The Glycocoll Theory of Gout
Excessive meat feeding in dogs, according to Kochmann, induces degenerative changes in the liver and kidneys. Similar tissue alterations were noted by Walker Hall in rabbits, after injection with hypoxanthine, while the same was observed by Kionka in mice. These findings suggest that, although anatomical lesions are not apparent in the livers of “gouty” men, it is at least probable that functional damage results from the overeating of meat.
Now, if glycocoll be added to a solution of (neutral) dialkali-urate, it expedites the appearance of the (acid) mono-alkali-urate, a reaction more noticeable with the sodium salt. Urea, in contrast to glycocoll, markedly inhibits the formation of the acid salt. But if glycocoll be added to a solution of the (neutral) dialkali-urate and urea, the latter parts to some extent with its powers in this respect, and the mono-alkali-urate is deposited.
It is reasonable, then, to suppose that if, as testified by Ignatowski and Walker Hall, glycocoll is present in gouty urine, it is also present in the tissue fluids of the gouty individual, and so the precipitation of uric acid is favoured. Glycocoll, normally, is almost entirely transmuted into urea by the urea-forming ferment of the liver.
Impressed by these considerations, Kionka advances the hypothesis that gout is due to:
(1) Functional changes in the liver, a depressed urea-ferment action.
(2) A deficient uric acid excretion by the kidney, possibly due to the changed uric acid combinations in the blood.
(3) These pathological conditions may be “hereditary” or “acquired,” from overeating, alcohol, lead, etc.
In other words, given deficient action of the urea ferment in the liver, then more glycocoll will be present in the blood-stream, and the uric acid may be thrown out of solution.[7]