dietary fatty acids for healthy adults

FROM THE ACADEMY

2212-2672/$36.00http://dx.doi.org/10.1016/j.jand.2013.11.001

136 JOURNAL OF THE ACADEMY OF NUTRITION AND DIETETICS

Position Paper

Position of the Academy of Nutrition and Dietetics:Dietary Fatty Acids for Healthy Adults

ABSTRACTIt is the position of the Academy of Nutrition and Dietetics (the Academy) that dietaryfat for the healthy adult population should provide 20% to 35% of energy, with anincreased consumption of n-3 polyunsaturated fatty acids and limited intake of satu-rated and trans fats. The Academy recommends a food-based approach through a dietthat includes regular consumption of fatty fish, nuts and seeds, lean meats and poultry,low-fat dairy products, vegetables, fruits, whole grains, and legumes. These recom-mendations are made within the context of rapidly evolving science delineating theinfluence of dietary fat and specific fatty acids on human health. In addition to fat as avaluable and calorically dense macronutrient with a central role in supplying essentialnutrition and supporting healthy body weight, evidence on individual fatty acids andfatty acid groups is emerging as a key factor in nutrition and health. Small variations inthe structure of fatty acids within broader categories of fatty acids, such as poly-unsaturated and saturated, appear to elicit different physiological functions. TheAcademy recognizes that scientific knowledge about the effects of dietary fats on hu-man health is young and takes a prudent approach in recommending an increase infatty acids that benefit health and a reduction in fatty acids shown to increase risk ofdisease. Registered dietitian nutritionists are uniquely positioned to translate fat andfatty acid research into practical and effective dietary recommendations.J Acad Nutr Diet. 2014;114:136-153.

POSITION STATEMENT

It is the position of the Academy of Nutritionand Dietetics that dietary fat for the healthyadult population should provide 20% to 35%of energy, with an increased consumption ofn-3 polyunsaturated fatty acids and limitedintake of saturated and trans fats. The Acad-emy recommends a food-based approachthrough a diet that includes regular con-sumption of fatty fish, nuts and seeds, leanmeats and poultry, low-fat dairy products,vegetables, fruits, whole grains, and legumes.

ª

HIS IS AN UPDATE OF THE (TFA) for healthy individuals. From ways that are difficult to delineate.

T2007 Dietary Fatty Acid Posi-tion Paper developed by theAcademy of Nutrition and Di-

etetics (the Academy; formerly theAmerican Dietetic Association) andthe Dietitians of Canada.1 This updateand the associated position reflectthe current opinions of the Academyand is based on the most current sci-entific literature with considerationof other academic or organizationalbody recommendations.2-6 The objec-tives of the current position paperare to provide information on specificfatty acids including structure, currentand recommended intakes, function,and impact on health. This positionpaper evaluates the evidence for bothbeneficial and adverse effects of die-tary fatty acids for the purpose ofproviding a rationale for intake levelsof total fat, n-3 and n-6 polyunsatu-rated fatty acids (PUFA), monounsatu-rated fatty acids (MUFA), saturatedfatty acids (SFA), and trans-fatty acids

this, a position has been developedthat will guide registered dietitian nu-tritionists (RDNs) in their practice anddietetic technicians, registered (DTRs)who work under the supervision ofthe RDN in counseling healthy individ-uals. As the stated position reflectsrecommendat ions for fat ty ac idintakes in the context of healthy indi-viduals, it will not provide dietaryguidance for chi ldren, pregnantwomen, or specific disease states.Fatty acids are the major form of

dietary fat and primarily exist infoods in the triglyceride form. Althoughfatty acids are often categorized bytheir saturation status (eg, mono-unsaturated, saturated), understandingthe role of individual fatty acidson health, rather than as a group,is important. Because of this, fattyacids will be presented individually inthe following order: polyunsaturated,monounsaturated, saturated, and trans.In addition, fatty acids are consumed asa part of foods that contain other nu-trients and dietary compounds; thesehave both additive and synergistic ef-fects on health and interact in complex

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Therefore, the roles of individual fattyacids within the broader context of foodand dietary patterns will be discussed.

FATTY ACID CLASSIFICATIONSYSTEMFatty acid structures vary considerablyby both hydrocarbon chain lengthand saturation status. Although carbonchain length can vary from 2 to 40 car-bons, most dietary fatty acids contain 12to 22 carbons.7 Fatty acids are oftencategorized into short chain (up to 6carbons), medium chain (8 to 12 car-bons), or long chain (>12 carbons).Although hydrocarbon chain length isan important determinant of function,fatty acids are often classified based onwhether or not the fatty acid carbonchain contains no double bonds (SFA),one double bond (MUFA), or more thanone double bond (PUFA), as well as theconfiguration of the double bonds (cisor trans). In addition, PUFAs are oftenfurther classified based on the positionof the first double bond from the fattyacid methyl terminus, creating n-3 andn-6 fatty acids. In n-3s, the first double

014 by the Academy of Nutrition and Dietetics.

http://dx.doi.org/10.1016/j.jand.2013.11.001

This Academy of Nutrition and Dieteticsposition paper includes the authors’ in-dependent review of the literature inaddition to a systematic review conduct-ed using the Academy’s Evidence AnalysisProcess and information from the Aca-demy’s Evidence Analysis Library. Topicsfrom the Evidence Analysis Library areclearly delineated. The use of anevidence-based approach providesimportant added benefits to earlier re-view methods. The major advantage ofthe approach is the more rigorous stan-dardization of review criteria, which min-imizes the likelihood of reviewer bias andincreases the ease with which disparatearticles can be compared. For a detaileddescription of the methods used in theEvidence Analysis Process, go to www.andevidencelibrary.com/eaprocess.

Conclusion Statements are assigned agrade by an expert work group based onthe systematic analysis and evaluation ofthe supporting research evidence:

� Grade I[Good� Grade II[Fair� Grade III[Limited� Grade IV[Expert Opinion Only� Grade V[Not Assignable

(because there is no evidence tosupport or refute theconclusion).

See grade definitions at: www.andevidencelibrary.com.

Evidence-based information for thisand other topics can be found at www.andevidencelibrary.com. Subscriptionsfor nonmembers are purchasable at:www.andevidencelibrary.com/store.cfm.

FROM THE ACADEMY

bond occurs at the third carbon of thefatty acid chain from the methyl (oromega) end, and in n-6s, the first dou-ble bond occurs at the sixth carbonin the fatty acid chain.8 Figure 1presents nomenclature and commonfood sources of dietary fatty acids. It isthe differences in chain length andsaturation status that dictate their per-formance in food and cooking, as wellas their role in the body and impact onhuman health and disease risk.

TOTAL FAT VS INDIVIDUALFATTY ACIDSTotal fat intake has been the primaryfocus of dietary recommendations,with increased emphasis on the healthimpact of individual fatty acids inrecent years. Total fat intake of 20% to35% of energy is recommended by theInstitute of Medicine and the Food andAgriculture Organization of the United

January 2014 Volume 114 Number 1

Nations (FAO) and is supported by the2010 Dietary Guidelines for Americans(DGA).5,9 The American Heart Associa-tion (AHA) and National CholesterolEducation Program recommend 25% to35% of daily calories from fat.3,4 Thesetotal fat intake recommendations arebased on evidence that indicates con-sumption outside of these ranges isassociated with a greater intake of en-ergy and SFA (fat intake >35%) orgreater intake in carbohydrate (fatintake <20%); higher intake of carbo-hydrate leads to increases in plasmatriglyceride and reductions in high-density lipoprotein (HDL) cholesterollevels. According to the National Healthand Nutrition Examination Survey(NHANES) 2009-2010, 33% of caloriesin the diets of both women and mencame from fat, which is near the rec-ommended upper limit of 35%.10 It isimportant to note that individualsoften eat more than their energy needs,and examining total fat intake as apercentage of calories might wellreflect more fat in the diet than is rec-ommended and necessary.Although total fat recommendations

have been emphasized, for example,low-fat diet (<20%); moderate-fat diet(20% to 35%); or high-fat diet (>35%),the importance of individual fatty acidshas been overlooked. Achieving intakeof total fat within the recommendedrange (20% to 35%) is an importantgoal, but the quality of fat in the diet isequally important. Altering fat con-sumption, for example, the unsatu-rated/saturated fat balance, instead ofreducing total fat might be more ad-vantageous to health and chronic-disease risk reduction.11 In tissues, anincrease in concentration of one fattyacid corresponds to the reduction ofthe same magnitude of another fattyacid.12 The displacement or replace-ment of the quality of fatty acid isimportant to consider.Recent recognition that individual

fatty acids have differing effects onhealth, even within the conventionalfat categories, has brought examinationof these fatty acids into the forefront.Although this reductionist viewpointallows for understanding specific fattyacid functions and is important indetermining which fatty acids are bestfor health, examination of the foodscontaining these fatty acids is alsoimportant. Knowledge of the individualfatty acids in foods provides a

JOURNAL OF THE ACAD

foundation for the RDN to make wholefood recommendations to their clients.The variety of fatty acids in commonfats and oils is provided in Table 1.Additional information on individualfatty acids in foods can be found at theUS Department of Agriculture’sNutrient Database (http://ndb.nal.usda.gov).13

DIFFERING, WIDE-RANGINGIMPACTS ON HEALTHThe structure of each fatty acid differs,so it is reasonable that individual fattyacids might have unique impacts onhealth. The impact of specific fattyacids on disease incidence is difficult toelucidate, as chronic disease developsover many years and is the culminationof many genetic and lifestyle factors.This complexity makes randomizedcontrolled trials of dietary in-terventions largely impractical, butthese trials, coupled with observa-tional, epidemiologic, and mechanisticstudies, provide valuable evidence onthe health effects of dietary fat andspecific fatty acids. Because healthyindividuals are the focus of this paper,the impact of fatty acid intake on thosewith chronic diseases is not discussed.However, despite not having estab-lished or diagnosed disease, “healthy”individuals can possess disease riskfactors (eg, elevated low-density lipo-protein [LDL] cholesterol, glucose,obesity) that are influenced by spe-cific fatty acid intake. Modulation ofknown and emerging risk factors, suchas chronic low-grade inflammation,through dietary fatty acid intake canbeneficially impact development ofcommon diseases, such as cardiovas-cular disease, diabetes, and depression,as well as emerging diseases, such asAlzheimer’s and dementia. For example,evidence from randomized clinical tri-als and observational studies provideconvincing argument that inadequateintake of long-chain n-3 fatty acids isassociated with an increased risk ofsudden cardiac death.14 Targeting mul-tiple risk factors through modulation ofdiet, specifically fatty acids, holdspromise for promoting public healthand attaining meaningful reductions indisease risk in healthy individuals.

