Effects of a diet low in excitotoxins on PTSD symptoms and related biomarkers

ABSTRACT

Post-traumatic stress disorder (PTSD) develops after trauma exposure and involves symptoms of avoidance, intrusive re-experiencing, mood and cognitive dysfunction, and hypervigilance. PTSD is often comorbid with Gulf War Illness (GWI), a neurological condition involving widespread pain, cognitive dysfunction, digestive problems, and other symptoms, in Gulf War veterans. PTSD tends to be more severe when comorbid with GWI. Low cortisol and elevated homocysteine levels have been found in PTSD, making them potential PTSD biomarkers. The low-glutamate diet, which aims to reduce excitotoxicity by eliminating the consumption of free glutamate and aspartate, has been shown to significantly reduce GWI and PTSD symptoms. This study examined whether changes in serum cortisol and homocysteine are associated with reduced PTSD severity in veterans with GWI after one month on the low-glutamate diet, and whether reducing the consumption of dietary excitotoxins was associated changes in PTSD and serum biomarkers. Data were analyzed for 33 veterans. No serum biomarkers significantly changed post-diet; however, cortisol increased as dietary excitotoxin consumption decreased, which held in a multivariable linear regression after adjustment for sex. Reduced dietary excitotoxin consumption was also associated with reduced hyperarousal symptoms, which held in a multivariable linear regression after adjustment for sex. Cortisol increase was associated with reduced avoidance symptoms after adjustment for change in BMI, and was marginally associated with overall PTSD reduction. Change in homocysteine was not significantly related to dietary adherence nor change in PTSD. Results suggest that reducing the consumption of dietary excitotoxins may normalize cortisol levels, which has been associated with alleviating PTSD.

KEYWORDS:

• Post-traumatic stress disorder
• Gulf War Illness
• low-glutamate diet
• glutamate
• homocysteine
• cortisol
• excitotoxins
• aspartate

Disclosure statement

No potential conflict of interest was reported by the authors.

Data availability statement

The data that support the findings of this study are available from the corresponding author, Kathleen Holton, upon reasonable request.

Additional information

Funding

This work was supported by Office of the Assistant Secretary of Defense for Health Affairs, through the Gulf War Illness Research Program: [Grant Number W81XWH-17-1-0457].

Notes on contributors

Sidney L. Murray

Sidney Murray is a doctoral student in the Behaviour, Cognition, and Neuroscience PhD program at American University. Her research interests include investigating the neurobiological underpinnings of the relationship between PTSD and eating disorders and using diet to treat these conditions. She earned her M.A. in Experimental Psychology from Appalachian State University and her M.S. in Neuroscience from American University.

Kathleen F. Holton

Dr. Kathleen Holton is a nutritional neuroscientist at American University who studies the negative effects of food additives and positive protective effects of micronutrients on neurological function. She specializes in the dietary modulation of glutamatergic neurotransmission.