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Bulletin #43 – High Performance Essential Fatty Acids

Parrillo Performance is proud to in-troduce another new supplement for body-builders – a concentrated source of essen-tial fatty acids. I have recommended fattyacid supplementation  for bodybuilders foryears, long before it became so popular.The details of fatty acid metabolism arequite complicated – far more complex thanprotein or carbohydrate metabolism – butthe basic concept is simple. Everybodyknows that vitamins and minerals Are nu-trients required by the body in small quan-tities. (thus the name “Micronutrients”)which provide for vital metabolic functions.Certain fats are similarly required by thebody in relatively small quantities. Since thebody cannot manufacture these fats by it-self, it is essential that they be obtained fromthe diet, and are therefore called essentialfatty acids (EFAs). The main function ofEFAs in the body is to provide buildingblocks for a class of hormones calledeicosanoids. The broad category ofeicosanoids is further subdivided into pros-taglandins, prostacyclins, leukotrienes, andthromboxanes.

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The eicosanoids are a com-plex group of hormones (over 100 differ-ent prostaglandins have been identified sofar) which are involved in controlling manymetabolic processes such as blood pres-sure, inflammation, fat metabolism, andblood clotting, to name a few. Eicosanoidsare made by all cells of the body and theircentral function is to communicate mes-sages to nearby cells to help coordinate andregulate the body’s metabolic activity. EFAsare also important structural componentsof cell membranes and thus are importantfor healthy skin. But before we get too deepinto the details, let’s talk about the basics.Since everybody makes such a big dealabout making sure to get enough vitaminsand minerals, why don’t we hear moreabout EFAs? Aren’t they just as important?Essential fatty acids are very important butthey don’t get much attention because EFAdeficiencies are relatively rare in America.Why? Because the average American getsabout 40% of his calories from fat, whichis more than enough to supply adequateamounts of EFAs.

About the only peopleyou hear of suffering from EFA deficiencyare burn or trauma patients, patients whohave had some sort of  intestinal bypasssurgery or intestinal resection, people witha fat malabsorption syndrome (that is, theycan’t absorb dietary fat very well), mal-nourished children, patients receiving pro-longed fat-free intravenous feeding, andduring high-protein, low-fat dietary supple-mentation to treat kwashiorkor (proteindeficiency) (1,2). Wait a second – whatwas that about high-protein, low-fat supple-mentation? Does that sound like your diet?Normally people don’t have to worryabout EFA deficiency in this country be-cause the typical diet contains so much fat.Furthermore, EFAs can be stored in bodyfat so a dietary deficiency won’t show upfor a long time. Extremely lean athletes,however, who follow a low-fat diet for aprolonged time are definitely at increasedrisk for fatty acid deficiency. Have I everactually seen any bodybuilders with theclinical symptoms of essential fatty aciddeficiency? You bet. Did their symptomsresolve after fatty acid supplementation?Yes – rapidly and dramatically. I rememberone female bodybuilder in particular whohad a problem with her skin getting dryand breaking out, and it got worse at con-test time.

After one week of Evening Prim-rose Oil (EPO) supplementation her skinwas completely clear. It was very dramatic,and you can imagine how happy she was.So what are the symptoms of EFA de-ficiency? In adults the first symptom is der-matitis – red, dry, scaly skin, especially onthe face (1-3). This condition will not berelieved by lotions or moisturizers – you’llsimply have red, scaly skin with lotion onit. The EFAs are required for the forma-tion of some components of normal,healthy skin, so moisturizers really won’thelp. Other problems include increased lossof water (from the skin), infertility, kidneydisease, liver disease (including decreasedATP production), decreased capillary re-sistance, increased fragility of red bloodcells (which can result in anemia), in-creased susceptibility to infections, anddecreased contractile strength of the heart(1,2). In infants EFA deficiency is evenmore serious and can include decreasedgrowth, dermatitis, and degenerativechanges in the kidney, liver, and lung (1,2).Recent evidence suggests that EFAs arealso required for normal development ofthe nervous system. Usually the problemdoesn’t get that far.

