Yo! Small fry! You lookin’ at me? You…lookin’…at…me?!
Listen up, you punk. It’s high time we cleared the air regarding inflammation and all of the nasty consequences thereof. I’ve been preaching this stuff as an underlying theme throughout much of my writing, since first coming to T-mag (now T-Nation) a few years ago.
We’re not just talking tendonitis and bursitis here, kids. The ramifications extend far beyond a week or two of purposely avoiding hit-heads (or skull crushers, if you will). It’s time we spell out just how subtle inflammation can be and how we can crush it into submission before we drop dead of a heart attack one day–fat, atrophied, glucose intolerant and depressed.
And so we come to the question: who has been around the wellness scene–not just bodybuilding or fitness per se–long enough to know what in the world of fatty acids is going on?
The benefits of controlling inflammation in our soft, hydrogenated culture are many. Of the number of lifestyle changes one can make, one comes to mind as paramount for me: DHA. That’s right, you putz. Docosahexaeneoic Acid (now you see why we just call it “DHA”) is a specific fatty acid in fish oil that’s central to reams of research and scientific conferences (the 2004 American Society of Exercise Physiologists meeting comes to mind). EPA and DHA have even trickled down to become the focus of pharmacology textbook chapters.
I’m frankly sick of rehashing the basics, but here they are, one more time…
Common Omega-6 oils in the face of low omega-3 intake lead to…
Arachidonic Acid production which leads to…
Prostaglandin E2 formation* which is a source of…
Inflammation, which can exacerbate…
Poor dietary carb metabolism,
Cardiovascular disease risk,
Mental depression (somewhat different mechanism),
Tendonitis and bursitis,
Full-blown diabetes risk,
*let’s not forget thromboxane A2 and leukotriene B4, both also contributory, as well as various related cytokines
Okay, so we’ve established that inflammation has a dietary link (such as omega-6 fatty acids and trans-fatty acids from hydrogenation), but what can we do? We can’t ditch all fats from the diet–that line of thinking has actually contributed to America’s obesity epidemic and may even lower Testosterone levels.(10) What we can do however, as any dolt could tell you, is change the type of fat we consume.
One approach is to replace a portion of the ever-present omega-6 fats (linoleic acid, predominant in corn oil, cottonseed oil, safflower oil and “vegetable oils”) and all trans fats (usually elaidic acid, a mutated form of healthy oleic acid) with natural, “cis” configured monounsaturated fatty acids (MUFA).
This is a big deal. Monounsaturated food sources, in addition to their antioxidant effects,(3, 11, 15, 21) don’t provide substrate for inflammatory biological molecules like typical omega-6 polyunsaturates do. Put more simply: No inflammatory “building blocks” equals no (or less) inflammation. Don’t choose foods that give inflammation a foothold when you have better choices. Have you seen the news regarding a major restaurant chain agreeing to a multi-million dollar settlement over failure to remove trans fats in their fryers expeditiously? There are consumer advocacy groups, specific to trans fats, out there who are cheering.
MUFA are actually being used in research to help all kinds of maladies, as described on our list above. Food as drug–I love it.
Inflammatory disorders are being targeted but one need only look to the large percentage of octogenarians strolling around Mediterranean countries for evidence of safety and effectiveness. So here’s another reminder, you dolts: The classic MUFA is oleic acid in olive oil and canola oil. There is a chapter in the upcoming International Society of Sports Nutrition textbook diagramming the positional and stereo-chemical aspects of various fats, including MUFA. I know it’s a decent resource because I wrote it… and a brainy T-Nation regular, “Cassanova” took part in its editing! (No, we don’t get royalties; it’s just a decent resource.)
But the MUFA approach, however necessary, can be overdone. For starters, MUFA are stored more readily than other types of fat.(7, 23) This calls for caution because no matter how healthy, at nine calories-per-gram they add up to lots of potentially problematic energy, fast.
I don’t want to be too alarmist, though; MUFA do rock. We just need to keep them in check, perhaps 30-50g total fat, maximum, per meal. So once again, here it is simply, you ingrates: oleic acid doesn’t provide substrate for inflammatory reactions like omega-6 fats do and it comes complete with benefits beyond even this.
But there are just other, more potent things we can do.
The obvious approach, for those in the know, is to ingest a couple grams of EPA and DHA each day. Although considered “high dose” by some standards, two or three grams of these fatty acids potently compete with (and defeat, if you will) the omega-6 fatty acid, linoleic acid for the enzyme cyclooxygenase and it’s relatives like lipoxygenase. Crack any medical physiology book or pharmacology text and take a look. There is both underlying biochemistry and promising speculation to be found. These texts are part of what is taught in classrooms around the world. In fact, here’s a quote:
“…near absence of significant adverse effects suggest that dietary alteration or supplementation to provide 1-4g/ day of eicosapentaenoic acid may be a beneficial addition to conventional treatment of these conditions.”
