ABSTRACT

Carrageenan has been widely used as a food additive in the Western diet for several decades. Its unique ability to solubilize milk proteins has led to its use in many processed foods, including both low-fat and high-fat and low-calorie and high-calorie foods. Hence, individuals who follow dietary recommendations with regard to cholesterol and calories may still have significant exposure to carrageenan. In experimental animal models, ingestion of carrageenan has been associated consistently with development of gastrointestinal ulcerations and neoplasms. It has been used as a model of human ulcerative colitis, an inflammatory bowel disorder that is pre-neoplastic. In addition, it has been used to induce inflammation in animal models of arthritis and pleuritis and to study effectiveness of anti-inflammatory therapies. Observation of cells exposed to carrageenan from inflammatory models and from tissue culture has demonstrated development of intracellular inclusions, consistent with incomplete metabolism of carrageenan within endosomes and lysosomes of the exposed cells, including macrophages, intestinal epithelial cells, and mammary cells in tissue culture. Subsequent vacuolation and disruption of the lysosomes appear to lead to cellular destruction due to release of the lysosomal contents. These changes may be associated with subsequent development of ulcerations and neoplasms.