If you're ready for another inflammatory and quite possibly insulting article on how we might tweak our diets to reduce the insidious nature of inflammation, read on. More muscle mass and less body fat might just be your reward. Oh, and you may want to grab a medical dictionary because this is one current and highly-referenced opus. What can we say? Get this man geeking-out and he'll bust through the wall of ignorance like the Kool Aid Man!
Liberals rule!
Bush is a dolt!
Buddhism is the one true path to enlightenment!
As you can see, some comments get pretty inflammatory. Politics, religion, and philosophy are notorious but what about nutrition? It too gets some people pretty hot under the collar. Talk about dietary supplements in general or controversial things like antioxidants, and emotions often cloud people's conclusions. They even get hacked off.
So what. This didn't deter us in Part 1 and it won't now either. In fact, if you recall, we upped the ante in this article's predecessor, with insults flying as we explored inflammation and dietary fats, you bonehead.
Okay, okay, I'll cut back on that type of inflammatory comment, I promise. It's time we get down to some new information surrounding optimal fat choices for health and physique. Then we'll round out the discussion with some supportive lifestyle tips to further control inflammation.
Reduce, Do Not Remove...
But first thing's first. Inflammation is not always "bad". It plays a necessary role in the body during such things as host defense from infections.(20) Thus, we want only moderate reductions in inflammatory immune function for our physique purposes. Even eating–that's right, merely ingesting and metabolizing food–has an inflammatory component.(7,42)
So, as with the traditional hormonal "villains" of bodybuilding, cortisol and estrogen, we must employ some wisdom. We don't want to erase these things entirely (regardless of any "inflammatory remarks" I might have made in Part I for effect). It's time to be serious. The problems arise when inflammation, either low-grade and chronic, or painful and acute, is allowed to run wild on us.
This unfortunately, more often than not, is the state of affairs in Western culture: heart disease, diabetes, and other low-grade inflammatory states are epidemic. And they begin earlier in life than many people think. These diseases, along with obesity and even cognition and mood are affected greatly by our diets. Did you know that simply being overweight kicks up inflammatory markers? So does a diet that's disproportionately heavy in omega-6 fat (the necessary but over-consumed linoleic acid).
And just as an illustration of how much inflammation interferes with dietary carbohydrate metabolism, did you know that merely ingesting aspirin improves glucose tolerance in Type II diabetics?(19) Since this occurs by different mechanisms, it's fascinating to me– just not practical.
Obviously, high-dose aspirin intake is not recommended on a continuing basis. If you're saying: "but I'm not diabetic" right now, good for you. Let me then offer a recent quote by Lobner and Fuchtenbusch (2004):
"Even minimal disturbances in glucose tolerance are associated with a chronic, generalized inflammatory reaction".
Hmm. So, although we're generally not diabetics, as a population of individuals who are adversely affected by inflammation from body composition, metabolism, and performance (injury) perspectives–to say nothing of disease risk–we need to be aware of it. And we need to be aware of how to combat it.
To better understand how the beneficial omega-3 fatty acids work (especially the more potent EPA and DHA), we can look at spanking new data on how the body metabolizes them. First however, let's lay some groundwork. For starters, EPA and DHA have only recently been examined separately.
Researchers now realize that these fatty acids can do different things in the body. For example, DHA, but not EPA, appears to lower blood pressure and heart rate.(28) We'll discuss much more later. These differing effects can help us fine tune and target their use specific to our needs while minimizing any undesirable effects.
Is There a Down side?
From a side effects perspective (if one can call it that at prudent doses), omega-3 fatty acids differ. One study revealed an 8% increase in LDL cholesterol after six weeks of DHA supplementation in "mildly hyperlipidemic men," which sounds a bit concerning until one sees that DHA also increased LDL particle size (a good thing).(29)
So, when added to a reduction in heart disease risk factors like inflammation, LDL oxidation,(12) and post-meal triglyceridemia (19-49% reduction with EPA and DHA, respectively), I'm not overly concerned. In fact, men have a bigger problem with post-prandial hypertriglyceridemia than women, so here's another male-specific bonus.
