2012. Recovery from Anorexia Nervosa Includes Neural Compensation for Negative Body Image. International Journal of Eating Disorders, 45, pp. 919-931

A genetic link to eating disorders?

Posted by a.marlow on October 7, 2012 at 5:00 AM Comments comments (0)

Two articles in recent editions of the International Journal of Eating Disorders paint us a very interesting, but also very puzzling, picture of the roles genes might play in the formation of eating disorders.

First, the positive role they might play: Soltenberg et al. in their study found that women who had a specific variant of the serotonin transporter gene SLC6A4 were more likely to respond to childhood trauma by developing eating problems in later life. (For those who don't know, serotonin is a brain chemical that is believed to regulate appetetite and mood, and whose abnormal functioning has been implicated in the formation and experience of eating disorders).

So far, so good- but another study by Munn-Chernoff et al. found, in contrast to the above referenced study, that there was no significant correlation between any variant of the SLC6A4 gene and either binge-eating or body weight concern.

So how can we reconcile these two seemingly conflicting studies? In reality, it is not that hard. Firstly, we need to consider that they were both looking at different things: Soltenberg et al. had a more general definition of eating problems, while Munn-Chernoff et al. were looking specifically at binge-eating and body weight concern. It is entirely possible that, had the latter group been looking for links with other kinds of disordered eating behaviour (such as the self-starvation shown by anorexics), they would have found a correlation.

Secondly, for what it's worth, both studies also looked at slightly different variants of the SLC6A4 gene. Soltenberg et al. focused their study on one particular variation of this gene (or 'allele*'), while Munn-Chernoff et al. conducted a more comprehensive study looking at seven different 'polymorphisms**' of this gene. You might expect, then, that the latter study would have more comprehensive results, and we can probably say that it did- but when saying that, it is important to remember the points made in the paragraph above about what specifically Munn-Chernoff et al. were looking for.

The picture that emerges, then, is a complicated one: which variant of the SLC6A4 gene you have can affect whether you contract an eating disorder later in life; however, this gene is not linked to either binge-eating or body image concern and only really determines how you'll react to childhood experiences, rather than completely determining the future state of your mental health.


Flummoxed by some of the terms in this blog post? Don't worry, so am I. I had to look these terms up:

allele: the term 'allele' refers to an alternative form of a gene.

polymorphism: in genetics, "genotype" refers to the instructions passed down in the genetic code, while "phenotype" refers to the actual behaviour and traits exhibited by the creature that has those genes. Genotype is thus determined only by genes, while phenotype is determined by genetic and environmental factors. Here, a different "polymorphism" of the SLC6A4 gene would refer to a different phenotype of that gene i.e. different observable traits in different people carrying the same gene. When a polymorphism is genetic, as it seems to be here, the different behaviour results from an alteration in the gene itself.

I'll freely admit that genetics is not my speciality, so if I've got some of this wrong, please do correct me in the comments section.



Munn-Chernoff, M. A. et al., 2012. "Examining associations between disordered eating and serotonin transporter gene polymorphisms", International Journal of Eating Disorders, 45(4), 556-561

Soltenberg, S., et al., 2012. "Association between the serotonin transporter triallelic genotype and eating problems is moderated by the experience of childhood trauma in women", International Journal of Eating Disorders, 45(4), 492-500