Neil McGregor

Neil R. McGregor, BDS, MDSc, PhD is a periodontist with an interest in ME/CFS research stemming from treating ME/CFS patients with temporomandibular dysfunction syndrome. He is a senior researcher at the Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Melbourne, Australia and an Adjunct Professor at Victoria University, Melbourne, Australia. Dr. McGregor was a former co-editor of the Journal of Chronic Fatigue Syndrome.

Books

 * 2014, Chapter Five in Advances in Clinical Chemistry, Vol. 66, published by Elsevier; "Metabolism in Chronic Fatigue Syndrome," by [[Christopher Armstrong | Christopher W. Armstrong], Neil R. McGregor, Henry L. Butt, and Paul R. Gooley]
 * 2006, Pediatric Chronic Fatigue Syndrome by [[Kenny de Meirleir], Neil McGregor, and Elke L.S. Van Hoof]

Notable studies
"'Abstract - Chronic fatigue syndrome (CFS) is a debilitating multisystem disorder characterised by long-term fatigue with a variety of other symptoms including cognitive dysfunction, unrefreshing sleep, muscle pain, and post-exertional malaise. It is a poorly understood condition that occurs in ~ 5 in every 1000 individuals. We present here a preliminary study on the analysis of blood samples from 11 CFS and 10 control subjects through NMR metabolic profiling. Identified metabolites that were found to be significantly altered between the groups were subjected to correlation analysis to potentially elucidate disturbed metabolic pathways. Our results showed a significant reduction of glutamine (P = 0.002) and ornithine (P < 0.05) in the blood of the CFS samples. Correlation analysis of glutamine and ornithine with other metabolites in the CFS sera showed relationships with glucogenic amino acids and metabolites that participate in the urea cycle. This indicates a possible disturbance to amino acid and nitrogen metabolism. It would be beneficial to identify any potential biomarkers of CFS for accurate diagnosis of the disorder.'"
 * 2017, The association of fecal microbiota and fecal, blood serum and urine metabolites in myalgic encephalomyelitis/chronic fatigue syndrome "Abstract - Introduction: The human gut microbiota has the ability to modulate host metabolism. Metabolic profiling of the microbiota and the host biofluids may determine associations significant of a host–microbe relationship. Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a long-term disorder of fatigue that is poorly understood, but has been linked to gut problems and altered microbiota. Objectives: Find changes in fecal microbiota and metabolites in ME/CFS and determine their association with blood serum and urine metabolites. Methods: A workflow was developed that correlates microbial counts with fecal, blood serum and urine metabolites quantitated by high-throughput ¹H NMR spectroscopy. The study consists of thirty-four females with ME/CFS (34.9 ± 1.8 SE years old) and twenty-five non-ME/CFS female (33.0 ± 1.6 SE years old). Results: The workflow was validated using the non-ME/CFS cohort where fecal short chain fatty acids (SCFA) were associated with serum and urine metabolites indicative of host metabolism changes enacted by SCFA. In the ME/CFS cohort a decrease in fecal lactate and an increase in fecal butyrate, isovalerate and valerate were observed along with an increase in Clostridium spp. and a decrease in Bacteroides spp. These differences were consistent with an increase in microbial fermentation of fiber and amino acids to produce SCFA in the gut of ME/CFS patients. Decreased fecal amino acids positively correlated with substrates of gluconeogenesis and purine synthesis in the serum of ME/CFS patients. Conclusion: Increased production of SCFA by microbial fermentation in the gut of ME/CFS patients may be associated with deleterious effects on the host energy metabolism
 * 2016, Widespread pain and altered renal function in ME/CFS patients "Abstract - 'Background: Widespread pain is noted in many patients with chronic fatigue syndrome (ME/CFS), fibromyalgia and temporomandibular disorders. These conditions usually start as a localized condition and spread to a widespread pain condition with increasing illness duration. Purpose: To aim was to assess the changes in biochemistry associated with pain expression and alterations in renal function. Methods: Forty-seven ME/CFS patients and age/sex-matched controls had a clinical examination, completed questionnaires, standard serum biochemistry, glucose tolerance tests and serum and urine metabolomes in an observational study. Results: Increases in pain distribution were associated with reductions in serum essential amino acids, urea, serum sodium and increases in serum glucose and the 24-hour urine volume; however the biochemistry was different for each pain area. Regression modelling revealed potential acetylation and methylation defects in the pain subjects. Conclusions: These findings confirm and extend our earlier findings. These changes appear consistent with repeated minor inflammatory-mediated alterations in kidney function resulting in essential amino acid deprivation and inhibition of protein synthesis and genetic translation within tissues.'"
