The fallacy of using DHA alone for brain trauma

I am constantly amazed by the lack of understanding by neurologists of basic essential fatty acid biochemistry in the treatment of brain trauma and concussions. They often blindly believe that the only omega-3 fatty acid that has any impact in the treatment of concussions is DHA alone. Their blind faith is based on the observation that you find a lot of DHA in the brain and little EPA. This obviously means that EPA must not be important for brain function. This is similar to stating the world is flat because it appears that way to the naked eye.

I have mentioned many times in my books that EPA and DHA have different functions, and that’s why you need both of these essential omega-3 fatty acids (1-4). This is especially true for the brain. EPA produces most of the anti-inflammatory properties of omega-3 fatty acids since it’s structurally similar to arachidonic acid (AA) as they both contain 20 carbon atoms with approximately the same spatial configuration. As a result, EPA can inhibit the enzymes that would otherwise produce pro-inflammatory eicosanoids from AA. It is AA that generates the inflammation caused by brain trauma. DHA, on the other hand, is primarily a structural component of neural tissue. They do different jobs, and that’s why you need both in combination.

So why isn’t there as much EPA in the brain compared to DHA? The reason is simple. EPA enters the brain just as quickly as DHA, but it is rapidly oxidized, whereas DHA is sent off to long-term storage in neural tissue (5-7). The lifetime of DHA in the human brain is measured in years, whereas the lifetime of the EPA is measured in days. So obviously when you kill an animal and look at the brain, you are not going to find very much EPA.

What complicates the issue is that if you only treat a concussion with DHA, some of the DHA will be converted to EPA. This gives the appearance that DHA is working to reduce inflammation. Since brain trauma and concussions generate inflammation in the brain, doesn’t it make more sense to provide as much EPA as possible to reduce the inflammation as opposed to supplementing only with DHA and hoping some fraction of it will be converted to EPA?

To answer that question, it is useful to look at two recent studies that used the same protocol to study inflammation induced by a concussion injury (8,9). The same total amount of omega-3 fatty acids was used to treat the animals after the concussion injury. One experiment used a 2:1 ratio of EPA to DHA, and the other experiment used only DHA. If the DHA was so important, then the animals treated with the DHA alone should have demonstrated three times the reduction of neuro-inflammation compared to the group that received omega-3 fatty acids containing only one-third as much DHA.

In fact, just the opposite was the case. The 2:1 EPA/DHA group demonstrated greater benefits compared to the DHA-alone group in reducing neuro-inflammation induced by a concussion. Why? EPA is a far more powerful anti-inflammatory agent than DHA. This is why in both studies the AA/EPA ratio was used as the marker of inflammation induced by the concussion injury. Since the AA/EPA ratio was decreased in both studies, this meant that some of the pure DHA was converted to EPA providing at least some anti-inflammatory actions. Thus giving 100 percent DHA is not exactly the most efficient way to decrease neuro-inflammation induced by a concussion injury. This is further emphasized by a recent study that indicated that 1 gram of DHA per day for an 18-month period had no impact in the cognitive improvement of Alzheimer’s patients (10), even though Alzheimer’s is known to be a neuro-inflammatory disease (11).

Does this mean that DHA is not important for brain repair? Of course not. This is because you need both EPA and DHA for optimal repair of brain damage after a concussion. You need the EPA to reduce the neuro-inflammation, and you need the DHA to help rebuild new neurons. But to give DHA alone without additional EPA to maximally reduce neuro-inflammation caused by concussions simply makes no sense.