Let's see, what else... those LDL particle size researchers I mentioned also revealed that EPA, but not DHA (4.0 g daily), tends to increase fasting glucose over six weeks.(29) That doesn't sound too good for over-enthusiastic EPA consumers, even if it's just a trend in the data. [I've spoken to researchers from one Canadian lab that suggest CLA may interfere somewhat with blood glucose handling as well, but those data are mixed so stay tuned.] I'll be waiting for more research in this regard because A.) The effect looks mild and B.) Fatty acids seem to have opposing effects depending on one's metabolic state (e.g. diabetic vs. healthy).(10)
There's also research on infection risk, although it's not overabundant. Harkening back to the immune suppression issue (which by the way is part of the way these fatty acids benefit us), let me just say that the state of the scientific research regarding resistance to infection is equivocal and even then seems to depend on what kind of infection, bacterial versus viral versus parasitic.(3)
Please go peruse relevant references as presented herein. DHA itself may decrease T-lymphocyte activation,(21) but not proliferation (44), so again we need to keep in mind that immunity is complex and its reduction can be good or bad depending upon whether one is looking to calm a hyperactive immune system (like many athletes) or rather to boost immune function (persons enduring frequent infections).
There's also the anti-thrombotic (anti-clotting) effect of fish oils (not always seen with DHA alone), but this too can be seen as helpful or harmful depending on one's viewpoint and other lifestyle and health factors.
Want more? Well, there's the ability of long chain n-3 fatty acids, in general, to reduce intra-myofibrillar triglycerides.(10) This could conceivably affect long duration aerobic performance adversely. Ergolytic effects have yet to be shown to my knowledge, however; it's just a plausibility considering the use of this fuel source in low-intensity exercise. (Normally the body stores a few hundred grams of fat as oil droplets right there within muscle fibers.)
Wait a minute, here... Hey! Mr. Luoma! Are you even listening? And you back there, Mr. Shugart! Straighten up and listen you punk or I'll slip sugar into your Benefiber container. What do think that'll do to your evening blood glucose levels, "Mr. Velocity Diet"?
Where was I? Ah yes, I had promised some spanking new data on how omega-3 fatty acids are metabolized. So here we go, realizing that its relative newness means much data from rodents and a lack of widespread consensus. Something that struck me as fascinating is that the actual mechanisms behind how these uncommon fats work, for example in conjunction with aspirin, is only now really coming to light.(4,5,36) The actual biochemical circuitry is being teased apart.
Molecules called resolvins and protectins among others, actually act to end the inflammatory biochemistry of the body! Imagine how this knowledge can help our inflamed, chronically-diseased and hydrogenated world. And guess what these bio-molecules can be made from? Duh! Oh, and while I'm on a nerdy roll, also consider that the putative anti-inflammatory, adiponectin appears to be helped by long chain monounsaturates and omega-3s but harmed by saturated fat.(13)
It seems that trans fats and omega-6 fats are not our only inflammatory concern. All this is important stuff but I don't want to belabor the issue, as it currently pertains almost entirely to the "why" and not the "how". Thus, I won't bore anyone with esoterica until researchers further develop the topic, potentially toward pharmaceutical applications. For now, look up the cited references if you're geeky enough!
Specific to You Ingrates...
But on to us warrior types. Getting more specific to bodybuilding, we might also consider the benefits of DHA on blood lipid profile (particularly if these transfer to "high-androgen males") and glucose tolerance. As we all know, those of us involved in physique sports/ lifestyles have special interests in optimizing T and training muscles to the point of soreness. But these endeavors, respectively, can lower serum HDL ("good cholesterol") and keep us from partitioning dietary carbs preferentially into muscle tissue.
