Wheat, Rye, Barley, and Oats
Early conclusions regarding the toxicity of cereal grains and their constituents were based mainly on the ability of a grain to produce malabsorption of fats in celiac patients. Despite the lack of the more sophisticated approaches available today, early test results generally seem convincing. Currently, examination of mucosal biopsy specimens has become fairly common. When a flattened mucosa is found, with loss of villous structure, wheat and other harmful grains are removed from the diet to see if improvement follows. If it does, a subsequent challenge and biopsy to test for relapse may follow, although subsequent challenge has come to be reserved for special circumstances (Walker-Smith et al. 1990) because supporting antibody tests (tests for circulating antigliadin and antiendomysium antibodies) have lessened the likelihood of misdiagnosis (McMillan et al. 1991). In recent years, however, the situation has become more complicated through recognition that a flattened mucosa may actually be an extreme response and that there are many gluten-sensitive people who show less obvious evidence of the disease (Marsh 1992a). Circulating antigliadin antibodies may be indicative of celiac disease or at least a related gluten-sensitive condition in the absence of any evidence of mucosal changes, particularly when symptoms are present (O’Farrelly 1994).
Relatively few subjects were used in the testing of some grains or grain fractions in early work. This has been a continuing problem, resulting largely from the difficulties inherent in the requirement for human subjects in celiac disease research. It has become fairly clear that response to challenge may vary greatly from one patient to another and for a single patient over time. Furthermore, a considerably delayed response to challenge is not unusual, even when the challenge is with wheat, presumably the most toxic of the cereal grains (Egan-Mitchell, Fottrell, and McNicholl 1978; Walker-Smith, Kilby, and France 1978).
The variations in response known to occur might explain the opposing conclusions arrived at by various investigators regarding the harmful effects of oats. For example, Dicke, H. A. Weijers, and J. H. Van de Kamer (1953) asserted that oats are toxic, whereas W Sheldon (1955) concluded that they are not. Part of the problem apparently arises from the relatively small proportion of avenins, the likely toxic fraction, in oat grain proteins (Peterson and Brinegar 1986): Avenins may make up only about 10 percent of the total protein in oats. Furthermore, when small numbers of subjects are involved, the average response of one group can be quite different from that of another. Because a negative response in one or a few patients might indicate only that the feeding time was too short, a clear positive response, as in the studies of oat protein toxicity by P. G. Baker and A. E. Read (1976), should perhaps be given more weight than a negative response, as in the study by A. S. Dissanayake, S. C. Truelove, and R. Whitehead (1974). The latter effort, however, included testing by intestinal biopsy - the more rigorous test - whereas the former did not.
A recent feeding trial using oats with 10 confirmed celiac patients produced no harmful effects as indicated by changes in mucosal architecture, endomysial antibody development, and infiltration of intraepithelial lymphocytes (Srinivasan et al. 1996).The relatively low percentage of avenins in oats may complicate this study in that a daily dosage of 50 grams (g) of oats was fed for 3 months. This would correspond to about 5 g of avenins per day. If 50 g of wheat had been fed instead, the patients would be eating at least 40 g of gliadins per day. Nevertheless, subsequent challenge of two of the patients with only 0.5 g of gluten per day produced evidence of intestinal damage. Thus, the toxicity of oats must be considered questionable on the basis of this latest study, as there are now two careful studies that showed no evidence of toxicity and only one study that was positive. It should also be emphasized that the supposedly positive study did not include biopsies.
In other cases, the test materials may not have been well defined. It is possible that the maize (corn) flour used in early testing was actually maize starch and relatively free of protein (Simoons 1981); the conclusion that maize proteins are not harmful may not have as rigorous a scientific base as is generally thought. There is, however, no obvious reason to question the apparent safety of maize.
A lack of sensitivity of the available testing methods, combined with inadequate test length, may have been responsible for the early conclusions that wheat starch is safe for celiac patients (Dicke et al. 1953). These conclusions, however, were challenged in later work (Ciclitira, Ellis, and Flagg 1984; Freedman et al. 1987a, 1987b; Skerritt and Hill 1990,1991) as a consequence of the development of sensitive monoclonal antibody tests for gliadins (but also see Booth et al. 1991). Such tests have demonstrated the presence of small amounts of gliadins in wheat starch preparations, although the question of how harmful these small amounts may be to celiac patients is controversial (Ejderhamn, Veress, and Strandvik 1988; Hekkens and van Twist-de Graaf 1990; Campbell 1992).
It may be that rigorous scientific studies have proved toxicity in celiac disease only for wheat (and wheat proteins). To a considerable extent, conclusions regarding the toxicity of rye and barley - and, conversely, the lack of toxicity for rice and maize - are not based on an adequate amount of rigorous scientific testing. (Rigorous studies of oats are beginning to appear, and these support an absence of toxicity for this grain.)
World History
