Position of the American Dietetic Association and Dietitians of Canada: Dietary Fatty Acids

tia ie

ABItetetiaforvidphacicreacifoothethafruleg(iedafisnooiltioundofatinenfulnizthehededucreintheaotameheapopJ A1599-1611.

POIttetCa

poofinfatpoAmetibafatdiewhteifatfatgetna

RulatreThsisin(SFan35accaninplewibopromaompocreacichnic acid (ALA), and increasing con-sumption of fish, particularly fatty

total fat, SFA, TFA, monounsatu-rated fatty acids (MUFA), and n-6and n-3 PUFA for healthy individu-als. The endpoints used to determine

oncauetaimcuvaassmesivlatinfldopotioR

aneathebrispeeaproemtioEva ucluingagIn(DNugu

FATFaetaFawhch(SFA), one double bond (MUFA), ormore than one double bond (PUFA),

from the methyl terminus of the fattyacid as n-6 or n-3 fatty acids. MUFAfound in the diet are largely n-9 fattyacids, with small amounts of n-7 fatty0002-8223/07/10709-0016$32.00/0d

2risks and benefits are based largely acids. The Figure presents the struc-oi: 10.1016/j.jada.2007.07.024

007 by the American Dietetic Association Journal of the AMERICAN DIETETIC ASSOCIATION 1599SITION STATEMENTis the position of the American Die-ic Association and the Dietitians ofnada that dietary fat for the adult

fish. This paper evaluates the evi-dence of benefits and adverse effects(or lack thereof) of dietary fatty acidsto issue dietary recommendations for

and the configuration of the doublebonds (cis or trans). In addition,PUFA are further classified based onthe position of the first double bondfrom thPosition of the

Dieti

STRACTis the position of the American Di-tic Association (ADA) and Dieti-ns of Canada (DC) that dietary fatthe adult population should pro-e 20% to 35% of energy and em-asize a reduction in saturated fattyds and trans-fatty acids and an in-ase in n-3 polyunsaturated fattyds. ADA and DC recommend ad-based approach for achievingse fatty acid recommendations;t is, a dietary pattern high inits and vegetables, whole grains,umes, nuts and seeds, lean protein, lean meats, poultry, and low-fatiry products), fish (especially fattyh high in n-3 fatty acids), and use ofnhydrogenated margarines ands. Implicit to these recommenda-ns for dietary fatty acids is thatsaturated fatty acids are the pre-minant fat source in the diet. Thesety acid recommendations are madethe context of a diet consistent withergy needs (ie, to promote a health-body weight). ADA and DC recog-e that scientific knowledge abouteffects of dietary fats on human

alth is incomplete and take a pru-nt approach in recommending a re-ction in those fatty acids that in-ase risk of disease, while promotingake of those fatty acids that benefitlth. Registered dietitians play a piv-l role in translating dietary recom-ndations for fat and fatty acids intolthful dietary patterns for differentulation groups.m Diet Assoc. 2007;107:e assocAmerican Dieteticns of Canada: D

pulation should provide 20% to 35%energy and emphasize a reductionsaturated fatty acids and trans-ty acids, and an increase in n-3lyunsaturated fatty acids. Theerican Dietetic Association and Di-tians of Canada recommend a food-sed approach for achieving thesety acid recommendations; that is, at high in fruits and vegetables,ole grains, legumes, nuts, lean pro-n (ie, lean meats, poultry, and low-dairy products), fish (especially

ty fish high in n-3 fatty acids), to-her with the use of nonhydroge-ted margarines and oils.

ecommendations for the intakeof dietary fat and fatty acidshave been made for healthy pop-

tions as well as for prevention andatment of chronic disease (1-12).e guidance issued generally is con-tent in recommending a decreasethe intake of saturated fatty acidsA) and trans-fatty acids (TFA),d in recommending 20% or 25% to% of energy from fat. This can beomplished by a reduction in SFAd TFA, which results in a decreaseenergy intake, or by partial or com-te replacement of SFA and TFAth unsaturated fatty acids and car-hydrates or to a lesser extent withtein within the recommendationsde for macronutrients. Recent rec-mendations also recognize the im-rtance of n-3 fatty acids. An in-ase in n-3 polyunsaturated fattyds (PUFA) can be attained byoosing fats and oils high in -linole-iationADA REPORTSAssociation andtary Fatty Acidslipid and lipoprotein responses be-se they respond to changes in di-ry fatty acids and because they areportant risk factors for cardiovas-lar disease (CVD). Moreover, ele-ted biomarkers of inflammation areociated with CVD and numeroustabolic disorders that are respon-e to dietary fat (13). Research re-ing the role of dietary fatty acids toammatory and immune disorderses not suggest that among healthypulations, different recommenda-ns are needed for fat and fatty acid.ecommendations for dietary fat

d fatty acids for treatment of dis-se or clinical practice are outsidescope of this paper. However, a

ef discussion of the relationship ofcific fatty acids to different dis-ses/conditions is provided when ap-priate. For those with hyperlipid-ia, the American Dietetic Associa-ns (ADAs) updated Hyperlipidemiaidence Analysis Library (14) providesseful Guide for Practice, which in-des recommendations for modify-dietary fatty acid intakes for man-

ing hyperlipidemia/dyslipidemia.addition, Dietitians of Canadas

Cs) Practice-based Evidence intrition service provides practiceidance (15).