If you have any skinproblems or a poor complexion you maywant to consider trying EFA supplementa-tion.Lately there has been some specula-tion that EFA supplementation may improvemuscle and strength gains during weighttraining, or decrease muscle loss duringcatabolic conditions. In my opinion the juryis still out on this issue; there’s just notenough information to know for sure yet.However, it would not surprise me at all ifit turns out to be true. I personally haven’t seen any dramatic changes in muscle massor strength following EFA supplementation.I think the main nutritional issues here arecalories and protein intake.So what are the EFAs and what aresome good food sources for EFAs? Mostdietary fat, as well as most fat stored inthe body, is in the form of triglycerides,also known as triacylglycerols. These largemolecules are comprised of three fatty ac-ids linked to a glycerol backbone. Fattyacids themselves are long hydrocarbonchains (the fatty part of the molecule) witha carboxylic acid group attached at one end(the acid part). Fatty acids are classifiedaccording to their length and their degreeof saturation.

Short chain fatty acids are2-4 carbon atoms in length, medium chainfatty acids (like CapTri) are 6-12 carbonatoms in length, and long chain fats are14-24 carbons long. The degree of satura-tion describes how many double bonds themolecule has. If the fatty acid moleculecontains no double bonds, it is said to be“saturated.” This term describes the ideathat the carbon atoms are saturated withhydrogen atoms; if a fatty acid moleculecontains carbon-carbon double bonds itmust give up some of the hydrogens, andis no longer “saturated.” Anyway, fats canbe either saturated, monounsaturated, orpolyunsaturated. Saturated fats are foundin animal fat and some vegetable sources,and are the kind most prone to be con-verted to cholesterol and clog up your ar-teries. There is no requirement for satu-rated fats in the diet and it’s best to limitthese as much as possible. As you can tellfrom the name, monounsaturated fats con-tain one double bond. These fats are notessential in the diet, but do not contributeto heart disease. The best source ofmonounsaturated fat is olive oil. Have youever wondered why the Mediterranean dietdoes not cause heart disease even thoughit contains as much fat as the Americandiet? The fat in the Mediterranean diet issupplied as olive oil, which does not pro-mote heart disease. The American diet ismuch higher in saturated fat (from meat,butter, and eggs).

Keep in mind that whileolive oil doesn’t cause atherosclerosis, itwill still make you just as fat as eating ani-mal fat.There are two essential fatty acids, andboth are polyunsaturated. This means theycontain multiple double bonds. One is calledlinoleic acid (an omega-6 fatty acid) andthe other is linolenic acid (an omega-3 fattyacid). The terms omega-6 and omega-3describe the location of the first doublebond from the methyl end of the molecule.Many vegetable oils contain linoleic acid(omega-6), including safflower oil, cornoil, soybean oil, and flax (linseed) oil,among others. The omega-3 fatty acids areabundant in fish oils; flax is the only veg-etable source containing a significantamount of omega-3. You can find theseoils (except fish oil) in the grocery store,but if you’re going to take them as a sourceof essential fatty acids you should be sureto use “cold pressed” oils. This means theoil was extracted without the applicationof heat, which can damage (oxidize, to bespecific) the oil. The oils you see at thegrocery store are extracted by pressingwith heat which increases the extractionefficiency, but damages the EFAs.

Also, ifyou’re using one of these oils as a sourceof EFAs don’t cook with it – this also canoxidize the oil and destroy its biologicalactivity. Just use the oil straight, or youcan make salad dressing out of it. You canfind cold pressed oils at good health foodstores. Most bodybuilders eat fish regu-larly, and fish are a great source of omega-3’s. If you don’t like fish, omega-3 cap-sules are available at health food stores.When you buy EFA supplements don’tshop for bargains, shop for the best. EFAsare delicate molecules and are easily dam-aged during preparation. There is a differ-ence in quality and purity between brands.There’s nothing wrong with using thecold-pressed oils mentioned above as asource of EFAs, but it’s not the ultimateway to go. I’ll explain why. First, thesevegetable oils are not pure EFAs, but merelycontain EFAs along with a bunch of otherfat (and calories) you don’t necessarilywant. a table of fatty acid composition ofvarious oils is included for your informa-tion (from Linder, reference 3). the bestsource of omega 6 is safflower oil, whichis 74% linoleic acid. The others are around50% or less. the second problem is thatEFAs are not the final biologically activecompound (such as eicosanoids) but aremerely the building blocks the body usesto make these hormones.  

