Framycetin and the Staphylococcus

While admitting the importance of the curative side of the work, one wonders if we are perhaps neglecting the preventive side, which might yield more eventual success. This would necessitate more work in regard to carriers. Hsia, Paine, and Driscoll' showed how heterozygotes of phenylketonuric patients could be detected by their low tolerance for phenylalanine, etc. Perhaps a well-worthwhile line of "treatment" on the preventive side would be to have a register of all phenylketonuric families and to practise some scientific marriage guidance in order to prevent, if possible, the matings of heterozygotes. I have been involved, successfully, in a little of this by "enlightened" families. All general practitioners might have knowledge of the phenylketonuric families in their practice and might recognize their responsibilities to them in this respect. With regard to the genetics of the condition, Penrose2 postulated that the condition was due to the action of a single autosomal recessive gene. One wonders what caused the gene to become defective so as to upset the enzyme which it controlled and so bring about the metabolic disturbance which resulted in the grave condition of phenylketonuria. I have noticed that in 50% of the families (albeit only eight families are involved) of my 10 phenylketonuric patients gross alcoholism appears in the parents or grandparents. Considering that alcohol is a liver poison and that the enzymatic action in the metabolism of phenylalanine takes place in the liver, one wonders what is the connexion between alcoholism and phenylketonuria, more especially since one considers gross alcoholism to be a form of metabolic disease rather than a psychiatric illness.-I am, etc., J. H. THOMPSON. Northgate and District Hospital. Morpeth. Northumberland.