S IN THE FOOD SUPPLYtty acids are the major form of di-ry fat (mainly as triglycerides).tty acids are classified based onether or not the fatty acid carbonain contains no double bonds

turlogsouthethenuS

amvegucSFandosteoiloil

F

SL l a

ic fMPS cho

Mc

enreary

tr

Pn

n

Figlipo

ADA REPORTS

160e of different fatty acids, their bio-ical actions, and common foodrces. Humans are unable to syn-size n-6 or n-3 fatty acids, thusse fatty acids are essential dietarytrients.FA are present in relatively highounts in animal fats and tropicaletable oils. Meat and dairy prod-ts contribute approximately 60% ofA in the diet in the United Statesd Canada. Animal fats contain pre-minantly palmitic acid (16:0) andaric acid (18:0). Tropical vegetables, such as palm kernel and coconut

atty acid classification Structure

aturated fatty acidsauric acid C12:0yristic acid C14:0almitic acid C16:0tearic acid C18:0

onounsaturated fatty acidsis-configurationPalmitoleic acid C16:1Oleic acid C18:1

ans-configurationElaidic acid C18:1

Vaccenic acid C18:1

olyunsaturated fatty acids-6 fatty acidsLinoleic acid C18:2

Arachidonic acid C20:4

Conjugated linoleic acid C18:2 (vari

-3 fatty acids-linolenic acid C18:3

Eicosapentaenoic acid C20:5Docosapenteonoic acid C22:5Docosahexaenoic acid C22:6

ure. Fatty acids in the food supplystrucprotein.s, contain high amounts of lauric res

0 September 2007 Volume 107 Number 9d myristic acid. SFA are formed byustrial hydrogenation (addition ofdrogen atoms to unsaturated bondsating saturated bonds) of vegeta-oils. Fully hydrogenated fats areh in stearic acid.artial hydrogenation results information of a large number of

sitional and geometric isomers ofnaturally occurring cis-fatty ac-

. A major TFA in industrially hy-genated oils is elaidic acid (t9-18:although many other trans-

mers are formed. TFA are presentruminant meat and milk fats as a

Biological actions

Raises total, LDLa, and HDLb cholesteroincreases some hemostatic/thrombotthat promote thrombosis

Does not increase total, LDL, and HDL

Decreases total and LDL cholesterol whsubstituted for saturated fat and dectotal cholesterol compared with dietacarbohydrate

Raises total and LDL cholesterol similasaturated fat, decreases HDL vs satuand raises the total-to-HDL ratio mosaturated fat; induces systemic inflaand endothelial dysfunction

Not established

Decreases total and LDL cholesterol

Precursor for eicosanoids (prostaglandithromboxanes, leukotrienes)

) Anti-cancer properties, decreases bodygrowing animals

Decreases cardiovascular risk throughmechanisms including platelet functiinflammation endothelial cell functioncompliance, arrhythmia

Decreases risk of sudden death througmechanisms including platelet functiendothelial cell function, arterial comand arrhythmia and has beneficial enervous system development and he

, function, and common food sources. LDLult of biohydrogenation of unsat- fatated fatty acids in the rumen. Thejor TFA in ruminant meat andlk is vaccenic acid (t11-18:1), withaller amounts of other TFA.UFA are present in vegetable,

t, and seed oils, as well as in meatsd dairy products. The major dietaryFA is oleic acid (18:1n-9). Oleicd is present in high amounts inve oil, canola oil, mid-oleic sun-wer oil, and other mid- and high-ic vegetable oils, peanuts, pista-ios, almonds, and avocados. PUFAfound in vegetable, nut, and seed

s with the amounts of n-6 and n-3

Common food sources

ndactors

Coconut oilButter fat, coconut oilMost fats and oils

lesterol Most fats and oils, cocoabutter, fully hydrogenatedvegetable oils

sesSome fish oils, beef fatMost fats and oils, nuts,

seeds, avocados

ed fat,o thanation

Partially hydrogenatedvegetable oils

Butterfat, meat

Liquid vegetable oils, nuts,seeds

Meat, poultry, fish, eggs

in Butterfat, meat

tiple

rterial

Flaxseed, canola oil,soybean oil, walnuts

ultiple

ncets on

Fish oil, algaeFish oil, algaeFish oil, algae

ow-density lipoprotein; HDLhigh-densityanindhycreblehigP

thepotheidsdro1),isoin

urmamismM

nuanMUaciolifloolechareoil

r toratre smm

ns,

ants fat

mulon,, a

h mon,pliaffecalth

ture lty acids varying greatly. The major

dielin(18thehigflo3nn-3seewapreamandit(adALcucelacieican6npaereasetachjorpoC

PUcuammiCLt11onLAclafooinglabanamanexelabingingtioT

diebleThtrienalenofKeintvidfating

FATThporthawhantriAm1TFTh(AHdabe1trivenmethaDiaSFprobenulimonareenintinhigtertakT

Gumediseta0.6PUmemavidmaeqfataleinfatyeayeag/dtha(12ab0.5potha10whtio

LAdieT

thainttheconetaofristiotheCotio(21tifiomweabpeMetrianmgwodupuThcenmawhwearseracorbragtwciatio

ADAciADgrointtotiointiocabbuprotoopagendreintom

ADA REPORTStary PUFA are the 18-carbon n-6oleic acid (LA) and the n-3 ALA. LA:2n-6) is the parent fatty acid ofn-6 fatty acids and is present inh amounts in soybean, corn, saf-wer, and sunflower oils. ALA (18:-3) is the parent fatty acid of thefatty acids and is highest in flax-d, canola and soybean oils, andlnuts. -Linoleic acid (18:3n-6) issent in foods in very smallounts, except for evening primrosed borage oils. The desaturation (ad-ion of double bonds) and elongationdition of carbon atoms) of LA andA to longer carbon chain PUFA oc-rs in phytoplankton and animalls. LA is elongated to arachidonicd (ARA), and ALA is converted toosapentaenoic acid (EPA; 20:5n-3)d docosahexaenoic acid (DHA; 22:-3) animal cells. Fish and seafood,rticularly fatty fish such as mack-l, herring, salmon, tuna, and trout,well as oysters, are the richest di-ry sources of the n-3 longer carbonain PUFA, EPA, and DHA. The ma-dietary sources of ARA are meat,

ultry, and eggs.onjugated linoleic acids (CLA) areFA in which the double bonds oc-r on adjacent carbons. Smallounts of CLA are present in thelk and meat of ruminants. A majorA is cis-9, trans-11 18:2, termed c9,18:2, which has one trans- and

