Doctors consider anorexia, bulimia and obesity as a mainly psychological problem, but new research shows that vitamin deficiencies and even allergies are often the hidden causes of eating disorders.
Eating disorders, whether they be the starvation regimes of anorexia and bulimia or the compulsive eating which leads to overweight and in some cases morbid obesity, are on the rise. Medical research has, frustratingly, not kept pace with the increase. For years the theory that people who suffer from these problems are mentally unstable, slothful or undisciplined has prevailed so much so that it is now difficult to find any practitioner who will acknowledge a possible biological basis for these disorders.
No one would deny the psychological component of eating disorders, but as a total diagnosis it is unsatisfactory. For instance, family background is often cited as a risk factor in eating disorders, with those coming from abusive or dysfunctional families having the highest risk. But we have to ask: how is it that there are women who come from abusive or dysfunctional families who do not develop into anorexics or turn to compulsive eating as a way of dealing with unresolved problems?
To the minds of many clinicians, “fat phobia” is still the central defining characteristic of anorexia and bulimia (Soc Sci Med, 1995; 15: 25-36; Int J Eat Dis, 1996; 1594: 317-34). But entrenchment in this attitude hasn’t moved us much closer to a cure. In one study, only 29 per cent of treated anorexics had shown significant recovery 20 years later, and approximately 15 per cent died from suicide or starvation (Br J Psych, 1991; 58: 495-502).
Equally, since there is not yet a medical cure for obesity, it is often easier to explain it away by blaming some weakness in the individual. Yet we know that simplistic solutions such as eating less and/or exercising more do not always produce results. Some theorists believe that exercise contributes little to weight loss (AM J Clin Nutri, 1993; 57: 127-34). This is because physical activity normally only accounts for a small proportion of an individual’s total energy expenditure. About 80 per cent of a person’s energy is used to maintain the resting physiological processes of the body and to digest food (Am J Clin Nutr, 1992; 55: 533S-7S).
At the same time, individuals can vary enormously in the way they can dissipate energy through diet induced thermogenesis (fat burning). When one study looked at pairs matched for sex, weight, age, height and activity level, it found that it was not uncommon for one member of a pair to be consuming twice as many calories as the other member without gaining more weight than the other (Br J Nutri, 1061; 15: 1-9).
It’s time to take a wider view.
Anorexia and bulimia affect nearly 1.2 million adolescent and young adults in the US, but only 5-10 per cent of these are males. In the UK, an estimated 1 per cent of teenagers are anorexic and 3 per cent, bulimic. Estimates of mortality can range from 1 to 5 per cent and are usually due to kidney failure, heart attack, dehydration or suicide (Nurse Pract, 1990; 15: 12-18, 21).
As stated before, recovery rates are not very encouraging. Although in one study over six years, 77 per cent of patients were classified as “recovered”, at the end of the study period the total risk of relapse among recovered anorexics was 48 per cent though none had more than one relapse. More worrying, the mortality rate was 17.8 times higher than expected, with bulimic patients having twice the risk of premature death as anorexics (Acta Psychi Scand, 1993; 19: 437-44).
Recent data suggests that imbalances in serotonin the hormone involved in the regulation of feeding and mood remain altered in anorexia patients, even after weight restoration (Arch Gen Psychi, 1991; 48: 556-62).
Few studies have explored potential links between multiple chemical sensitivity and anorexia. Women use more highly perfumed products (toiletries and household cleaners) than men, and it is possible that an assault on the olfactory nerves from petrochemicals, which cross the blood brain barrier, can create chronic problems physical and psychological (Toxicol Ind Health 1992; 8: 181-202), in much the same way as glue sniffing. These things may be causes in their own right, or they may simply be the things which increase an individual’s vulnerability.
Although many of the symptoms of anorexia mimic those of mercury poisoning, there is little information other than anecdotal on any possible links with sources of mercury toxicity, such as from dental amalgam and vulnerability to slimming disorders. WDDTY panellist Jack Levinson has commented that he has seen young girls diagnosed with eating disorders recover once their amalgam fillings were removed. Excess mercury, he says, blocks the body’s absorption of zinc, and there are many studies which confirm that zinc deficiency could be a biological cause of anorexia.
Zinc deficiency and anorexia are similar conditions. Both tend to affect females between ages 12 and 25, and both are characterized by weight loss, changes in appetite and taste, yellowish skin pigmentation, depression and loss or irregularity of menstruation.