–Payan, D. and Katzung, B., Basic and Clinical Pharmacology, p. 551.
Fascinating. And well-established enough to be in a variety of academic textbooks, presented as fact. But the body is complex and EPA cannot “do it alone.” As we’ll soon explore, dietary DHA, along with its specific benefits, can also significantly enhance EPA concentrations in tissues, even if the reverse isn’t necessarily true.(4,6) This fact should be interesting for those persons who might have exclusive interest in EPA supplementation.
In fact, DHA currently appears to be a better choice in some ways. Hence, we’ll look at DHA-specific effects in Part II. For now here’s two nifty quotes:
“In the DHA group, serum phospholipid DHA increased by 69% and EPA increased by 29%, indicating retroconversion of DHA to EPA. In the EPA group [however]…DHA decreased 15%, suggesting that EPA is not elongated to DHA in humans”
–Grimsgaard, S., et al. Am J Clin Nutr, 66(3): 649-659.
“Long-term docosahexaenoic acid supplementation to patients with XLRP [an eye condition] was associated with no identifiable safety risks in this 4-year clinical trial”
–Wheaton, D., et al. Arch Opthalmol, 121(9): 1269.
But back to some biochemistry. Without getting too chewy, in the presence of omega-3 fatty acids, the cyclooxygenase enzymes in bodily tissues (and their relatives) end up making prostaglandins of the 1 and 3 series (as well as thromboxanes of the 3 series and leukotrienes of the 5 series), all of which are good news for reducing inflammation, thrombosis, chemotaxis muscle catabolism, and body fat.
Research is ongoing as to the full extent of benefits that result from EPA and DHA ingestion but it’s clear even now that hundreds if not thousands of physicians and researchers are convinced enough to supplement them. Even the rightfully conservative American Heart Association is on board.(1) There is so much empirical evidence mounting that researchers are making the move to start classifying DHA in particular–as essential to human health, just like vitamins and minerals are.(13)
Hey, are you listening, punk? You, in the back row! Which fatty acid may soon become essential for humans?
Ahem. So you see, low-grade, systemic inflammation is a big deal and it’s being forced out of the closet, particularly as fatty acid essentiality comes fully to bear. It stuns me at times that cigarette manufacturers take so much heat (as they should), but fast food purveyors and convenience food sellers continue to pump pro-inflammatory junk fats into the population.
It doesn’t take a consumer advocate to know these are known to be extremely harmful, sometimes with effects similar in magnitude to cigarettes, and yet they are everywhere. Conversely, we have few choices of potently healthy omega-3 fats; we must make the effort to deliberately seek them out. Most of us (particularly men; see reference 5) may be able to use DHA, for example, to improve our physiques and health simultaneously. And this just isn’t true of all supplements.
Muscle sports and athletics in general can be abusive and pro-inflammatory so EPA and perhaps more importantly DHA look like appropriate nutritional support. Inflammation, as just one addressable factor, can be low-grade, long-term and unnoticeable, or it can be acute and exercise-induced. To be fair here, we need to note that there are data out there on carbed-up, experienced runners showing no effect on the acute phase response post-marathon, using 3.6g of a mostly EPA supplement.(25).
Perhaps this is because trained endurance athletes already have a 42% lower omega-6 to omega-3 ratio simply due to training adaptations.(2) Whatever the case, I think that decades of research suggesting effects supportive of improved body comp and athletic recovery are impossible to ignore (such as anti-inflammatory effects, cartilage preservation, improved glucose tolerance in “healthies,” improved fat metabolism, mood elevation, nerve protection/ enhancement, blood flow and others). We’ll reference much of this in a follow-up article. Hopefully you can make some conclusions and decisions of your own, as you continue reviewing available literature.
But I feel like we need a few more statements on exercise stress and inflammation. Don’t want more? Tough. I’m breaking out the mental floss. Many, many athletes need augmented dietary support. Although one can find differences in magnitude and even small distinctions between certain biological markers, the body’s stress response, or acute phase response to physical insult is quite similar between bodybuilding training and, say elective surgery or skeletal trauma!
Put simply, the overload principle dictates that we must ask ever more of ourselves if we are to improve, and if you’re anything like me, “overload” is often an understatement.
So while I wait for long-term, DHA-focused, athlete-specific literature to reach print, I will continue with what I consider a “best practice” approach. This currently includes at least 3-6 fish oil capsules most days (I’ve been known to take up to 10), depending on where I’m at in a 5 year macro-cycle.
