My view that mongolism is caused by fœtal hyperthyroidism ceasing at birth, is based on the theory that if the known actions of hyperthyroidism on the embryos of animals, as proved by feeding experiments and otherwise, were at work on the human fœtus, the characteristic features of the mongol would be produced. Fœtal hyperthyroidism could not fail to cause abnormal endocrine inter-reaction, and it has been said that in every mongol some endocrine disturbance can be demonstrated. The action hyperthyroidism has on frog embryos, including the cutting out of the later stages of normal development and growth, and the action thyroxin has in retarding cell division and embryonic development, would explain the general arrest of growth and development of the mongol, including that of the skull and the brain. The same actions would also account for the coincident congenital anomalies, e.g., congenital heart lesions, cleft palate, hypospadias, undescended and undeveloped testicles, primitive hands and feet, syndactyly of fingers and toes, atresia of anus, spina bifida, etc.; these are also manifestations of arrested development, and in favour of a common cause for the local and the general defects, are the facts that both are symmetrical, and that there is a parallelism between the amount of general physical defect, the number of anomalies, and the degree of amentia.
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