NEED FOR KNOWLEDGEFatty acids can no longer be viewed ingeneral categories, such as saturated

EMY OF NUTRITION AND DIETETICS 137

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Name Common abbreviationa Nomenclature Common food sourcesb

Polyunsaturated fatty acids PUFA

n-3

a-linolenic acid ALA C18:3 Flax, chia, walnuts, canola oil

Stearidonic acid SDA C18:4 GMOc soybean oil

Eicosapentaenoic acid EPA C20:5 Fish and seafood

Docosapentaenoic acid DPA C22:5 Fish and seafood

Docosahexaenoic acid DHA C22:6 Fish and seafood

n-6

Linoleic acid LA C18:2 Soybean oil, corn oil, shortening

g-linolenic acid GLA C18:3 Not commonly found in food

Arachidonic acid ARA C20:4 Meat, poultry, eggs

Conjugated linoleic acid CLA C18:2 (variants) Ruminant meat and dairy

Monounsaturated fatty acidsd MUFA

Palmitoleic acid C16:1 Macadamia nuts, blue-green algae

Oleic acid C18:1 Olive oil, canola oil, beef tallow, lard, avocado

Saturated fatty acids SFA

Carprylic acid MCTe C8:0 Coconut oil, palm kernel oil

Capric acid MCT C10:0 Coconut oil, palm kernel oil

Lauric acid MCT C12:0 Palm kernel oil, coconut oil

Myristic acid C14:0 Beef tallow, cocoa butter

Palmitic acid C16:0 Palm oil, most fats and oils

Stearic acid C18:0 Meat (lard, beef tallow), fully hydrogenatedvegetable oils

Trans-fatty acids TFA

Elaidic acid C18:1, t9 Partially hydrogenated vegetable oils

Vaccenic acid C18:1, t11 Butterfat, meataOnly fatty acids with common abbreviations are listed.bFood sources of naturally occurring fatty acids are listed (with exception of GMO soybean oil); fortified food andsupplement sources can be found in body of paper.cGMO¼genetically modified organism.dOnly monounsaturated fatty acids (MUFA) in the cis configuration are listed. MUFAs with trans configuration are listedunder trans fatty acids.eMCT¼medium-chain triglyceride.

Figure 1. Nomenclature and common food sources of dietary fatty acids.

FROM THE ACADEMY

and unsaturated, because individualfatty acids within these categorieshave different influences on healthstatus and disease risk. For example,both stearic acid (18:0) and palmitic

138 JOURNAL OF THE ACADEMY OF NUTRIT

acid (16:0) are saturated fats, differingonly in chain length by two carbons,but they appear to have different ef-fects on circulating LDL cholesterol.15

Another example is the difference

ION AND DIETETICS

between the location of the first dou-ble bond on the fatty acid carbonchain. Whether the double bond islocated on carbon number 3 or 6 (asin n-3 and n-6 PUFA) makes a


Table 1. Fatty acid profiles of select animal and vegetable fats and oilsa

Lipid Quantity SFAb 8:0 10:0 12:0 14:0 16:0 18:0 MUFAc 18:1 PUFAd 18:2 18:3

EPAe

DPAf

DHAg ARAh TFAi

Avocado oil 1 Tbsp 11.9 0.0 0.0 0.0 0.0 11.3 0.7 72.6 69.9 13.9 12.9 1.0 0.0 0.0 0.0

Beef tallow 1 Tbsp 46.8 0.0 0.0 0.9 3.5 23.5 17.8 39.3 33.9 3.8 2.9 0.6 0.0 0.0 0.0

Butterj 1 Tbsp 53.6 5.1 2.6 2.7 7.8 22.6 10.4 22.0 20.8 3.2 2.9 0.4 0.0 0.0 0.0

Canola oil 1 Tbsp 7.6 0.0 0.0 0.0 0.0 4.4 6.8 65.1 63.5 29.0 19.6 9.4 0.0 0.0 0.4

Coconut oil 1 Tbsp 11.8 1.0 0.8 6.1 2.3 1.1 0.4 0.8 0.8 0.2 0.2 0.0 0.0 0.0 0.0

Corn oil 1 Tbsp 12.9 0.0 0.0 0.0 0.0 10.6 1.8 27.6 27.4 54.7 53.5 1.2 0.0 0.0 0.3

Flaxseed oil 1 Tbsp 9.0 0.0 0.0 0.0 0.1 5.1 3.4 18.5 18.3 67.9 14.3 53.4 0.0 0.0 0.1

Grapeseed oil 1 Tbsp 9.6 0.0 0.0 0.0 0.1 6.7 2.7 16.1 15.8 69.9 69.6 0.1 0.0 0.0 —

Lard 1 Tbsp 36.9 0.0 0.1 0.2 1.3 22.4 12.7 42.5 38.8 10.5 9.6 1.0 0.0 0.0 0.0

Olive oil 1 Tbsp 13.7 0.0 0.0 0.0 0.0 11.2 1.9 72.4 70.7 10.4 9.7 0.7 0.0 0.0 —

Palm oil 1 Tbsp 49.3 0.0 0.0 0.1 1.0 43.5 4.3 37.0 36.6 9.3 9.1 0.2 0.0 0.0 —

Palm kernel oil 1 Tbsp 81.5 3.3 3.7 47.1 16.4 8.1 2.8 11.4 11.4 1.6 1.6 0.0 0.0 0.0 —

Rice bran 1 Tbsp 19.7 0.0 0.0 0.0 0.7 16.9 1.6 39.3 39.1 35.0 33.4 1.6 0.0 0.0 —

Salmon oil 1 Tbsp 19.9 — — — 3.3 9.9 4.3 29.0 17.0 40.3 1.5 1.0 31.3 0.7 —

Soybean oil 1 Tbsp 15.7 0.0 0.0 0.0 0.0 10.4 4.4 22.8 22.6 57.7 51.0 7.1 0.0 0.0 0.5

aListed as percent of total fatty acid content. Based on 13.6 g fatty acids/tablespoon (Tbsp). Cells without numbers did not have data in US Department of Agriculture Nutrient Database.bSFA¼saturated fatty acid.cMUFA¼monounsaturated fatty acid.dPUFA¼polyunsaturated fatty acid.eEPA¼eicosapentaenoic acid.fDPA¼docosapentaenoic acid.gDHA¼docosahexaenoic acid.hARA¼arachadonic acid.iTFA¼trans-fatty acid.jButter contains 16% water and therefore the percentages are unable to be directly compared with percentages of the other fats/oils.

FROM THE ACADEMY

remarkable difference in biologicalfunction (eg, vasoconstriction vs va-sodilation). Therefore, understandingthe breadth of information whiledelineating specifics about individualdietary fatty acids is essential. RDNshave the opportunity and re-sponsibility to translate research intopractice for the population at large.National organizations specializing inevidence-based dietary recommenda-tions are valuable resources. Table 2summarizes intake recommendationsfor dietary fatty acids.This section of the position paper

includes the results of a systematic re-view of literature conducted using theAcademy’s Evidence Analysis Processand information from the Academy’sEvidence Analysis Library. In thisprocess, expert work groups identifieddietetic practice�related topics, priori-tized and selected questions, per-formed systematic reviews, and


developed and rated a conclusionstatement for each question. Theworkgroups used the Academy’s pro-cess to answer a total of three ques-tions related specifically to dietaryfatty acids.

PUFAsSpecific Fatty Acids and FoodSourcesPUFAs are triglycerides that containfatty acids with two or more (poly)double bonds. PUFAs are liquid at roomtemperature and, because they are notsolid fats, they are often referred to asoils. In recent decades, researchershave discovered that the function ofPUFAs in human nutrition differ basedon the fatty acid structure. The mostcommon PUFAs are n-3 and n-6, andbecause humans cannot synthesizethem, they are considered essentialdietary nutrients.

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Dietary fatty acids are oxidized asfuel; incorporated in plasma phospho-lipids, lipoprotein particles, and cellmembranes; or stored as triglycerides.The most abundant PUFAs in the dietare a-linolenic acid (ALA; 18:3n-3) andlinoleic acid (LA; 18:2n-6); both ofthese fatty acid hydrochains are 18carbons in length and are consideredthe parent fatty acids for n-3 and n-6,respectively.

n-3 and n-6 fatty acids are long-chain fatty acids (18 carbons andlonger) and are distinguished withineach group by chain length. In the n-3family, ALA and stearidonic acid (SDA;18:4n-3) are considered the shorter-chain n-3s, while eicosapentaenoicacid (EPA; 20:5n-3), docosapentaenoicacid (DPA; 22:5n-3), and docosahexa-enoic acid (DHA; 22:6n-3) are thelonger-chain n-3s. ALA occurs in plantfoods such as nuts, particularly walnutsand flax, chia and hemp seeds, and


Table 2. Dietary fatty acid intake recommendationsa

OrganizationTotalfat (%) PUFAb (n-3) PUFAc (n-6) MUFAd SFAe TFAf

2010 Dietary Guidelinesfor Americans

20-35 Use oils to replace solid fats where possibleIncrease the amount and variety ofseafood consumed by choosingseafood in place of somemeat and poultry

Use oils to replace solidfats where possible

Replace solid fatswith MUFAs, possiblythrough adopting aMediterraneandietary pattern

<10% As low aspossible

US DietaryReference Intake

20-35 AIg for ALAh is 1.1-1.6 g/day or 0.6%-1.2%of intake; up to 10% can be EPAiþDHAj