e cis-bond, compared to the all cis-, which is c9,c12 18:2. CLA are notssified as TFA for the purpose ofd labeling, or in regulations relat-to TFA in Canada. The trans-fateling rules in the United Statesd Canada do not differentiateong TFA from ruminant animalsd industrial hydrogenation, but dompt conjugated dienes (CLA) fromeling. Thus, all trans fats, includ-ruminant trans fats, but exclud-CLAs, are included on the Nutri-

n Facts label, regardless of origin.he fatty acid composition of commontary fats and oils are presented in Ta-1 (available at www.adajournal.org).e USDepartment of Agricultures Nu-nt Data Laboratory (16) and the Ca-dian Nutrient File (17) provide excel-t resources on the nutrient contentfoods, including fatty acids. Theep It Managed database (18) is aneractive software program that pro-es information about the n-3 and n-6ty acid content of 9,000 food serv-

s. theTY ACID RECOMMENDATIONSe Dietary Reference Intake (DRI) re-t on macronutrients recommendedt SFA and TFA be as low as possibleile consuming a diet that providesadequate intake of all essential nu-ents (12). The Dietary Guidelines forericans 2005 (9) recommended0% of calories from SFA, and thatA consumption be as low as possible.e American Heart AssociationsA) Diet and Lifestyle Recommen-

tions recommended that SFA intake7% of calories, and that TFA be% of calories (5). Likewise, the Nu-tion Recommendations and Inter-tions for Diabetes 2007 (1) recom-nd that SFA be 7% of calories andt TFA be minimized. The Canadianbetes Association recommended thatA be10% of calories and that use ofcessed foods containing SFAandTFAlimited (http://www.diabetes.ca/Files/tritional_guide_eng.pdf). The upperit of 35% calories from fat was baseddata to show that higher fat intakesassociated with a greater intake of

ergy and SFA. The lower limit for fatake was set tominimize the increaseplasma triglyceride and decrease inh-density lipoprotein (HDL) choles-ol levels that occurs with high in-es of carbohydrates.he DRI report and the Dietaryidelines for Americans 2005 recom-nd an acceptable macronutrienttribution range of 5% to 10% di-ry energy from n-6 PUFA, and% to 1.2% of energy from n-3FA, but did not set a Recom-nded Dietary Allowance or Esti-ted Average Requirement for indi-ual fatty acids. The DRI report oncronutrients (12) provided an Ad-uate Intake (AI) for n-6 and n-3ty acids, which is an intake equiv-nt to the observed median intakethe United States. The AI for n-6ty acids is 17 g/day for men 19 to 50rs, 12 g/day for women 19 to 50rs. The AI for ALA is 1.6 and 1.1ay for men and women 19 to oldern 70 years of age, respectively). These intakes are equivalent toout 5% to 6% energy from LA and% energy from ALA. The DRI re-rt on macronutrients also notedt EPA and DHA can provide up to% of total dietary n-3 fatty acids,ich is based on median consump-n patterns for these fatty acids in

United States. Mean intakes of yea

September 2007 Journal ofand ALA are about 5% and 0.5% oftary energy in Canada (19).his position paper emphasizest the AI are the observed medianakes of n-6 and n-3 fatty acids forUS population, and should not befused with the Recommended Di-ry Allowance or with those intakesfatty acids that confer the lowestk of disease. For primary preven-n of coronary heart disease (CHD),US Dietary Guidelines Advisory

mmittee (20), AHA (5,6), the Na-nal Heart Foundation of Australia), and the United Kingdom Scien-c Advisory Committee (10) all rec-mend two servings of fish perek, preferably fatty fish, providingout 450 to 500 mg EPA and DHAr day. The National Health anddical Research Council (2006) Nu-ent Reference Values for Australiad New Zealand recommend 610/day for men and 430 mg/day formen for chronic disease risk re-ction (http://www.nhmrc.gov.au/blications/synopses/_files/n35.pdf).e National Academies (22) re-tly recommended that adolescentles, adult males, and femaleso will not become pregnant, asll as adult males and females whoe at risk of CVD consume two 3-ozvings of fish per week. The reportknowledged that females who aremay become pregnant or who areeastfeeding, and children up toe 12 may benefit from consumingo 3-oz servings of seafood, espe-lly those with higher concentra-ns of EPA and DHA.

A and DC Position on Fat and FattydsA and DC concur with other expertups in recommending a dietary fatake for adults in the range of 20%35% energy, emphasizing a reduc-n of SFA and TFA, and an increasen-3 PUFA. These recommenda-ns for specific fatty acids are appli-le to children over 2 years of age,t should be followed with age-ap-priate total fat and energy intakessupport normal growth and devel-ment. For children 1 to 3 years ofe, a total fat intake of 30% to 40% ofergy is recommended, and for chil-n 4 to 18 years of age, a total fatake of 25% to 35% of energy is rec-mended. For children under 2

rs of age, cows milk, if fed, should

the AMERICAN DIETETIC ASSOCIATION 1601

betiobahigtotD

egythecanfatteiateingsurefihiganraiResucartuteriHooveoftimrean-6toevionintme4%(32OrWotoNunaFatomeR

intaromalisofdisproeicceptoThfavdisverCoredhaint

chbeityglySosanthemaalslev(28A

ceprantri1.2ALisshbleundraofextwiF

conananwemaproDHanDHbeforpleabfecnoT

inmegutallowistPrFovirthetioviswhyouswbeelscushpo

canmapetiosmThAganronmekgwhyoutiothamawisutypforM

admebyanmaEPconronpo(45giotiosocconponaB

preinfclilesbresuenfroamme(46wosu0.2ofDH

FATWhrislipplalow

ADA REPORTS

160full-fat milk. The recommenda-ns for total fat for children aresed on a gradual transition fromh-fat intakes during infancy to theal fat recommendation for adults.ecreasing SFA and TFA is a strat-for reducing the energy content ofdiet. Alternatively, SFA and TFAbe replaced with unsaturated

ty acids, and/or carbohydrate, pro-n. Replacing SFA with unsatur-d fat avoids the triglyceride-rais-effect when carbohydrates are

bstituted for SFA. Complex and un-ned carbohydrates result in aher fiber intake and can attenuate,d even prevent, the triglyceride-sing effect of low-fat diets (23-25).placing SFA with protein also re-lts in lower triglycerides than whenbohydrates are used as the substi-e (26). MUFA avoid the HDL-low-ng effects of diets high in n-6 LA.wever, uncertainty surrounds therall risk-to-benefit of high intakesMUFA vs LA; consensus on the op-al intake of LA has not beenched. The recommended range forPUFA in the United States is 5%10% of energy (7-9,12) based ondence of beneficial effects of PUFACVD and diabetes (27-31). Otherernational groups have recom-nded lower intakes of n-6 PUFA ofto 8% [European Commission

