Dr. Naviaux has responded to some comments on the groundbreaking paper, “Metabolic Features of Chronic Fatigue Syndrome”.

In this response he addresses the need for metabolic studies in other disease groups, whether metabolic studies determine the initial cause of sysmptoms, and how dauer states relate to what is seen in CFS.

We thank Vogt et al. for their comments (1). We respond to their three points in order. First, we are aware of the need to extend future metabolomics studies to include other disease groups. We stated this fact in the discussion of ref. 2 and are validating the results in independent cohorts. The detailed biochemical phenotype or signature that we found provides a first glimpse at a previously hidden biology. For example, disturbances in sphingolipid metabolism have important implications for immunobiology and neuroendocrine regulation relevant to myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS) (3). Sphingolipids are important mediators of the cell danger response (CDR) (4), and the CDR is an important regulator of the behavioral and functional changes produced by infection, and associated with sickness behavior (5). The biochemical phenotype of ME/CFS is distinct from other diseases that Vogt et al. (1) named. For example, in heart failure, metabolomics shows that long chain acyl-carnitines are increased (6), but these long chain acyl-carnitines were not changed in ME/CFS (2). In our view, chemistry and metabolism underlie all aspects of human biology. Our studies show that metabolomics can be used as a new lens to reveal unexpected biology that was invisible before…

Robert Naviaux, et all

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