When Dr Rita Bakan and her colleagues at the British Columbia Institute of Technology conducted a clinical trial that used zinc supplementation to treat anorexia, they found that patients who received the supplement gained weight “significantly faster” than those who received a placebo (Townsend Letter for Docs, Nov 1993: 1154). In another study, those taking supplements also showed weight gain (Acta Psychi Scand, 1990; 361 (Suppl): 14-17).
Other practitioners have also assessed the zinc link (see Schauss, AG et al, Nutrients and Brain Function: 1987: 151-62; Ann Nutri Metab, 1992; 36: 197-202; J Clin Psychi, 1993; 54: 63-6) and found it a relevant factor in anorexia. One study concluded that anorexics have a lower intestinal uptake of zinc than normal subjects (Lancet, 1985; 1: 1041-42). Other studies have shown that anorexics and bulimics are deficient in zinc due to a variety of reasons lower dietary intake, impaired absorption, vomiting, diarrhea or binging on low zinc foods. Since zinc deficiency results in decreased food intake, it can be concluded that the acquired zinc deficiency of bulimics and anorexics could exacerbate their altered eating behaviour (J Clin Psychi, 1989;50: 456-9; see also J Am Coll Nutri, 1992; 11: 694-700).
Many bulimics perceive themselves as being uncomfortably full thus the rationale behind induced vomiting or abusing laxatives. In one study, normal weight female bulimics who had abstained from binge eating and purging for at least a month were studied. What the researchers found was that they had irregularities in the hormonal process that regulates fluid volume in the body a fact which may be relevant to their behaviour (J Clin Endocrinol and Metab, 1992; 74: 1277-83).
Pre existing hormonal imbalances are also common in anorexics. Indeed, amenorrhea develops in many patients before the onset of substantial weight loss has occurred, and age inappropriate gonadotrophin secretion patterns are present in some patients who are weight recovered (see Pirke, KM et al, The Psychobiology of Anorexia Nervosa, New York: Springer-Verlag, 1984; 46-57).
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).
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.
This process of errors is cumulative, says Bates, and may begin in infancy. Signs of IMED are apparent in babies who have feeding problems, colic or some kind of chronic indigestion, diarrhea, allergies, eczema and an inability to tolerate certain foods such as cow’s milk. Later they may show a tendency towards chronic bronchitis and middle ear infections.
In school they may have learning disabilities or hyperactive behaviour. The process takes its toll over the years. By adulthood there may be more complaints: irritability, joint pain, noticeable fatigue, depression and migraines, gastritis, ulcers and heartburn. Any chronic inflammatory disease of the upper or lower gastrointestinal tract is a significant sign.
Bates’ theory sits well with the inroads made into the link between blood type and diet. The theory goes that dietary lecithins can trigger different allergic responses in different individuals, depending on their blood type (J Nutri Med, 1991; 2: 45-64; Am J Clin Nutri, 1980; 33: 2338-45; see also D’Adamo, J, One Man’s Food is Someone Else’s Poison, Marek, 1980). If food lecithins pass undigested into the gastrointestinal tract, they are either recognized as self or non self by the body’s immune system. Cooking eliminates a large percentage of dietary lecithins, but not all. Some, such as those present in wheat, tomato, carrot, corn, banana, peanuts, pumpkin seeds and avocado, are highly heat resistant.
Although not specifically centred around obesity, the research into serotyping and diet shows that certain blood groups react badly to certain types of foods, resulting in allergies, inflammation and leaky gut as well as wasting diseases such as Crohn’s disease (Townsend letter for Docs, Nov 1996: 74-7).
Another theory is that, for a variety of reasons we wrongly interpret our body’s needs. Dr. Fereydoon Batmanghelidj, author of Your Body’s Many Cries for Water (Global Health Solutions, 1994) believes that many common illnesses today are the result of a profound kind of dehydration. Infants recognize thirst and cry out when they need liquid. But, he says, as we grow older we become unused to drinking water, and gradually the thirst signals are misinterpreted or over ridden. As they grow up, children learn to drink sodas, colas and juices instead of simple water. Adults respond to the body’s thirst with tea, coffee and alcohol all of which dehydrate the body further (Independent, January 11, 1994. The body then responds by releasing more anti diuretic hormone, and a vicious cycle is instigated.
If food sensitivity and/or dehydration theories are correct, obesity could be seen as not just excess fat, but a kind of waterlogging which occurs as the body tries to restore balance.