)], 5% to 8% (Food and Agricultureganization of the United Nations/rld Health Organization [11]), 3%4% [The Japan Society for Lipidtrition (33)], and 2% to 3% [Inter-tional Society for the Study oftty Acids and Lipids (34)] of energymeet essential fatty acid require-nts.ecommendations for lowering theake of n-6 PUFA have centeredund concerns that high intakesy antagonize n-3 PUFA metabo-m, contribute to an increased riskinflammatory, immune, and otherorders associated with an excessduction of n-6 fatty acidderivedosanoids, and may increase sus-tibility of tissue and plasma lipidsoxidative modification (35,36).

us, ALA, EPA, and DHA, whichorably affect risk of CVD and othereases (37), could be affected ad-sely by high n-6 fatty acid intakes.nsensus on the beneficial effect ofucing LA intakes on human healths not been reached (38). Higher LA

akes can play an important role in (w

2 September 2007 Volume 107 Number 9olesterol-lowering (39), may haveneficial effects on insulin sensitiv-(40), and may reduce plasma tri-cerides in some individuals (41).me n-6 fatty acidderived eico-oids also have important effects inresolution of inflammation and

rkers of CVD and CVD events areo lowest in individuals with highels of both n-6 and n-3 fatty acids,42).DA and DC concur with the ac-table macronutrient distributionge of the DRI report on macronu-ents (12) for ALA, which is 0.6% to% of energy. The median intake ofA in the United States and Canada0.5% energy. The intake of TFAould be reduced to as low as possi-. SFA should be replaced with cis-saturated fat or complex carbohy-tes to maintain a total fat intake20% to 35% of energy. To a limitedent, SFA calories can be replacedth protein.ish and Shellfish. ADA and DCsider that n-3 PUFA from fish areimportant part of a healthful diet,d recommend two servings perek, preferably fatty fish. Approxi-tely 8 oz of cooked fish per weekvides about 500 mg/day EPA andA. For vegans who do not consumey preformed sources of EPA andA, additional research is needed

fore recommendations can be madethese fatty acids, including sup-ments. It is important to note thesence of reported adverse health ef-ts in this population that consumesfish.he presence of some contaminantsfish, including dioxins and methylrcury, has raised concern. Federalidelines for avoiding environmen-contaminants in fish should be fol-ed (the US Food and Drug Admin-ration and the Environmentalotection Agency (43); Canadianod Inspection Agency (44)]. The En-onmental Protection Agency andUS Food and Drug Administra-

n have issued a joint consumer ad-ory for pregnant women, womeno could become pregnant andng children not to eat shark,ordfish, king mackerel, or tilefishcause of their higher mercury lev-. Up to 12 oz per week of low-mer-ry fish are recommended, such asrimp, canned light tuna, salmon,llock, and catfish. As albacore

hite) tuna has more mercury than terned light tuna, these risk groupsy eat up to 6 oz of albacore tunar week. These same recommenda-ns apply to young children, butaller portions should be served.e Canadian Food Inspectionency, different from the US Foodd Drug Administration and Envi-mental Protection Agency, recom-nds a maximum intake of 0.20 g//day for pregnant women, womeno could become pregnant, andng children. A report from the Na-nal Academies (22), which statest pregnant women or women whoy become pregnant should staythin Federal advisories for con-mption of specific fish and seafoodes, and state/regional advisorieslocally caught fish.any of the fish noted in federal

visories as containing high levels ofrcury are not commonly consumedCanadian women and children,

d other fish not noted in the reportsy contain methyl mercury. TheA and DHA content of commonlysumed fish and amounts of envi-mental contaminants has been re-rted by Mozaffarian and Rimm). Adherence with federal (and re-nal) advisories on fish consump-n will help achieve the benefits as-iated with fish and seafoodsumption without increasing ex-sure to environmental contami-nts.reast Milk. Human milk is theferred source of nutrition for allants under 6 months of age, unlessnically contraindicated. Infantss than 1 year of age who are notastfed should be fed human milkbstitutes that contain at least 4%ergy from LA and 0.75% energym ALA, which are the minimumounts of LA and ALA recom-nded in formulas for term infants), and both DHA and ARA. Formen who wish to use a humanmilkbstitute, DHA should be at least% of total fatty acids and the levelARA should not be lower thanA.

TY ACIDS AND HEALTHile many factors contribute to thek of CHD, the important lipid andoprotein risk factors includesma (or serum) total cholesterol,-density lipoprotein (LDL) choles-

ol, HDL cholesterol, triglycerides,

anterliplipmasesingmoestovecengiemeon

SFAEppotak(27shchcrelesmg53cre0.0difacihaingwhefftermythecauterSFindme

MUOlles(7,hyideinvlesstutes22suterchtha(49T

an

InaciofanlevbrecanaciginC

MUrecn-6rectheomtiograEvBloTrthariehigpaingesdie(64hu

TFAHiciarisdefatdehaofofterdecreLDTFtersmenflawhTF(74E

poallanCliMUmethu

ruthaisC

fatincangenertthapaC-g/dstrCLsitmedadustuThabdieefihigmerecpaF

rivduplewisombySFadgieSF

PUTh(AimEaLAtorityincpoCVanordtheroltheinchan-6uteWe

ADA REPORTSd the ratio of total to HDL choles-ol. Despite the significance of lipid/oprotein risk factors, many non-id factors, including inflammatoryrkers, are also important for as-sing CHD risk (47). Thus, target-multiple risk factors holds the

st promise for attaining the great-reduction in disease risk. More-r, because inflammation plays atral role in many diseases, strate-s to reduce elevated inflammatorydiators may have beneficial effectsmany other diseases.

