122 



CHOLINE 



of alcoholism is as much non-portal as that of choline deficiency. It must 

 therefore be conceded that the architectures of both lesions are essentially 

 similar. The distinction of portal from non-portal cirrhotic lesions has been 

 heightened by the anatomical nomenclature employed, but is apparently 

 only one of degree. 



If the validity of these arguments is accepted, evidence based on dietary 

 studies would strongly suggest that alcoholic cirrhosis in man is indeed due 



^ S> W$ 



Fig. 20. The field indicated bj- the white arrow in the lower left portion of Fig. 19 

 is enlarged in this photomicrograph. A small bile duct occupies the center of the 

 field, and at the bottom a terminal portal venule is seen in tangential section. There 

 is no fibrosis present. As in the rat, with regard to these functional!}^ periportal areas, 

 the fibrosis is non-portal. X800. 



in large part to the dietary deficiency of the lipotropic agents. Clinicians 

 might be richly rewarded were they to accept this as a working hypothesis 

 on which to base well-controlled studies designed to test its validity. The 

 results may well necessitate modification of the views presented in this 

 chapter, for it is quite possible that toxic substances, both organic and 

 inorganic, in commercial spirits may play an important role in the effects 

 of alcohol-containing drinks on man. 



There is no evidence at present that extrahepatic lesions involving the 

 kidney, the eye, or the cardiovascular system of choline-deficient animals 

 have any clinical counterparts, despite some suggestions to the contrary. 



