Trauma symptoms
PTSD
Also searched as PTSD.
PTSD is not a condition that happens to involve poor fear extinction — it is defined by it. The trauma memory forms normally; what fails is the brain's ability to learn the cue is now safe. On a two-day protocol, learning the extinction can be near-normal and recalling it the next day fails. Amygdala runs hot, the hippocampus and the prefrontal brake run cold. And it is not only a mind condition: it raises hypertension, doubles type-2 diabetes risk and adds 27% to cardiovascular events.
In depth
Trauma-linked persistence of the threat response long after the threat. Its endocannabinoid signature is a divergent pair — stress lowers anandamide while raising 2-ag — which a single arrow cannot represent.
What drives it
Fear extinction reduces it.
PTSD is characterized by an inability to extinguish fear memories. A clinical characteristic of PTSD is persistently elevated fear responses to stimuli associated with the traumatic event. doi 10.1111/j.1601-183X.2012.00801.x · PMC2787650
Stress & cortisol increases it.
PTSD is a trauma- and stressor-related disorder; a clinical characteristic is persistently elevated fear responses to stimuli associated with the traumatic event. doi 10.1111/j.1601-183X.2012.00801.x · PMC2787650
Supports BDNF signaling reduces it.
In the PTSD animal model BDNF was higher in prelimbic cortex and amygdala and lower in infralimbic cortex and every hippocampal subfield — elevated where fear is expressed, depleted where the extinction brake lives. doi 10.1111/j.1601-183X.2012.00801.x · PMC2787650
Sympathetic drive increases it.
Sympathetic hyperactivation is a documented feature of PTSD and part of its cardiovascular mechanism. doi 10.31083/RCM44081 · PMC11065026
Calms inflammation increases it.
Informatics analysis of PTSD, CVD and T2DM risk genes identified shared signaling pathways emphasising the NF-kB complex and downstream proinflammatory signaling; 36 PTSD risk genes overlapped with CVD risk genes and 15 with T2DM. doi 10.31083/RCM44081 · PMC11065026
Oxidative stress increases it.
Oxidative stress is named among the interconnected biological pathways in the PTSD-cardiovascular link (PMC11065026; doi 10.31083/RCM44081; PMC12569545; PMC12851403; PMC10200052). Verbatim: “Currently, oxidative stress and neuroinflammation attract increasing attention as important mechanisms of MD and PTSD”. doi 10.31083/RCM44081 · PMC11065026
Mood (serotonin) reduces it.
Sertraline, paroxetine, fluvoxamine and citalopram have received FDA support for the treatment of PTSD symptoms. Treatment response to these agents is estimated at 15%-30%, with small effect sizes, and there is a tendency to relapse on discontinuation. doi 10.1176/appi.focus.20220088 · PMC9567733
Social bonding hormone reduces it.
The neuropeptide oxytocin modulates key neural substrates, namely the amygdala and PFC, implicated in PTSD, learning and memory, and fear extinction. MDMA's therapeutic effect involves increased serotonergic activity and the release of oxytocin and BDNF in key memory and emotional circuits. doi 10.1176/appi.focus.20220088 · PMC9567733
What it drives
It increases Calm under stress.
A clinical characteristic of PTSD is persistently elevated fear responses to stimuli associated with the traumatic event. doi 10.1111/j.1601-183X.2012.00801.x · PMC2787650
It reduces Mood.
PTSD is characterized by persistently elevated fear responses with exaggerated amygdala and diminished hippocampal and vmPFC activation — the same circuit disruption implicated in negative affect. doi 10.1111/j.1601-183X.2012.00801.x · PMC2787650
It reduces Sleep.
Sleep disturbance and nightmares are core to the trauma-related symptom cluster. doi 10.1111/j.1601-183X.2012.00801.x · PMC2787650
It increases Lowers cortisol.
Stress-induced extinction impairments contribute to relapse of fear in patients undergoing exposure therapy; the HPA axis is named as a system altering fear extinction through BDNF modulation. doi 10.1111/j.1601-183X.2012.00801.x · PMC2787650
It increases Calms body-wide inflammation.
Trauma- and stressor-related disorders are associated with elevated peripheral inflammatory markers. doi 10.1111/j.1601-183X.2012.00801.x · PMC2787650
It reduces Heart & blood pressure.
PTSD is associated with a 27% increase in cardiovascular events or cardiac-specific mortality, a 47% increased risk of heart failure, and is recognized as an independent risk factor, predictor and even a cause of cardiovascular disease. doi 10.31083/RCM44081 · PMC11065026
It increases Blood pressure.
PTSD was associated with subsequent hypertension (OR=3.0, 95% CI 2.9-3.1), remaining significant after adjustment for comorbidities and sociodemographic variables (OR=1.9, 95% CI 1.8-2.0). doi 10.31083/RCM44081 · PMC11065026
It increases Type 2 diabetes.
PTSD increased T2D risk and was associated with worse glycemic control; meta-analyses report a 30-50% increased incidence, and the association persists after adjusting for obesity and physical inactivity. doi 10.31083/RCM44081 · PMC11065026
It reduces Metabolic health.
A meta-analysis of 9 studies and over 9,000 subjects found people with PTSD had almost doubled risk for comorbid metabolic syndrome; PTSD symptom severity predicts risk in a fashion. doi 10.31083/RCM44081 · PMC11065026
It reduces Lowers cholesterol.
PTSD provokes classical cardiovascular risk factors including high cholesterol and triglycerides. doi 10.31083/RCM44081 · PMC11065026
It reduces Blood flow (nitric oxide).
PTSD provokes endothelial dysfunction and platelet hyperaggregation. doi 10.31083/RCM44081 · PMC11065026
It increases Oxidative stress.
Interconnected biological pathways explaining the PTSD-CVD association include systemic inflammation, endothelial dysfunction, platelet hyperreactivity, coagulation abnormalities and oxidative stress. doi 10.31083/RCM44081 · PMC11065026
It increases Sympathetic drive.
Chronic sympathetic activation and reduced parasympathetic tone are named among the interconnected pathways linking PTSD to cardiovascular disease. doi 10.31083/RCM44081 · PMC11065026
It reduces Alcohol recovery.
PTSD has high comorbidity with tobacco and alcohol use disorders. doi 10.31083/RCM44081 · PMC11065026
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.