5%-10% of intake;AI for LAk is 12-17 g/day

As low as possible As low aspossible

Academy of Nutritionand Dietetics

20-35 0.6%-1.2% of intake as ALA;500 mg EPAþDHA/day

3%-10% of intake 15%-20% of intake Goal of <7%,maximumintake of 10%

<1%

American HeartAssociation

25-35 Eat fish (particularly fatty fish)at least 2�/week

LA as 5%-10% of intake Replace animalfats in the diet

<7% <1%

WHO/FAOl 20-35 0.5%-2% of intake; minimum 0.5%from ALA; 250 mg EPAþDHA/day

AI for LA is 2%-3% of intake Intake at nomore than 10%of energy; shouldbe replacedwith PUFAs

<1%

EFSAm 20-35 AI for ALA is 0.5% of intake;250 mg EPAþDHA/day

AI for LA is 4% of intake As low as possible As low aspossible

ISSFALn ALA 0.7% of intake; minimum500 mg EPAþDHA/day

AI for LA 2% of intake

aPercentages based on total energy intake that meets the needs of the individual.bPUFA¼polyunsaturated fatty acids.cValues reported for total n-6 PUFA unless indicated.dMUFA¼monounsaturated fatty acids.eSFA¼saturated fatty acids.fTFA¼trans-fatty acids.gAI¼Adequate Intake. AI is a recommended average daily nutrient intake level, based on experimentally derived intake levels or approximations of observed mean nutrient intake by a group (or groups) of apparently healthy people that are assumedto be adequate. An AI is established when there is insufficient scientific evidence to determine an Estimated Average Requirement.hALA¼a-linolenic acid.iEPA¼eicosapentaenoic acid.jDHA¼docosahexaenoic acid.kLA¼linoleic acid.lWHO/FAO¼World Health Organization/Food and Agriculture Organization.mEFSA¼European Food Safety Authority.nISSFAL¼International Society for the Study of Fatty Acids and Lipids.

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FROM THE ACADEMY

vegetable oils, such as canola and soy-bean oils. SDA is not typically foundin food; very small amounts occurin fish and uncommon plant sources(eg, echium, black currant). In theUnited States, the soybean has beengenetically modified to produce oilcontaining SDA n-3; the SDA-rich soy-bean oil has Generally Recognized asSafe approval in the United States.16

EPA, DPA, and DHA occur in fatty fishand seafood, and the best sources aresalmon, sardines, tuna, herring, andtrout. An abundance of foods fortifiedwith EPA and/or DHA from either ma-rine or algal sources are now available;called functional foods, examplesinclude soy milks and juices, cookingoils, spreads, snack foods and even fishsticks, where fortification is in thebreading. Availability of functionalfoods varies by region. Eggs can containshorter or longer-chain n-3s, as deter-mined by the chicken feed. Most of theresearch on long-chain n-3s has usedEPA and DHA. DPA is a lesser known n-3; it occurs in fatty fish along with EPAand DHA but is particularly rich in sealmeat, a traditional food of Eskimos andother cultures. Interest in new orunique health contributions from DPAis growing. The predominant and bestunderstood n-3 fatty acids are ALAfrom plants and EPA and DHA from fishand seafood.In the n-6 family, LA and g-linolenic

acid (GLA; 18:3n-6) are shorter-chainfatty acids, and arachidonic acid (ARA;20:4n-6) is a longer chain. Longer-chain n-3 and n-6 fatty acids (�20carbons) are sometimes called highlyunsaturated fatty acids. LA occurs inplant foods; the richest sources aresoybean, corn, and safflower oils. GLAis not found to any great extent infoods and is available through dietarysupplements from borage and eveningprimrose oil. The best sources of ARAare meat, poultry, and eggs.Conjugated linoleic acid (CLA) is an

18-carbon n-6 PUFA that occurs insmall amounts in the milk (about 0.3%to 0.6% total dairy fat) and meat of ru-minants. A conjugated fatty acid is onein which the double bonds occur onadjacent carbons. The two major CLAforms are cis-9, trans-11 18:2 (c9, t1118:2) and the trans-10, cis-12 18:2(t10,c12 18:2). There is usually more c9,t11 18:2 in food, while supplementstypically contain an equal mixture ofboth forms. For the purpose of food


labeling, CLA is classified as an n-6 fattyacid and not a TFA. One pilot studyreported intake of CLA from foods at94.9 mg/day in healthy adults in NorthAmerica.17

Within the n-3 and n-6 families, theshorter-chain and longer-chain fattyacids make different contributionsto human nutrition. ALA n-3 is pre-dominantly used as a fuel source for b-oxidation and only a small portion isconverted to longer-chain fatty acids.18

Desaturase and elongase enzymes arerequired for the conversion of shorter-chain to longer-chain fatty acids. Itwas originally believed that theshorter-chain fatty acids readily con-verted to the longer chains, butcontemporary research indicates thatn-3 conversion from short chain tolong chain in humans is very limited;ALA converts to EPA at a rate of 5% to15%, and <1% of ALA reliably convertsto DHA.19,20 Rate of conversion of theseessential fatty acids is determined bythe presence of and competition for thedesaturase and elongase enzymes andis further influenced by other factors,including sex, diet, health status, andgenetics.21-24 This explains the interestin genetically engineered SDA; moreSDA than ALA is converted to EPAbecause with SDA, the rate-limitingconversion step requiring delta-6desaturase is bypassed. Conversion,however, is limited; two publishedhuman trials reported that about 17% ofSDA converts to EPA and there is noconversion from SDA to DHA.25,26 As aresult, SDA is best considered an EPA-only precursor.27

Individuals who follow a vege-tarian or vegan diet and include nomarine foods in their diet willconsume ALA because of its widedistribution in plant-sourced foods.Through conversion, ALA will providesome EPA but little, if any, DHA.19

Emerging science suggests there isindividual variation in conversionrate of fatty acids, influenced by ge-netics and dietary habits, includingthe presence of other fatty acids inthe diet. Those who follow a vege-tarian diet might be more efficient atn-3 conversion, but this has not beenconfirmed.22,28

As 20-carbon PUFAs, EPA n-3 andARA n-6 function as eicosanoids. Ei-cosanoids are bioactive mediators andprecursors for prostaglandins, throm-boxanes, and leukotrienes. Eicosanoids

JOURNAL OF THE ACAD

are considered hormone-like sub-stances because they are producedwhen stimulated, rapidly utilized andmetabolized, and not stored in cells.Prostaglandins, thromboxanes, andleukotrienes are involved with amyriad of physiological and homeo-static activities, including inflamma-tion modulation, platelet aggregation,cell growth and proliferation, smoothmuscle contraction, and vasoconstric-tion and vasodilatation. EPA, ARA,and DHA are also involved with geneexpression, cytokine activity, cellsignaling, and immune modulation.The eicosanoids produced from EPAand ARA differ from each other instructure, and they function in com-plementary metabolic pathways. Ei-cosanoids produced from ARA havehigh biological activity and areconsidered more potent than EPA-derived eicosanoids. For example,prostaglandins produced from ARApromote inflammation, serve as vaso-constrictors, and stimulate plateletaggregation, and prostaglandins pro-duced from EPA function as vasodila-tors and anti-aggregators. Eicosanoidsderived from ARA are mostly pro-inflammatory but have some anti-inflammatory effects. A balance ofeicosanoid synthesis in tissues isoptimal. Resolvins and neuroprotectins,derived from EPA and DHA, respec-tively, are a new class of modulatorsthat appear to have anti-inflammatoryand neuroprotective activity.8,29 Fi-nally, DHA is a structural component ofred blood cell membranes and exists inhigher concentrations in retina tissue,neuronal cells, liver, and testes.30

PUFAs FROM SUPPLEMENTSn-3 supplements are widespread in themarketplace. The most common sup-plement forms of ALA are flax and chiaseed oils. SDA supplements from algaeare being synthesized. EPA and DHAsupplements are made from fish oil(typically anchovy, menhaden, andsalmon oils), cod liver oil, krill oil,and squid (calamari) oil. GenerallyRegarded as Safe status of up to 3 g/dayof EPA and DHA from fish oil inhealthy people was obtained in 1997.31

Vegetarian sources of EPA and DHA areavailable from algal sources, andgenetically engineered supplementsare under development. GLA n-6 sup-plements are most often sourced from


FROM THE ACADEMY

borage and evening primrose oils. CLA,the conjugated n-6 supplement, issynthesized from vegetable oils.

Current Intake of PUFAsNHANES 2009-2010 provided infor-mation on dietary intake of n-3s andn-6s among adults.10 NHANES reportedmean daily intake of ALA among maleswas 1.77 g and 1.38 g among females.Mean daily intake of EPA among menwas 40 mg and 30 mg for women.Mean daily intake of DHA was 80 mgfor men and 60 mg for women. There islittle difference between mean intakesby sex, race/ethnicity, and income.These values have remained quite sta-ble as reported in the last NHANES dataset (NHANES III 1988-94). For n-6s, themean daily intake of LA among menwas 17.84 g and among women,13.33 g.This represents an increase as previousNHANES III data reported a mean dailyconsumption of LA at 14.1 g. Dailyconsumption of ARA was reported as180 mg for men and 120 mg forwomen.Economic disappearance data for

each year from 1909 to 1999 was usedto estimate consumption of food com-modities per capita.32 With regard ton-3, availability of ALA increased from0.39% to 0.72% of energy. In 1909, thegreatest dietary sources of ALA werefats, dairy, pork, beef, and grains; by1999, sources were soybean oil, dairy,fats, other oils, beef, shortening, andnuts. Availability of EPA and DHA hasremained virtually unchanged. Resultsfor n-6, however, were strikinglydifferent. The availability of LAincreased 158%, from 2.79% of energyin 1909 to 7.21% of energy in 1999(based on current fatty acid analysis).In 1909, the primary food sources of LAwere fats, pork, grains, shortening, oils,and nuts. Ninety years later they weresoybean oil, fats, shortening, other oils,poultry, and nuts. The availability ofARA has remained unchanged.