References

  1. Sears B. “The Zone.” Regan Books. New York, NY (1995)
  2. Sears B. “The OmegaRx Zone.” Regan Books. New York, NY (2002)
  3. Sears B. “The Anti-inflammation Zone.” Regan Books. New York, NY (2005)
  4. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  5. Chen CT, Liu Z, and Bazinet RP. “Rapid de-esterification and loss of eicosapentaenoic acid from rat brain phospholipids: an intracerebroventricular study.” J Neurochem 116: 363-373 (2011)
  6. Chen CT, Liu Z, Ouellet M, Calon F, and Bazinet RP. “Rapid beta-oxidation of eicosapentaenoic acid in mouse brain: an in situ study. “Prostaglandins Leukot Essent Fatty Acids 80: 157-163 (2009)
  7. Umhau JC, Zhou W, Carson RE, Rapoport SI, Polozova A, Demar J, Hussein N, Bhattacharjee AK, Ma K, Esposito G, Majchrzak S, Herscovitch P, Eckelman WC, Kurdziel KA, and Salem N. “Imaging incorporation of circulating docosahexaenoic acid into the human brain using positron emission tomography.” J Lipid Res 50: 1259-1268 (2009)
  8. Mills JD, Bailes JE, Sedney CL, Hutchins H, and Sears B. “Omega-3 fatty acid supplementation and reduction of traumatic axonal injury in a rodent head injury model.” J Neurosurg 114: 77-84 (2011)
  9. Bailes JE and Mills JD. “Docosahexaenoic acid reduces traumatic axonal injury in a rodent head injury model.” J Neurotrauma 27: 1617-1624 (2010)
  10. Quinn JF, Raman R, Thomas RG, Yurko-Mauro K, Nelson EB, Van Dyck C, Galvin JE, Emond J, Jack CR, Weiner M, Shinto L, and Aisen PS. “Docosahexaenoic acid supplementation and cognitive decline in Alzheimer disease: a randomized trial.” JAMA 304: 1903-1911 (2010)
  11. Akiyama H, Barger S, Barnum S, Bradt B, Bauer J, Cole GM, Cooper NR, Eikelenboom P, Emmerling M, Fiebich BL, Finch CE, Frautschy S, Griffin WS, Hampel H, Hull M, Landreth G, Lue L, Mrak R, Mackenzie IR,McGeer PL, O’Banion MK, Pachter J, Pasinetti G, Plata-Salaman C, Rogers J, Rydel R, Shen Y, Streit W, Strohmeyer R, Tooyoma I, Van Muiswinkel FL,Veerhuis R, Walker D, Webster S, Wegrzyniak B, Wenk G, and Wyss-Coray T. “Inflammation and Alzheimer’s disease.” Neurobiol Aging 21: 383-421 (2000)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

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About Dr. Barry Sears

Dr. Barry Sears is a leading authority on the impact of the diet on hormonal response, genetic expression, and inflammation. A former research scientist at the Boston University School of Medicine and the Massachusetts Institute of Technology, Dr. Sears has dedicated his research efforts over the past 30 years to the study of lipids. He has published more than 30 scientific articles and holds 13 U.S. patents in the areas of intravenous drug delivery systems and hormonal regulation for the treatment of cardiovascular disease. He has also written 13 books, including the New York Times #1 best-seller "The Zone". These books have sold more than 5 million copies in the U.S. and have been translated into 22 different languages.

4 thoughts on “The fallacy of using DHA alone for brain trauma

  1. This is an excellent bit of information. This is important for all of us to know. I did not know any of this and stumbled onto your article while trying to figure out what kind of omega 3 supplement to buy. There are so many permutations and combinations available out there!

    But I was horrified that some people would actually, deliberately injure an animal to prove something. We have to find humane ways to “prove” things or to understand the workings of the human body. That the above information was gained by animal abuse does not mean that this knowledge could not have been obtained otherwise. All we need is the will. But with the easy availability of millions of hapless animals, why bother…

    • I personally prefer to do only clinical experiments with humans. This is one of the few times in more than 30 years of research that I had to use an animal to demonstrate the reduction of neuro-inflammation in the brain. It was a necessary experiment to set the foundation for further experimentation in humans.

  2. How much EPA/DHA would you recommend for the treatment of concussion? Are you following AA/EPA ratios and if so, how often are you checking this ratio? Thank you for your input.

  3. Alrighty then.

    Maybe it’s not only concussions where the brain sucks up/oxidizes EPA like crazy. Maybe this is happening in normal, undamaged brains, too. Or do I misunderstand you in the first place.

    For research, how about locating some human brains which have been damaged, and start from there? Where there is a will, there is a way. I would go on welfare and live under a bridge before I deliberately harm an animal who never did anything to me. Where did scientists all get the idea in the first place that DHA was more important? Obviously they were looking at human brains somewhere along the line and found lots of DHA and little or no EPA, but a truly smart scientist could easily conclude the reverse of what most of them did. To me the correct conclusion is the logical one.

    In any case, this is all very interesting.

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