The diagnosis of the Chronic Fatigue Syndrome (CFS), also referred to as Myalgic Encephalitis (ME)  when associated with fibrobromyalgia, is usually based on diagnostic criteria from history taking. e Fukuda criteria  have been updated and re ned by several other systems [3,4], but the validity of these tools is hard to certify since there is no “gold standard” to compare with. When patients present the signs and symptoms suggesting a particular diagnosis, but the disease is not found, they should be categorized as su ering from a “nondisease” . e latter requires a different therapeutic strategy.
Definite diagnostic and biological markers of ME/CFS are either lacking or are difficult to apply for screening purposes. Probably the study of the metabolome most closely approaches the required accuracy for detecting the biological disturbances alleged to be associated with ME/CFS . ere is good evidence that CFS is due to a systemic immune disorder  whereby oxidative, immunological and epigenetic mechanisms may increase the activity of the pyruvate dehydrogenase kinase (PDHK) and inhibit the pyruvate dehydrogenase activity. is will result in reduced aerobic pyruvate metabolism in the Krebs cycle [8,9]. e anaerobic escape route which uses lactate dehydrogenase (LDH) to generate lactate and lactic acid is engaged, including the Cori cycle of gluconeogenesis , in order to temporarily compensate for the paucity of aerobic energetic ATP production (Figure 1).
This pathogenic hypothesis reconciles all clinical, biological and theoretical observations, and may explain the increased lactate concentration in blood a er oral glucose intake observed in some patients (Figure 2). Based on this concept the author has developed a composite nutriceutical containing the sodium salt of one of the halogenated organic acids present in a particular genus of algae, vitamin B1, alfa lipoic acid, acetyl-l-carnitine, and the oxidoreductase ubiquinone Q10 (patent pending).