Eating 2-anorexia Flashcards
Anorexia: some facts: What is it?
The situation when someone tries to keep their weight as low as possible, for example by starving themselves or exercising excessively. How often does it occurs? Around 1 in 250 women and 1 in 2,000 men will experience anorexia nervosa at some point. The condition usually develops around the age of 16 or 17.
Social factors:
Social isolation, family dynamics, maternal criticism. Social messages promoting a specific type of body image.
Anorexia is a multi-factorial disorder: There is no ‘anorexia’ gene. Rather, genetically heritable personality traits and social factors predispose certain individuals to anorexia. There is a broader phenotype featuring perfectionism, rigidity, tendency to behavioural constraints. Subsequently, dieting starts & maintains a self-reinforcing cycle of anxiety, weight loss and neurobiological changes
Possible causes of anorexia: Psychological factors:
Obsessive-compulsive behaviour (OCD), anxiety, depression. Childhood anxiety is an important genetically-mediated pathway towards the development of anorexia, which is reflected in onset of OCD (Kaye et al, 2004). OCD and anorexia can coexist but no sufficient cases support the causal link between the two. It is also unclear if OCD is cause or consequence of anorexia.
Possible causes of anorexia: Biological factors:
Twin studies show that 50% -80% of variance in anorexia can be explained by genetic factors (but these values are not always consistent). Altered satiety / hunger hormones: Ghrelin (“I’m hungry”): High levels in anorexia. Leptin (“I’m not fat”): Low levels in anorexia. Altered HPA axis: this is hyperactive in anorexia, and cortisol levels are raised to reflect a state of chronic stress. A mental disorder with genetic basis mediated by an altered brain transmitter system may pre-disposes some people to develop anorexia (Kaye et al, 1991; 2004). Hypothesis extensively tested but no consistent support. It is unclear whether these biological factors are cause or consequence of anorexia.
The neurobiological changes observed in anorexia are probably not the source of the initial problem, but it is hard to dissociate if they are a cause or effect. Animal models suggest these neurobiological changes are likely to be an effect rather than a cause of anorexia. Severe dieting in ‘healthy’ humans results in the same chemical state as anorexic, e.g. severe alterations of mood, feeding, body image etc.
What reinforces anorexia:
Eating less food is linked to reward. Physiological reasons why patients experience “reward” when first dieting. Corticotropin-releasing factor (CRF) is released when food intake is reduced. This activates the pituitary–adrenal axis (ACTH-cortisol secretion), Which in turn enhances dopamine (DA) release from the ventral striatum (nucleus accumbens, NAC). The ventral striatum acts as a ‘reward‘ system. CRF also activates dopamine-cell bodies in the mesencephalon (VTA, ventral tegmental area), Level of serotonin (linked to OCD) is elevated in A (Kaye et al,1997). Subsequently, anorexic behaviour is maintained because it is conditioned to the stimuli that provided the reward.
Conclusions: Obesity and anorexia are eating disorders with commonalities (multi-factorial disorders characterized by abnormal relation with food, and abnormal body weight) as well as differences (in the role of genes, emotions, body image, role of social and cultural factors).
The Minnesota Starvation Study: Keys et al, 1950
36 young men underwent very restrictive caloric intake for 6 months. Participants were selected from over 100 volunteers for having the highest levels of physical and psychological health, as well as the most commitment to the objectives of the experiment. Following the restricted diet, volunteers experiences were the same as those of patients with eating disorders, e.g. dramatic physical, psychological, and social changes, sometimes continuing during the rehabilitation or re-nourishment phase. Standardized personality testing (Minnesota Multiphasic Personality Inventory) revealed that semi-starvation resulted in significant increases on the Depression, Hysteria, and Hypochondriasis scales.
Settling-point theory: biology of fat cells
A lot of work is being done on the biology of fat cells. Researchers in Sweden recently discovered that people tend to drop out of weight loss programmes – not when they had attained their target weight – but when their fat cells had reached normal size. For two people of the same height, this could occur at greatly different weights. One person may have more fat cells than the other.
Some overweight children and morbidly obese adults are known to have more fat cells than usual. This is called hyperplastic obesity. Fat cells are usually formed at two critical periods of a person’s life – in early childhood and at puberty. We now know that new fat cells can be formed at any time of life if weight is gained rapidly or if fat cells grow to over 50% of their normal size.
Similarly, if people try to reduce their weight to the point where their fat cells shrink below normal size, the organism starts to behave as if starving (even if they eat fairly well). People with fat cells below normal size display all the usual symptoms of people with eating disorders (craving food, being obsessional and ritualistic). So there is obviously some kind of biological pressure to keep fat cells at approximately their normal size, even if technically this means that a person may be culturally “overweight. This provides evidence for the Set Point Theory which is described below.
