Ácido láctico en el cerebro en el SFC!! (fallo mitocondrial)

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Ácido láctico en el cerebro en el SFC!! (fallo mitocondrial)

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Más evidencia sobre el fallo mitocondrial en el SFC! Un estudio demuestra el exceso de ácido láctico en una parte del cerebro de los enfermos de SFC, que sugiere fallo mitocondrial, pues el ácido láctico es un metabolito de la respiración anaeróbica, que se incrementa al no poder utilizar bien el O2 para crear energía en forma de ATP...Por si a alguien le quedan dudas de este fallo energético, que ya se encuentra hasta en el cerebro (lógico, por otra parte...)

S.
Ventricular cerebrospinal fluid lactate is increased in chronic fatigue syndrome compared with generalized anxiety disorder: an in vivo 3.0 T (1)H MRS imaging study.

Mathew SJ, Mao X, Keegan KA, Levine SM, Smith EL, Heier LA, Otcheretko V, Coplan JD, Shungu DC.

Department of Psychiatry, Mount Sinai School of Medicine, New York, NY, USA.

Chronic fatigue syndrome (CFS) is a controversial diagnosis because of the lack of biomarkers for the illness and its symptom overlap with neuropsychiatric, infectious, and rheumatological disorders. We compared lateral ventricular volumes derived from tissue-segmented T(1)-weighted volumetric MRI data and cerebrospinal fluid (CSF) lactate concentrations measured by proton MRS imaging ((1)H MRSI) in 16 subjects with CFS (modified US Centers for Disease Control and Prevention criteria) with those in 14 patients with generalized anxiety disorder (GAD) and in 15 healthy volunteers, matched group-wise for age, sex, body mass index, handedness, and IQ. Mean lateral ventricular lactate concentrations measured by (1)H MRSI in CFS were increased by 297% compared with those in GAD (P < 0.001) and by 348% compared with those in healthy volunteers (P < 0.001), even after controlling for ventricular volume, which did not differ significantly between the groups. Regression analysis revealed that diagnosis accounted for 43% of the variance in ventricular lactate. CFS is associated with significantly raised concentrations of ventricular lactate, potentially consistent with recent evidence of decreased cortical blood flow, secondary mitochondrial dysfunction, and/or oxidative stress abnormalities in the disorder.
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