Dietary Recommendations forPUFAsThe 2005 Daily Reference Intakesrecommend 5% to 10% energy from n-6and 0.6% to 1.2% of energy from n-3,but it did not set a Recommended Di-etary Allowance (RDA) or EstimatedAverage Requirement for either. Thereport did provide an Adequate Intake(AI) for n-6 and n-3. The AI for n-6 is 17


g/day and 12 g/day for men andwomen 19 to 50 years, respectively;the AI for ALA is 1.6 g/day and 1.1 g/dayfor men and women age 19 to olderthan 70 years, respectively.9 These in-takes are equivalent to 5% to 6% energyfrom LA and 0.5% energy from ALA.Recognizing that differences in meta-bolic function among n-3s existed, theDaily Reference Intake report notedthat EPA and DHA could provide up to10% of ALA intake. It is important torecall that AI recommendations areobserved median intakes for the USpopulation, not an RDA or an intake offatty acids shown to confer lower riskof disease.The DGA recommend that adults

consume 8 oz or more of seafoodper week, or about 20% of the re-commended intake of protein foodsfrom a variety of seafood (fish andshellfish). For primary prevention ofcoronary heart disease (CHD), theAHA,33 the National Heart Foundationof Australia,34 and the United KingdomScientific Advisory Committee,35 allrecommend at least two servings offish per week, preferably fatty fish,providing an average daily intake of450 to 500 mg EPA and DHA. The samerecommendation of two or more serv-ings per week is suggested by theAmerican Psychiatric Association36 forsupport of mental health. An increasedintake of nuts and seeds is also rec-ommended. Because these foods havegreater caloric density, they shouldreplace servings of meat and poultryand/or be consumed in small portions.5

The World Health Organization/Foodand Agricultural Organization estab-lished an upper Acceptable Macronu-trient Distribution Range (AMDR) fortotal PUFAs at 11% energy. Theyrecommend total n-3 intake of 0.5% to2% energy, with a minimum require-ment of >0.5% energy from ALA toprevent deficiency, and 250 mg EPAand DHA/day for men and nonpregnantwomen.6 For LA n-6, they recommendan estimated average requirement of2% energy, an AI of 2% to 3% energy, andan AMDR of 2.5% to 9%. The lowerlevels in the range are to prevent defi-ciency, and the upper level is suggestedas part of healthy diet for long-termcardiovascular health. The EuropeanFood Safety Authority recommends anAI of 0.5% energy for ALA and an AI of250 mg EPA and DHA for primaryprevention in healthy adults. For n-6,

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the European Food Safety Authorityrecommends an AI of 4% energy for LA;they do not give a Dietary ReferenceValue for ARA.37 The International So-ciety for the Study of Fatty Acids andLipids recommends a healthy intake ofALA n-3 as 0.7% energy and for car-diovascular health, a minimum of 500mg/day of EPA and DHA n-3. They alsorecommended an AI of LA n-6 at 2%energy.38

In 2004, the Food and Drug Admin-istration (FDA)39 approved a QualifiedHealth Claim for n-3 fatty acids andheart disease, stating: “Supportive butnot conclusive research shows thatconsumption of EPA and DHA n-3 fattyacids may reduce the risk of CHD. Oneserving of [name of food] provides [x]grams of EPA and DHA n-3 fatty acids.”The FDA also approved a QualifiedHealth Claim for nuts and heart diseaseas well as walnuts and heart disease,stating: “Scientific evidence suggestsbut does not prove that eating 1.5ounces per day of most nuts [such asname of specific nut] as part of a dietlow in saturated fat and cholesterolmay reduce the risk of heart disease.”The FDA made the same statement forwalnuts.40

Based on recent literature, increasingconsumption of PUFAs with a partic-ular focus on increasing n-3 intake (ie,striving to consume two or moreservings of fatty fish per week to pro-vide at least 500 mg EPA and DHA perday, and aiming toward an intake of atleast 0.5% to 2% energy as n-3 fattyacids and 5% to 10% energy as n-6 fattyacids per day) is desirable.

PUFAs and Healthn-3 Fatty Acids. The role of n-3 fattyacids in heart health is one of the moststudied areas of nutrition science. Ob-servations specific to long-chain n-3fatty acids were first made in the 1960swhen epidemiologists observed thatGreenland Eskimos and native Alaskanshad a low incidence of CHD, althoughthey consumed large amounts of fat. Inthe 1970s, death rates from heart dis-ease among males aged 45 to 64 yearswere 40% in the United States andnearly 35% in Denmark, yet only 5% inGreenland.41 Compared to the Danes,Greenland Eskimos had higher bloodlevels of saturated fat and lower levelsof PUFAs, cholesterol, and triglycerides,even though both groups ate about the


FROM THE ACADEMY

same amount of total fat (Danes 40%;Eskimos 37%). The Greenland Eskimosalso had considerably higher bloodlevels (up to 16%) of the n-3 fatty acidEPA. The researchers noted more of aqualitative than quantitative differencewith respect to fatty acid composition inthe diets.42 Based on these findings, aswell as observations in countries thatconsume large amounts of fish such asJapan, associations between fish con-sumption and overall cardiovascularmortality and sudden cardiac deathhave been noted. According to a 2011meta-analysis, observational and ran-domized clinical trial evidence suggeststhat fish or fish oil consumption canalso reduce inflammation, improveendothelial function, normalize heartrate variability, improve myocardialrelaxation and efficiency, and, at higherdoses, limit platelet aggregation.43 Inaddition, inverse relationships betweenblood levels of n-3 and risk for suddencardiac death have been observed.44,45

Habitual fish consumption is associ-ated with lower risk of CHD andischemic stroke and, among the generalhealthy population, those who consumea modest amount of fish or fish oilproviding �250 mg EPA and DHA/dayhave a 36% lower risk of fatal heartdisease.14 These benefits have not beenshown among those who eat commer-cially fried fish or fish sandwiches; thismight be a reflection of the type offish commonly fried, as it tends to belower in EPA and DHA content. None-theless, researchers have shown thatconsumption of nonfried fish is associ-ated with higher EPA and DHA bloodlevels.46,47

In addition to providing long-chainn-3s, fish provides lean protein, vita-mins, and minerals. Due to theconcern of potential methylmercurycontamination in fish, in 2004 the USDepartment of Agriculture48 recom-mended pregnant women and chil-dren under 5 years old limit fishconsumption and avoid the followingtypes of fish: shark, swordfish, kingmackerel, and tilefish. Since then, anextensive risk-to-benefit analysisconcluded that, with the exception ofselect fish, such as those included inthe US Department of Agricultureadvisory, the health benefits of fishconsumption outweigh potentialrisks.49 At this time, however, the USDepartment of Agriculture advisoryremains in effect. Although fish oil


supplements have been shown to beequally effective as fish at increasingtissue levels of EPA and DHA,50 it isunclear whether benefits observed inthose with habitual fish consumptioncan be fully reproduced with refinedfish oil supplements. Clinical researchhas shown that supplementing withrefined fish oil can help reduce tri-glycerides and improve blood pressureand heart rate levels.51-55

The benefits of ALA independent ofEPA and DHA are not well documented;but, because it is plant sourced, ALA ismore readily available in the diet andis a particularly important source ofPUFAs for vegetarians. Studies investi-gating cardiovascular benefits of ALA inthe healthy population have shownmixed or inconsistent results.56,57 Dietsrich in ALA have been reported tolower lipid levels, reduce vascularinflammation, and reduce blood pres-sure in those with elevated cholesterollevels.58,59 Interestingly, an 11-countrystudy in Europe reported reductionsin CHD in countries that consumedALA-rich canola oil compared to coun-tries that consumed primarily sun-flower oil, which contains no ALA.60

Walnuts are a particularly rich sourceof ALA and several studies have re-ported benefits from ALA by includingwalnuts and a variety of nuts in thediet.61-63 Plant-sources of n-3s havealso been shown to have a protectiveeffect on bone metabolism.64 However,a cardioprotective blood level of long-chain n-3s (EPA and DHA) cannot beachieved by consuming ALA alone.65,66

Health benefits of SDA independentof EPA and DHA are unclear. Althoughlittle is known about the biological ef-fects of SDA, incorporating geneticallyengineered SDA into the food supply ismotivated by barriers to fish con-sumption and global concerns for sus-tainability. Modulating lipid levels withEPA and DHA require relatively highdoses; preliminary studies indicatethat consuming SDA at a bioequivalentdose of EPA (approximately 4 g SDA¼approximately 1 g EPA) has littleimpact on circulating lipids.26,27

Depression is an increasingly com-mon mental health disorder. It can bechronic or recurrent, and the impact onindividuals, families, caregivers, com-munities, and the work force is signif-icant. It is the leading cause ofdisability worldwide and is predictedto be among the top three leading

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causes of burden of disease by 2030.67

An association between fish consump-tion and incidence of major depressionwas first reported in 1998.68 Sincethen, a link between low levels of long-chain n-3 fatty acids and depressionhas been observed in a number of tri-als.69-73 The recommendation by theAmerican Psychiatric Association toconsume fatty fish at least twice aweek reflects these findings.36

Some level of cognitive decline isconsidered normal with aging andlower levels of DHA have beenobserved in individuals with cognitivedecline and Alzheimer’s disease.74-77

The results of studies examining therelationship between long-chain n-3son cognitive decline have beenmixed.78-80 The Academy’s EvidenceAnalysis Library recently examined thisquestion (see Figure 2); 6 of the 14studies analyzed reported positive as-sociations between EPA, DHA, or fishconsumption and decreased risk ofcognitive decline. Results varied basedon amount and source of EPA and DHAconsumed and, perhaps more impor-tantly, the state of cognitive healthat the outset of the study. A studyevaluating healthy middle-aged adultsshowed that DHA but not ALA or EPAwas associated with better perfor-mance on cognitive tests, such asnonverbal reasoning, mental flexibility,memory, and vocabulary.81

Essential fatty acids are potentiallypotent anti-inflammatory agents and,as such, clinical evidence has shown arole for EPA and DHA in reducingsymptoms of rheumatoid arthritis.82,83

Currently, there is interest in the roleof fatty acids in immune health, in partbecause long-chain fatty acids appearto influence proteins directly involvedwith immune cell activation.29,84

Despite promising results from animalmodels and cultured tumor cell lines,no clear relationship between dietaryintake of EPA and DHA and risk forcancer have been demonstrated.65

n-6 Fatty Acids. LA is the most highlyconsumed PUFA in the Western dietand is found in virtually all commonlyconsumed foods. LA is the metabolicprecursor of ARA and there is concernthat LA consumption can enrich tissueswith ARA and contribute to over-production of bioactive eicosanoids,thereby increasing inflammatorymarkers and/or chronic disease risk.