To formeicosanoids from linoleic acid, the firstthing that happens is the linoleic acid isconverted to gamma-linolenic acid (GLA).This conversion is carried out by an en-zyme called delta-6-desaturase. No prob-lem, except for the fact that your bodymakes less and less of delta-6-desaturaseas you age. The activity of this enzymedeclines markedly, making this conversioninefficient. This is why I recommendEvening Primrose Oil (EPO) as a bettersource of EFAs. The evening primrose is asmall flowering plant that grows in En-gland. Evening Primrose Oil contains GLAand therefore bypasses the delta-6-desaturase step. This turns out to be a wayto provide EFAs in a minimal amount offat calories, so it doesn’t upset your per-contest diet strategy. So EPO is a morepotent source of EFAs than even saffloweroil for two reasons: it’s more concentratedin total omega-6, which means there’s less“garbage” fat, plus it bypasses the limitingdelta-6-desaturase step by supplying GLAdirectly. Each 500 mg EPO capsule pro-vides 45 mg GLA and 365 mg linoleic acid,so it’s almost pure EFAs.How do I take EPO? Take from twoto six capsules a day with meals. What doI look for? You may notice an improve-ment in the appearance of your skin, espe-cially if you were deficient in linoleic acidor if your level of delta-6-desaturase is low.It’s kind of like taking vitamins.

A vitamindeficiency produces a characteristic dis-ease state which is reversed when the de-ficiency is corrected. However, if you al-ready have adequate vitamin levels thentaking extra doesn’t really make any dif-ference. (The exception may be the anti-oxidants, vitamin C, beta-carotene, and vi-tamin E, where there is some evidence thattaking more than the minimum amount re-quired to prevent a deficiency state mayactually confer additional benefits.) If you are borderline deficient in EFAs and havesome minor skin problems, then takingEPO will probably help. If you consistentlyfollow a low fat diet (10% of calories fromfat or less), if you are very lean, or if youhave minor skin problems EPO is definitelyworth a try. At the very least it will ensureyou don’t develop an omega-6 deficiencywhile following a very low fat diet. Thepeople who claim that EFAs may be the“missing link” you’re looking for to packon more muscle are probably exaggeratingin most cases. My philosophy is that therole of supplements is to increase cellularnutrient levels beyond what can be obtainedfrom a healthy diet of regular foods. Foodwill always be the cornerstone of soundnutrition – don’t lose sight of the impor-tance of your diet.

The only supplements Iknow of that can really affect your bodycomposition beyond what can be obtainedfrom regular foods are CapTri and Creat-ine.Are there any toxic effects from tak-ing too much EPO? No, EPO is completelynontoxic. There are some potential sideeffects, which include headaches and(paradoxically) your skin breaking out(pimples). These are a result of the effectsof the class 2 prostaglandins which aremade from arachidonic acid, a metaboliteof GLA. These effects are completelyblocked by aspirin, which stops the con-version of arachidonic acid into prostag-landins. If you should notice these prob-lems, simply take two aspirin and decreasethe number of capsules you take.That’s about all the practical “how to”information you need to incorporate EFAsinto your diet. The Parrillo EPO supple-ment was developed specifically to pro-vide a concentrated source of EFAs so youdon’t have to eat a tablespoon of oil everyday. By supplying GLA directly we alsobypass the rate limiting step in the metabo-lism of omega-6 fatty acids, meaning youneed to take even less to get the same ef-fect. The rest of this month’s article willcenter around a discussion of prostaglan-dins and other hormones produced fromEFAs.Prostaglandins are a family of hor-mones whose levels are determined by diet(3). Prostaglandins have potent functionsin regulating blood pressure, inflammation,and platelet aggregation (blood clotting).

