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Suicide Deaths of Active-Duty US Military and Omega-3 Fatty-Acid Status: A Case-Control Comparison

J Clin Psychiatry 2011;72(12):1585-1590
10.4088/JCP.11m06879

Background: The recent escalation of US military suicide deaths to record numbers has been a sentinel for impaired force efficacy and has accelerated the search for reversible risk factors.

Objective: To determine whether deficiencies of neuroactive, highly unsaturated omega-3 essential fatty acids (n-3 HUFAs), in particular docosahexaenoic acid (DHA), are associated with increased risk of suicide death among a large random sample of active-duty US military.

Method: In this retrospective case-control study, serum fatty acids were quantified as a percentage of total fatty acids among US military suicide deaths (n = 800) and controls (n = 800) matched for age, date of collection of sera, sex, rank, and year of incident. Participants were active-duty US military personnel (2002–2008). For cases, age at death ranged from 17–59 years (mean = 27.3 years, SD = 7.3 years). Outcome measures included death by suicide, postdeployment health assessment questionnaire (Department of Defense Form 2796), and ICD-9 mental health diagnosis data.

Results: Risk of suicide death was 14% higher per SD of lower DHA percentage (OR = 1.14; 95% CI, 1.02–1.27; P < .03) in adjusted logistic regressions. Among men, risk of suicide death was 62% greater with low serum DHA status (adjusted OR = 1.62; 95% CI, 1.12–2.34; P < .01, comparing DHA below 1.75% [n = 1,389] to DHA of 1.75% and above [n = 141]). Risk of suicide death was 52% greater in those who reported having seen wounded, dead, or killed coalition personnel (OR = 1.52; 95% CI, 1.11–2.09; P < .01).

Conclusion: This US military population had a very low and narrow range of n-3 HUFA status. Although these data suggest that low serum DHA may be a risk factor for suicide, well-designed intervention trials are needed to evaluate causality.

J Clin Psychiatry

Submitted: January 24, 2011; accepted March 9, 2011.

Online ahead of print: August 23, 2011 (doi:10.4088/JCP.11m06879).

Corresponding author: Joseph R. Hibbeln, MD, USPHS, Section of Nutritional Neurosciences, Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcoholism and Alcohol Abuse, National Institutes of Health, 5625 Fishers Lane, Rm 3N-07, MSC 9410, Bethesda, MD 20892 (jhibbeln@mail.nih.gov).