While we have apparently, definite knowledge of the function of the liver in regard to glycogenosis, we are almost entirely ignorant of the function with regard to fats and proteins and practically unable, in any given case, to test the function of the liver, excepting with regard to its power to retain carbohydrates. Even the accumulation of empiric knowledge with regard to the effect of foods upon the liver, is tedious and uncertain. Thus, whatever is said in this chapter is largely hypothetic and many of the ideas regarding the subject are doubtless mere notions.

Biliousness is a term used vaguely and sometimes merely as a euphemism for constipation or even diarrhoea. Suppositi-tiously, it signifies biliary torpor, with accumulation in the system of biliary waste. But, as it is not attended with the obvious retention of biliary pigment which is, at once, the most toxic and most conspicuous ingredient of the bile, this condition may not exist at all, and at any rate, it is impossible to justify the diagnosis in any given case. The writer has found it impossible to verify the apparent corroboration of this conception, by the supposed enlargement of the liver, most of the cases in which the liver has been stated to be enlarged, not yielding this sign on careful examination by palpation with allowance for the thickness of the abdominal wall, or by auscultatory percussion, or X-ray shadow. In most cases of so-called biliousness, indicanuria is found, along with other signs of intestinal putrefaction and it is obvious that the value of calomel and other cholagogues - which have been experimentally demonstrated not to increase the flow of bile - is easily explained on the hypothesis that so-called biliousness is an intestinal toxaemia.

Nearly every statement regarding "biliousness " can be transferred to the conception of intestinal toxaemia, viz., that it it due to overeating, especially of rich, greasy foods, meats, crustaceans etc.; that malt liquors and strong alcoholic beverages should be avoided; that the bowels and stomach should be cleared out and that feeding should be intermitted for a day or two and should then be begun with eggs, milk if it does not disagree, fresh vegetables, cereals, juicy fruits and little meat and that of the simplest and most digestible kind.

Catarrhal Jaundice (cholangitis) is virtually an extension of a duodenitis. Abstention from food for a few days, with an abundance of water, especially alkaline water plain or carbonated is advisable, unless the patient is much reduced, when the nourishment appropriate to the next period should be instituted. This consists of peptonized milk, or junket, buttermilk, egg water, raw custard without liquor, beef juice, or the proprietary meat juices in certain cases. Fats should be reduced to a minimum and sugar should be used in small quantities after resuming solid food but too much meat should not be given. Cereals, stewed fruits without sugar or seeds, or even orange, lime, lemon and pine-apple juice may be given, and chicken breast, gelatin preparations or meat jellies, oyster stew without butter are appropriate.

In any serious lesion of the liver, there is usually the indication for abundant nutrition and the counterindication afforded by the impaired condition of the liver and the alimentary canal. The best compromise is the diet appropriate for chronic enteritis, with due regard to the gastric condition which is usually catarrh and hypochlorhydria.

Abscess of the liver is usually part of the morbid anatomy of pyaemia or a sequela of sepsis of the biliary ducts, incident to typhoid, paratyphoid and colon bacillus infection, or is due to haematogenic sepsis in the course of dysentery of different kinds. The prophylactic and therapeutic relations of diet are more or less susceptible of successful application, except that if hepatic abscess develops, treatment is usually unsuccessful.

Syphilitic, Tuberculous, Ecchinococcic, Leucocythaemic, Amyloid and similar lesions of the liver, may or may not interfere markedly with the hepatic function and the general digestive powers of the body. The ability to digest fats can be determined to some degree by examination of the faeces, sometimes quite easily by macroscopic examination or extraction with gasoline which normally yields from a gram or two of faeces only enough fat to grease a sheet of toilet paper. Sugar digestion and assimilation can be judged crudely by the non-development or development of glycosuria (See Diabetes). The ability to utilize proteins must be determined by the state of gastric digestion, microscopic examination of the stools, urinary waste and symptomatology. No positive rules can be laid down for any serious lesion, with regard to any kind of foods but, usually a diet of milk, cereals, small quantities of tender fresh meats, proprietary foods, and stewed fruits or fresh fruit juices, may be employed and nutrition should be forced so far as possible in proportion to the digestive powers.

True Fatty Metamorphosis of the liver usually occurs as a fulminant process in phosphorus poisoning, as the result of toxaemia in pregnancy or without explanation, in yellow fever and occasionally in other infections. The regimen, is therefore that of yellow fever or other acute infection, or nil and the prognosis is so bad that the diet makes almost no difference in the result.

Feeding experiments resulting in the deposit in the liver and elsewhere of the specific fat employed, have cast considerable doubt on the former view of the distinction between fatty infiltration and metamorphosis and have led to the very practical but as yet undecided question as to the propriety of using appreciable quantities of fat when the liver is vulnerable.

Fatty Degeneration usually accompanies Hepatic Sclerosis and hence, from the yellowing tint produced, the more common term Cirrhosis. For practical purposes, we may distinguish (1) fatty changes accompanying marked interstitial changes - cirrhosis or sclerosis; (2) fatty infiltration, usually affecting various viscera, not causing especially marked functional disturbances and usually occurring as part of obesity; (3) non-fulminant fatty change hitherto considered as a true metamorphosis; and (4) fulminant fatty degeneration or icterus gravis. The first two will be diagnosed clinically as hepatic sclerosis and obesity, respectively and the dietetic reigmen and etiologic relations will be discussed under those titles. The last has already been considered. The third is scarcely diagnosticable and is vaguely considered under the headings of cloudy swelling and degenerations under general pathologic changes.