idemiologic studies have shown asitive association between the in-e of SFA and the incidence of CHD,48,49), and clinical studies haveown that SFA raise total and LDLolesterol (40,50). For every 1% in-ase in energy from SFA, LDL cho-terol levels increase by 1.3 to 1.7/dL (0.034 to 0.044 mmol/L) (51-), and HDL cholesterol levels in-ase by 0.4 to 0.5 mg/dL (0.010 to13 mmol/L) (54). Individual SFAfer in their effects (55,56). Lauricd (12:0) and myristic acid (14:0)ve a greater total cholesterol rais-effect than palmitic acid (16:0),

ile stearic acid (18:0) has a neutralect on total, LDL, or HDL choles-ol (53,54,57). Lauric acid, but notristic or palmitic acid, decreasestotal-to-HDL cholesterol ratio be-se of an increase in HDL choles-ol (54). Foods contain mixtures ofA, thus, selecting foods based onividual SFA content is not recom-nded.

FAeic acid lowers total and LDL cho-terol when it replaces SFA8,12,58). When compared to carbo-drate, MUFA decrease triglycer-s, increase HDL cholesterol, and isersely related to total-to-HDL cho-terol ratio. A meta-analysis ofdies with individuals with diabe-showed that high-fat diets with

% to 33% energy from MUFA re-lted in lower plasma total choles-ol, verylow-density-lipoproteinolesterol, and triglyceride levelsn did low-fat, high-carbohydrate% to 60% energy) diets (59).he association between MUFA

d risk of cancer is inconsistent (60). mesome studies, food sources of oleicd were associated with a lower riskbreast cancer (61,62), but meta-alysis found that tissue oleic acidels were positively associated withast cancer (63). Because oleic acidbe synthesized in vivo, tissue oleicd is not necessarily of dietary ori-.urrent recommendations forFA were derived by consideringommendations for SFA, TFA, andand n-3 PUFA, then deriving a

ommendation for MUFA based onamount needed to obtain the rec-mended intake of total fat. Na-nal Cholesterol Education Pro-m Expert Panel on Detection,aluation, and Treatment of Highod Cholesterol in Adults (Adulteatment Panel III) recommendst MUFA not exceed 20% of calo-s. There is an increasing trend forher MUFA in many foods, due inrt to use of fats with higher MUFAplace of TFA. Some evidence sug-ts an adverse effect of high MUFAts on atherosclerosis in animals), but this has not been observed inmans.

gh intakes of TFA have been asso-ted with an increase in the relativek of coronary artery disease, CHDath rate, and risk of fatal and non-al myocardial infarction, and sud-n death (27,65-70). Clinical trialsve shown a dose-dependent effectTFA over the range of 0.5% to 10%energy in increasing LDL choles-ol levels (12). Relative to SFA, TFAcrease HDL cholesterol and in-ase the TC-to-HDL cholesterol andL-to-HDL cholesterol ratios (54).A also increases other coronary ar-y disease risk factors, such asall dense LDL, postprandial lipids,dothelial function, and systemic in-mmatory mediators (71-73), all ofich may contribute to the effect ofA on CHD mortality and morbidity,75).vidence of no relationship and a

sitive association between industri-y produced TFA and cancer (76-79)d diabetes (80) has been reported.nical studies with the major transFA (vaccenic acid) in ruminantats and milks have not been done;s, evidence to support a recom-

ndation for the intake of fat from EP

September 2007 Journal ofminant meats and dairy productst differs from those based on SFAinsufficient.LA, in ruminant meat and dairys, have unique biological effects,luding decreased fat deposition,d anticarcinogenic, antiathero-ic, and immune-modulating prop-ies (81). There is some evidencet CLA supplements (3 g/day) im-ir insulin sensitivity (82), increasereactive protein [t10,c12 CLA, 3.4ay (83)], and increase oxidativeess and insulin resistance [c9,t11A, 3 g/day (84)] in those with obe-y and metabolic syndrome. Supple-ntation with about 2 g CLA pery may reduce milk fat secretionring lactation (85), although otherdies have not confirmed this (86).ese doses are above those attain-le from usual foods; thus, whethertary CLA provides any health ben-t is not clear. Consumption ofher-fat dairy and red meats as aans to increase CLA intake is notommended because of the accom-nying increase in SFA.oods containing industrially de-ed TFA should be minimized. Re-cing TFA in some foods, for exam-, pastry that requires solid fat,thout increasing SFA is complex. Ine foods, TFA have been removedreplacement with fats higher inA. The current recommendationsvise that TFA replacement strate-s not result in a higher TFA andA (87).

FAe n-6 (LA and ARA) and the n-3LA, EPA, and DHA) fatty acids areportant in many aspects of health.rly studies focused on diets rich inin reducing plasma lipid risk fac-s and CVD morbidity and mortal-(31). More recently, there has beenreased understanding of the im-rtance of n-3 fatty acids in reducingD risk, in neurological function,d in inflammatory and immune dis-ers. ALA, EPA, and DHA differ inir metabolic and physiologicales, and the relative importance ofdifferent n-3 fatty acids remains

ompletely understood. Concerns been raised that a high dietary:n-3 fatty acid ratio may contrib-to many diseases associated withstern diets. Because the intake of

A and DHA are much lower than


foranicatheScreaofwhcreetaplaintcenvermibyinacicauachofforingALdasolacin

alsenplaan43fecPrchmafrobysimlesmuchboantotchcreto-alsmeanastiotypStutiogluCotheganuint

inshigbeT

n-6canrebanimhaanancluintofcerFothePUstocreinincfar(33relCHdifH

beoftor(10LDoxifroMUtosucreanerninenoftherentoconacctioiscrewitofavincrediebeernis

cretiothaareinfln

inaverconcia(10theintasseveanThStucrewiinffatNuthaALristhothecarsuwienlesoftie(11conofin(11M

thaprotioiesassprolenALofdeevebinpro(952.1pointInHeterfro

ADA REPORTS

160LA and ALA, increases in EPAd DHA intake that have physiolog-l effects do not substantively alterdietary n-6:n-3 fatty acid ratio.

