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).<\/p>\n
https:\/\/www.nature.com\/articles\/s41598-025-24099-0<\/a><\/p>\n https:\/\/www.utsouthwestern.edu\/newsroom\/articles\/year-2025\/nov-gulf-war-illness.html<\/a><\/p>\n “…\u201cOur research shows that these veterans don\u2019t have damaged neurons, which would be incurable, but an energy imbalance, which suggests that their disabling symptoms might respond to novel treatments<\/strong><\/span>,\u201d said study leader\u00a0Robert Haley, M.D.<\/a>, Professor of\u00a0Internal Medicine<\/a>\u00a0in the\u00a0Division of Infectious Diseases and Geographic Medicine<\/a>\u00a0and in the\u00a0Peter O\u2019Donnell Jr. School of Public Health<\/a>\u00a0at UT\u00a0Southwestern. He co-led the study with Sergey Cheshkov, Ph.D., former Assistant Professor of\u00a0Radiology<\/a>\u00a0at UT\u00a0Southwestern 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\u00a0Southwestern.”<\/p>\n “…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\u2019t have GWI<\/strong><\/span>. However, MRS technology available at the time couldn\u2019t 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<\/span><\/strong><\/span>. 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<\/strong><\/span>. Because mitochondrial dysfunction in the brain causes chronic neuroinflammation, this finding explains nearly all the symptoms of GWI<\/span><\/strong><\/span>, Dr. Haley said. He and his colleagues are currently studying how low-level sarin gas exposure causes mitochondrial dysfunction<\/strong><\/span>. This research may eventually lead to treatments that calm this chronic neuroinflammation, bringing relief to those with GWI.”<\/p>\n