Some good news just in for the holidays. For decades, military veterans with this conditions have been told that they have “organic brain damage”, for which not much can be done other than managing symptoms. The study below finally provides evidence that, yet again, a mysterious, chronic, debilitating and “incurable” conditions is nothing but a mitochondrial hypofunction in disguise. As such, it should be readily treatable with pro-metabolic interventions. The study even mentions a limited human trial with CoQ10 producing modest improvements for patients with this conditions. I suspect that the CoQ10 dose used in the study was grossly inadequate as several human studies demonstrated that in another brain condition (Parkinson Disease) the CoQ10 doses considered clinically relevant (200mg-400mg daily) are woefully inadequate and for established severe mitochondrial dysfunction doses in the range of 1g-2g daily may be needed. In addition, CoQ10 may not be the best option here as it only targets a single complex of the electron transport chain (ETC). Quinones targeting more steps of OXPHOS would likely be more beneficial, and so should be co-factors such as NAD+ that boost mitochondrial function and glucose oxidation. As such, I would suggest trying a combination of vitamin B1, B3, and a more broad-spectrum quinone such as methylene blue, emodin, vitamin K, thymoquinone, etc. Neurosteroids such as pregnenolone and progesterone would also likely come in handy as they play a role in both mitochondrial function as well as dampening neuro-inflammation. Finally, good ol’ aspirin would also likely be beneficial and it has already been shown to reverse symptoms and structural changes in another severe neurological condition (Alzheimer Disease).
https://www.nature.com/articles/s41598-025-24099-0
https://www.utsouthwestern.edu/newsroom/articles/year-2025/nov-gulf-war-illness.html
“…“Our research shows that these veterans don’t have damaged neurons, which would be incurable, but an energy imbalance, which suggests that their disabling symptoms might respond to novel treatments,” said study leader Robert Haley, M.D., Professor of Internal Medicine in the Division of Infectious Diseases and Geographic Medicine and in the Peter O’Donnell Jr. School of Public Health at UT Southwestern. He co-led the study with Sergey Cheshkov, Ph.D., former Assistant Professor of Radiology at UT Southwestern and now Research Scientist/Physicist in the Sammons BrainHealth Imaging Center at The University of Texas at Dallas, and Richard W. Briggs, Ph.D., retired Professor of Radiology at UT Southwestern.”
“…Their initial study showed that veterans with GWI had a lower NAA/tCr ratio than those who had also served in the war but didn’t have GWI. However, MRS technology available at the time couldn’t distinguish whether this ratio was due to relatively lower NAA or higher tCr, which have opposing implications: Decreased NAA suggests a process that stems from nerve damage, while increased tCr suggests a process that stems from mitochondrial dysfunction. In the new study, researchers used state-of-the-art MRS equipment and techniques to measure the NAA/tCr ratio in 39 Persian Gulf War veterans with GWI and 16 without. They found that the lower NAA/tCr ratio in veterans with GWI is due to increased tCr. Because mitochondrial dysfunction in the brain causes chronic neuroinflammation, this finding explains nearly all the symptoms of GWI, Dr. Haley said. He and his colleagues are currently studying how low-level sarin gas exposure causes mitochondrial dysfunction. This research may eventually lead to treatments that calm this chronic neuroinflammation, bringing relief to those with GWI.”
https://scienceblog.com/exhausted-cell-batteries-not-dead-neurons-may-drive-gulf-war-illness/
“…The chemistry fits with other clues. Animal studies using sarin-like compounds have documented behavioral changes, calcium overload, and mitochondrial injury lasting well beyond initial exposure. Studies in Gulf War veterans using phosphorus MRS have shown that muscle phosphocreatine recovers slowly after exercise—a direct measure of impaired mitochondrial ATP production. Small trials with coenzyme Q10, which supports mitochondrial function, have produced modest symptom improvements….Haley’s group argues that these pieces form a coherent picture. Mitochondria fail to sustain normal energy output. Cells lean harder on the creatine kinase buffer system, depleting phosphocreatine and raising free creatine. ATP shortages and mitochondrial stress trigger release of danger signals that activate microglia and drive chronic inflammation. The elevated myo-inositol in Gulf War illness fits that scenario of ongoing glial activation.”
