TGI Friday! Our weekly round-up of recently published research abstracts | 28 August 2015

August 28, 2015

From BMC Medicine, 1 April 2015 (open access)

The many roads to mitochondrial dysfunction in neuroimmune and neuropsychiatric disorders

Gerwyn Morris(1,*) and Michael Berk(2,3,4,5).
1) Tir Na Nog, Bryn Road seaside 87, Llanelli, Cardiff, Wales SA152LW, UK.
2) IMPACT Strategic Research Centre, School of Medicine, Deakin University, PO Box 291, Geelong 3220, Australia.
3) Orygen Youth Health Research Centre and the Centre of Youth Mental Health, Poplar Road 35, Parkville 3052, Australia.
4)The Florey Institute for Neuroscience and Mental Health, University of Melbourne, Kenneth Myer Building, Royal Parade 30, Parkville 3052, Australia.
5)Department of Psychiatry, University of Melbourne, Level 1 North, Main Block, Royal Melbourne Hospital, Parkville 3052, Australia.



Mitochondrial dysfunction and defects in oxidative metabolism are a characteristic feature of many chronic illnesses not currently classified as mitochondrial diseases. Examples of such illnesses include bipolar disorder, multiple sclerosis, Parkinson’s disease, schizophrenia, depression, autism, and chronic fatigue syndrome.


While the majority of patients with multiple sclerosis appear to have widespread mitochondrial dysfunction and impaired ATP production, the findings in patients diagnosed with Parkinson’s disease, autism, depression, bipolar disorder schizophrenia and chronic fatigue syndrome are less consistent, likely reflecting the fact that these diagnoses do not represent a disease with a unitary pathogenesis and pathophysiology. However, investigations have revealed the presence of chronic oxidative stress to be an almost invariant finding in study cohorts of patients afforded each diagnosis. This state is characterized by elevated reactive oxygen and nitrogen species and/or reduced levels of glutathione, and goes hand in hand with chronic systemic inflammation with elevated levels of pro-inflammatory cytokines.


This paper details mechanisms by which elevated levels of reactive oxygen and nitrogen species together with elevated pro-inflammatory cytokines could conspire to pave a major road to the development of mitochondrial dysfunction and impaired oxidative metabolism seen in many patients diagnosed with these disorders.

From Medical Hypotheses, 21 August 2015.

Mitoprotective dietary approaches for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Caloric restriction, fasting, and ketogenic diets

Courtney Craig
Private Practice, Queens, NY, United States


Myalgic Encephalomyelitis/Chronic Fatigue Syndrome is an idiopathic illness characterized by debilitating fatigue and neuro-immune abnormalities. A growing body of evidence proposes mitochondrial dysfunction as a central perpetrator of the illness due to activation of immune-inflammatory pathways that burden the mitochondria.

Under a model of mitochondrial dysfunction, this paper explores dietary strategies that are mitoprotective.

Studied for decades, the cellular mechanisms of ketogenic diets, fasting, and caloric restriction now reveal mitochondria-specific mechanisms which could play a role in symptom reduction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.

Future research should examine the physiological effects of these dietary strategies in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.

From the Journal of Rehabilitation Research and Development, August 2015.

Timed loaded standing in female chronic fatigue syndrome compared with other populations.

Jan b Eyskens (1,*), Jo Nijs (2), Kristiaan D’Août(3), Alain Sand (4), Kristien Wouters(5,6), Greta Moorkens(1,6)
1) Department of Internal Medicine, Antwerp University Hospital, Antwerp, Belgium;
2) Pain in Motion Research Group; Departments of Human Physiology and Physiotherapy, Vrije Universiteit Brussel, Brussels, Belgium; and Department of Physical Medicine and Physiotherapy, University Hospital Brussels, Brussels, Belgium;
3) Department of Musculoskeletal Biology, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, UK; Department of Biology, University of Antwerp, Antwerp, Belgium;
4) Nuclear Medicine, AZ Jan Palfijn, Ghent, Belgium;
5) Department of Scientific Coordination and Biostatistics, Antwerp University Hospital, Antwerp, Belgium;
6) Faculty of Medicine and Health Science, University of Antwerp, Antwerp, Belgium


Patients with chronic fatigue syndrome (CFS), like patients with osteoporosis, have similar difficulties in standing and sitting. The aim of the study was to compare combined trunk and arm endurance between women with CFS (n = 72), women with osteoporosis (n = 30), nondisabled women (n = 55), and women from non-industrialized countries (n = 58) using the timed loaded standing (TLS) test.

TLS measures how long a person can hold a 1 kg dumbbell in each hand in front of him/her with straight arms. TLS was higher in the industrialized nondisabled population than in the non-industrialized study population (p < 0.001) and in patients with osteoporosis (p = 0.002). TLS was lower in patients with CFS than in nondisabled controls (p < 0.001).After adjustment for age, body height, and weight, combined trunk and arm endurance was even lower in CFS than in osteoporotic patients more than 25 yr old (p < 0.001). In CFS, TLS was lower compared in the non-industrialized group (p = 0.02).Since only women were studied, external validity of the results is limited to adult female patients with CFS. TLS revealed a specific biomechanical weakness in CFS patients that can be taken into account from the onset of a rehabilitation program. We propose that influencing the quality, rather than the quantity, of movement could be used in the rehabilitation.

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