The recent CDC efforts to better characterize CFS using a large data set resulted in the simultaneous publication of 14 research papers in the Journal of /Rsrch/Pharmacogenomics in April, 2006. This complex effort which involved almost 20 researchers, many of them working for free, is the first to attempt to integrate gene expression with laboratory and clinical data. It could re-orient our thinking on CFS. Below you can find a laymen’s summaries of these papers.
Pharmacogenomics I: Overview- Vernon and Reeves, the two principal investigators, provided an overview of the project.
Pharmacogenomics II: Allostatic Load and CFS – This is the first time allostatic load – an measure of the health of the stress response – has been measured in CFS. These researchers examined data from multiple systems in the body (endocrine, sympathetic nervous, immune, cardiovascular) to assess if the allostatic stress response has been impaired in CFS, and, if so, where.
- Hypocortisolism, Artifact or Central Factor in CFS? – The hypocortisolism (low cortisol levels) found in CFS has apparently played a major role in convincing the CDC to devote a good deal of research funding to examine the stress response in CFS. This paper explores the evidence for hypocortisolism in CFS looks at it’s possible causes and effects. Finally it looks at whether hypocortisolism plays a secondary or central role in CFS.
- Do CFS Patients Have Selfish Brains? – The authors of the allostatic load papers on CFS propose that an altered energy ‘set point’ in the brains of CFS patients may be at the heart of CFS. In this Selfish Brain paper we explore the theory behind the idea of energy ‘set points’ in the brain.
Pharmacogenomics III: The Gene Expression Papers – The CDC pioneered gene expression studies in CFS and gene expression was at the heart of the Wichita effort. These three papers present the most complete and complex efforts yet at understanding the genetic activity present in CFS.
Pharmacogenomics IV: The Gene Polymorphisms in CFS – There is no evidence that mutations in a single gene can cause CFS but more and more evidence is emerging that in CFS, like other complex diseases, a group of gene mutations may predispose one to getting the disease. The gene mutation studies in the Pharmacogenomics studies are the most comprehensive yet done.
Pharmacogenomics V: The Subsets in CFS – There may be no more important issue in CFS than identifying the subsets present in it. Several researchers believe that until the subsets in CFS are identified research efforts in CFS will be problematic at best. This, the most extensive effort to uncover the subsets in CFS yet attempted, utilized clinical, laboratory, gene mutation and gene expression data.
The CAMDA Conference -The analyses of the 2003 CDC Wichita data did not stop with the publications in the Pharmacogenomics Journal. An international group of researchers took their shot at this large data set at the 2006 Critical Assessment of Microarray Data Analysis (CAMDA) Conference. This conference, devoted to expanding our understanding of and utilization of gene microarray data, featured an array of sometimes mind-bogglingly sophisticated ways of examining this data. The top paper at the conference may have found a biomarker for CFS.