While there's no current research to my knowledge specific to these exact situations (fish oils administered to well-trained bodybuilders who are boosting T or using "negatives"), there is indirect evidence that looks promising in the long run. For example, DHA can raise the HDL2 subfraction of good cholesterol by about 29% (strangely EPA actually reduces HDL3 by 6.7%).(29) Truth be told, there are tons of data out there on the generally beneficial effects of fish oils on serum lipids in general, mostly focused on serum triglycerides, or for you biochemists, "triacylglycerols" (TAG). The lipid data I've been discussing here corroborated these other studies with an18-20% reduction in serum TAG.
Also from a cardiac standpoint, one of the clearest benefits of fish oil (DHA in particular) is its anti-arrhythmic effect. This is well documented as the principle reason for less cardiac death in fish oil consumers. The anti-arrhythmic effects and the blood pressure-reducing effects of DHA (28) may also be interesting to those who use dietary stimulants pre-workout or to those like me with a family history of irregular heart beat and hypertension.
Along these same lines, the mechanism for the anti-hypertensive effect of DHA, that's not present from EPA (at 4.0g daily for 6 weeks), may appeal to bodybuilders pursuing a pump or anyone interested in improved circulation (recovery, body fat extraction, etc.): vasodilation.(27) The work I'm referring to here involves improved forearm blood flow, which you might agree is pretty applicable to what bodybuilders might look for.
And lastly, there is at least one study floating around out there supporting the notion that the inflammation from eccentric exercise ("negatives") is attenuated after 14 days of supplementation with a DHA + vitamin E + flavanoid supplement.(33) Now, this is indeed data that's directly applicable to weight lifters.
For us, lower interleukin-6 and C-reactive protein are good things. And these effects are supported by data in non-athletes that reveal a relationship between the DHA content of white blood cells and lower CRP.(25) But let's not totally ignore the other beneficial fish fatty acid, EPA. The ratio of EPA:DHA supplementation that may best reduce catabolic, inflammatory IL-6, without interfering with other immune parameters, was reported in one study to be 1.0:2.5, with the "threshold" dose as low as 0.44-0.94g daily.(44) After our investigation here, one doesn't have to be a clear-minded, educated liberal to see several potentially protective effects as bodybuilders pursue their goals.
What? I forgot something? Thanks for nitpicking. I always appreciate the know-it-all input of a brainwashed conservative like yourself...
Yes, okay, I also mentioned muscle glucose metabolism. Fish oils have been shown to prevent a decrease in PI3 kinase (a part of cellular insulin signaling that falls with both high fat diets and muscle micro-trauma.(11,10) While there's no guarantee that this will "fix" the metabolic aberrations related to these self-imposed experiences (remember, research never "proves" anything but rather just offers evidence), such data do make for hopeful discussion. Imagine the muscle growth if we could functionally shuttle glucose, amino acids, and energy into damaged, resistant muscles that otherwise endure a slow and prolonged recovery period.
And powerlifters might be hopeful as well. Of the many functional foods and supplements that appeal to bodybuilders, considerably fewer appeal to powerlifters. Such guys, with whom I've trained for many years, primarily focus on nervous system recovery. This is where DHA as a separate entity really gets research attention. And then there are the effects on cartilage and inflammation that could reduce/ treat osteoarthritis and lengthen career longevity. But I think these are stories for another day.
Putting It Together
So to summarize our little exploration, excessive inflammation and related health effects are major problems in the Western world. These problems underlie epidemic diseases from hypertension to heart disease to diabetes–and even beleaguer athletes in unique ways.
