Michael Maes

Michael Maes, M.D., Ph.D., is a clinician at Revitalis, in Waalre, Netherlands, as well as a researcher at IMPACT Strategic Research Center, Barwon Health, Deakin University, School of Medicine, Geelong, Victoria, Australia. He is, also, affiliated with the Department of Psychiatry, Chulalongkorn University, Bangkok, Thailand and Health Sciences Graduate Program, Health Sciences Center, State University of Londrina, Brazil.

His special interests include: Behavorial Systems Biology, major depression, inflammatory illnesses and chronic fatigue syndrome.

Neuro-Inflammatory and Oxidative Fatigue (NIOF) Theory
In 2015, Maes developed a new case definition of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) called Neuro-Inflammatory and Oxidative Fatigue (NIOF) "based on pattern recognition methods and using neuro-immune, inflammatory, oxidative and nitrosative stress (neuro-IO&NS) biomarkers as external validating criteria." These biomarkers include "IgM / IgA responses against LPS [lipopolysaccharides] of gut commensal bacteria (leaky gut), IgM responses to O&NS modified neoepitopes, autoimmunity to serotonin, plasma interleukin-1 (IL-1) and serum neopterin." Maes sees a "significant overlap between NIOF and chronic fatigue syndrome although NIOF criteria were much more restrictive."

Professor Maes proposes the ME/CFS, as well as other chronic diseases, can be treated by lessening the Neuro-Inflammatory and Oxidative Fatigue with foods and supplements that decrease inflammation and repair leaky gut such as curcumin, N-acetyl-cysteine ​​(NAC), glutamine, zinc, and omega-3 oils.

Books

 * 2011, Nooit Mer Moe (English translation: 'Tired No More, CFS Unmasked) 

Published Studies

 * 2006, Increased serum IgA and IgM against LPS of enterobacteria in chronic fatigue syndrome (CFS): indication for the involvement of gram-negative enterobacteria in the etiology of CFS and for the presence of an increased gut-intestinal permeability.
 * 2008, Normalization of leaky gut in chronic fatigue syndrome (CFS) is accompanied by a clinical improvement: Effects of age, duration of illness and the translocation of LPS from gram-negative bacteria (Abstract - full text upon request)
 * 2009, A review on cognitive behavorial therapy (CBT) and graded exercise therapy (GET) in myalgic encephalomyelitis (ME) chronic fatigue syndrome (CFS): CBT/GET is not only ineffective and not evidence-based, but also potentially harmful for many patients with ME/CFS
 * 2009, Coenzyme Q10 deficiency in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is related to fatigue, autonomic and neurocognitive symptoms and is another risk factor explaining the early mortality in ME/CFS due to cardiovascular disorder (Abstract)
 * 2011, Increased IgA responses to the LPS of commensal bacteria is associated with inflammation and activation of cell-mediated immunity in chronic fatigue syndrome
 * 2012, Evidence for inflammation and activation of cell-mediated immunity in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): increased interleukin-1, tumor necrosis factor-α, PMN-elastase, lysozyme and neopterin. (Abstract)
 * 2012, Myalgic Encephalomyelitis (ME), Chronic Fatigue Syndrome (CFS), and Chronic Fatigue (CF) are distinguished accurately: results of supervised learning techniques applied on clinical and inflammatory data (Abstract)
 * 2013, In myalgic encephalomyelitis/chronic fatigue syndrome, increased autoimmune activity against 5-HT is associated with immuno-inflammatory pathways and bacterial translocation (Abstract)
 * 2013, Case definitions and diagnostic criteria for Myalgic Encephalomyelitis and Chronic fatigue Syndrome: from clinical-consensus to evidence-based case definitions (Full text)
 * 2014, Review Article - "Mitochondrial dysfunctions in Myalgic Encephalomyelitis / chronic fatigue syndrome explained by activated immuno-inflammatory, oxidative and nitrosative stress pathways"
 * 2014, The emerging role of autoimmunity in myalgic encephalomyelitis/chronic fatigue syndrome (ME/cfs)
 * 2014, Oxidative and Nitrosative Stress and Immune-Inflammatory Pathways in Patients with Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS) (Full Text)
 * 2015, A new case definition of Neuro-Inflammatory and Oxidative Fatigue (NIOF), a neuroprogressive disorder, formerly known as chronic fatigue syndrome or Myalgic Encephalomyelitis: results of multivariate pattern recognition methods and external validation by neuro-immune biomarkers. (Abstract)
 * 2015, Central pathways causing fatigue in neuro-inflammatory and autoimmune illnesses (Full Text)
 * 2016, Nitrosative Stress, Hypernitrosylation, and Autoimmune Responses to Nitrosylated Proteins: New Pathways in Neuroprogressive Disorders Including Depression and Chronic Fatigue Syndrome (Abstract)
 * 2016, The role of microbiota and intestinal permeability in the pathophysiology of autoimmune and neuroimmune processes with an emphasis on Inflammatory Bowel Disease, Type 1 Diabetes and Chronic Fatigue Syndrome (Abstract)
 * 2017, Mechanisms Explaining Muscle Fatigue and Muscle Pain in Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): a Review of Recent Findings (Abstract)
 * 2018, Recognizing the leaky gut as a trans-diagnostic target for neuro-immune disorders using clinical chemistry and molecular immunology assays (Abstract)

Talks & Interviews

 * 21 August 2013, Dr Michael Maes: The Immune Pathophysiology of ME/CFS/FM - seminar given at Emerge Australia (formerly ME/CFS Australia (Victoria)) at The Alfred Hospital

Online Presence

 * PubMed
 * ResearchGate
 * LinkedIn
 * Onward thru the Fog blog article about Dr. Maes' research