Question: What is the effect of eicosapentaenoic acid (EPA)/docosahexaenoic acid (DHA) from supplemental and dietarysources on cognitive decline in adults?

Conclusion: Based on 14 studies (1 case-control, 3 cross-sectional, 6 prospective cohort, and 4 randomized controlled trials)primarily of healthy elderly subjects or those matched for incident dementia, results are mixed. Six of the 14 studies found apositive association of EPA, DHA, or fish consumption and a decreased risk of cognitive decline. The majority of the studiesincluded large populations of elderly subjects measuring either blood levels of EPA and DHA and fish consumption. Results varybased on dose of supplementation or dietary consumption of fish, EPA, or DHA. Further research is needed to determinewhether EPA, DHA, and fish consumption has a protective effect for all-cause dementia. There is some evidence that ApoE e4carrier status should be factored into future studies.

Gradea II¼Fair

Question: What is the effect of linoleic acid (LA) on the risk of diabetes mellitus and/or insulin resistance in adults?

Conclusion: There is fair evidence that LA status is inversely associated with risk of type 2 diabetes mellitus. Limited studies haveshown an inverse relationship between LA status and risk factors for type 2 diabetes mellitus including insulin resistance,metabolic syndrome, inflammation, nerve function/neuropathy, and the liver enzyme, alanine transaminase, as a marker of liverfat.

Grade II¼Fair

Question: What is the effect of conjugated linoleic acid (CLA) on body composition and weight loss in healthy adults?

Conclusion: Fair evidence indicates that 3 to 6 months of CLA supplementation results in a decrease in fat mass and an increasein fat-free mass in healthy adults; however, fair evidence indicates that CLA does not affect body weight.

Grade II¼FairaAcademy of Nutrition and Dietetics Evidence Analysis Library Grade Definitions and Chart: http://andevidencelibrary.com/content.cfm?content_id¼11.

Figure 2. Questions, conclusions, and grades from the Dietary Fatty Acids Evidence Analysis Project of Academy of Nutrition andDietetics’ Evidence Analysis Library.

FROM THE ACADEMY

However, a 2011 review reported thatdecreasing dietary LA up to 90% did notsignificantly correlate with change inARA tissue levels and, similarly,increasing dietary LA levels did notincrease ARA levels substantially. A2012 systematic review of randomizedcontrolled trials that assessed theimpact of LA on biologic markers ofchronic inflammation among healthyadults also reported no evidence thatLA increased inflammatory markers.85

Nevertheless, emerging evidence in-dicates significant racial differences inconversion rate of LA to ARA, particu-larly between those of European andAfrican descent, making this animportant area for further learning.86

With regard to GLA, a linear relation-ship between dietary GLA and in-creases in plasma and serumphospholipid ARA levels has beenmeasured.87

An AHA advisory published in 2009summarized evidence on n-6 con-sumption, particularly LA and CHD risk.It reported that consuming 5% to 10% ofenergy from n-6 PUFAs reduced the


risk of CHD relative to lower intakes.88

A more recent meta-analysis, however,challenges this conclusion.89

Evidence from animal studies sug-gests a beneficial role for CLA forweight loss. However, results fromsupplementation trials using intakelevels of CLA unattainable from food(1.8 to 4.5 g/day) have been mixed.90-92

The Academy’s Evidence Analysis Li-brary recently reviewed this question(see Figure 2). Impaired insulin sensi-tivity has been reported in some butnot all studies using CLA supplemen-tation in those with obesity and meta-bolic syndrome.91-93

MUFAsSpecific Fatty Acids and TheirFood SourcesMUFAs are present in a wide variety offoods, including vegetable, nut, andseed oils, as well as meats and dairyproducts. By definition, MUFAs containone double bond; this double bondvaries in location but is frequentlylocated at carbon nine from the methyl

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end of the fatty acid hydrocarbonchain. MUFAs also differ based on chainlength, and although these fatty acidscan exist from 10 to 32 carbons, themajority exist as an 18-carbon fattyacid in the form of oleic acid.

Oleic acid contains one double bondat carbon nine, with the double bondexisting in the cis position (18:1 c-9).One of the most abundant fatty acidsfound in foods, oleic acid is present inhigh amounts in olive and canola oils(see Table 1), as well as in avocadosand almonds (9.8 g/avocado half and8.8 g/1 oz almonds, respectively).Although these food sources aregenerally well known, at least 30% ofthe fatty acids in beef tallow, lard, andpalm oil are oleic acid, and >20% ofthe fatty acids in both soybean andcorn oil are oleic acid.13 As a result,oleic acid is the most abundantlyconsumed fatty acid in the Americandiet at 12% energy intake.10

Several other MUFAs exist but arepresent in foods in low quantities. OneMUFA that naturally exists in lowerquantities in foods is erucic acid, a


http://andevidencelibrary.com/content.cfm?content_id=11



FROM THE ACADEMY

22-carbon fatty acid that contains onedouble bond at carbon 9 (22:1, c-9).Food sources of erucic acid includerapeseed and other plants from theBrassicaceae family, including kale andbroccoli. Canola oil is produced fromrapeseed, but removal of erucic acidthrough genetic modification hasessentially eliminated the erucic acidcontent in canola oil and subsequentlyfrom the diet.In addition to n-9 MUFAs, an n-7

MUFA with a purported health benefitis palmitoleic acid, containing 16 car-bons with one double bond at carbon 7from the methyl end (16:1, c-7). Pal-mitoleic acid is not commonly found infoods, but is a product of palmitic acid(16:0) metabolism in the body. Foodsthat naturally contain palmitoleic acidinclude certain blue-green algae, mac-adamia nuts (3.7 g/oz; 17% of fat con-tent), and sea buckthorn oil. Althoughthe fatty acids mentioned have onedouble bond that exists in the cis for-mation, MUFAs can exist in the transconformation as a result of industrialhydrogenation; most often these TFAexist as 18:1, t-9. TFAs will be discussedin the trans-fat section of this article.Although additional MUFAs exist, thequantities consumed through diet arenegligible and therefore will not bediscussed.

MUFAs from SupplementsSupplementation with MUFA is notcommon practice and is not supportedby authoritative bodies. However,MUFAs are available in supplementform. Despite its abundance in variousfoods and oils, oleic acid from olive oilis marketed as a dietary supplement.Given the quantity of oleic acid incommon food oils (9.6 g per Tbsp oliveoil; 8.3 g per Tbsp canola oil; 3 g perTbsp soybean oil), supplementing witholive oil does not provide appreciablequantities compared to the commondaily diet. Oleic acid from olive oil canalso be found in supplements contain-ing the combination of n-3, n-6, andn-9 fatty acids; given the abundantsupply of both n-6 (18:2) and n-9 (oleicacid; 18:1) in the diet, the supple-mental use of this combination is notsupported. In addition to oleic acid,palmitoleic acid is currently beingmarketed as an n-7 fatty acid supple-ment with claims of preventing orreducing heart disease.


Current Dietary Intake of MUFAsNHANES 2009-2010 reports the dietaryintake of MUFA for both men andwomen was 12% of total energy. Thisrivals SFA intake (11%) and is nearlydouble that of PUFA intake (7%).10 Of allthe fatty acid categories, MUFAs areconsumed the most, comprising 36% oftotal fat intake. The majority (93%) ofMUFA consumption is oleic acid atapproximately 27 g/day; second to thisis palmitoleic acid at 1.2 g/day. MUFAintake has remained relatively stablewith an average daily intake of 30.9 gin 2001-2002 vs 28.7 g in 2009-2010.No differences in MUFA intakecurrently exist between sex, race, andincome. Global consumption of MUFAis variable but approximates intake inthe United States.94

MUFA RecommendationsMUFA intake recommendations byauthoritative bodies exist as generalguidelines. There is no AMDR forMUFAs. Although the DGA do notrecommend a specific amount of MUFAto consume each day, they do recom-mend replacing solid fats with oils richin PUFAs and MUFAs, possibly throughadopting a Mediterranean dietarypattern.5 Similarly, the AHA’s 2006 Dietand Lifestyle Recommendations forcardiovascular disease (CVD) riskreduction in the general populationstated PUFAs and MUFAs shouldreplace animal fats in the diet, with atotal fat intake of 25% to 35% of energyintake.3 To date, the most specificrecommendation for MUFAs hasbeen the Adult Treatment Panel III(2004) recommendation, which statesup to 20% of energy intake as MUFA,thereby comprising a majority of therecommended 25% to 35% of total fatintake.4 No specific recommendationsexist for MUFA intake with regard tocancer or diabetes prevention.Most US authoritative bodies have

not provided percentage intake rec-ommendations for MUFA; instead,appropriate consumption levels needto be extrapolated from the quantity offat remaining from total fat intakerecommendations after PUFA and SFArecommendations are met. Indeed, arecent FAO report indicated that MUFAintake be calculated by difference (To-tal fat [%E]�SFA [%E]�PUFA [%E]�TFA[%E]).6 This quantity determinedthrough calculation by difference

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allows for up to 15% to 20% of totalenergy. While considering intake rec-ommendations for total fat and fattyacids (discussed in their respectivesections), one can extrapolate thatMUFAs can comprise 9% to 29% of en-ergy in our diet, assuming currentintake levels of saturated and trans fat.For example, assuming no change fromcurrent consumption of saturated andtrans fat (approximately 12% com-bined), then MUFA intake should notbe more than 17% of energy in order toavoid consumption above intake rec-ommendations for total fat. This isimportant, as excess consumption ofenergy-dense nutrients, such as fattyacids, can lead to weight gain and,depending on type of fatty acid, bedetrimental to health. Based oncurrently available information, con-sumption of MUFA at a moderate level(15% to 20%) to account for appropriatePUFA intake, while keeping within 20%to 35% of energy as fat is desirable.

MUFAs and HealthAlthough current MUFA intake at 12%of energy falls within total fat recom-mendations and supports recom-mended PUFA intake, investigating theimpact of MUFA in the diet is war-ranted. This is important becausespecific intake recommendations forMUFA are limited, specific healthbenefits of MUFAs are unclear, andrecent emphasis on olive oil con-sumption by health professionals andthe media can result in increases inMUFA intake. Understanding the roleof MUFAs within the context of sub-stitutions for other macronutrients isalso important. With consumption ofoleic acid at 93% of total MUFA intake,oleic acid is the primary focus in thissection.

