Another area of speculation with a substantial following is concerned with nutrition. The nutritional theories divide in the same way as the viral theories. Some postulate prenatal nutritional deficiencies, which have caused developmental abnormalities and others argue that schizophrenia is caused by a deficiency in the current diet of the patient. Whereas the first group of theories generally do not have a direct remedy, the second group often does.
A considerable amount of research has focussed on historically recorded famines, and these events have been used to explore a hypothesised link between the starvation of pregnant mothers and schizophrenia in offspring. The Dutch Winter Famine of 1944–1945 provided Dutch researchers with the opportunity to explore this connection, and one group has concluded that starvation during pregnancy can be a factor in the development of schizoid personalities in offspring.
Researchers give four reasons for supporting the prenatal nutrition hypothesis: 1) the known effects of prenatal starvation are not incompatible with the observed features of schizophrenia; 2) brain abnormalities can develop as a result of these events; 3) general malnutrition has also been observed to cause abnormalities in areas of the brain that have been linked to schizophrenia; 4) it is known that proper prenatal nutrition is essential for the correct development of the fetal nervous system. But no hard evidence has yet been found to support this type of hypothesis. Indeed, there appears to be no evidence of a relatively high incidence of schizophrenia in countries where malnutrition has been endemic for generations. Nevertheless this area seems particularly attractive to some researchers, and the Dutch Winter Famine has been linked statistically to a two-fold increase in the risk of schizophrenia.
Amongst the second group of nutritional theories, which argue that schizophrenia is caused by deficiencies in the diets of adult schizophrenics, one theory claims that schizophrenia can be rectified with a high wheat diet. But this recommendation is directly contradicted by another theory which recommends avoiding wheat products.
The kinds of cereal grain from products customarily eaten may be a factor in the production of psychiatric symptoms. There might be a relationship between schizophrenia and coeliac disease, a disease of known sensitivity to wheat and sometimes to milk. The wheat and rye-eating areas of the world have the highest incidence of schizophrenia, with oats and barley areas next, followed by the rice-eating areas (with approximately 60% of the incidence of the wheat areas). In sorghum and maize-eating areas the incidence of schizophrenia was approximately 25% of the wheat areas and in the highlands of New Guinea a practically nil incidence is found. Here no grains are eaten. William Philpott, an American psychiatrist, found that half his sample of schizophrenic patients could not tolerate milk and 64% were wheat sensitive.
The confusion over whether wheat might have a beneficial or detrimental effect on people inclined towards psychosis is fairly typical of the many contradictions that surround schizophrenia. Perhaps this particular area of confusion might in part be explained by the well-known relationship between vitamin B12 deficiency and pellagra, a disease that affects the skin, the digestive and nervous systems, and which commonly presents with schizophrenia-like symptoms.
In 1937, Elvehjen identified niacin deficiency as the cause and niacin the cure for pellagra, after which large numbers of pellagra psychotics recovered and were found not to be schizophrenic. As a result of this discovery, niacin is now routinely added to bread.
Despite the length of time that this association between vitamin B12 deficiency and psychotic symptoms has been known contemporary researchers still occasionally announce its re-discovery. One recent example from Singapore reported a case study involving an observed link between vitamin B12 deficiency, anaemia and schizophrenia, and recommended supplementing neuroleptic medication to compensate.
Next: Genetic Theories
 J. O. Davis and H. S. Bracha, ‘Famine and schizophrenia: first-trimester malnutrition or second-trimester beriberi’, pp. 1–3.
 H. W. Hoek et al., ‘Schizoid personality disorder after prenatal exposure to famine’, pp. 1637–9.
 A. S. Brown et al., ‘Neurobiological plausibility of prenatal nutritional deprivation as a risk factor for schizophrenia’, pp. 71–85.
 E. Susser et al., ‘Schizophrenia after prenatal famine. Further evidence’, pp. 25–31.
 R. S. Smith, ‘The GI T-lymphocyte theory of schizophrenia: some new observations’, pp. 27–30.
 Brian Hyfryd, ‘Neglect of the Body to the Detriment of the Patient: Management Notes’, pp. 47–53.
 James S. Howard, ‘Requiem For Schizophrenia’, pp. 148–55.
 S. M. Ko, and T. C. Liu, ‘Psychiatric syndromes in pernicious anaemia—a case report’, pp. 92–4.