The levels of various prostaglandins aredeterAined by the balance of essential fattyacids in the diet and by the balance of in-sulin to glucagon (which is in turn deter-mined by the ratio of carbohydrate to pro-tein in the diet). The sensitivity of prostag-landin levels to essential fatty acid con-sumption is a result of substrate level regu-lation, while the enzymes involved in pros-taglandin production may be activated orrepressed insulin and glucagon.Prostaglandins, prostacyclines, throm-boxanes, and leukotrienes form a class ofhormones collectively known aseicosanoids, derived from unsaturated C20fatty acids (C20 describes a fatty acid mol-ecule 20 carbon atoms in length). Prostag-landins are made in all tissues of the bodyand experience very high turnover, whichmeans they are rapidly made and subse-quently destroyed. Prostaglandins havepotent effects in regulating blood pressure,inflammation, smooth muscle contraction,and erythrocyte (red blood cell)deformability. Prostaglandins arecyclopentanoic acids which differ from oneanother in the structure of the substitutedcyclopentane ring (1,3). Prostaglandins fallinto three general categories based on thenumber of double bonds they contain,which in turn is a consequence of the de-gree of desaturation of their parent fattyacids. Class 1 prostaglandins (PG1) con-tain three double bonds and are derivedfrom C20:3 (an omega-6 fatty acid). Class2 prostaglandins (PG2) contain four doublebonds and arise from C20:4 (also anomega-6 fatty acid). Class 3 prostaglan-dins (PG3) are made from C20:5 (anomega-3 fatty acid) and contain five doublebonds.There are many different prostaglan-dins which exert a variety of effects. Themost predominant and best characterizedof the class 1 prostaglandins is PGE1. It isa very potent vasodialator and it increasescAMP levels. Thus it has the effect of low-ering blood pressure and increasing freefatty acids (EFA). This means it promotesrelease of fatty acids from body fat stores,thus increasing use of stored body fat asenergy. It also possesses anti-inflammatoryproperties. Class 2 prostaglandins are de-rived from arachidonic acid (C20:4) andare the most abundant class of prostaglan-dins. Some PG2’s act as vasodialators whilesome are vasoconstrictors. A vasodialatorincreases the size of blood vessels thusreducing blood pressure, while a vasocon-strictor makes blood vessels smaller andincreases blood pressure.

Many class 2prostaglandins promote inflammation.Class 3 prostaglandins generally have lesspotent effects than classes 1 and 2, so willnot be emphasized in this discussion.Arachidonic acid (AA) serves as theprecursor for class 2 prostaglandins. Whilenecessary for life, this family of prostag-landins produces undesirable effects whenoverproduced. These include an increasein blood pressure and inflammation. Oncearachidonic acid is formed, it is difficult (if not impossible) to control the balanceof vasodialators and vasoconstrictorswhich will be produced from it. PGE1, onthe other hand, has the effect of loweringblood pressure and has no undesirable sideeffects. The strategy of the Parrillo diet isto provide the fatty acid precursors whichwill allow some arachidonic acid (and thusPG2’s) to be formed, but to tip the balancein favor of PGE1. As with all matters ofhomeostasis, balance is the key. By favor-ing production of PGE1 desirable resultscan be achieved in terms of lowering bloodpressure and reducing inflammation.

The ultimate precursor for both class1 and 2 prostaglandins is the omega-6 fattyacid linoleic acid. This is converted togamma-linolenic acid (GLA) by delta-6-desaturase. Since many individuals lackoptimum levels of this enzyme (delta-6-desaturase activity decreases with age), itmay be prudent to supplement the diet withGLA directly (from Evening Primrose Oil).Optimal doses probably range from 30-120mg GLA/day. GLA is then converted todihomo-gamma-linolenic acid (DGLA) byan enzyme called elongase. DGLA servesas the direct precursor of PGE1. Alterna-tively, DGLA may undergo conversion toarachidonic Acid by delta-5-desaturase.Conversion of DGLA to PGE1 and arachi-donic acid to PG2 is catalyzed by the en-zyme cyclooxygenase, the target of aspi-rin and other nonsteroidal anti-inflamma-tory drugs. These drugs work by acetylat-ing (and inactivating) cyclooxygenase, lim-iting the production of class 2 prostaglan-dins. This is how aspirin and Motrin workto relieve headaches and muscle soreness.The delta-5-desaturase activity isstimulated by insulin and repressed by glu-cagon and eicosapentaenoic acid (EPA, anomega-3 fatty acid in fish oil). The properbalance of insulin to glucagon (controlledin response to the ratio of carbs to proteinin the diet) will thus serve to inhibit arachi-donic acid synthesis. Furthermore, con-sumption of EPA also limits AA produc-tion.

