Increased 8-hydroxy-deoxyguanosine, a marker of oxidative damage to DNA, in major depression and myalgic encephalomyelitis / chronic fatigue syndrome. — CFSMEATLAS
Increased 8-hydroxy-deoxyguanosine, a marker of oxidative damage to DNA, in major depression and myalgic encephalomyelitis / chronic fatigue syndrome.
Maes, Michael, Mihaylova, Ivanka, Kubera, Marta et al. · Neuro endocrinology letters · 2009
Quick Summary
This study measured a marker of DNA damage in the urine of people with ME/CFS, depression, both conditions together, and healthy controls. Researchers found that people with both ME/CFS and depression had the highest levels of this DNA damage marker, and the damage correlated with fatigue severity and flu-like symptoms. This suggests that oxidative stress—a type of cellular damage from harmful molecules—may play a role in both conditions.
Why It Matters
This study provides biochemical evidence that oxidative stress and DNA damage accompany ME/CFS, particularly in patients with concurrent depression. These findings support the hypothesis that inflammatory and oxidative pathways contribute to ME/CFS pathophysiology, potentially opening avenues for targeted antioxidant interventions. The link between oxidative damage and cardiovascular and neurological complications also has important prognostic implications for ME/CFS patients.
Observed Findings
Residualized urinary 8-OHdG levels were significantly higher in patients with both depression and ME/CFS compared to normal controls and to patients with either condition alone.
Urinary 8-OHdG levels correlated significantly with fatigue severity scores on the Fibromyalgia and CFS Rating scale.
Urinary 8-OHdG levels correlated with sadness and flu-like malaise symptoms.
49% of variance in urinary 8-OHdG excretion was explained by creatinine, indicating proper adjustment methodology is critical.
Inferred Conclusions
Oxidative stress and oxidatively generated DNA damage are elevated in both major depression and ME/CFS, particularly in patients with comorbid disease.
IO&NS (inflammatory and oxidative & nitrosative stress) pathways are implicated in the pathophysiology of both disorders and may explain their overlapping features.
Oxidative DNA damage may contribute to increased cardiovascular morbidity and neurodegenerative processes observed in both depression and ME/CFS.
Remaining Questions
Is elevated oxidative DNA damage present before ME/CFS onset, or does it develop as a consequence of illness?
What specific sources drive oxidative stress in ME/CFS—mitochondrial dysfunction, immune activation, or other mechanisms?
What This Study Does Not Prove
This study does not prove that oxidative DNA damage causes ME/CFS or depression—only that it is associated with these conditions. The cross-sectional design cannot establish whether elevated DNA damage precedes illness onset or results from it. Additionally, a single morning urine sample may not capture variability in oxidative stress over time, and findings may not generalize to all ME/CFS populations.
Tags
Symptom:PainFatigue
Biomarker:Blood Biomarker
Method Flag:Weak Case DefinitionSmall SampleExploratory OnlyMixed Cohort