Access Psychology Hannah Butler

The biological explanation of Anorexia nervosa The biological explanation for Anorexia Nervosa can be explained by using the Biomedical model which suggests that psychological problems have physical causes. There are 3 ways in which the biomedical model suggests how psychological disorders can be caused either by Genetics Neurochemistry (abnormal brain chemistry) Brain (abormal brain functioning or structure)

Genetics It is suggested that Eating disorders (ED’s) tend to run in families which would lead us to think that it is genetic causes that cause ED’s. Kaye (1999) found that 10% of ED patients have a relative who also have an ED. However, there is 90% of patients that this didn't occur in which is a lot higher which would suggest that there is other causes why people develop a ED so it is difficult to tell if it is genetic or partly to do with the environment.

Evaluation: Holland et al (1988) Used as evidence to support this

Neuroanatomy The dual hypothalamic theory of eating explains how the lateral hypothalamus (LH) and the ventromedial hypothalamus (VMH) act to regulate our feeling of hunger and satiety. It would seem possible that problems with these structures may cause abnormal patterns of eating, perhaps having the set- point for hunger set too low.

Malfunctioning of the hypothalamus Malfunctioning of the HYPOTHALAMUS has been linked to anorexia, as this part of the brain is important in regulating eating. Animal experiments involving lesions in particular parts of the hypothalamus have led to animal either over-eating or starving. Kaplan & Woodside (1987) showed that when the neurotransmitter noradlrenaline acts on part of the hypothalamus, animals begin eating & show a marked preference for carbohydrates. The neurotransmitter serotonin, by contrast, seems to induce satiation & suppress the appetite.

NORADRENALINE – LEADS TO EATING SEROTONIN – SUPPRESSES APPETITE LATERAL HYPOTHALAMUS (LH) = PRODUCES HUNGER VENTROMEDIAL HYPOTHALAMUS (VMH) = DEPRESSES HUNGER A malfunction here may be the cause of loss appetite in some, and over-eating in others. For anorexics, it is as if their VMH is jammed in the ON position.

Karl Lashley (1938) Suggested that eating is not just a relax action. Used hungry rats to support his belief that neural mechanisms are involved in decision making. He cut out areas of their brain to see the different effects that they had on their ability to negotiate a maze successfully and reach the food placed at the exit as a reward. Rats whose ventro-medial hypothalamus (VMH) had been lesioned developed overeating and obesity.

Findings Lashley (1938) found that the hypothalamus played a vital role in the regulating of food intake. The Lateral hypothalmus was found as the main hunger centre and the Ventro-medial hypothalmus as the main satiety centre. Critisims: We can not carry out a experiment similar to this on humans as it is not ethical, but can we relate rats and humans together? No evidence in humans for structural damage to appetite related hypothalamic regions

Biochemical factors Serotonin is a neurotransmitter that helps regulate mood and is associated with many behaviours such as Hunger, sleep, secular response, anxiety and perception and this can be increased from containing starch from food. It is mainly associated with happiness and lifting mood when there is enough serotonin, but if there are low levels then this is when the individual can turn aggressive and in a bad mood. Abnormally high levels of serotonin lead to acute anxiety (continual fight or flight mode), constant state of feeling overwhelmed or insomnia. So by reducing the level of calorie intake to starvation level, the result would be calming or the individual would feel like they are regaining control causing serotonin levels to drop.

The acts of restricting food can lead to a disruption in serotonin levels, which could create a completely new problem to deal with, this could be depression or anxiety which are well known side effects of under eaters or over eaters. Studies suggest that there are genetic pre- dispositions to serotonin disruptions that appear to run in some families. However, there are individuals that live with too little amounts of serotonin and they do not develop a ED which would suggest that there is individual differences. So basically, a change in serotonin levels would result in starvation as a sufferer would want to get back to that calm and relaxed state. Fitcher and Pirke (1995) found normal individuals who were starved had changes in neurotransmitter and hormone levels (starvation hypothesis).

Holland et al 1984 Aims: To establish whether there is any genetic basis for the eating disorder Anorexia Nervosa (AN) A variety of data suggest that Anorexia may have a genetic basis. This study aimed to explore this possibility by comparing incidence of anorexia in identical (MZ) and non-identical (DZ) twins. Since twins are raised in the same environment, similarity may be due to nature or nurture. However, if MZ twins are more similar, this implies that genes play a greater role.

