PTSD (post-traumatic stress disorder) may be more likely to occur in the presence of pre-existing inflammation according to a study just published in JAMA Psychiatry. Noting that earlier studies have demonstrated an association of PTSD with peripheral inflammation, the authors set out to…

“…determine whether plasma concentration of the inflammatory marker C-reactive protein (CRP) helpspredict PTSD symptoms.”

The authors examined pre and post-deployment data on combat-related trauma for 1861 subjects and PTSD symptoms for 1617 in the Marine Resiliency Study, using the Clinician-Administered PTSD Scale (CAPS) as a metric for PTSD symptoms. The data demonstrated a correlation between inflammation and risk of PTSD:

“We determined the effects of baseline plasma CRP concentration on postdeployment CAPS using zero-inflated negative binomial regression (ZINBR), a procedure designed for distributions, such as CAPS in this study, that have an excess of zeroes in addition to being positively skewed. Adjusting for the baseline CAPS score, trauma exposure, and other relevant covariates, we found baseline plasma CRP concentration to be a highly significant overall predictor of postdeployment CAPS scores: each 10-fold increment in CRP concentration was associated with an odds ratio of nonzero outcome (presence vs absence of any PTSD symptoms) of 1.51 and a fold increase in outcome with a nonzero value (extent of symptoms when present) of 1.06.”

Medpage Today: Psychiatry quotes Paul E. Schulz, MD, of the University of Texas Health Science Center in Houston:

“Schulz said the inflammation-PTSD relationship was definitely plausible on the basis of several lines of research. For example, he told MedPage Today in an email, previous traumatic brain injury is a known risk factor for PTSD, and the mechanism may involve chronic brain inflammation resulting from the injury. Other lines of research have implicated immunological factors in promoting susceptibility to PTSD, he said.”

It certainly stands to reason that chronic brain inflammation from autoimmune or traumatic causes would render the brain more susceptible to stress-related anxiety disorders.Medscape also quotes the authors:

“”If peripheral inflammation contributes to the development of PTSD, interventions to decrease inflammation, such as dietary or lifestyle modifications, might ameliorate the severity of this disorder,” they wrote.”

The authors of the study conclude:

“A marker of peripheral inflammation, plasma CRP may be prospectively associated with PTSD symptom emergence, suggesting thatinflammation may predispose to PTSD.”

Practitioners reading this post are likely aware of the anti-inflammatory and calming virtues of magnesium but may not have seen the study just published in the European Journal of Clinical Nutrition offering evidence that magnesium lowers CRP:

“The aim of this study was to quantitatively summarize the association of dietary magnesium (Mg) intake with serum C-reactive protein (CRP) levels in the general population.”

They examined data from observational and experimental studies in PubMed, EMBASE, Google and hand searches of related reference lists for the likelihood of having serum CRP greater than or equal to 3”‰mg/l and used meta-regression was to determine the linear association of dietary Mg intake and CRP levels. The data showed a significant association between higher magnesium and lower CRP:

“A data set derived from seven cross-sectional studies including 32,918 participants was quantitatively assessed. A weighted inverse association between Mg intake and serum CRP levels was observed from four cross-sectional studies. The pooled OR of having CRP greater than or equal to 3 ”‰mg/l was 1.49 on comparing the lowest to the highest group of Mg intake from three studies with the data available. Qualitative assessmentamong five intervention studies also showed a potential beneficial effect of Mg intake on serum CRP levels.”

These authors conclude:

“This meta-analysis and systematic review indicates that dietary Mg intake is significantly and inversely associated with serum CRP levels. The potential beneficial effect of Mg intake on chronic diseases may be, at least in part, explained by inhibiting inflammation.”

Clinical note: considering that PTSD is characterized by SNS (sympathetic nervous system) hyperarousal and inflammation, and that magnesium is ”˜nature’s SNS calming mineral’ that supports PSNS (parasympathetic nervous system) function and has a natural anti-inflammatory effect, magnesium is certainly worthy of consideration in the case management of PTSD.

Magnesium measurement and dosage considerations: Serum magnesium and even RBC membrane magnesium are poor indicators of tissue magnesium status. When objective determination of tissue mineral status is required the Exa Test is definitive. Both clincians and patients should bear in mind that magnesium needs can fluctuate due to stress, inflammation and other causes, and the latter can learn to adjust their dosage as needed. Moreover, magnesium assimilation can be impaired by gut epithelial microinflammation and stomach acid blocking medications. Some earlier studies on magnesium and muscle cramps, a common clinical indicator of suboptimal magnesium status related to the role of magnesium in regulating neuromuscular excitability, are flawed by dosages that were too low.