The Gulf War, which took place in the Persian Gulf region between August 1990 and February 1991, involved about 700,000 US soldiers. According to estimates, one-third of these people developed chronic illnesses as a result of their deployment. Headaches, insomnia, cognitive impairment, fatigue, & nbsp, muscle ache, joint pain, and gastrointestinal distress are just a few of the ailments brought on by this illness, also known as Gulf War Illness( GWI ). There have been theories put forth as potential causes that include exposure to toxins like nerve gas, burn pits, and excessive pesticide exposure.
Inflammation and mitochondrial impairment have been suggested as the disease’s two potential causes. These hypotheses were directly tested with patient samples in recent research that was published in Scientific Reports. In this small study, fifteen unaffected people and nineteen GWI patients were compared. According to the research, GWI is caused by mitochondrial dysfunction rather than inflammation. According to the study’s authors, mitochondria should be the main therapeutic target for treatments.
This represents a radical rethinking of GWI’s pathology. According to the study’s author, Beatrice Golomb, MD, PhD, a professor of medicine at the UC San Diego School of Medicine, this discovery could change the lives of veterans who have long struggled to receive effective care.
The study’s participants’ muscle biopsies were used by the researchers to evaluate mitochondrial respiratory chain function ( MRCF ) and high-sensitivity C – reactive protein ( hsCRP ), two markers of peripheral inflammation. Patients with GWI were found to experience symptoms that matched the severity of mitochondrial impairment rather than inflammation.
According to a statistical analysis, mitochondrial dysfunction was linked to seventeen of the twenty most common GWI symptoms. Only one symptom, though, was connected to inflammation.
Only in the GWI patients was it discovered that mitochondria ‘ capacity to transform fat into energy, a process known as fatty acid oxidation, was connected to inflammation. Inflammation can result from fatty acid oxidation, which can cause cell death. This might suggest that GWI patients’ increased inflammation is being caused by mitochondrial dysfunction.
According to Golomb,” Inflammation does seem to be associated with GWI, but our research suggests that it’s actually a side effect of the main problem, which is impaired cell energy.”
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Many GWI symptoms can also be explained by mitochondrial dysfunction. Muscle aches and fatigue may result from mitochondria not producing enough fuel from fat. Additionally, it was discovered that muscle symptoms correlated with the degree of fatty acid oxidation in the patient’s mitochondria. Cognitive symptoms may result if mitochondria do not produce enough sugar-based fuel. Cognitive symptoms in GWI patients were also found to be correlated with mitochondrial dysfunction connected to sugar-based fuel production.
The researchers are optimistic that better treatments can be created and used on patients now that there is concrete evidence to back up the mitochondrial hypothesis.
Scientific Reports from the University of California, San Diego