Orthorexia – a new type of eating disorder?

You might have heard some of the negativity in the press recently about so called ‘clean eating’ and it’s advocates, who promote a lifestyle which involves cutting out any processed food and often entire food groups (gluten/dairy etc). This is not because of any medical reason, but simply just to be as ‘healthy’ as possible. I’m not going to go anymore into the debate around clean eating today (there’s too much to say, and several people have done it already) but I’ve mentioned it here as it has been linked to a rise in a condition known as orthorexia.

Orthorexia nervosa (so called by Steven Bratman, 1996) is characterised by a fixation with healthy food consumption. More than just dieting, sufferers will become obsessed with healthy food, and food will become preoccupying and a source of anxiety. Other problems often caused by this disorder include social isolation due to having to have complete control over their food intake, and some nutrient deficiencies caused by an extremely limited diet.

image from http://www.thefullhelping.com/neda-week-2014-considering-orthorexia

People with orthorexia (like some who ‘eat clean’) will often cut whole food groups or types of food out of their diet, thinking this will benefit their health. Common foods to be avoided are those which include artificial colours, flavours or preservatives, or foods perceived as containing too much sugar, or salt (Catalina et al., 2005). Orthorexics will also develop strict rules about food, which may also extend to rituals around food preparation (Chaki et al, 2013).

However, despite it’s increasing recognition, orthorexia isn’t listed as an official disorder by the DSM-V diagnostic manual for mental illness. As it is a relatively new disorder, research on orthorexia is lacking compared to other eating disorders such as anorexia or bulimia. There is some debate about whether orthorexia is a subtype of one of these existing eating disorders (Zamora et al, 2005), an eating disorder in it’s own right (Bratman & Knight, 2000), or a type of obsessive-compulsive disorder (e.g. Mathieu, 2005). Alternatively, some researchers view it as a combination of the above e.g. Brytek-Matera (2012) who describes orthorexia as “a disturbed eating habit which is connected with obsessive-compulsive symptoms.”

As researchers are still unclear how to categorise orthorexia, it is unsurprising it hasn’t yet made it in the DSM-V. However, despite it’s absence, Bratman & Knight (2000) have developed some guidelines for diagnosing orthorexia. These include:

  • preparing healthy food overtaking other activities in life, with sufferers spending over 3 hours a day thinking about or preparing food
  • following a very strict and restrictive diet plan
  • a healthy diet becoming linked to self-esteem, and feelings over superiority over others who do not follow such a strict regime
  • the nutritional value of a meal becoming more important than it’s taste or the joy from eating it

Orthorexia can be treated successfully, with a combination of cognitive behaviour therapy and medication such as SSRIs (a type of antidepressant) being shown to be effective in some cases (Mathieu, 2005). This study also suggested that orthorexics responded better to treatment than suffers of other eating disorders, perhaps due to their concerns and increased awareness about their health.

There is no question that more research needs to be done to establish more data on people living with this condition, which will enable preventative measures and effective treatments to be developed.



Phobias Part 2 – treatments

This week’s post is the second in a 2 part series about phobias, and will focus on different types of treatment, and what works. If you haven’t already, read part 1 (see here) for more information on types of phobias and possible causes.

If you’r a regular reading of my blog, you may remember that a while back I did a post on Cognitive Behavioural Therapy (CBT) and how that can be used to treat people with phobias. The main principle is to reduce the anxiety felt by encountering the phobia stimulus, be it crowds, flying, or needles. By teaching the patient breathing exercises to help them relax and working to change the thoughts (cognitions) about the phobic stimulus, therapists can help the patient to work towards overcoming their fear. The behavioural part of this technique is gradual exposure to the thing the patient is afraid of, whilst the patient works hard to control their breathing and stay calm. This exposure can help towards changing thoughts which contribute to the phobia such as ‘if I’m in a room with a dog it will bite me’, which in turn reduces fear.

For example, take a look at the diagram below which shows how phobias remain if the fears aren’t challenged. If therapy targets the thoughts, and tests the fear, then it is likely the phobia will be treated successfully.


Another form of exposure therapy which has been used to treat phobias is known as ‘flooding’. Unlike in CBT, where the individual is gradually exposed to their fear, in this technique they are put straight in the worst situation they could imagine. This uses more behavioural techniques – as the body cannot sustain a physiological stress response for a long period of time, people begin to notice they feel calmer, even though they are in the presence of their fear. An example would be putting someone who was scared of birds in a room full of them! This also enables the individual to confront their worst fear and learn that nothing bad happens when they are in that situation.

