This letter is in response to Trojian et al.’s review (1); specifically, those commentaries regarding omega-3 fatty acids (ω-3). The review included multiple instances of incorrect and inappropriate citations (e.g., see reference [69, 117,118]), contradictions, and in our opinion misrepresentation of emerging preclinical evidence in favor of ω-3.
Animal models of traumatic brain injury (TBI) clearly demonstrate that ω-3 administration before (2) and after (3) insult confers neuroprotective qualities. The authors would have been correct to state that no study, to date, has examined the difference between prophylactic and postinjury administration of ω-3s, in contrast to “animal data do not show added benefit from preloading DHA (docosahexaenoic acid)” which is incorrect and inappropriately cited (e.g., see reference 15, 111). A unique pathological consequence of TBI is a reduction in the quantity of neuronal DHA after injury (4) and deficiency of brain DHA content, induced by dietary restriction, heightens the pathophysiological response to injury (5). Failure on the part of those authors to acknowledge the relevant literature concerning prophylactic administration is of concern when the authors’ concluding remarks state that “despite the lack of data,” if used “we would suggest it (DHA) be used postinjury” as such statements may lead to broad policies that inhibit practitioners from supplementing those athletes at risk for sports-related concussion. Moreover, most individuals in the United States do not meet the recommended dietary intake for ω-3 (6), compounding concerns for the authors’ statements based on available evidence. The only iatrogenic effects, as noted by those authors’ include “belching, bad breath, fishy burp, heartburn, nausea, and loose stools,” and the theoretical risk of bleeding, which is likely unfounded (7).
Further, while it is a forgivable offense that the authors failed to recognize the purpose of the only human trial to date, the comment suggesting that “Further work is therefore needed to see if more DHA makes you more likely to become concussed while playing football” is irresponsible. There is a paucity of data suggesting that Sports Related Concussions (SRCs) can be prevented without rule changes and/or complete cessation of sport (8). Based on the authors’ flawed logic, football helmets should not be worn given that data do not support a reduction in injury severity or number of SRCs when used (8). The only published human trial to date, which demonstrated a potential neuroprotective effect of ω-3, was not designed to determine if ω-3 prevent SRC, as interpreted by the authors; rather the aim was to determine if ω-3 attenuated elevations of an established biomarker of neurological injury (9). Subconcussive impacts, in the absence of an SRC diagnosis, result in quantifiable pathophysiological changes (10) and may have important implications for long-term brain health, including the development of chronic traumatic encephalopathy (11).There is no doubt a lack of human trials. However, there are inherent limitations in the study of SRCs in humans, most notably the heterogeneity of injury. In closing, we find the authors’ conclusions contradictory and would appreciate an appropriately cited response.
Jonathan M. Oliver, PhD
Sports Concussion Research Group Department of Kinesiology Texas Christian University Fort Worth, TX email@example.com
Anthony J. Anzalone, MS
Sports Concussion Research Group Department of Kinesiology Texas Christian University Fort Worth, TX
Margaret T. Jones, PhD
Division of Health and Human Performance George Mason University Manassas, VA
K. Michele Kirk, MD
Sports Concussion Research Group Department of Kinesiology Texas Christian University Fort Worth, TX Department of Sport Medicine Texas Christian University Fort Worth, TX Department of Sport Medicine John Peter Smith Hospital Fort Worth, TX
David A. Gable, MSc
Sports Concussion Research Group Department of Kinesiology Texas Christian University Fort Worth, TX Department of Sport Medicine Texas Christian University Fort Worth, TX
Yanqin Gao, PhD
State Key Laboratory of Medical Neurobiology and Institute of Brain Science Fudan University China
William S. Harris, PhD
Department of Internal Medicine University of South Dakota Sioux Falls, SD
Henrik Zetterberg, MD, PhD
Clinical Neurochemistry Laboratory Institute of Neuroscience and Physiology The Sahlgrenska Academy at University of Gothenburg Mölndal, Sweden Department of Molecular Neuroscience UCL Institute of Neurology Queen Square London, UK
The authors declare no conflict of interest and do not have any financial disclosures.
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