Christopher Armstrong

Christopher William Armstrong, is a post doctorate student in the Department of Biochemistry and Molecular Biology and a Bio21 Molecular Science & Biotechnology Institute researcher at the University of Melbourne, Melbourne, Australia with an interest in the dysfunction of energy metabolism of people with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).

Awards

 * 2016 Ramsay Award Program grant recipient, sponsored by the Solve ME/CFS Initiative. This grant, shared with Geraldine Cambridge, University College London, and Fane Mensah, University College London, will focus on the metabolic analysis of B-Cell maturation in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Books

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

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

Talks and interviews

 * 2017, Community Symposium on the Molecular Basis of ME/CFS - 2017
 * Speech title- "ME, metabolism and I"


 * 23 Nov 2016, Inside Story Podcast - "In Melbourne, progress on Chronic Fatigue Syndrome"
 * 20 Oct 2016, [[Solve ME/CFS Initiative] Webinar with Christopher Armstrong, on recent metabolomics studies]
 * 15-16 June 2016, Speaker at the International Conference on Fibromyalgia and Chronic Pain. Speech title: "The impact of the gut microbiome on host fatigue in ME/CFS patients"

Online presence

 * Scholar Google
 * ResearchGate

Learn more

 * 3 Feb 2017, "How Gut Bacteria Is Helping To Unpack Chronic Fatigue Syndrome: Can improving a person's gut health help?" by Emma Brancatisano in The Huffington Post
 * Bio21 Molecular Science & Biotechnology Institute webpage on Armstrong's work - "Gutted by bad gut bugs" by Florienne Loder