Thanks for reading – there won’t be a post next week as I’ve got 2 interviews but I’ll be back the week after!


Hi everyone, this week’s post will be the first of two – all about phobias. This first post will cover causes and types of phobias, and the next on will talk more about treatments. And, as no post about phobias is complete without a quick phobia quiz – what do you think these phobias are? (scroll down for answers!)

  1. Agrizoophobia
  2. Suriphobia
  3. Enetophobia
  4. Coulrophobia
  5. Phasmophobia


by BromeliaCarnivor


  1. Fear of wild animals
  2. Fear of mice
  3. Fear of pins
  4. Fear of clowns
  5. Fear of ghosts


Although some of these phobias are unusual, some are more common than others – with Arachnophobia (fear of spiders) probably being one of the most well known. However, there is an important distinction between people who simply don’t like spiders, and would prefer not to be in the same room as them, or not want to touch them, and people who are  afraid of spiders i.e. have Arachnophobia. Sufferers of this phobia will experience extreme anxiety and panic if they come into contact with a spider, or even just look at a picture of one. This is a much more severe reaction.

According to the mental health charity Mind, there can be different reasons for a phobia to develop, from learned experiences to genetics. However, although it is true that some people develop phobias after a bad experience e.g. developing a fear of driving after a car crash, this does not occur for everyone with a phobia. Phobias can also be learnt, from observing other people’s reactions, for example if when you were young your older sibling always screamed and ran away from wasps, you might learn to do the same and develop a phobia of them, even if you’ve never been stung.

One famous (and very unethical) experiment on whether a baby could be given a specific phobia was carried out in the 1920’s by Watson & Raynor. The infant – ‘Little Albert’ had no fears or phobias at the start of the experiment, and the researchers wanted to investigate whether he could be given a phobia of white rats. As this picture shows, before the experiment started, he wasn’t frightened.


This study used principles of classical conditioning to give him a phobia – every time he was given a white rat, a loud noise was made by striking a metal bar with a hammer. Understandably, this noise scared him and made him cry. After this happened several times, he began to become upset when he was presented with the rat alone – the rat had become the conditioned stimulus (to read more about classical conditioning, see my blog post here). They also found that his phobia become generalised to other things that were white an furry, such as a white rabbit or when the experimenter wore a big white beard! No one is really sure what happened to Albert after this experiment, and whether his phobia continued into the rest of his life. It’s safe to say however that experiments like this one would not be allowed to take place now.

Thanks for reading and don’t forget to check back next week for Phobias Part 2.

Obsessive Compulsive Disorder

It’s not unusual for people to say they’re ‘a bit OCD’ when they check they’ve locked the front door, or that they turned appliances off before they go on holiday. However, there is an important distinction between these behaviours and OCD, which can cause significant disruption to sufferer’s lives. OCD is a psychological disorder which affect about 1.2% of the population (ocduk.org), and is characterised by obsessions and compulsions, which cause great distress and are very time consuming.

Obsessions are recurrent and persistent thoughts or images, which cannot be controlled by the individual. They are not just excessive worries about actual problems.

Compulsions are repetitive behaviours carried out by the individual to try to reduce the anxiety caused by the obsessive thought.

However, as illustrated by the figure below, these symptoms cause the distress to continue in a cycle of OCD.


There are 4 main types of OCD symptoms: washers, orderers, checkers, and hoarders. These factors are stable across time (Mataix-Cole et al, 2002) and are thought to be associated with different genes.

Treatments for OCD:

Pharmacological treatments for OCD include SSRIs (a type of antidepressant) and antipsychotics. Behavioural treatments include exposure therapy, and response prevention – to stop sufferers from performing the compulsive rituals. Foa et al (2005) found that a combination of these therapies was the most effective treatment.

Thank you for reading, and let me know if you would like a more in-depth post about the genes and brain areas implicated in OCD.


Hi everyone, I hope you liked my last post on how children develop a theory of mind – this post follows on, and talks about children with autism (if you haven’t read that post, find it here https://freudforthought.wordpress.com/2015/08/06/theory-of-mind/).

Autism is a neurodevelopmental disorder, which has a prevalence of 60 per 10,000 children under 8 in the UK (Baird et al, 2000). Characteristics of autism include impairments in social interactions, communication, and imaginative behaviours. Also, individuals with autism tend to like to stick to routine, and can become distressed if their routine changes. However, autism is a spectrum, and sufferers can have a range from very mild, to severe impairments. For example, the disorder formerly known as Asperger’s Syndrome had all the characteristics of autism, but without the language difficulties (however this is now no longer recognised as a separate disorder).