Further, omega-3 fatty acids, and DHA in particular, are powerful substances that combat inflammatory effects without literally erasing them. Thus they appear to be a worthy addition to a strength athlete's nutrition support regimen in general. Low-carb dieters may also have interest in both the insulin sensitivity-preserving effects and reductions in body fat deposition.(10,31) Of these populations, men in particular may benefit, as Testosterone doesn't offer the same DHA-boosting favor to the body as estrogens do. That is, men have about 15% lower proportion of DHA than women.(14)
EPA and DHA are unusual in that they are under-consumed dietary components that have relatively few contaminant-free food sources in our modern (polluted) world. Deliberately seeking safer sources such as canned salmon and/or supplements is reasonable since even typical, once-per-day fish intake doesn't provide enough.(35, 40) Here is a quote by Simopoulos (2002):
"The importance of omega-3 fatty acids in the diet is now evident, as well as the need to return to a more physiologic omega-6/ omoega-3 ratio of about 1-4/1 rather than the ratio of 20-16/1 provided by current Western Diets. In order to improve the ratio of omega-6 / omega-3 essential fatty acids, it will be necessary to decrease the intake of omega-6 fatty acids from vegetable oils and to increase the intake of omega-3 fatty acids by using oils rich in omega-3 fatty acids and increase the intake of fish to two to three times per week or take supplements."
Getting proactive in seeking out the weaker but uniquely important "other" omega-3 fat, linoleate, can help too– as can reducing coffee to under 200cc daily. (Listen, I love my java too, but check out a new study by Zampelas, et al. Am J Clin Nutr 2004; 80(4): 862.) Flavored teas (1) and Yogi Tea "Decaffe Roast" are increasingly becoming my alternatives at home. Putting these practices together with a considerable monounsaturated fat intake (primarily olive and canola oils), at least some "cardio" and body fat reduction if over-fat, will help keep inflammation from interfering with your health and physique.
Now beat it; I don't want to see you hanging around after the reference list like last time.
NOTE1: It is important to keep a critical mind. As most of you already know, I am compensated for my work with Biotest and T-Nation. This includes consultation on the new lipid product. As always, read, learn and think for yourselves!
NOTE2: When digging through research on your own, consider that there is much debate over which fat to use as a "placebo". This choice affects the data greatly and there's no one best comparison because all fatty acids have pharmaceutical-like effects.
NOTE3: Before you even ask, I am neither a liberal nor a devout Buddhist. The comments were meant simply to inflame some of you, as per the article's theme. I do however, think that TC and Chris would be trouble in a classroom.
References and Further Reading
1. Amarakoon, A., et al. Endotoxin induced production of interleukin-6 is enhanced by vitamin E deficiency and reduced by black tea extract. Inflamm Res. 1995; 44(7):301-5.
2. Anderson, A., et al. Fatty acid profile of skeletal muscle phospholipids in trained and untrained young men. Am J Physiol Endocrinol Metab 2000; 279(4):E744-51.
3. Andersen, M. and Fritsche, K. (n-3) Fatty Acids and Infectious Disease Resistance. J. Nutr. 132: 3566–3576, 2002. .
4. Arita, M. et al. Stereochemical assignment, antiinflammatory properties, and receptor for the omega-3 lipid mediator resolvin E1. 2005 Mar; J Exper Med, 201(5): 713-722.
5. Bannenberg, G., et al. Molecular Circuits of Resolution: Formation and Actions of Resolvins and Protectins. J Immunol 2005, 174: 4345-4355.
6. Berringer, T., et al. Supplemental DHA favorably alters HDL and LDL subclasses in patients with low HDL. American heart Association Scientific Sessions 2003; Session AOP. 15.2 Human Lipoprotein Metabolism II #1461.
7. Burdge, G. and Calder, P. Plasma cytokine response during the postprandial period: a potential causal process in vascular disease? Br J Nutr. 2005 Jan;93(1):3-9.
8. Conquer, J. and Holub, B. Supplementation with an algae source of docosahaxaenoic acid increases (n-3) fatty acid status and alters selected risk factors for hart disease in vegetarian subjects. J Nutr. 1996; 126(12):3032-9.