ientific consensus has not beenched on whether current intakesLA are too high, and it is unclearether associations between an in-ased risk of disease and high di-ry n-6:n-3 fatty acid ratios are ex-ined by high n-6, low n-3 fatty acidakes, or effects of their ratio. Re-t studies have suggested that con-sion of ALA into EPA is not deter-ned by the ratio of LA to ALA, butthe absolute amounts of ALA or LAthe diet (88). Use of n-6/n-3 fattyd ratios is also problematic be-se an identical ratio can beieved with very different amountseach fatty acid class (89). There-e, because of the difficulty in apply-one ratio across diets varying inA, EPA, and DHA, the recommen-tions in this paper focus on the ab-ute intakes of n-6 and n-3 fattyds.-6 Fatty Acids. Early clinical tri-found that 13% to 21% dietary

ergy from PUFA decreased totalsma cholesterol by 13% to 15%,d decreased CHD events by 25% to%, although there was a lack of ef-t on all-cause mortality (90-92).edictive equations based onanges in blood cholesterol esti-ted that an increase of 1% energym PUFA reduces total cholesterol0.9 mg/dL (0.023 mmol/L), while ailar intake of SFA raises total cho-terol by approximately twice asch (51,52). PUFA increase HDLolesterol when substituted for car-hydrate, although less than SFAd MUFA (54). Because PUFA loweral cholesterol and increase HDLolesterol, the net effect is a de-ase in the total-to-HDL and LDL-HDL cholesterol ratios. PUFA mayo have beneficial effects on glucosetabolism and insulin resistanced, hence, on type 2 diabetes (80,93),suggested by the inverse associa-n of vegetable fat and PUFA withe 2 diabetes in the Nurses Healthdy (80) and the inverse associa-n between PUFA and fasting bloodcose levels in the Italian Ninemmunities Study (94). However,Canadian Diabetes Association

ve a D-level evidence rating to thetrition recommendation for PUFA

ake of 10% of energy because of tai

4 September 2007 Volume 107 Number 9ufficient clinical evidence thath LA has beneficial effects in dia-tes (95).he possibility that high intakes ofPUFA may increase the risk ofcer, gallstones, CHDmortality, ce-ral infarction, hyperinsulinemia,d subsequent insulin resistance, ormune and inflammatory disorderss been raised (33,35,96-99). Meta-alysis of 16 case-control studiesd seven major cohort studies con-ded that it is unlikely that a highake of LA substantially raises riskbreast, prostate, or colorectal can-(96). The Health Professionals

llow-Up Study showed that men inhighest vs lowest quintile of

FA intake had a lower risk of gall-ne formation (100). In contrast, in-ased LA intake from 1950 to 2000Japan has been associated with anreased morbidity from cerebral in-ction and ischemic heart disease,97,98). Similarly, there is a linearationship between n-6 PUFA andD mortality among populations inferent countries (101).igh intakes of n-6 PUFA have

en proposed to increase productionproinflammatory and proaggrega-y eicosanoids derived from ARA2), and increase susceptibility ofL and tissue lipids high in LA todative modification (103). LDLm subjects consuming LA-rich vsFA-rich diets is more susceptibleoxidative modification (35). Con-mption of oils high in LA has in-ased in the United States, Canada,d other countries following West-ized diets (104), with an increaseLA intakes from about 3% dietaryergy in the 1930s to current intakesabout 5% to 6% dietary energy inUnited States and Canada. Cur-t evidence does not support a needincrease LA intakes in individualssuming LA at the lower end of theeptable macronutrient distribu-n range. However, whether benefitattained by recommending a de-ase in LA intakes for individualsth intakes above the median of 5%6% energy is unclear. One positionors a decrease in the intake of LAfavor of MUFA and ALA. A de-ase in LA would also reduce thetary ratio of LA to ALA, which hasen suggested to be too high in West-diets (105). An alternate position

that current intake of LA be main-

ned, and that n-3 fatty acids in- ofased. In support of the latter posi-n, recent studies have suggestedt n-6 and n-3 fatty acids togetherassociated with the lowest level ofammation (28,42).-3 Fatty Acids. ALA, the predom-nt dietary n-3 fatty acid, is con-ted to EPA and DHA, although theversion of ALA to EPA and espe-lly to DHA is very low in humans6-110). Epidemiologic studies inUnited States reported that ALA

akes of 0.53 to 2.8 g per day wereociated with a reduced risk of CVDnts, fatal ischemic heart disease,d all-cause mortality (111-113).e Health Professionals Follow-Updy reported that a 1% energy in-ase in ALA intake was associatedth a 40% lower risk of myocardialarction, after adjustment for totalintake (69), while results from therses Health Study (114) foundt women in the lowest quintile ofA intake had a 38% to 40% lowerk of sudden cardiac death thanse in the highest two quintiles. InLyon Diet Heart Study, postmyo-dial infarction patients who con-med a Mediterranean-style dietth 0.81% energy from ALA, 8.3%ergy from SFA and 217 mg/day cho-terol had a 50% to 70% lower riskrecurrent heart disease than pa-nts consuming an AHA step 1 diet5). Recent epidemiologic studiestinue to support a beneficial effectdietary ALA on CVD, particularlythe presence of a low fish intake6).eta-analysis have raised concernt ALA may increase the risk ofstate cancer (117). Nine observa-nal studies (four prospective stud-and five nonprospective studies)essed the relationship betweenstate cancer incidence or preva-ce, and intake or blood levels ofA, and reported an increased riskprostate cancer (1.70; 95% confi-nce interval: 1.12 to 2.58). How-r, in prospective studies, the com-ed estimate of relative risk forstate cancer incidence was 1.32% confidence interval: 0.80 to8). A subsequent study also re-rted no association between ALAake and prostate cancer risk (118).addition, subjects in the Lyon Dietart Study who consumed a Medi-ranean diet with 0.8% of energym ALA did not have increased risk

prostate cancer (119). Most evi-

deALE

decrefibofstudethipaofepStaofdeiscmgofDHfatmemoassitystrfisAerapreratpotalpoE

posocanconanrecexprecevefro11suananD

sysanshfatblosevtempotioorcog(13Fr

inph47allthenitlesweinZuuaabnoW

raptiorecfathefer

PRThvelattfattiocondielacPUthrtanALbydeTFhahefrobioacinothaUnothbrasombreposuverA