Oleic acid can be synthesized in vivo,so measuring serum oleic acid as amarker of health does not reflectintake. Although there is an inability toassess MUFA status, MUFA intakehas been linked to alterations inmarkers of health and disease, such asreducing LDL cholesterol, triglycerides,total cholesterol to HDL ratio, andincreasing HDL cholesterol.95 In thecontext of macronutrient replacement,oleic acid lowers total and LDL choles-terol when it replaces SFA (12:0through 16:0 SFAs).96 Comparedto carbohydrate, MUFA decreases


FROM THE ACADEMY

triglycerides, increases HDL choles-terol, and is inversely related to total-to-HDL cholesterol ratio. In addition,compared to diets with �12% MUFA,dietary regimens with high amounts ofMUFA (>12%) resulted in lower fatmass, systolic blood pressure, and dia-stolic blood pressure.97

Despite evidence reporting healthbenefits from MUFA consumption,some recent studies have questionedthese benefits. From a pooled analysisof 11 cohort studies, Jakobsen and col-leagues reported in 2009 that PUFAsare a preferred energy source over bothMUFA and carbohydrate; the analysisdid not show that MUFA provided car-dioprotection.98 In addition, whencoronary mortality was assessed over30 years, serum MUFA levels werepositively associated with coronarydeath.99 In contrast, however, there is alarge body of evidence reporting healthbenefits from consuming a Mediterra-nean diet (ie, a dietary pattern thatincludes olive oil at approximately 20%of energy intake).100-102 Recent evi-dence also suggests benefits from oliveoil consumption for obesity, accordingto a 14-point screener for adherence tothe Mediterranean diet (PREDIMED[Prevención con Dieta Mediterránea]trial).103 The finding that, compared toa low-fat diet, a Mediterranean dietenriched with either olive oil or nutsreduced the incidence of major car-diovascular events104 supports poten-tial health benefits from olive oil; itshould be noted that although thesubjects in this study were free ofheart disease, they were at high car-diovascular risk and might not beconsidered healthy adults, whichis the focus of this article. Finally,and as recognized in the previouslymentioned PREDIMED trial,103 olive oilis only one component of the Medi-terranean diet. Because the dietarypattern also emphasizes vegetablesand fruits, n-3 fatty acid-rich foods,nuts, low-fat dairy, and moderate redwine intake, reported benefits of aMediterranean diet on CVD risk factorscannot be attributed solely to theMUFA content. Indeed, nut consump-tion has been shown to reduce totalcholesterol, LDL cholesterol, and post-prandial hyperglycemia compared tomeals high in carbohydrates.61,105

In summary, MUFA consumption canbe beneficial when replacing carbohy-drate and saturated fat, but not as


beneficial when replacing PUFAs.Although MUFA is shown to have pos-itive impact on surrogate markers, thepotential impact of MUFA intake aloneon disease outcomes, such as CVD ordiabetes, remains unclear. Further un-derstanding of the precise role ofMUFAs on health and disease whenconsumed within the context of aneating pattern (eg, Mediterranean diet)is warranted. Although most of theresearch on MUFAs has focused on riskof CVD and associated biomarkers, therelationship between MUFAs and can-cer has been investigated. The Amer-ican Cancer Society guidelines statethat olive oil is not associated with anincreased risk of cancer and likely has aneutral effect on cancer risk.106

SFAsSpecific Fatty Acids and FoodSourcesSFAs are fatty acids that are fully hy-drogenated. SFAs do not contain doublebonds between carbon atoms in thefatty acid hydrocarbon chain andtherefore have a linear chain, a struc-tural property that allows the individ-ual fatty acids to tightly pack and existat a solid state at room temperature.SFAs vary in length, but mostcommonly exist in the food supplybetween 12 and 18 carbons: lauric acid(12:0), myristic acid (14:0), palmiticacid (16:0), and stearic acid (18:0). Lesscommon in the food supply areshorter-chain SFAs, specifically caprylic(8:0) and capric (10:0). These aremedium-chain triglycerides (MCTs), inthe category of fatty acids that are 8-12carbons in length.SFAs originate primarily from animal

sources, including meats, eggs, andbutter, or from processed food prod-ucts containing naturally saturatedvegetable oils. Animal fats such asbutter, lard, and beef tallow predomi-nantly contain palmitic acid (16:0) andstearic acid (18:0) (see Table 1). Spe-cifically, food fats high in stearic acid(18:0) include beef tallow (19% of fatas 18:0) and cocoa butter (33% of fat as18:0). It should be noted that stearicacid does not negatively impact serumcholesterol levels; as a result, foodshigh in stearic acid can affect health inways different from other SFAs.107

Although the primary sources of SFAsare animal products, tropical vegetableoils such as palm and palm kernel

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oil are commonly used in processedfoods, principally because of theirphysical properties. Although palm oiland palm kernel oil both originatefrom the oil palm tree, these oils havedifferent fatty acid profiles; palm oilcontains 49% of fat as SFA (primarily16:0) and palm kernel oil contains 82%of fat as SFA (primarily 12:0). In com-parison, 87% of the fatty acids in co-conut oil (from the coconut palm) aresaturated, with 12:0 in the highestconcentration. Although coconut oil isnot commonly used in processedfoods, new food products on the mar-ket (eg, milk, spreads, yogurt) con-taining coconut oil are touting thepurported health benefits of MCTs (seesection on SFAs and Health). In addi-tion to SFA that occur naturally infoods, vegetable oils are industriallyhydrogenated (the process of addinghydrogen atoms to unsaturated bondsto create saturated bonds) to producefats that have properties ideal for foodproduction. In this process of creatingfully hydrogenated fatty acids (SFA),partially hydrogenated fatty acids(TFAs) are also produced.

SFAs from SupplementsSFAs are not commonly marketed insupplement form; MCTs are an excep-tion. MCT supplements contain pri-marily 8:0 and 10:0 fatty acids incapsule or liquid form. However, someMCT supplements are derived fromcoconut oil. More than 50% of the fattyacids in coconut oil are MCTs (58.7% are6 to 12 carbons in length) and due tothis are marketed as having health-promoting properties. It is importantto note that supplemental MCT oil isused for medical nutrition therapyin patients who lack the ability toproperly metabolize longer-chainlipids. Although the MCT oil used forpatient care often originates from co-conut or palm oil and might containprimarily 12:0 (rather than 8:0 or 10:0)as its fatty acid source, individuals witha medical indication for MCTs differfrom the needs of the healthy individ-ual. Caution should be taken whenconsidering MCT supplements as theimpact of the different MCT fatty acidson human health are not fully eluci-dated and many over-the-countersupplements do not identify whichfatty acids they contain (see section onSFAs and Health).


FROM THE ACADEMY

Current Dietary Intake of SFAsOn average, both men and womenconsume 11% of energy from SFAs; thisis higher than the recommendationfrom most authoritative bodies toconsume <10% of energy as SFA.10 Nodifferences in saturated fat intake existbased on race/ethnicity (range of 10.0%to 11.3% of intake) or income. The ma-jority of saturated fat consumed is frompalmitic acid (16:0) and then stearicacid (18:0) (54% and 25% of saturatedfat intake, respectively).10 Food sourcesof SFA in the American diet, listed asgreatest to least, are cheese, pizza,grain-based desserts, and dairy-baseddesserts; together these foodscomprise 31% of SFA intake.5 Moststearic acid is consumed from grain-based desserts, cheese, and variousmeats.2 From a global perspective,saturated fat intake (based on foodavailability) varies by continent andcountry, with lower intakes in Asia(3.1% to 10.6% of kilocalories) to higherintakes in Europe (8.9% to 16.5%). Withthe diversifying population of theUnited States, identification of globalSFA intake and the specific food sour-ces is important.94 Finally, because en-ergy intake is often greater than energyneed, evaluating SFA intake solely as apercentage, rather gram quantities,provides a somewhat limited view.

SFA RecommendationsNo current AI or RDA exist, in partbecause SFA is synthesized in the bodyto meet physiological needs andbecause of the recognized role of SFA inCVD.9 The AMDR states that SFA shouldbe as low as possible while consuminga nutritionally adequate diet. The DGArecommend that <10% of calories comefrom saturated fat and should bereplaced with MUFA and PUFA; <7%SFA intake was suggested for furtherreduction of CVD risk.5 The guidelinesalso recommend limiting foods thatcontain solid fats (SFA and TFA), sugars,and sodium; this is especially impor-tant as these foods comprise 19% oftotal energy intake.The AHA’s Diet and Lifestyle Recom-

mendations (2006) recommendedSFA intake be <7% of calories (approx-imately 16 g based on a 2,000 kcal diet)for the general population for CVD riskreduction.3 In addition, the AHA andAmerican College of Cardiology re-cently released a report indicating a


dietary pattern that achieves 5% to 6%of calories from saturated fat best forthose that want to achieve lipidlowering.108 In 2010, the FAO reportedthat SFA intake should be no morethan 10% of energy and replaced withPUFAs.6 Although the American Dia-betes Association has a recent positionon fat in diabetes management, norecommendations exist for SFA in pri-mary prevention of either diabetes orcancer. A current American Cancer So-ciety guideline, however, recommendslimiting consumption of red and pro-cessed meats, recognizing their role asmajor contributors to total and satu-rated fat intake. Based on recent liter-ature and consensus, the goal forSFA intake for the population shouldbe 7% to 10% of total energy. The cur-rent intake of SFA at 11% exceedsthe amount recommended for healthyindividuals.