 * 2015, Metabolic profiling reveals anomalous energy metabolism and oxidative stress pathways in chronic fatigue syndrome patients "'Abstract - Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating long-term multisystem disorder with a central and inexplicably persistent fatigue symptom that is unable to be relieved by rest. Energy metabolism and oxidative stress have been recent focal points of ME/CFS research and in this study we were able to elucidate metabolic pathways that were indicative of their dysfunction. Blood and urine samples were collected from 34 females with ME/CFS (34.9 ± 1.8 SE years old) and 25 non-ME/CFS female participants (33.0 ± 1.6 SE years old). All samples underwent metabolic profiling via 1D 1H Nuclear magnetic resonance spectroscopy and quantitated metabolites were assessed for significance. Blood glucose was elevated while blood lactate, urine pyruvate, and urine alanine were reduced indicating an inhibition of glycolysis that may potentially reduce the provision of adequate acetyl-CoA for the citric acid cycle. We propose that amino acids are being increasingly used to provide an adequate carbohydrate source for the citric acid cycle. We suggest that this is via glutamate forming 2-oxoglutarate through an enzyme that deaminates it and subsequently elevates blood aspartate. Dysfunctional energy metabolism appears to have impacted creatinine and its elevation in urine suggests that it may be used as an alternative for anaerobic ATP production within muscle. A decrease in blood hypoxanthine and an increase in urine allantoin further suggest the elevation of reactive oxygen species in ME/CFS patients. These findings bring new information to the research of energy metabolism, chronic immune activation and oxidative stress issues within ME/CFS.'"
 * 2012, NMR metabolic profiling of serum identifies amino acid disturbances in chronic fatigue syndrome
 * 2011, The Biochemistry of Chronic Pain and Fatigue
 * 2009, Increased d-lactic Acid intestinal bacteria in patients with chronic fatigue syndrome
 * 2000, Blood parameters indicative of oxidative stress are associated with symptom expression in chronic fatigue syndrome
 * 1997, A Preliminary Assessment of the Association of SCL-90-R Psychological Inventory Responses with Changes in Urinary Metabolites in Patients with Chronic Fatigue Syndrome"Abstract - 'A previous investigation of a cohort of 20 chronic fatigue syndrome (CFS) patients revealed an increased urinary excretion of an unusual metabolite, tentatively identified as amino-hydroxy-N-methyl-pyrrolidine (coded CFSUM1) and β-alanine, compared with 45 control subjects. The relative abundances of both CFSUM1 and β-alanine were positively associated with the core diagnostic symptoms of CFS and associated changes in amino and organic acid excretion. The psychological attributes of these CFS patients and controls were assessed in this study by using the Symptom Check List-90-revised (SCL-90-R) psychological inventory. The CFS patients had increases in the SCL-90-R. somatization, obsessive compulsive, depression, anxiety and phobic anxiety dimension scores. Nineteen of 20 CFS patients had somatization T-scores ≥ 63 (P < 0.0001), suggestive of a somatization disorder. Multiple regression analysis indicated that somatization was the most important SCL-90-R-defined dimension discriminating CFS from control subjects. Depression and anxiety were not found to be important inter-group determinants. The dimension scores were each related to specific changes in the urinary excretion of organic and amino acids, suggesting that each is biochemically distinct and has an organic basis. Cluster analysis of dimension profiles revealed that the profile with increased prevalence (P < 0.0001) in CFS patients was associated with increased excretion of CFSUM1 (P < 0.005) and had increases in somatization, obsessive compulsion and depression dimension scores. The PSDI as a measure of SCL-90-R symptom severity was positively correlated with CFSUM1 (model P < 0.003). CFSUM1 was also the primary correlate for the somatization dimension (model P < 0.0008), but was not associated with any other SCL-90-R-defined dimension. Another unidentified urinary metabolite, coded UM 15, was the primary correlate for depression (model P < 0.0004) and was associated with multiple dimension elevations by both cluster and logistic regression analysis; the excretion of this compound was unrelated to CFSUM1. These results indicated that, in this CFS cohort, the SCL-90-R defined psychological changes were strongly associated with changes in the biochemical homeostasis of patients, suggestive of an organic basis to CFS.'"

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 * Meet the Scientists: Dr Neil McGregor