[Food allergies]. / Lebensmittelallergien.

Food allergies are not a phenomenon of our time. The public and published opinion characterize food allergies as an accompanying symptom of our modern industrial society. However, many years before our time, Hippocrates (400 B.C.) and Lucrezius (1. Century A.D.) had described symptoms of illness which seemed to be due to food-allergies and intolerances. Today, allergies (especially food allergies) are often depicted as having increased excessively and that this increase seems to result from harmful substances in the environment, residues, food additives or may even be due to food manufacturing processes. It is estimated that the frequency of all types of allergic illnesses at this time in West-Germany is between 10-20 percent. Taking into consideration all degrees of difficulty, the number of people with food allergies lies under 10 percent of the population, although exact numbers in this area are missing. It is undisputed that food allergies are induced as a result of some of the foreign substances mentioned. However, the predominant share of food allergies occur as a result of natural food substances. The trend towards less processed foods has especially increased the risk of food allergies, since for example unmodified protein may contain more possible allergens than the corresponding protein which has been denatured by heating. The wide distribution of "new" foods from exotic countries and the enormous expansion in the variety of seasonings is also thought of as a cause for many allergies. One cause for more allergens reaching our abundantly set tables is the increased distribution and range of products resulting from expansion of national and international trade. Allergy, which to some extent is due to a malfunctioning immune system, activates certain defense mechanisms in the body. Food or more precisely its contents, then becomes an alien substance or antigen for the body against which it builds certain antibodies to "stay in a good state of health". These antibodies cause typical allergic reaction such as nausea, vomiting, diarrhea, urticaria and difficulty in breathing, after a certain food has been eaten. We must differentiate between food allergies and incompatibility (food intolerances). The body does not produce antibodies for the latter. Unlike food allergies, intolerances can disappear with time.

Effect of functional stimulation on ascorbate content in phagocytes under physiological and pathological conditions.

Neutrophil polymorphonuclear leucocytes and macrophages contain 10-40 times increased intracellular ascorbate concentrations compared to plasma. A slight decrease of ascorbate content could be observed in total white blood cells and in monocytes upon stimulation with opsonized zymosan. These decreases were more pronounced in peritoneal and alveolar macrophages from rats. In patients with rheumatoid disease whose phagocytes are exposed to a constant challenge, significantly lowered intracellular ascorbate contents were found in neutrophils and mononuclear cells. Surgical and thermal trauma in rats depressed intracellular ascorbate levels in peritoneal macrophages. These results are indicative of an essential role ascorbic acid plays in phagocytic cells.

Studies on the metabolic conversion of ascorbate.

In the intact animal guinea pigs metabolize (1-14C)ascorbic acid much faster to (14C)carbon dioxide (peak exhalation at 30 min) than rats (peak exhalation at 2 to 3 h) following single oral administration, but total excretion was comparable. This finding might be related to the differences in the absorption mechanism of ascorbic acid in these species. The large difference in retention capacity of ascorbic acid in the liver is suggested to be due to multiple recirculation of ascorbic acid in the guinea pig when compared to the rate. Homogenate preparations of rat stomach, small intestine or liver as well as cultured intestinal microbial flora did not cause metabolic degradation on incubation with (1-14C)ascorbic acid to (14C)carbon dioxide. It is therefore suggested that the observed excretion of (14C)carbon dioxide is due to spontaneous non-enzymatical reaction in liver and possible other tissues. Analysis of ascorbic acid metabolites formed on incubation by analytical isotachophoresis suggests that ascorbic acid is a rather stable substrate whereas dehydroascorbate and 2,3-diketogulonic acid are rapidly degraded. This allows the assumption that in vivo metabolism of ascorbic acid might not involve dehydroascorbic acid. Our data do not support the hypothesis that ascorbic acid undergoes presystemic metabolism to carbon dioxide in the intestinal wall.