SFAs and HealthThe linear structure of SFA and itsability to tightly pack in cell mem-branes, along with its signaling prop-erties, have consequences oftenconsidered detrimental to health. Aswith the other fatty acid groups, indi-vidual SFAs have differing impacts onhealth. The SFAs 12:0, 14:0, and 16:0have similar effects on serum lipopro-teins; specifically, they increase LDLcholesterol.15 In contrast, stearic acid(18:0) has a neutral impact on LDLcholesterol.107 However, because stea-ric acid is consumed in foods thatshould otherwise be limited (eg, grain-based desserts, cheese, processedmeat), it is prudent to make the sameintake recommendations for stearicacid as the other SFAs. When evalu-ating the impact of replacing SFA withcarbohydrates on CVD risk, SFA in-creases LDL cholesterol but lowers tri-glycerides and raises HDL cholesterol,and apolipoprotein B is not changed.Inclusion of 12:0, 14:0, or 16:0 in-creases LDL cholesterol and HDLcholesterol when replacing carbohy-drate at 5% of the diet; however, arecent pooled analysis of large cohortstudies indicate there is a significantlygreater relative risk for CHD with car-bohydrate intake vs SFA intake.98

When stearic acid is replaced by car-bohydrate, there is a nonsignificantchange in these CVD risk factors.95 Inaddition, replacing SFA with PUFA

JOURNAL OF THE ACAD

lowers CVD risk by approximately 10%(5% energy substitution).109 There islimited evidence about any impact ofsaturated fat on inflammation. Despitedocumented influence of saturated faton surrogate disease markers, the ef-fect of saturated fat intake on diseaseend points is not clear. A recent sys-tematic review reported insufficientevidence to link saturated fat intakewith CHD.110 Several studies showthat reducing fat consumption, espe-cially saturated fat, can reduce riskfor diabetes with improvements inweight111,112; however, this is not sup-ported by other trials.

Although known to be an importantcomponent of breast milk, MCTs aregaining in popularity among healthyadults. Unlike longer chain SFAs, MCTsare transported in portal circulationand more readily oxidized through theb-oxidation pathway. That these fattyacids are oxidized rather than stored astriglyceride in the body could be ad-vantageous. The oxidation rate ofMCTs, as well as their impact on ther-mogenesis, has been shown to bebeneficial in decreasing adiposity andimproving weight loss when comparedto olive oil.113,114 However, these resultswere from supplementation with oilcontaining 8:0 and 10:0 and not 12:0fatty acids. New food products con-taining coconut oil and other palm oils(eg, milk, spreads, yogurt) are toutinghealth benefits of MCTs. Given that 44%of coconut oil is 12:0 and 16% is 14:0,and these fatty acids are hypercholes-terolemic, consumption of coconutproducts is not currently recom-mended.115 There is, however, cause tofocus on the impact of differentMCT fatty acids in human health. Asresearch is completed, the Academywill disseminate findings to RDNs withappropriate recommendations.

Dietary patterns that are high insaturated fat include the Western di-etary pattern, characterized as high intotal fat, saturated and trans fat, refinedcarbohydrate, and sodium. Althoughdistinguished in part by its saturatedfat content, saturated fat is only onecomponent of the Western dietarypattern. The saturated fat content ofred meat can contribute to disease risk,but other components such as iron,sodium, and compounds created whencooking red meat can also contribute.Compared to red meat, consumptionof fish, poultry, dairy products, and


FROM THE ACADEMY

nuts is associated with a lower riskof CHD when the same servings areconsumed.116 Although this riskreduction could be due to a reductionin heme iron, sodium, or saturated fat,or an increase in PUFA, examiningwhole foods rather than individualcomponents is important. In addition,although evidence on the impact ofSFAs on disease end points such asheart disease, diabetes, and cancer ismixed, replacing of SFA with PUFAinstead of refined carbohydrate appearsto be beneficial. Finally, decreasing SFAwithout caloric replacement is aneffective strategy for reducing total en-ergy content of the diet and promotinghealthy body weight.

TFAsSpecific Fatty Acids and FoodSourcesPartial hydrogenation results in theformation of a large number of posi-tional and geometric isomers of thenaturally occurring cis-fatty acids. Amajor TFA in industrially hydrogenatedoils is elaidic acid (18:1, t9), althoughmany other trans isomers are formed.TFA are present in ruminant meatand milk fats as a result of bio-hydrogenation of unsaturated fattyacids (18:2 and 18:3) in the rumen. Themajor TFA in ruminant meat and dairyproducts are c9,t11-CLA, with vaccenicacid (18:1, t11), predominating at 50%to 80% of total ruminant TFA (rTFA)produced. Recent efforts to increasec9,t11-CLA content in ruminants hasincreased the presence of rTFA in bothmeat and dairy products.117 As previ-ously stated, CLA is classified as an n-6fatty acid and not a TFA and, therefore,will not be discussed here. Sources ofcommercially partially hydrogenatedTFA include hydrogenated vegetableand marine oils; these oils have beencommonly used in commercial bakedgoods. Although the TFA content infoods has decreased recently (throughfood reformulation), it is important tomonitor the type of fat used to replaceTFA, as it might be SFA.An FDA labeling requirement that

went into effect in 2006 required foodlabels to list TFA on their NutritionFacts panel (on a separate line underthe saturated fat listing) when presentat 0.5 g or more per serving. Dietarysupplements were also required to listTFA in the Supplement Facts panel. If


the TFA content is <0.5 g per serving,then TFA does not need to be listed.Consumption of foods that contain TFAbut at <0.5 g per serving contribute tooverall TFA intake, so foods commonlycontaining TFA should continue tobe limited (eg, commercial pastries,cookies, fast food). In addition, the FDAhas recently issued a Federal Registernotice preliminarily determining thattrans fats (partially hydrogenated oils)are no longer “generally recognized assafe,” or GRAS. RDNs should monitorthe determination of the FDA regardingGRAS status of trans fats and what thismeans to the availability of trans fats tothe consumer.

TFA from SupplementsNo TFA supplements currently exist, astheir negative health impacts arewidely known. However, this excludesCLA, considered a TFA, as the cis-9,trans-11 CLA isomers contain a transbond at cis-11. Although nutritionalsupplements in liquid or powder formcan contain trans fats, and must declareit on the label if �0.5 g per serving, themajority of the products do not containappreciable quantities.

Current Dietary Intake of TFAsRecent intake data estimates that TFAintake is 3 to 4 g/day in North America;intake is similar in northern Europeancountries and less in eastern Asiancountries (<1 g/day). This is a reductionfrom previous consumption, which wasestimated to be 10 g/day worldwide.118

Data from the European TRANSFAIRstudy indicate that in the United States,1.2 g/day of TFA originates from rumi-nants. This is comparable with othercountries, as consumption of rTFA inEurope ranges from 0.8 to 1.7 g/day.119

More recent evidence (2007) reportsthe consumption of rTFA is 20% of totalTFA intake, with most (85%) of thiscoming frommilk fat. Recent analysis ofNHANES 2003-2006 dietary data indi-cate industrially produced TFA intake at1.3 g per person per day.120 This is areduction from4.6 g per day, as stated inthe FDA ruling (2003), which estab-lished labeling requirements for TFAintake; this reflects a reduction ofTFAs in processed foods. TFA intakeis declining; a recent comparisonusing NHANES data indicated a 58%decrease in serumTFA levels from2000-2009.121

ION AND DIETETICS

TFA RecommendationsThe 2005 Daily Reference Intake hasnot set an AI or RDA for TFAs. No upperlimit is set, as any TFA intake increasesCHD risk; in light of this, intake of TFAshould be kept as low as possible.9 TheDGA also recommend TFA consump-tion to be as low as possible, especiallyby limiting foods that contain syntheticsources of TFA, such as partially hy-drogenated oils, and by limiting othersolid fats.5 The AHA’s Diet and LifestyleRecommendations advocate that TFAbe <1% of calories.3 In 2008, the FAO/World Health Organization recom-mended a TFA upper limit (both rumi-nant and industrially produced) to be<1% of energy; a 2010 reportacknowledged that the <1% recom-mendation might need to be revisiteddue to unknown distribution of intakeand potential negative impact on sub-groups with higher consumption.6

TFAs and HealthThe impact of TFA intake is generallyundisputed. There is convincing evi-dence that consumption of commercialpartially hydrogenated vegetable oilsincreases CHD risk factors, as well as inmetabolic syndrome and diabetes risk.For example, trans-C18:1 increasedserum levels of lipoprotein(a), anatherogenic protein associated withapolipoprotein B�containing lipopro-teins; as this is the most commonlyconsumed TFA, this finding may beimportant with regard to risk of diseasein healthy individuals.122 Limitedresearch has examined the differentimpacts of industrially produced TFAand rTFA on CHD risk. The amount ofTFA is also relevant when consideringthe impact on disease risk markers. At3.7% of energy, both ruminant and in-dustrial TFA have been shown to haveadverse effects on blood lipids, specif-ically increases in LDL cholesterol anddecreases in HDL cholesterol. However,when examined at lower doses (1.5% ofenergy from rTFA or 0.8% total TFA), nosignificant differences in blood lipids orlipoproteins were seen.123 A relation-ship between trans fats and cancer hasnot been determined.106 In summary,foods containing industrially derivedTFA should be minimized. Due torecent changes in commercial foodcomposition, there is less TFA in foods.Nonetheless, consumers should becognizant of potential TFA in processed


FROM THE ACADEMY

foods and limit fast food in the diet inorder to reduce TFA intake, ideally to<1% of energy. Replacing TFA withother fatty acids or carbohydrate is animprovement, but replacing TFA withPUFA is most beneficial for health.

