Exploring the neurobiological impact of combat trauma on veterans
Every day, approximately 17 to 24 American military veterans die by suicide—a staggering statistic that reveals a hidden crisis among those who have served their country. Combat veterans are particularly vulnerable, with suicide rates 1.5 times higher than non-veterans despite comprising only 8.5% of the U.S. population 1 2 . Behind these devastating numbers lies a complex neurobiological story of how combat trauma alters brain chemistry, circuitry, and function, creating perfect conditions for suicidal thoughts and behaviors to emerge.
17-24 veterans
die by suicide each day in the United States
For decades, research focused primarily on psychological explanations for veteran suicide, but cutting-edge neuroscience is now revealing physical changes in the brain that occur during military service that contribute to this elevated risk. From hormonal imbalances to altered brain connectivity, the neurological legacy of combat is helping researchers develop more effective prevention strategies and treatments for those who carry invisible wounds from their service 1 8 .
Combat trauma can disrupt the delicate balance of neurochemicals that regulate mood, stress response, and impulse control. Several key biomarkers have been identified that distinguish veterans who attempt suicide from those who don't:
Dehydroepiandrosterone (DHEA) and its sulfate form (DHEA-S) are neurosteroids that help protect the brain from stress. Studies have found that combat veterans with a history of suicide attempts have significantly lower levels of both DHEA and DHEA-S compared to non-attempters 1 .
The endocannabinoid system, which helps regulate emotional processing and stress recovery, shows significant alterations. Researchers found that 2-arachidonoylglycerol (2-AG) blood concentrations were higher among suicide attempters 1 .
Neuropeptide Y (NPY), a neurotransmitter associated with resilience and stress buffering, shows paradoxical changes. Contrary to expectations, veterans who had attempted suicide had higher NPY levels than non-attempters 5 .
Research shows platelet serotonin is significantly lower in suicidal veterans with PTSD, which may contribute to increased impulsivity and difficulty with mood regulation 3 .
| Biomarker | Function | Change in Suicide Attempters | Potential Impact |
|---|---|---|---|
| DHEA/DHEA-S | Neuroprotection, stress resilience | Significant decrease | Reduced buffering against stress |
| 2-AG | Endocannabinoid signaling | Increased | Disrupted emotional processing |
| Anandamide (AEA) | Stress response modulation | Lower in those with ideation | Reduced ability to manage stress |
| Neuropeptide Y (NPY) | Resilience, stress adaptation | Increased | Possible compensatory mechanism |
| Serotonin | Mood regulation, impulse control | Decreased platelet serotonin | Increased impulsivity, depression |
Neuroimaging studies have revealed that suicidal thoughts and behaviors are associated with specific alterations in brain structure and function. The most consistent findings involve regions responsible for emotion regulation, decision-making, and impulse control 8 .
| Brain Region | Primary Functions | Role in Suicidal Behavior |
|---|---|---|
| Ventral Prefrontal Cortex (VPFC) | Emotion regulation, reward processing | Generation of suicidal ideation |
| Dorsal Prefrontal Cortex (DPFC) | Cognitive control, planning | Transition from ideation to attempt |
| Anterior Cingulate Cortex (ACC) | Conflict monitoring, emotion regulation | Switching between emotional states |
| Insula | Interoception, emotional awareness | Body awareness of distress |
| Hippocampus | Memory formation, stress regulation | Contextualizing experiences |
"Damage or reduced volume in the ventral prefrontal cortex may contribute to the excessive negative and blunted positive internal states that stimulate suicidal thinking." 8
One crucial study led researcher Leo Sher and colleagues examined neurobiological differences between combat veterans with and without a history of suicide attempts 1 .
The findings revealed striking neurobiological differences:
| Biomarker | Non-Attempters | Suicide Attempters | Statistical Significance | Clinical Implications |
|---|---|---|---|---|
| DHEA | Higher levels | Significantly lower | p < 0.05 | Reduced stress resilience |
| DHEA-S | Higher levels | Significantly lower | p < 0.05 | Loss of neuroprotection |
| 2-AG | Lower levels | Elevated | p < 0.05 | Disrupted stress signaling |
| Anandamide (AEA) | No correlation with ideation | Negative correlation with ideation | p < 0.05 | Possible protective factor |
| Suicidal Ideation (SSI) | Lower scores | Significantly higher | p < 0.01 | Persistent suicide risk |
Research shows that social experiences during deployment significantly impact suicide risk years after veterans return home 3 .
Soldiers who report strong unit cohesion before deployment have a lower risk of post-deployment mental disorders and suicidal ideation 3 .
Combat veterans often experience multiple traumatic brain injuries (TBIs) from blast exposures, falls, or other combat-related incidents 7 .
Research shows that Iraq and Afghanistan veterans with multiple TBIs are about twice as likely to report recent suicidal ideation compared to veterans with one TBI or none at all 7 .
"Veterans with three or more mild TBIs often show slowed processing speed and memory difficulties that may make it challenging to access and use past experiences to solve current problems and imagine future outcomes, leading to increases in hopelessness and suicidal ideation." 7
The growing understanding of the neurobiology underlying suicidal behavior in combat veterans offers hope for more effective prevention strategies and treatments. By identifying specific biological vulnerabilities—whether in neurosteroid function, brain circuitry, or stress response systems—researchers are moving closer to objective biomarkers that could help identify at-risk veterans before they reach crisis point 1 8 .
This research may also lead to novel treatments targeting the biological underpinnings of suicide risk. Medications that modulate neurosteroid levels or endocannabinoid signaling, neuromodulation approaches that normalize activity in disrupted brain circuits, and interventions that specifically address cognitive deficits from TBIs could all emerge from this work 1 7 .
Ultimately, reducing veteran suicide will require integrating our understanding of neurobiological risk factors with attention to social, psychological, and environmental influences. As research continues, we move closer to a future where we can honor veterans' service by providing care that addresses both the visible and invisible wounds they carry home from combat 2 3 .