9. Conquer, J and Holub, B. Supplementation with an algae source of docosahexaenoic acid increases (n-3) fatty acid status and alters selected risk factors for heart disease in vegetarian subjects. J Nutr. 1996; 126(12):3032-9.
10. Delarue, J., et al. N-3 long chain polyunsaturated fatty acids: a nutritional tool to prevent insulin resistance associated to type 2 diabetes and obesity? Reprod Nutr Dev 2004; 44(3): 289-99.
11. DelAguila, L., et al. Muscle damage impairs insulin stimulation of IRS-1, PI 3-kinase, and Akt-kinase in human skeletal muscle. Am J Physiol Endocrinol Metab. 2000 Jul;279(1):E206-12.
12. deRuiz, G. et al. Habitual fish intake is associated with decreased LDL susceptibility to ex vivo oxidation. Lipids 2002 Apr;37(4):333-41.
13. Fernández-Real, J., et al. Circulating Adiponectin and Plasma Fatty Acid Profile. Clinical Chemistry. 2005;51:603-609.
14. Giltay, E., et al. Docosahexaenoic acid concentrations are higher in women than in men because of estrogenic effects. Am J Clin Nutr 2004; 80(5):1167-1174.
15. Grimsgaard, S., et al. Effects of highly purified eicosapentaenoic acid and docosahexaenoic acid on fatty acid absorption, incorporation into serum phospholipids and post-prandial triglyceridemia. Lipids 1998; 33(2): 131-138.
16. Grimsgaard, S., et al. Highly purified eicosapentaenoic acid and docosahexaenoic acid in humans have similar triacylglycerol-lowering effects but divergent effects on serum fatty acids. Am J Clin Nutr. 1997; 66(3):649-59.
17. Grimsgaard, S., et al. Effects of highly purified eicosapentaenoic acid and docosahaxaenoic acid on hemodynamics in humans. Am J Clin Nutr 1998; 68:52-59.
18. Hansen, J., et al. Effects of highly purified eicosapentaenoic acid and docosahexaenoic acid on fatty acid absorption, incorporation into serum phospholipids and postprandial triglyceridemia. Lipids. 1998 Feb;33(2):131-8.
19. Hundal, R., et al. Mechanism by which high-dose aspirin improves glucose metabolism in type 2 diabetes. J Clin Invest. 2002 May;109(10):1321-6.
20. Kelly, D., et al. Docosahexaenoic acid ingestion inhibits natural killer cell activity and production of inflammatory mediators in young healthy men. Lipids, 34(4): 317-324, 1999.
21. Kew, S., et al. Effects of oils rich in eicosapentaenoic and docosahexaenoic acids on immune cell composition and function in healthy humans. Am J Clin Nutr. 2004; 79(4):674-81.
22. Kremer, J., et al. Fish-oil fatty acid supplementation in active rheumatoid arthritis: a double-blinded, controlled, crossover study. Ann Intern Med 106: 497-503, 1987.
23. Lobner K. and Fuchtenbusch, M. Inflammation and diabetes. MMW Fortschr Med. 2004; 146(35-36):32-3, 35-6.
24. Lowery, L. Dietary Fat and Sports Nutrition: A Primer. Journal of Sports Science and Medicine. 2004; 3(3): 106-117. Accessible at: http://www20.uludag.edu.tr/%7Ehakan/sbtd/ vol3/n3/1/v3n3-1abst.php.
25. Madsen, T., et al. C-reactive protein, dietary n-3 fatty acids, and the extent of coronary artery disease. Am J Cardiol 2001;88(10):1139-42.
26. Morcos, N. and Camilo, K. Acute and chronic toxicity study of fish oil and garlic combination. Int J Vitam Nutr Res 2001; 71(5):306-12.
27. Mori, T., et al. Differential effects if eicosapentaenoic acid and docosahexaenoic acid on vascular reactivity of the forearm microcirculation in hyperlipidemic, overweight men. Circulation 2000; 102(11): 1264.
