Not Ill Enough

Imagine living with depression. It affects every aspect of your life, from your work to the time you spend with your family. You experience intrusive negative thoughts. You begin to suffer from insomnia, which in turn increases feelings of anxiety. Imagine living with depression, but being told you are not ill enough to qualify for mental health treatment.

This scenario is unfortunately far too common in those seeking help for mental illness. Adult mental health services are often only able to treat the most severely ill, with their treatment focus on those with severe and enduring mental illnesses, such as psychosis or bipolar disorder (McGorry, 2007). This has led to strict eligibility criteria to be put in place when assessing whether someone is suitable to be cared for at their service, something thought to be in part due to a lack of funding and resources (Belling, 2014). If someone visits A&E with a broken arm we don’t wait for it to get worse before we treat it, so why does this happen if someone goes to their doctor with signs of an eating disorder? A recent investigation by the British Medical Associate found waiting lists of up to 2 years in some parts of the UK, (BMA, 2018). Once again this shows the disparity between our attitudes to physical vs mental healthcare.

According to the eating disorder charity BEAT, some people had to wait an average of 182 days to access care in some areas of the UK. This is despite all evidence pointing to the advantages of early intervention: an individual with an eating disorder is 50% less likely to relapse if they can access treatment early. Treatments have also been shown to be more effective if accessed at an early stage (BEAT, 2018).


This problem isn’t just specific to the UK – one study of carers with mental illness in Australia found that they had to push for their relatives to access appropriate care, with one of the main barriers being that they were not ill enough to be admitted to hospital for their mental health, in some cases despite being suicidal (Olasoji, 2017). Another study looked at the treatment gap in different countries (the percentage difference between the numbers needed treatment and those receiving treatment for it) and found the treatment gap for major depression to be between 36% in the Netherlands to 73% in Finland (Kohn et al, 2004). The international nature of this disparity in mental health care shows how global attitudes to mental illness need to change to allow people to access appropriate treatment as soon as they need it.

Young people can also experience disruption to care due to not meeting the eligibility thresholds in adult services, despite being eligible in the children’s service. In contrast to adult mental health services having high thresholds for care, those at children and adolescent mental health services can be much lower. Children’s services are generally perceived as being more supportive and nurturing than adult services, with a focus on treating emotional and developmental disorders, including autism and ADHD (McGorry, 2007). However this means that when young people reach the upper age limit of children’s services (at around 16-18 years old), they cannot be transitioned to adult care, as they do not meet the eligibility threshold. Therefore at this transition boundary, young people can ‘fall through the gap’ between services despite still being unwell. One study in Ireland estimated that two-thirds of young people do not receive a referral to adult services, despite still being unwell when they reached the upper age limit of children’s services (McNicholas et al, 2015). Those who do receive a referral can still experience a gap in care: adult services can have waiting lists of up to 6 months (Hovish et al, 2012).

It is clear that something needs to change to ensure that people with mental illness are able to access timely and appropriate support, without having to wait for their condition to get worse in order to qualify for treatment.

Please share and let me know your thoughts using the hashtag #MHAW18 and help raise awareness.



image reference: [accessed 13/05/18]

Belling, R., Mclaren, S., Paul, M., Ford, T., Kramer, T., Weaver, T., Hovish, K., Islam, Z., White, S. & Singh, S. P. 2014. The effect of organisational resources and eligibility issues on transition from child and adolescent to adult mental health services. Journal of health services research & policy, 19, 169-176. %5Baccessed 13/05/18]

Hovish, K., Weaver, T., Islam, Z., Paul, M. & Singh, S. P. 2012. Transition experiences of mental health service users, parents, and professionals in the United Kingdom: a qualitative study. Psychiatric rehabilitation journal, 35, 251.

Kohn R, Saxena S, Levav I, Saraceno B (2004). The treatment gap in mentalhealth care. Bulletin of the World Health Organization 82, 858-866

McGorry, P. D. 2007. The specialist youth mental health model: strengthening the weakest link in the public mental health system. Medical Journal of Australia, 187, S53.

McNicholas, F., Adamson, M., Mcnamara, N., Gavin, B., Paul, M., Ford, T., Barry, S., Dooley, B., Coyne, I. & Cullen, W. 2015. Who is in the transition gap? Transition from CAMHS to AMHS in the Republic of Ireland. Irish Journal of Psychological Medicine, 32, 61-69.

Olasoji, M., Maude, P. and McCauley, K., 2017. Not sick enough: Experiences of carers of people with mental illness negotiating care for their relatives with mental health services. Journal of psychiatric and mental health nursing24(6), pp.403-411.



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

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.


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, 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.



Eating Disorders

This is a topic I’ve been interested in for some time, and would love to do more research on. Here is an overview of the two restrictive types of eating disorders: anorexia nervosa and bulimia nervosa.

Anorexia is thought to be a relatively modern disorder, however it has been recognised as an eating disorder since the 19th Century, whereas bulimia has only been recognised since 1980. Anorexia is categorised by significantly restricted food intake coupled with a distorted body image. This eating disorder affects 1 in 200 adolescents, with 90% of the sufferers female. Sufferers of bulimia nervosa consume large amounts of food and then purge, either by forcefully vomiting or laxative abuse. This eating disorder is rare in men, and affects up to 3% of young women.

There are several different biological theories about the cause of eating disorders. If eating disorders have a genetic link, then abnormal relationships with food should be found amongst the close relatives of a sufferer of an eating disorder. A recent study found that the female relatives of an anorexia nervosa sufferer have an 11.4 times higher chance of having an eating disorder compared to the female relatives of someone who does not have the disorder.

One of the possible biological causes of eating disorders could a biochemical imbalance in the brain. The hypothalamus is a small cone shaped structure in the brain which connects to the pituitary gland via the pituitary stalk (see picture below).

The hypothalamus is the area of the brain responsible for maintaining homeostasis – part of which involves regulating appetite and thirst (Damage to the ventromedial hypothalamus has been linked to overeating, while damage to the lateral hypothalamus has been shown to cause starvation).

However, not every sufferer of an eating disorder has damage to their hypothalamus. The hypothalamus also regulates the secretion of neurotransmitters in the brain, and there is evidence to show that abnormally low or high levels of these neurotransmitters, in particular serotonin could be a contributing factor to eating disorders. Serotonin is involved in regulating hunger and satiety, and serotonergic disfunction has been found to increase susceptibility of eating disorders (Kaye et al).

One of the treatments for bulimia involves patients taking drugs called SSRIs which increase the amount of serotonin at synapses (like the one shown in the cartoon below). Taking these drugs has been shown to lessen the binging and purging symptoms of the disorder, although it is likely that other therapy is needed for a sufferer to completely recover.


However, although there are biological factors which can cause an individual to develop an eating disorder, there must be other factors which can also play a part. This is shown by the fact that there isn’t a 100% correlation between identical twins who have the disorder. There is also evidence that cases of eating disorders are rising, which has been blamed on the shift in culture towards favouring skinny models and celebrities.

Ogden (1992) analysed the physical features of female fashion models over a 20 year period, and found that models became taller, with a decrease in hip and bust size relative to waist size, giving a more androgynous body shape. These findings correlate with an increase in eating disorders, suggesting that there could be a causal relationship between them.

This was just a brief overview of the causes of eating disorders, although a single cause has yet to be identified. It is likely that an interaction of biological and social factors can cause someone to develop anorexia or bulimia. As eating disorders have the highest mortality rate of any mental illness, it is vital that more research is done in order to develop effective treatments and help more people overcome these conditions.