Criteria for social impairments include lack of eye contact during interactions, and the lack of voluntarily sharing interests and enjoyment with others. Communication impairments include a delay of language development, and a lack of varied pretend play. Finally, examples of repetitive behaviour include sticking to rituals, and a preoccupation with the parts of objects. As mentioned in my last post, some of these behaviours can be explained by deficits in a theory of mind, which is a theory proposed by Baron-Cohen et al.

As well as the traditional theory of mind tasks, they also carried out more advanced experiments, called ‘reading the eyes’ tasks. In these, adults with autism were shown pictures of people’s eyes, and had to work out the emotion the eyes were showing. They found that autistic participants made more errors than controls without the disorder. However, it is worth noting that this task is challenging to normally developed adults – see how you get on from the picture below!


One other interesting thing about autism is that it is more common in males than females, with a 3:1 ratio. Baron-Cohen (2003) therefore outlined his theory that autism is an extreme form of the male brain. This theory states that everyone has either a male or female brain, regardless of their actual gender, with the male brain being better at systemising, and the female brain better at empathising. As autistic individuals can struggle showing empathy, and are generally interesting in how things work, he hypothesised that autism reflects the male brain. Despite the terms ‘male’ and ‘female’, he found that about 17% of men had a ‘female’ brain, with the same percentage of women having a ‘male’ brain. Many people also have a balanced brain, showing aspects of both.

I kind of get why he came to this conclusion, but I think that this theory is very oversimplified, and that there is actually no need for the terms ‘male’ or ‘female’ at all – especially as people can have aspects of both, and that the brain type has nothing to do with gender! Might be one theory to take with a pinch of salt…

But what do you think? Let me know in the comments and thanks for reading!

Body Dysmorphia in Anorexia

Okay, so there hasn’t been a post in a while, no thanks to my dissertation – an 8,000 word essay on “Is there a neuro-cognitive basis of body dysmorphia in anorexia nervosa”. While I doubt many people would actually want to read the whole thing, this is a fascinating topic, so this post will be a (very) shortened version – hope you enjoy!


Firstly, if you’d like more information about anorexia and other eating disorders, check out my previous post https://freudforthought.wordpress.com/2014/01/27/eating-disorders/, which gives a pretty good background.

So what is body dysmorphia? Basically, I was trying to find out if there was any abnormality in the brain which causes sufferers of anorexia to feel as though they are fat, when in fact they are seriously underweight. It is important to find this out, as if body dysmorphia is not treated in anorexic patients,  it could prevent full recovery by maintaining restricted eating patterns (Heilbrun & Friedburg, 1990). Having body dysmorphia also makes suffering from anorexia more likely, therefore early intervention could prevent people from developing the disorder.

The Multidimensional Model of Body Dysmorphia

I focused on evaluating the multidimensional model of body dysmorphia in anorexia, which was proposed by Cash and Deagle (1997). This states that there are two main processes underlying body dysmorphia:

– Perceptive: involves deficits in perceptual processing of body stimuli, and less activation in areas of the brain involved in perceiving body image.

– Attitudinal: split into affective and cognitive components. The affective component states that anorexia sufferers show more activation of the amygdala to body stimuli, which suggests increased emotional involvement and possibly a fear response to body-related stimuli. The cognitive component states that sufferers overestimate their body size due to inaccurate body schema.

Perceptive Component

In order to find out whether anorexic patients have abnormal perceptual body processing, you first need to look at how healthy people process their body image. Downing et al (2001) found that the extrastriate body area (EBA) in the posterior and inferior temporal sulcus is active during body shape perception in the healthy population. Another area – the fusiform body area (FBA) has been identified (Taylor and Downing, 2011). These are shown in the image below:

eba and fba

These areas are thought to detect changes in body shape (Aleong and Paus, 2009), which could explain why anorexic patients don’t recognise their thinner body shape. The first study which showed that these areas could be dysfunction in anorexia was carried out by Uher et al (2005). They used fMRI to measure neural activity while healthy, anorexia nervosa and bulimia nervosa participants were presented with line drawings of overweight, underweight or normal female bodies. They found less activity in the EBA in anorexic women, which suggests a functional abnormality in this area.


Affective Component

The two key pieces of evidence for this are increased amygdala activation to body images (Seeger et al, 2002), and more anxiety in AN patients when shown body images, compared to controls (Friedrich et al, 2006). Seeger et al found that anorexic patients show a more activation of the amygdala when they are presented with distorted pictures of their own body. This suggests a higher emotional involvement in body images as the amygdala has been shown to be involved in emotion processing (e.g. Birbaumer et al, 1998).Friedrich et al found that AN patients show more anxiety than healthy controls when shown pictures of thin models, which again suggests higher levels of emotion caused by body images.