28. Mori, T., et al. Docosahexaenoic acid but not eicosapentaenoic acid lowers abulatory blood pressure and heart rate in humans. Hypertension 1999; 34:253-260.
29. Mori, T., et al. Purified eicosapentaenoic and docosahexaenoic acids have differential effects on serum lipids and lipoproteins, LDL particle size, glucose, and insulin in mildly hyperlipidemic men. Am J Clin Nutr 2000; 71(5): 1085-1094.
30. Muskiet, F., et al. Is docosahexaenoic acid (DHA) essential? Lessons from DHA status regulation, our ancient diet, epidemiology and randomized clinical trials. J Nutr 2004; 134:183-186.
31. Nakamura, M., et al. Metabolism and functions of highly unsaturated fatty acids: an update. Lipids 2001; 36(9):961-4.
32. Oken, H., et al. Low dose algal docosahexaenoic acid reduces triglycerides and raises HDL cholesterol in healthy adults. American heart Association Scientific Sessions 2003; Session AOP. 15.1 Human Lipoprotein Metabolism #630
33. Phillips, T., et al. A dietary supplement attenuates IL-6 and CRP after eccentric exercise in untrained males. Med Sci Sports Exerc 35(12): 2032-2037.
34. Pickup, J. Inflammation and activated innate immunity in the pathogenesis of type 2 diabetes. Diabetes Care. 2004; 27(3):813-23.
35. Rupp, H., et al. Risk Stratification by the "EPA+DHA Level" and the "EPA/AA Ratio"Focus on Anti-Inflammatory and Antiarrhythmogenic Effects of Long-Chain Omega-3 Fatty Acids. Herz. 2004 Nov;29(7):673-685.
36. Serhan, C., et al. Resolvins: A Family of Bioactive Products of Omega-3 Fatty Acid Transformation Circuits Initiated by Aspirin Treatment that Counter Proinflammation Signals. 2002 Oct; J Exper Med 196(8): 1025-1037.
37. Schmidt, M. and Duncan, B. Diabesity: an inflammatory metabolic condition. Clin Chem Lab Med. 2003; 41(9):1120-30.
38. Simoncikova, P., et al. Comparison of the extrapancreatic action of gamma-linolenic acid and n-3 PUFAs in the high fat diet-induced insulin resistance. Endocr Regul 2002 Dec;36(4):143-9.
39. Simopoulos, A. Omega-3 fatty acids in inflammation and autoimmune diseases. J Am Col Nutr 2002; 21(6):495-505.
40. Sujata L. Association of Dietary Fish and n-3 Fatty Acid Intake With Hemostatic Factors in the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Arterioscler Thromb Vascr Biol 1998; 18:1119-1123.
41. Theobald, H. et al. LDL cholesterol-raising effect of low dose docosahexaenoic acid in middle aged men and women. Am J Clin Nutr 2004; 79(4): 558-563.
43. Vidgren, H., et al. Incorporation of n-3 fatty acids into lipid fractions, and erythrocyte membranes and platelets during dietary supplementation with fish, fish oil, and docosahexaenoic acid-rich oil among healthy young men. Lipids. 1997; 32(7):697-705.
Wallace, F., et al. Comparison of the effects of linseed oil and different doses of fish oil on mononuclear cell function in healthy human subjects. Br J Nutr. 2003 May;89(5):679-89.
44. Wallace, J. If heart disease is an inflammatory disease, what about the risk factors? Am Soc Exerc Physiol Natl Mtg. April 2, 2004.
45. Yudkin, J., et al. Inflammation, obesity, stress and coronary heart disease: is interleukin-6 the link? Atherosclerosis 2000 Feb;148(2):209-14.
46. Zhender, M., et al. Further glycogen decrease during early recovery after eccentric exercise despite a high carbohydrate intake. Eur J Nutr. 2004 Jun;43(3):148-59. Epub 2004 Jan 06.
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