DHwiTFsumehigbean

intofsinfooT

pe10ALARabinffraapme(15shdonaothcreinfbrepolevscosu(15Sturepqudremo34naerstioT

poDHunCethevelDHterwo(16twanextingwhwefislonmospiwetiocomfanoth

ADA REPORTSnce suggests no adverse effect ofA and risk of prostate cancer.PA and DHA reduce risk of sud-

n cardiac death, possibly by in-asing the threshold for ventricularrillation, which is a leading causesudden death (120,121). Recentdies in patients with implantedfibrillators, however, caution thats effect may not be present in thistient population (122). The intakeEPA and DHA from fish in fiveidemiologic studies in the Unitedtes associated with the lowest riskcoronary events, including CHDath, primary cardiac arrest, andhemic heart disease death was 496per day (123-127). A daily intakeapproximately 500 mg EPA andA is equivalent to about 8 oz ofty fish per week. Other recentta-analyses reported that five orre servings of fish per week wasociated with a lower CHD mortal-(128) and a lower incidence of

oke (129) when compared with noh or fish less than once per month.recent systematic review of the lit-ture of primary and secondaryvention studies with 1 year du-ion with fish or fish oils also re-rted reduced rates of all-cause mor-ity, cardiac and sudden death, andssibly stroke (130).pidemiologic studies have re-

rted that high fish intakes are as-iated with a reduced risk of breastd colorectal cancer (131), which issistent with evidence that EPAd DHAmay reduce markers of colo-tal cancer (60,131,132) and reduceression of genes involved in colo-tal cancer cell growth (133). How-r, a recent review of 20 cohortsm seven countries that evaluateddifferent types of cancer found nobstantial association between plantd marine-derived n-3 fatty acidsd incidence of cancer (134).HA is important in the nervoustem, including the retina. Clinicald epidemiologic studies haveown that low dietary intakes of n-3ty acids and low plasma or redod cell DHA are associated witheral neurological and visual sys-problems (135-137). Three recent

pulation studies found an associa-n between higher intakes of DHAEPA and DHA and lower risk ofnitive decline or verbal fluency8-140). Men and women in the

amingham Heart Study who were higthe top quartile of plasma phos-atidylcholine DHA levels had a% reduction in risk of developing-cause dementia (138). Likewise, inAtherosclerosis Risk in Commu-

y Study (140), higher plasma cho-teryl ester levels of EPA and DHAre associated with a lower declineverbal fluency. Similarly, in thetphen Elderly Study (139), individ-ls who consumed fish had consider-ly less 5-year cognitive decline thannconsumers.hile research in these areas isidly increasing, sufficient informa-n is as yet unavailable to suggestommendations for dietary n-3ty acids with respect to mentalalth or visual problems that are dif-ent from those based on CVD.

EGNANCY, LACTATION, AND INFANCYe importance of DHA in neural de-opment and function has focusedention on the importance of n-3ty acids during pregnancy, lacta-n, and infancy. Observational andtrolled clinical studies show thattary PUFA during pregnancy andtation influences the transfer ofFA across the placenta andough breast milk (141,142). Impor-t questions are whether dietaryA can provide sufficient amountsconversion through the elongation-saturation pathway, and whetherA from hydrogenated n-6 mayve adverse effects on the mother orr infant. An intake of 2% energym the n-6 LA prevents clinical andchemical signs of essential fattyd deficiency in infants (143), andevidence is available to suggestt LA intakes are inadequate in theited States or Canada. On theer hand, the lower blood lipid andin levels of DHA in infants fede formulas lacking DHA than inast-fed infants (144,145) raises thessibility that inadequate dietarypplies of n-3 fatty acids can ad-sely influence infant development.n inverse association of TFA withA in newborn infant blood andth growth has been reported, andA may be deposited in infant tis-es or converted to other unusualtabolites (146-148). TFA levels ash as 18% of milk fatty acids haveen reported in the United Statesd Canada (149-151), which is

her than in Europe, where dietary tio

September 2007 Journal ofakes of TFA are lower (148). LevelsTFA in human milk have decreasedce the introduction of trans-fatd labeling (148,152).he conversion of ALA to DHA ap-

ars to be very low in humans (107-9). Newborn infants can convertA to EPA and DHA, and LA toA, and there is no evidence of met-olic immaturity in this pathway inancy (106,153,154). Although thectional conversion of ALA to DHApears to be higher in women thann, and increases during pregnancy5), intervention studies haveown that increased intakes of ALAnot increase levels of DHA in preg-nt women or infants (156). On theer hand, higher maternal DHA in-ases the transfer of DHA to theant both before birth and viaast milk after birth (142,157). Asitive association between bloodels of DHA in infants and higherres on measures of neural and vi-al maturation has been reported8-162). The Avon Longitudinaldy of Parents and Children (163)orted that the verbal intelligenceotients were higher among chil-n 6 months to 8 years of age ofthers who consumed more than9 g seafood per week during preg-ncy than among children of moth-who reported no seafood consump-n.he long-term benefits of early ex-

sure to n-3 fatty acids (EPA andA) on later child development arecertain (76,164-166). The Harvardnter for Risk Analysis extrapolatedresults of studies on cognitive de-opment of infants fed formula withA to suggest that increasing ma-nal DHA intake by 100 mg/dayuld increase child IQ by 0.13 points7). However, a linear relation be-een DHA intake and IQ is unlikely,d nutrient requirements cannot berapolated from formula to lactat-women. Studies in Denmark in