The effects of omega-3 fatty acids(fish oil) in reducing blood pressure, in-creasing erythrocyte deformability, andreducing platelet aggregation are probablymediated by their suppressive effect onarachidonic acid synthesis.As mentioned, PGE1 is a potentvasodialator and thus reduces blood pres-sure. PGE1 also activates adenylate cyclaseand thus acts to mobilize fat stores. Ade-nylate cyclase makes the intermdediatecyclic AMP, or cAMP, which stimulatesuse of fat for energy. This is the same waythe hormone adrenaline (epinephrine) anddrugs like ephedrine, caffeine, andclenbuterol mediate their fat-burning effect.PGE1 decreases blood viscosity by increas-ing erythrocytes (red blood cells)deformability. PGE1 reduces platelet ag-gregation (blood clotting). These all con-fer a protective effect against coronaryartery disease. In addition, PGE1 stimu-lates growth hormone release, which in turnpromotes use of fat for energy and parti-tions nutrients into the lean compartment(4-7). Among the class 2 prostaglandins,some are vasodialators and some are vaso-constrictors. Many promote inflammationand have an immunosuppressive effect.Since it is impractical to direct the synthe-sis of “good” class 2 prostaglandins andrepress the “bad” ones, the strategy of theParrillo diet (high protein, moderate carbs)involves simply limiting arachidonic acidsynthesis.

By increasing the balance of class1 to class 2 prostaglandins, beneficial ef-fects can be achieved while avoiding theundesirable effects of excess class 2 pros-taglandins.Glucagon promotes use of fat for en-ergy and generation of PGE1, while inhib-iting synthesis of series 2 prostaglandins.The balance of essential fatty acids in thediet (ratio omega-3 to omega-6) influencesthe balance of prostaglandins produced.Omega-3 fatty acids provide EPA whichalso inhibits delta-5-desaturase. By consum-ing a high protein, moderate carbohydratediet you can control the ratio of insulin toglucagon so as to favor the production ofPGE1 while limiting excess formation ofclass 2 prostaglandins.I warned you, the metabolism of EFAsis very complicated. I’ve just covered someof the basics. All you need to remember isthat EFAs are required for your body tomake some very important hormonesEvening Primrose Oil and the Importance of Essential Fatty Acidswhich are involved in controlling bloodpressure, blood clotting, inflammation, andfat metabolism, among other things. Peoplefollowing a low fat diet may be at risk fordeveloping essential fatty acid deficiencies.Parrillo EPO is a high-tech EFAsupplement designed to provide EFAs with-out excess non-essential fats. It provides away for bodybuilders and other athletes tooptimize their EFA metabolism while stillmaintaining a low fat diet. Parrillo EPO -another tool to help you optimize your nu-trition.


1. Paige DM. Clinical Nutrition. C.V.Mosby Company, St. Louis, 1988.

2. Shils ME, Olson JA, and Shike M.Modern Nutrition in Health and Disease.Lea & Febiger, Philadelphia, 1994.

3. Linder MC. Nutritional Biochemis-try and Metabolism with Clinical Applica-tions. Elsevier Science Publishing Com-pany, New York, 1991.

4. Hertelendy F, Todd H, Ehrhart K,and Blute R. Studies on growth hormonesecretion IV. In vivo effects of prostaglan-din E1. Prostaglandins 2: 79-91, 1972.

5. Hertelendy F and Keay L. Studieson growth hormone secretion VI. Effectsof dibutyrl cyclic AMP, prostaglandin E1,and indomethacin on growth and hormonesecretion by rat pituitary tumor cells inculture. Prostaglandins 6: 217-225, 1974.

6. McKeown BA, John TM, andGeorge, JC. The effect of prostaglandinE1 on plasma growth hormone, free fattyacids and glucose levels in the pigeon. Pros-taglandins 8: 303-314, 1974.

7. Dray F, Kouznetzova B, Harris B,and Brazeau P. Role of prostaglandins ongrowth hormone secretion. Adv. Prostag-landin and Thromboxane Res. 8: 1321,1980.

2018-03-13T11:10:36+00:00 May 27th, 2009|Technical Supplement Bulletins|

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