Despite the current hypotheses for its causation, the exact cause of endmyocardial fibrosis is unknown. However, endomyocardial fibrosis being a disease of the low socio-economic groups who feed on low protein high carbohydrate diets consisting exclusively of cassava in Uganda and the demonstration by the author of a bimodal age distribution among the female patients and monomodal pattern in the male patients, led the author to suspect protein deficiency and cassava as aetiological factors thereby attributing the first mode to the increased but unmet protein needs for childhood growth and the second mode to the increased but unmet protein needs for pregnancies and lactation in the 20-40 year age groups. Consequently a new hypothesis that "prolonged ingestion of tuber (cassava/tapioca) crops associated with extreme deprivation of protein causes EMF" was formulated. In order to verify this hypothesis, three Cercopithecus aethiops were fed on uncooked banana diet while another three were fed on uncooked cassava and hearts harvested for histology whenever the animal health deteriorated. Changes in the endomyocardium included cell vacuolation, interstitial fibrosis and endocardial thickening by the 130th day in the animals on cassava but the animals on bananas were free from such changes. By the 160th day, the former exhibited marked thickening of the endocardium, interstitial fibrosis, fibrous septa formation, pappillary muscle fibrosis as well as apical fibrosis of the left ventricle, which findings occur in the human disease. Calcification and inflammatory cells were absent. A repeat of the experimental feeding with cassava using a batch of five animals, one of which survived up to seven months revealed cardiac findings similar to those seen at 160 days. Thus, the pathogenetic process, hitherto obscure, begins with cardiac cell necrosis followed by fibrosis consequent upon the failure of cardiac cell repair due to protein deficiency caused by the protein free cassava diets since the animals on bananas, which also lacked protein did not develop similar changes. The low plasma amino acid profiles in EMF prone subjects, the poor blood supply and the great apical mechanical stress are incriminated for the severe apical lesions. This study shows that the disease can be experimentally induced in the monkey thereby validating the postulated hypothesis.