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JOSEPH GOLD, MD
Syracuse, NY

Arch Surg. 1987;122(7):850.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—In their recent article, Dempsey and coauthors¹ discussed various proposals for the pathogenesis of cancer cachexia, but they omitted what is, perhaps, the most significant proposal, namely, the establishment of a systemic energy-losing cycle in the interplay of tumor glycolysis and host gluconeogenesis, which I first proposed in 1968 and subsequently elaborated in further studies.^2,3 This mechanism involves the production of lactic acid by the tumor and subsequent conversion of lactate, amino acids, and glycerol to glucose, chiefly in the liver, at great energy expense to the host. Paraphrasing this mechanism in regard to lactic acid, Burt and coauthors⁴ set forth in 1981:

One consequence [of increased Cori cycle activity] is an energy-wasting cycle between host and tumor [reference to original concept¹]. In this situation, the host supplies glucose to the tumor, which it avidly consumes and anaerobically produces lactate. This lactate is . . . [Full Text PDF of this Article]

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