The Global Deficiency of Omega-3—What Are Your Cell Membranes Made Of?
Chris Oswald
NUTRITION
Modern society is in a health crisis, and much of it has to do with what people eat every day. In a very short period, we have moved from a diet of fresh fruits and veggies, lean meats, and unrefined grains, to meals that aie highly processed and generally come from a box, bag, or can. These food products are so highly processed that they will not spoil for years to come. The negative health consequences of this shift are hard to overstate. It has created a perfect storm resulting in many of the poor states of health we witness daily.
As a clinician, when I think about the foundational systems of a healthy individual, I go to the health of the cell. Humans have between 60 and 100 trillion cells in their bodies. Each cell membrane is essential for the ability of the cell to hold a proper structure and communicate with the rest of the body. Every one of these cell membranes is made up of essential fatty acids (EFA), which are nutrients acquired exclusively through diet. When the cell membrane is not working well, widespread impacts on health aie felt and seen.
The ciment Western diet attacks cell membranes on two fronts. First, it is almost devoid of the healthy omega-3 fats eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which are essential to healthy cells and bodies. Second, the diet is full of arachidonic acid (AA), which has been shown to be increased in many chronic disease states.1 In fact, omega-3 deficiency is such a large problem that in 2011 the Global Summit on Nutrition, Health, and Human Behavior stated unanimously, “Brain and heart disorders resulting from LC-Omega-3 (EPA +DHA) deficiency are the biggest challenges to the friture of humanity.”2
The importance of adequate, balanced levels of EPA and DHA can’t be underestimated. Several biochemical processes, with effects on nearly every tissue in the body, ai e highly dependent on the fatty acid content of the cell membrane. Eicosanoid modulation is a process highly involved in the inflammatory response and its eventual resolution. Not to mention the additional impact that inflammation has on immune function within the human body as well.3 The endocannabinoid system (ECS) deals with the CB 1 and CB2 receptors, which aie plentiful throughout the body, especially in the brain. Its operation has wide-ranging effects on satiety, addiction, cravings, and pain.4
Imbalance of the cell membrane is linked to the specific EFAs taken in via diet and supplementation. A higher ratio of AAto EPA results in the creation of eicosanoids, which exert a powerful inflammatory influence and make it difficult to create the eicosanoids important for the resolution stage of an inflammatory event. This connection is more along the lines of how the body responds to inflammation within the body, but another consideration is why the inflammation is present in the first place. This state of EFA imbalance can often be traced back to poor food choices and positive energy balance, or taking in too many calories. The impact of food choices is long felt by the fact that the body has to determine how to handle the excess, which many times results in a slow, insidious rise in the levels of systemic inflammation. The underlying biochemical processes have a tremendous amount to do with the development of visceral obesity and obesity in general.5
The complex, whole-body interaction of long-chain polyunsaturated fatty acids clearly indicates that balanced EFAs have the potential to dramatically affect overall health across time. Research points to their importance in the areas of cardiovascular health, cerebrovascular health, neurological health, and much more.6 There is good reason to limit dietary AA intake to help support a more appropriate balance with the omega-3 s EPA and DHA.
In addition to understanding how serious EFA deficiency and imbalance in the cell membrane can be, it is also important for clinicians to be able to identify a problem when a patient walks into the office. In practice, I generally assume, due to prevailing dietary practices, that most everyone has some sort of imbalance. Lab analysis is the ideal way to be certain about a patient’s EFA status. It looks at the fatty acid content of red blood cells by measuring whole blood, or with a simple blood spot test (which can easily be done in any office environment). The test results include the ratio of omega-6 to omega-3 fatty acids, and the ratio of AAto EPA. Data concerning the other omegas 3 and 6 will also be provided, but just knowing the aforementioned ratios will give you an excellent foundation to determine an appropriate recommendation.
When the cell membrane integrity needs a bit of support, it is easy to develop a plan to maintain good EFA nutrition. Even without lab data, it is very safe to provide recommendations of up to two grams of EPA+DHA daily, with some studies reporting even higher doses being well tolerated for long periods, even in the presence of many medications. The human body does need AA because there ai e several important processes for which it is responsible. One of these is its impact on cholesterol metabolism,7 so when using higher doses the clinician must remember that there can be too much of a good thing. During treatment, it’s important to be aware of balancing the cell membrane with the appropriate amount of EPA/DHA versus AA. The great part of laboratory analysis is that it becomes very easy to determine dosing requirements. After detennining healthy levels of EFAs in the cell membrane, the test can be performed again, in many cases six months later, to determine the appropriate dose for the patient in order to ensure the best outcome.
Omega-3 deficiency is a global problem. As clinicians, we need to understand the broad support that the essential fatty acids EPA and DHA offer human health. We aie
the front line with a deeper understanding of why and how omega-3 fish oils work. This knowledge is the first step of harnessing their power to truly support the health of the many patients we see every day.
References:
1. Mozaffarian, I)., Lemaitre, R. N, King, I. B., Song, X., Huang, H, Sacks, F M., Siscovick, D. S. (2013). Plasma phospholipid long-chain co-3 fatty acids and total and cause-specific mortality in older adults: A cohort study. Annals of Internal Medicine, 158(7), 515-25. doi: 10.7326/0003-4819-1587-201304020-00003
2. Consensus Statement. Omega-3 Summit. Global Summit on Nutrition Health and Human Behavior, n.d. Web. 08 May 2015. http://www.omega3summit.org/pdf/ConsensusStatements.pdf>.
3. Si-Tahar M, Tou qui L, Chi gnard M. Innate immunity and inflammation— two facets of the same anti-infectious reaction. Clinical and Experimental Immunology. 2009; 156(2): 194-198.
4. McPartland, J. M., Guy, G. W., & Di Marzo, V. (2014). Care and feeding of the endocannabinoid system: A systematic review of potential clinical interventions that upreguíate the endocannabinoid system. PLoS ONE, 9(3). doi: 10.1371/journal.pone. 0089566
5. Masoodi, M., Kuda, O., Rossmeisl, M., Flachs, P, & Kopecky, J. (2015). Lipid signaling in adipose tissue: Connecting inflammation and metabolism. Biochi mica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, 1851(4), 503-518. doi:10.1016/j. bbalip.2014.09.023
6. Chilton, F. H., Murphy, R. C., Wilson,
B. A., Sergeant, S., Ainsworth, H., Seeds, M. C., & Mathias, R. A. (2014). Diet-gene interactions and PUFA metabolism: A potential contributor to health disparities and human diseases. Nutrients, 6(5), 1993-2022. doi: 10.3390/nu6051993
7. Demetz, E., Schroll, A., Auer, K, Heim,
C. , Patsch, J. R., Eller, P, Uboldi, P. (2014). The Arachidonic Acid Metabolome Serves as a Conserved Regulator of Cholesterol Metabolism, 20(5), 787-798. doi: 10.1016/j. cmet.2014.09.004
Christopher Oswald, D.C., C.N.S. is a chiropractor, certified nutrition specialist and a graduate of Northwestern Health Sciences University. He practices in Wisconsin, focusing on whole body care for those suffering from head and neck pain. He is an Advisory Board Member of Nordic Naturals, and the National Association of Nutrition Professionals.
