In addition, both anorexics and bulimics have been shown to have delayed gastric emptying in other words it takes longer for food to leave the stomach (Int J Eating Disor, 1992; 11: 163-72; see also Robinson, PH, Gastric Function and Eating Behaviour in Anorexia and Bulimia Nervosa, in Walsh, BT (ed), Eating Behaviour in Eating Disorders, American Psychiatric Press, 1988; 125-40). This can also contribute to feelings of fullness and motivate the individual to diet or to purge more strenuously.

In one study, delayed gastric emptying was linked, not to the effects of starvation or vomiting, but to factors not related to nutrition such as high rates of depression and anxiety. This was particularly true in bulimics (Lancet, 1995; 364: 1240).

Obesity/obsessive eating

The American public spends $33 billion each year in weight control efforts without any real effect (BMJ, 1995; 346: 134-5). Some researchers have estimated that by the year 2030, 100 per cent of adults in the USA will be overweight (JAMA, 9194; 272: 205-11). In many ways, obesity is a more insidious disorder. Its prevalence in some 15 per cent of the adult population in the UK and some 33 per cent of the adult population in the US (JAMA, 1994; 272: 205-11) means we often do not treat it as a serious illness.

Often the results of research into fat busting drug cures resemble the same kind of yo yo between poles which obese individuals experience when they diet. For instance, two major trials done around the same time on cimetidine (Tagagel), a wonder substance which promised to melt the pounds away, showed either that it had no effect at all (BMJ, 1993; 306: 1093-96) or that it led to reduced hunger, reduced food intake and subsequent weight loss (BMJ, 1993; 306: 1091-93).

Similarly inconsistent results have been found with investigations of a genetic explanation for obesity. Only a few years ago the papers were ablaze with the miracle story of fat laboratory mice who, when injected with leptin, the byproduct of the Ob gene, lost 12 per cent of their body weight and practically all of their body fat in four days (Science, 1995; 269: 540-3, 543-6, 546-9). The conclusion was that within obese individuals this gene is defective and so they have less leptin circulating in their bodies.

Not long after this study appeared, two other studies showed that very obese people, particularly women, have 80 per cent more leptin circulating in their bodies (Nature Med, 1995; 1: 905-53, 953-6). These findings were further echoed by a study in the New England Journal of Medicine which found that obese men and women have leptin levels up to four times higher than healthy controls (N Eng J Med, 1: 1996; 334: 292-5).

As if to underline the fact that data from animal studies cannot be easily extrapolated to humans, scientists have yet to explain why it is that the mice bred to produce no leptin were fat, while "normal" fat people seem to overproduce it.

Further, the theory that fat people have high levels of leptin and anorexics have low levels of leptin was disputed when one research team measured leptin levels in a group of anorexics.

What they found was that a third of the group had leptin levels in the normal range one of these individuals had the lowest body mass index of the group (BMJ, 1995; 346: 1624-5).

Perhaps the most fruitful avenue of exploration for obese individuals is that of food sensitivities. Obesity can be linked, for instance, to persistent hunger. According to Charles E Bates, author of Beyond Dieting: Relief from Persistent Hunger, Victoria, Canada: Tsolum River Press, 1994), delayed, or non IgE, food allergy may be at the root of obsessive eating habits. He believes obesity may be a symptom of an immune mediated eating disorder, or IMED, which is caused by a combination of digestive system and immune system errors.