Method 45 pairs of female twins were interviewed where at least one twin had had anorexia. The interviews established the clinical characteristics observed as well as the occurrence of eating disorders in any close relatives. Records were also made of body mass and length of amenorrhoea, and questions asked about drive to be thin and body dissatisfaction. In order to determine whether twins were identical or not, a blood test was used. There were 25 MZ twins and 20 DZ twins in the study.

Findings There was significantly higher concordance in the MZ twins; 25 (56%) of the MZ twins were concordant for anorexia whereas only 1 (5%) of the DZ twins was. There was significantly more anorexia in relatives studied than found in the normal population. The rate of anorexia in the population in general is 0.1%. The study found 6 cases of anorexia among first-degree relatives (4.9%) and in the second- degree relatives there were 2 cases (1.2%). The measures of body mass, amenorrhoea, drive to be thin and body dissatisfaction indicated that these were heritable as there was greater similarity between MZ and DZ twins.

Conclusions The findings from all three different methods of analysis suggest that anorexia has a large genetic component. The figure of heritability may be as large as 80%; in other words, 80% of the variation in anorexia is due to genetic factors and 20% to environmental factors. This high figure may be partly explained in terms of how genetic factors interact with the environment. What is inherited is a genetic sensitivity to environmental factors.

Strengths of study Many measurements were used for analysis in this study such as blood tests, body mass and clinical interviews-in depth data. A more recent study by Bulik et al (2000) concluded that anorexia is 56% genetic, supporting Holland’s suggestion that there is a strong genetic link.

Weaknesses of study One difficulty with studies of anorexia is that the actual diagnosis in any individual is not that certain. Some individuals suffer both anorexia and bulimia, though not always at the same time. This means that the genetic susceptibility may be to ‘develop eating disorders’ rather than anorexia in particular. Gorwood et al (1988) suggest that if we want to identify the genetic causes of anorexia, we need to identify the distinct subtypes more clearly.

Twins don’t just share the same genes – they also share cultural and family values, and the environment for MZ twins is more similar than for DZ twins. Therefore, physiological and environmental factors are confounded. Indeed, the 56% concordance rate in MZs might be entirely due to their more similar upbringing than DZs.

Small sample - many twin studies involve a small sample size. Holland et al studied only 25 MZ and 20 DZ twins, and it is estimated that 15,000 pairs would be needed for a definitive, genetic study. The low occurrence of both twin births and eating disorders make this unlikely.

Eating Disorder Treatment: Medication for Anorexia Medication is used less frequently to treat anorexia compared to other eating disorders because there is little evidence that shows it works. The best medicine for anorexia nervosa is food. However, when medication is called for, antidepressants are typically prescribed to treat underlying mental health problems. Fluoxetine (Prozac) may help people with anorexia overcome their depression and maintain a healthy weight once they have gotten their weight and eating under control. Fluoxetine is in a class of drugs called selective serotonin uptake inhibitors (SSRIs). These drugs increase serotonin levels, a brain chemical connected to mood.

Kaye et al (2001) Kaye et al. (2001) is notable for its long duration and placebo-controlled evaluation of fluoxetine (Prozac), previously found to be effective in bulimia nervosa (Bacaltchuk et al., 2000). Kaye et al. studied 35 subjects with restricting and restricting-purging types of anorexia nervosa recruited during an inpatient program and followed them for one year. Weight gain and psychological measures (core eating disorder symptoms, depression, anxiety, obsessions and compulsions) improved only in the 10 patients who remained on fluoxetine treatment.

Dropouts were much higher in the placebo group (84% versus 37%). The high refusal rate and small numbers limited conclusions from the study. The authors postulated that there may be a relative serotonin "resistance" due to a compromised release of serotonin from presynaptic storage in underweight individuals with anorexia nervosa. The authors argued that this may reverse with weight gain and may explain the greater efficacy of SSRIs in normal-weight people with eating disorders.

There is insufficient evidence at this stage to support antidepressant therapy in combination with psychotherapies and various nutritional rehabilitation programs alone. As patients with anorexia nervosa are in a compromised physical state due to the effects of starvation, low dosage and caution is recommended in the use of most psychotropics and other agents, including antidepressants, for which there is limited evidence of efficacy