Abstract
Background: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) affects approximately 250,000 people in the UK. The condition varies in severity causing long-term physical and cognitive fatigue which is not alleviated by rest. Whilst the pathology is not understood, recent evidence suggests metabolic abnormalities may be associated with the manifestation of symptoms, particularly involving the metabolism of glucose and energy production. The use of ketone bodies as an alternative energy substrate may be beneficial to people with ME/CFS, in order to by-pass the glycolytic pathway, enhance energy production and reduce fatiguing outcomes. Study Design and Methods: Using a pragmatic collective case study with repeated measures methodology we investigated the feasibility of following a ketogenic diet and potential effects of the high fat, low carbohydrate diet on response to physical activity in people with ME/CFS (n=3) and healthy controls (n=3) using a submaximal exercise stress test both with and without dietary intervention. Exercise tolerance (mins), rate of oxygen consumption (VO2) to workload (75W), respiratory exchange ratio (RER), rate of perceived effort (RPE) and lactate response were measured throughout and descriptive statistics performed. Results: We found that the ketogenic diet was followed, with compliance higher in the pwME/CFS. Variations in response following the ketogenic diet was observed across individuals in minutes performed, VO2, HR, RER, and RPE post diet but the KD only limited exercise capacity in the control individuals. Individuals responded differently to the KD but group trends have been reported as means and standard deviation. The KD resulted in a decrease in RER at submax in the controls with a mean change of 0.07 from baseline (0.86 ± 0.1) to post intervention (0.79 ± 0.1) compared to a mean change of 0.02 in the ME/CFS from baseline (1.03 ± 0.1) to post intervention (1.01 ± 0.1). A decrease in VO2 (L/min) at submax showed a mean change of 0.06 (L/min) in the pwME/CFS at baseline (1.34 ± 0.1) to post intervention (1.27 ± 0.2) compared to a mean change of 0.07 (L/min) in the controls at baseline (1.40 ± 0.3) to post intervention (1.33 ± 0.2). HR (bpm) at submax decreased in all individuals, with a mean change of 4 (bpm), with pwME/CFS at baseline (139 ± 8.2) to post intervention (135 ± 14) and control individuals at baseline (107 ± 7.8) to intervention (103 ± 3.2). RPE at submax decreased in the pwME/CFS from baseline (6 ± 1.0) to post intervention (5 ± 2.1) whereas the controls increased from baseline (2 ± 1.0) to post intervention (3 ± 1.5). Conclusion: Our observations suggest individualised but metabolic flexibility in healthy individuals is achievable via dietary manipulation showing the ability to switch from glucose to fats under controlled conditions. The different response in substrate utilisation in individuals with ME/CFS suggests that potential metabolic abnormalities may be present in ME/CFS. Further investigation is now warranted in order to assess whether the KD is beneficial for people with ME/CFS
Highlights
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a chronic neurological health condition that affects approximately 250,000 people in the UK
Whilst the pathology is not completely understood, emerging evidence indicates people with ME/CFS have bio-energetic impairments which may be related to mitochondrial dysfunction (MD) and abnormal substrate metabolism which may associate with the manifestation of symptoms [3, 4]
The study was a pragmatic collective case study with a repeated measures methodology that lasted for a total of three weeks, with two testing visits separated by a one-week self-guided dietary intervention
Summary
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a chronic neurological health condition that affects approximately 250,000 people in the UK. Nicolson and Ellithorpe [9] previously suggested that pwME/CFS may have an increased susceptibility to cellular oxidative stress, resulting in the loss of electron transport chain function due to the accumulation of reactive oxygen species Under these conditions, glycolysis would increase and result in abnormal lactate production and cellular damage. Limited net energy available to cells may result in anaerobic metabolism This was later supported by Booth et al [10] who suggested that this possible compensatory glycolysis mechanism in pwME/CFS results in the need for additional ATP in order to convert lactate back to pyruvate. Further investigation is warranted in order to assess whether the KD is beneficial for people with ME/CFS
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