Cognitive Component

This states that AN patients have unrealistic body schema, which causes them to view themselves as being fatter than they actually are. But why do AN have larger body schema? One theory is that it could be caused by rapid weight loss, meaning the body schema is not updated. This was first shown by Guardia et al (2010), who, as body schema are involved in action, investigated how anorexic patients estimate body size in relation to actions. This study used a doorway aperture method – participants had to imagine whether or not they could walk through an doorway of varying sizes at normal speed and without turning sideways. They found that anorexic patients significantly overestimated their shoulder width compared to controls, which suggests a dysfunctional body schema.

Another study (Metral et al, 2014) found that anorexic patients act like they are fatter than they are too. This used the same method as the one described above. However, instead of just imagining whether or not they could pass through an aperture, participants had to then actually carry out that action.


Therefore, it is likely that a combination of all these factors causes patients with anorexia to view themselves as being fatter than they actually are, and continue to restrict their diet as they believe they need to lose weight. It is therefore vitally important to break this cycle by treating body dysmorphia, in order to allow anorexic patients to view their true body size, and enable them to make a full recovery.




This blog post will look at what hallucinations are, what causes them, and what can be do to help people who suffer from them. Normally, we are pretty good at identifying what’s real in the environment, but occasionally this processing is distorted, and people see things which aren’t there. This is a hallucination, and the most common type is auditory.


Although they are a symptom of schizophrenia, they can occur in people without the condition, and factors such as drug use, sleep or sensory deprivation or bereavement can make them more likely to occur.

It has been hypothesised that hallucinations are caused by an internal event being misattributed to an external source. For example, internal speech is thought to originate from something external, and so is experienced as hearing a voice. Evidence to support this comes from a study by McGuire et al (1993) who found increased blood flow to Broca’s area during auditory hallucinations – this is an area of the brain involved in language production.

This externalising bias is thought to be caused by impairments in self-monitoring, which means that sufferers do not identify the sense of effort or intention behind their actions. Evidence for this comes from studies such as one carried out by Johns et al (2001), which ask patients to speak words out loud into a microphone. The words are then played back to the individual, some distorted and some in another person’s voice. The patient then has to identify whether or not they spoke the word. This study found that patients with hallucinations were more likely than healthy controls to identify their speech as someone else’s.


One of the most successful ways to treat hallucinations is using cognitive therapy, which involves challenging people’s beliefs about their voices. At first this is done using a hypothetical contradiction, before progressing to directly questioning their beliefs.

A new form of therapy to treat hallucinations has recently been developed, and involves the use of technology. Leff et al (2013) helped patients develop an avatar which resembled the voice their hear, and the patient was encouraged to stand up to the voice. The therapist spoke as the voice, and gradually changed their responses so that the avatar was under the control of the patient. This technique was found to reduce hallucinations more than traditional methods.

However, most of the research has only focused on auditory hallucinations, whereas they can occur in any sensory modality. Therefore, more needs to be done to develop successful therapies for these other types of hallucinations.


Thanks for reading!


Can you imagine constantly feeling as though people are plotting against you, or that they are watching you and spreading rumors? These are common symptoms of people who suffer from delusions, which is turn is a symptom of schizophrenia.

Delusions are defined as implausible, unfounded and strongly held beliefs which are personal to the individual and are extremely preoccupying and distressing to them (Freeman, 2007). There are 3 main types:

  1. Grandiose: beliefs that they have a special talent or are related to someone special
  2. Persecutory: beliefs that they are going to come to some harm which is intended by others
  3. Reference: beliefs that others are watching them or deliberately spreading ideas about them

One of the most influential models of delusions is the Threat-Evaluation Model (Freeman et al, 2002). This states that there are 3 main psychological processes which lead to uncertainty, and in turn to a delusion – shown in the flow chart below:

threat anticipation


The first of these processes is deficits in reasoning; in particular they jump to conclusions rather than considering all the evidence.

This has been shown by the Beads Task – participants are presented with 2 jars filled with 2 different coloured beads in opposite proportions e.g. 85 red, 15 blue in one; 15 red and 85 blue in the other.

The jars are then hidden from view, and the experimenter picks out beads from one of the jars one by one. The participants’ task is to work out which jar the beads are from. Several studies have found that schizophrenia patients need fewer draws to make a decision, compared to healthy participants, suggesting that they have a tendency to jump to conclusions.