Are 10 capsules too much? At a 30% combined EPA + DHA content, not really. My intake amounts to a maximum of 3.0g from those 10 full capsules. It’s inefficient to be sure, and one might even speculate that combining EPA with DHA can be counter-productive in some ways, but this is currently my approach. It’s actually far less than the huge 6-10 g daily EPA + DHA recommendations that I hear from many gurus and trainers… those who are less tempered by many years of consuming literature and participating in research.
Okay; enough talk. I’m not sorry if you find my remarks… inflammatory. I’ll continue to write you ingrates a reality check in Part II, coming at you when I’m good and ready. At that time we’ll delve into more advanced topics like protectins and resolvins, the newly-discovered metabolites of omega-3 fats that literally act to end inflammation, among other things. We’ll also discuss differences in EPA vs. DHA and why men in particular may benefit more from the latter.
If I’m in a less foul mood, I’ll even throw in a few new dietary tricks that can be supportive to proper lipid ingestion as part of a comprehensive anti-inflammatory, health and physique program. Maybe.
I’m out of here.
SPECIAL NOTE: In truth, I don’t really believe anyone here to be small or doltish or ungrateful in any way. (It’s just the article’s theme, you sensitive guy, you.) I fully realize how dedicated, built and brainy the readers of the Think Tank actually are. That’s why I spend my time writing nerdy referenced articles that could probably be minimally modified for use as term papers! (Insert Jedi gesture: you didn’t just see any comment about term papers…). You see, this is as much a learning experience for me as it is for you and I’m glad to have people with our unique values to investigate sports nutrition with me. I love you guys; somebody give me a hanky…
References and Further Reading:
1. American Heart Association. (2002) AHA Scientific Statement: Fish Consumption, Fish Oil, Omega-3 Fatty Acids and Cardiovascular Disease, #71-0241 Circulation. 106, 2747-2757. Available from URL: http://www.americanheart.org
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. Berry, E.M., et al. (1991). Effects of diets rich in monounsaturated fatty acids on plasma lipoproteins–the Jerusalem Nutrition Study: high MUFAs vs high PUFAs. Am J Clin Nutr. 53(4):899-907.
4. 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.
5. 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.
6. 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.
7. Guo, W., et al. Esterification of free fatty acids in adipocytes: a comparison between octanoate and oleate. Biochem J. 2000 Jul 15;349(Pt 2):463-71.
8. 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.
9. 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.
10. 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.
11. Mataix, J. Tissue specific interactions of exercise, dietary fatty acids, and vitamin E in lipid peroxidation. Free Radic Biol Med. 1998; 24(4):511-21.
12. 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.
13. 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.
14. Nakamura, M., et al. Metabolism and functions of highly unsaturated fatty acids: an update. Lipids 2001 Sep;36(9):961-4.
15. Ramirez-Tortosa, M.C., et al. Effect of extra-virgin olive oil and fish-oil supplementation on plasma lipids and susceptibility of low-density lipoprotein to oxidative alteration in free-living spanish male patients with peripheral vascular disease. Clin Nutr. 1999; 18(3):167-74.
16. Rassmussen, O., et al. Favourable effect of olive oil in patients with non-insulin-dependent diabetes. The effect on blood pressure, blood glucose and lipid levels of a high-fat diet rich in monounsaturated fat compared with a carbohydrate-rich diet Ugeskr Laeger 1995; 20;157(8):1028-32.
17. 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.
18. Salway, J. Metabolism at a glance. Blackwell Scientific Publications: London. 1994.
19. Siess, W., et al. Platelet-membrane fatty acids, platelet aggregation, and thromboxane formation during a mackerel diet. Lancet 1980; 1: 441-444.
20. 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.
21. Sola, R., et al. Oleic acid rich diet protects against the oxidative modification of high density lipoprotein. Free Radic Biol Med 1996; 22(6):1037-45.
22. 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.
23. Summers, L., et al. Uptake of individual fatty acids into adipose tissue in relation to their presence in the diet. Am J Clin Nutr. 2000;71(6):1470-7.
24. Thomsen, C., et al. Comparison of the effects on the diurnal blood pressure, glucose, and lipid levels of a diet rich in monounsaturated fatty acids with a diet rich in polyunsaturated fatty acids in type 2 diabetic subjects. Diabet Med 1995; 12(7):600-6.
25. Toft, A., et al. N-3 polyunsaturated fatty acids do not affect cytokine response to strenuous exercise. J Appl Physiol 2000; 89: 2401–2406.
Are you still here? That’s the end. Go home.