Emerging Population ResearchNutrition research is the basis forongoing revisions in dietary recom-mendations. Large and long-term in-vestigations into the impact of specificfatty acid groups on public health areemerging. In a recent study, associa-tions between type of dietary fatintake—PUFA, MUFA and SFA—and CHDrisk were assessed using data from 11American and European cohort studiesto address the question of the bestmacronutrient substitution for SFA inthe diet. From follow-up data over 4 to10 years including 344,696 persons,researchers identified that replacingSFA with PUFA was preferable to MUFAand carbohydrate for reducing CHDrisk; a 5% decrease in SFA that wasreplaced with PUFA showed an inverseand significant relationship withCHD.98 The EPIC (European ProspectiveInvestigation of Cancer)-Norfolk studyinvolving 25,639 individuals reportedblood levels of SFA were positivelyassociated with CHD risk, while an in-verse association was seen with PUFAlevels.11 In addition, a 2012 study froma prospective cohort among 91,981women in the Nurses’ Health Studyreported that consumption of PUFAs asa proportion of fat was inversely asso-ciated with risk of sudden cardiacdeath, independent of traditional CHDrisk factors.12 Together, these datasupport dietary guidelines to replaceintake of SFAs with n-3 and n-6 PUFAs.American and international health

and government organizations agreewith recommendations to consume7% to 10% of total calories as SFAand restrict consumption of transfat. The optimal intake of MUFA is un-determined, and the optimal amount ofn-3 and n-6 fats to consume within thePUFA category also remains unan-swered. Many but not all fats and oilsthat contain n-6 fatty acids also containsome plant-based n-3s. Physiologicaldifferences between plant-basedand marine-source n-3s exist andexperts agree that increasing intakeof n-3 is warranted. An upper intakelevel of 2% energy as n-3 and 10%


energy as n-6 is recommended, but itmight also be time to review theserecommendations.124,125

Role of the RDN and DTR TeamFat is a valuable macronutrient in hu-man health. RDNs and DTRs, under thesupervision of the RDN, can help cli-ents set and maintain realistic goals forintake of total fat and fatty acids,thereby influencing lifelong health andweight. This requires providing guid-ance on the quantity and quality ofdietary fat in addition to meal planningand food preparation. The guidingphilosophy is to encourage food-basedconsumption first and supplementssecond. Monitoring total fat is impor-tant because it is abundant in the dietand contributes to excessive energyintake; however, it aids absorption offat-soluble nutrients and providesdesirable cooking and sensory quali-ties. Monitoring type of fatty acid isimportant because they each havedifferent biological effects in the bodyand some are essential in humannutrition. Recommendations for spe-cific foods (eg, avocados) or fatty acids(eg, more n-3) might be more practicalthan general statements. The conceptof caloric density is relevant becausefat contains 9 calories per gram, morethan double the calories per gram ofprotein and carbohydrates. Replacingfat with less calorically dense foodsor without caloric replacement,within the context of adequatenutrition, are effective strategies forlimiting excess energy intake; helpingpatients make appropriate sub-stitutions is equally important. Under-standing, for example, that individualswho consume fried fish tend toconsume higher amounts of SFA andTFA is useful when offering guidance.47

Providing clients with helpful tools andresources, for example, how to choosesnack foods with less SFA or fish thatis recommended by environmentalorganizations, will support ongoinghealthful choices. Teaching consumershow to understand and apply NutritionFacts labels and ingredient lists haslasting results.In addition to current knowledge, in-

formation on how fatty acids influencehealth through gene expression isforthcoming. Forexample, both the typeand amount of PUFA influence peroxi-some proliferator-activated receptor

JOURNAL OF THE ACAD

activity and its regulation of lipidmetabolism, including lipogenesis,oxidation, and transport.126 In addi-tion, research on how an individual’sgenetic variation influences fatty acidutilization is underway; this workwill provide rationale and directionfor future individualized dietary pre-scriptions. For example, individualscarrying >2 signal transducer andactivator of transcription 3 (STAT3)risk alleles have increased risk ofobesity with a SFA intake of >15.5%of energy, compared with those with�1 risk allele.127 Knowledge gained inthis area of research will enable RDNsto customize diets for optimal healthoutcomes.

Nutrition science has moved beyondfat as a macronutrient; a commandingknowledge of food sources and healthimpact of individual fatty acids is avital piece of RDN training andcontinuing education. It is essentialthat RDNs understand the currentliterature on dietary fat and fatty acidsand build knowledge as science ex-pands. Translating fat and fatty acidliterature into dietary recommenda-tions is a complex process yet highlysuited for the skills and trainingofRDNs.New technologies are changing thetypes of fatty acids in the food supply:new sources of fatty acids are beingdiscovered, structural changes withinthe fatty acids and how they are posi-tioned within the triglyceride moleculeare being made, and genetically engi-neered fatty acids are being incorpo-rated into new foods. As modified fattyacids and their sources become avail-able, RDNs will be called on to pro-vide leadership and guidance in areaswhere the science is still emerging.

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of Canada. Position of the American Di-etetic Association and Dietitians of Can-ada: Dietary fatty acids. J Am Diet Assoc.2007;107(9):1599-1611.

2. National Cancer Institute. Sources ofsaturated fat, stearic acid, & cholesterolraising fat among the US population,2005e06. Risk Factor Monitoring andMethods website. http://riskfactor.cancer.gov/diet/foodsources/sat_fat/. Updated2010. Accessed August 2012.

3. American Heart Association NutritionCommittee, Lichtenstein AH, Appel LJ,et al. Diet and lifestyle recommenda-tions revision 2006: A scientific state-ment from the American HeartAssociation nutrition committee. Circu-lation. 2006;114(1):82-96.


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4. National Cholesterol Education Program(NCEP) Expert Panel on Detection, Eval-uation, and Treatment of High BloodCholesterol in Adults (Adult TreatmentPanel III). Third report of the NationalCholesterol Education Program (NCEP)Expert Panel on Detection, Evaluation,and Treatment of High Blood Cholesterolin Adults (Adult Treatment Panel III)final report. Circulation. 2002;106(25):3143-3421.

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7. The nomenclature of lipids (recommen-dations, 1976) IUPAC-IUB Commissionon Biochemical Nomenclature. BiochemJ. 1978;171(1):21-35.

8. RatnayakeWM, Galli C. Fat and fatty acidterminology, methods of analysis andfat digestion and metabolism: A back-ground review paper. Ann Nutr Metab.2009;55(1-3):8-43.

9. Food and Nutrition Board Institute ofMedicine. Dietary Reference Intakes forEnergy, Carbohydrate, Fiber, Fat, FattyAcids, Cholesterol, Protein, and AminoAcids. Dietary Fats: Total Fat and FattyAcids. Washington, DC: National Acade-mies Press; 2005:422-541.

10. US Department of Agriculture, AgriculturalResearch Service. Nutrient intakes fromfood: Mean amounts consumed per indi-vidual, by gender and age, what we eat inAmerica, NHANES 2009-2010. http://www.ars.usda.gov/ba/bhnrc/fsrg. Updated2012. Accessed September 4, 2012.

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15. Nicolosi RJ. Dietary fat saturation effectson low-density-lipoprotein concentra-tions and metabolism in various animalmodels. Am J Clin Nutr. 1997;65(5suppl):1617S-1627S.

16. Center for Food Safety and AppliedNutrition, Office of Food Additive Safety.Agency response letter GRAS notice no.GRN 000283. September 4, 2009.

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18. Sinclair AJ, Attar-Bashi NM, Li D. What isthe role of alpha-linolenic acid formammals? Lipids. 2002;37(12):1113-1123.

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21. Simopoulos AP. Genetic variants in themetabolism of omega-6 and omega-3fatty acids: Their role in the determina-tion of nutritional requirements andchronic disease risk. Exp Biol Med (May-wood). 2010;235(7):785-795.

22. WelchAA, Shakya-ShresthaS, LentjesMA,Wareham NJ, Khaw KT. Dietary intakeand status of n-3 polyunsaturated fattyacids in a population of fish-eating andnon-fish-eatingmeat-eaters, vegetarians,and vegans and the product-precursorratio [corrected] of alpha-linolenic acidto long-chain n-3 polyunsaturated fattyacids: Results from the EPIC-Norfolkcohort. Am J Clin Nutr. 2010;92(5):1040-1051.

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26. Lemke SL, Vicini JL, Su H, et al. Dietaryintake of stearidonic acid-enriched soy-bean oil increases the omega-3 index:Randomized, double-blind clinical studyof efficacy and safety. Am J Clin Nutr.2010;92(4):766-775.

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28. Gibson RA, Neumann MA, Lien EL,Boyd KA, Tu WC. Docosahexaenoic acidsynthesis from alpha-linolenic acid isinhibited by diets high in polyunsaturatedfatty acids. Prostaglandins Leukot EssentFatty Acids. 2013;88:139-146.

29. Calder PC. N-3 polyunsaturated fattyacids, inflammation, and inflammatorydiseases. Am J Clin Nutr. 2006;83(6suppl):1505S-1519S.

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33. Kris-Etherton PM, Harris WS, Appel LJ;AHA Nutrition Committee. AmericanHeart Association. Omega-3 fatty acidsand cardiovascular disease: New rec-ommendations from the American HeartAssociation. Arterioscler Thromb VascBiol. 2003;23(2):151-152.

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FROM THE ACADEMY

This Academy of Nutrition and Dietetics position was adopted by the House of Delegates Leadership Team on April 16, 2007 and December 18,2008. This position is in effect until December 31, 2017. Requests to use portions of the position or republish in its entirety must be directed tothe Academy at [email protected].

Authors: Gretchen Vannice, MS, RDN (Consultant, Santa Cruz, CA); Heather Rasmussen, PhD, RD (Rush University Medical Center, Chicago, IL).

Reviewers: Research dietetic practice group (DPG) (Elizabeth Droke, PhD, RD, LN, South Dakota State University, Brookings, SD); Public Health/Community Nutrition DPG (Lori A. Kaley, MS, MSB, RD, LD, SA Sutherland Group, Hanover, NH); Quality Management Committee (Barbara Kamp,MS, RD, Johnson and Wales University, North Miami, FL); Mary Pat Raimondi, MS, RD (Academy Policy Initiatives & Advocacy, Washington, DC);Dietitians in Integrative and Functional Medicine DPG (Elizabeth Redmond, PhD, MMSc, RDN, Genova Diagnostic, Atlanta, GA); Paula Ritter-Gooder, PhD, RDN, CSG, LMNT (University of Nebraska, Lincoln, NE); Ahlam B. El Shikieri, PhD, MBA (Taibah University, Al Madinah, Al Muna-warah, Saudi Arabia); Martha Valverde, PhD, RD, LDN (Mansfield University, Mansfield, PA).

Academy Positions Committee Workgroup: Connie B. Diekman, MEd, RD, LD, FADA (chair); Andrea Hutchins, PhD, RD; Kimberly B. Heidal, PhD, MHS,RD, LDN (content advisor).

We thank the reviewers for their many constructive comments and suggestions. The reviewers were not asked to endorse this position or thesupporting paper.

January 2014 Volume 114 Number 1 JOURNAL OF THE ACADEMY OF NUTRITION AND DIETETICS 153

mailto:[email protected]

dietary fatty acids for healthy adults

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