The second of these processes is anomalous experiences – these are often internal and do not have an immediate explanation, so patients attribute them to external sources. For example, Zimbardo et al (1981) used hypnosis to induce a hearing problem in participants, with half told why, and half not. They found that the participants who were not told about their hearing problem had more paranoid thoughts during a social interaction.

The last process is emotions – depression and low self-esteem are thought to cause a negative bias when interpreting events, which can lead to delusions. Freeman et al (2003) showed this using a virtual reality study, in which participants had to go on a virtual tube journey. The avatars on the tube were programmed to behave neutrally, however 1/3 participants had persecutory thoughts about them, e.g. they looked intimidating. The researchers concluded that this is caused by higher levels of anxiety and interpersonal sensitivity.


I hope you liked this brief overview of this complex topic – check back soon for more posts!


Post – traumatic stress disorder, or PTSD is a type of anxiety disorder which is characterised by:

  • reexperiencing the trauma (intrusive thoughts)
  • avoidance and numbing
  • increased arousal

It has a lifetime prevalence of about 8%, and is more likely to occur in women than men.

It differs from other anxiety disorders as it is anxiety about something which has happened in the past, whereas other ADs are about something which could happen in the future.


This has been explained by the Cognitive Theory of PTSD (Ehlers & Clark, 2000), which states that the sufferer views the traumatic event in a way which produces a sense of serious current threat – they believe they are still in danger.

This is caused by 2 processes:

  • appraisal of the trauma
  • the nature of the traumatic memory and its link to other autobiographical memories.

They could believe they are still in danger as they could interpret the world as being a very dangerous place, or thinking that it was something about them in person that caused the traumatic event to happen.

These processes generate situational fear and avoidance, and therefore maintain fear and anxiety.

The 2nd process which contributes to anxiety is that the memory of the trauma is often poorly elaborated – it is muddled up and not integrated with other past memories. Foa & Riggs (1993) found that sufferers of PTSD can have difficulty intentionally remembering the traumatic event, but have regular involuntary ‘flashbacks’ which are very vivid and emotional. These memories are experienced as being in the present, so act as a source of current threat.

Cognitive therapy for PTSD therefore aims to change the individual’s appraisal of the trauma, so they don’t think the threat is current, as well an integrating the memory into other past experiences. It also encourages sufferers not to try and repress the intrusive memories, as this can actually have the opposite effect and make them think about it more. Finally, it aims to reduce safety behaviours such as avoiding reminders of the trauma e.g. not travelling by car after being in a car accident.

Cognitive Behavioural Therapy is the NICE recommended therapy for PTSD and has been shown to be more successful than other therapies such as drugs or counselling.


Thank you for reading!


Can you imagine only being able to see one thing at a time?

This is the struggle faced by patients with Simultanagnosia – an extremely rare visual disorder. The reason this is so rare is that it is caused by damage to the posterior parietal cortex (shown in light blue below) but on BOTH sides of the brain.




The damage to the brain is thought to cause deficits in grouping stimuli, although this is thought to be due to impaired attention rather than impaired perception. 

For example, Luria (1959) found that if patients were shown a star of David with one triangle blue, one red, they only reported seeing one of the triangles, however if the triangles were the same colour, they saw the whole shape.




This result is interesting, because both shapes take up exactly the same amount of space on the retina, which shows that this disorder isn’t caused by a restricted visual field.

Patients also show a bias for local rather than global stimuli – this means they focus on small details rather than the overall shape.

This was shown in an experiment by Shalev et al (2008). The stimuli used were big letters made up of little letters e.g. lots of little H’s forming one big H. Healthy participants are quicker at identifying the big letter when it is made up from little letters that are the same, compared to when they are different, e.g. a big H made of little D’s.

However, Simultanagnosia patients do not show this pattern of results – instead they are faster at identifying the small letters regardless of whether they are the same as the big one.



As you can see from this graph, Simultanagnosia patients get a high percentage of single letters correct, but are impaired for the global (big) letter when it is made of smaller ones, regardless of whether they are the same or not.

One way to help patients see more than one item is to group items together.

For example, although patients cannot read text, they can read single words as the letters are grouped together. Hall et al (2001) found that familiarity of words also helps them be identified, as patients are bad at reading non-words. They also presented patients with acronyms (e.g. NHS) presented in capitals (familiar form) or in lower case (unfamiliar form). They found that Simultanagnosia patients could only recognise the acronyms when they were in capitals, showing that familiarity helps patients recognise the global form.


Thank you for reading!