ich women with low fish intakesre supplemented with 4.5 g/dayh oil (equivalent to 1.3 g/day n 3ger carbon chain PUFA) for 4nths after delivery found that de-te higher blood lipid DHA, therere no advantages to visual matura-n, but passive vocabulary and wordprehension were lower in the in-ts at 1 year of age (168,169). Iner studies, maternal supplementa-

n with 200 mg/day DHA for the


fireffbuopfanilawoeffnetivwameARbowapreing(17fisna

mebetiginfARtiaersstubeingsiotioinfanthesispreDHfanwirantiocludesivART

soumoabARrecfouARnokeARhupoefffanforDHcor

ROPRFATHEAThetiuaachpaingtioskalsset2),fer

T etetto tedb

To

S

M tota

n-

n-

n-

aTbNc2dT2DofweSfMgPhA

ADA REPORTS

160st 4 months of lactation also had noect on infant visual maturation,t psychomotor, not mental, devel-ment test scores were higher in in-ts at 30 months of age (170). Sim-rly, supplementation of pregnantmen in Norway with fish oil had noect on early measures of infantural maturation (158), but cogni-e development at 4 years of ages increased (166). Fish oil supple-ntation in pregnancy may reduceA in both mothers and their new-rn infants (171). Reduced growths reported in three studies withterm infants fed formula contain-DHA from fish oil without ARA2-175). The risks and benefits ofh oil supplementation during preg-

able 2. Recommendations by the American Dital fat (for adults) and saturated, monounsaturaased on a 2,000 calorie dietab

tal fatcd

20% of energy25% of energy30% of energy35% of energyFatty acid/fatty acid class % of energy

FAe (as low as possible)3% of energy7% of energy10% of energyUFAf (provides remaining fatty acids to meet8% of energy14% of energy20% of energy25% of energy6 PUFAg (3% to 10% of energy)3% of energy5% of energy7% of energy10% of energy3 PUFA-ALAh (0.6% to 1.2% of energy)0.6% of energy0.9% of energy1.2% of energy3 PUFAlong-chain PUFA

rans-fatty acids should be as low as possible.umbers are rounded to nearest whole number.7 g oils recommendedUS Department of Agriculture Foohe Acceptable Macronutrient Distribution Range for total fa5% to 35% of energy for children 4 to 18 years. The Acceptaietary Reference Intake is 5% to 10% energy from n-6 PUFAdeficiency, and intakes of n-6 fatty acids in the range of 3hen the intake of n-3 fatty acids is at least 0.7% energy.FAsaturated fatty acids.UFAmonounsaturated fatty acids.UFApolyunsaturated fatty acids.LA-linolenic acid.ncy and lactation, or in infants as a vis

6 September 2007 Volume 107 Number 9ans to increase infant DHA ares unclear.lthough some epidemiologic andervention studies have suggestedt higher intakes of EPA and DHAassociated with a small increase

gestational length and reduced risksome pregnancy-associated compli-ions (158,176,177), other studiesve not confirmed a benefit ongth of gestation, preeclampsia,ampsia, or gestational hyperten-n (158,171,178-181). Thus, currentdence does not support a recom-ndation to increase EPA and DHAreduce risk of preterm delivery orgnancy-associated complications.ince 1990, the impact of formulastaining DHA or DHA plus ARA on

ic Association and Dietitians of Canada for, n-6, n-3, and polyunsaturated fatty acids

Amount

44 g56 g67 g78 g

7 g16 g22 g

l fat)18 g31 g44 g56 g

7 g11 g16 g22 g

1.3 g2.0 g2.7 g500 mg

ide.30% to 40% of energy for children 1 to 3 years andacronutrient Distribution Range provided by the 2002kes of 3% energy from n-6 fatty acids prevents signs5% energy will support a n-6:n-3 ratio of about 4:1ual maturation and neurodevelop- wwnt in term and preterm infants hasen extensively studied. Some inves-ators have shown benefits in termants fed formulas with DHA andA, or DHA from birth, or after ini-l breastfeeding (182,183), but oth-have not (184). However, most

dies assessed neurodevelopmenttween 6 and 24 months, an age dur-which there is latency in expres-

n of minor neurological dysfunc-n (185). Evidence that pretermants benefit from inclusion of DHAd ARA in formula fed throughoutfirst year after birth is more con-

tent (184,186,187), and formula forterm infants now includes bothA and ARA. Formulas for term in-ts with ARA and DHA are alsodely available. One review of 6 of 10domized controlled trials of addi-n of DHA and ARA to formula con-ded no substantial effect on infantvelopment, and that more-expen-e formula with added DHA andA is not necessary (188).he preferred and recommendedrce of nutrition for infants under 6nths is human milk, and the avail-ility of infant formulas containingA and DHA does not change thisommendation. Some studies havend benefits of including DHA andA in formulas for term infants, andadverse effects of feeding mar-

ted infant formula containing bothA and DHA in amounts found inman milk are known. Because ofssible benefits and lack of adverseects, it is recommended that all in-ts who are not breastfed be fed amula containing both ARA andA through at least the first year ofrected age.

LE OF FOOD AND NUTRITIONOFESSIONALS IN IMPLEMENTINGTY ACID RECOMMENDATIONS FORLTHe special expertise of registered di-tians (RDs) is important to individ-lize dietary recommendations toieve optimal food-based dietarytterns. The complexity of translat-fat and fatty acid recommenda-

ns requires the knowledge andills of food and nutrition profession-. Once specific targets have beenfor total fat and fatty acids (Tablethen the type and amount of dif-ent fats (Table 1, available atmethuA

intthaareinofcathaleneclsioevimetopreS

con

d Gut isble M. Inta% tow.adajournal.org) to be included

togoabeguproeasuthethemealstioendieC

toingaciawresabetaFatratiothecomalsdieA

etatantopagPUcaleaingscitheetaqu

Ref1

2

3

4

5

6

7

8

9

10

11

12

13

14

16

17

18

19

20

21

22

23

24

25

26

27

28

29

ADA REPORTSmeet the total fat and fatty acidls in an energy-controlled diet candetermined. For all fatty acids, theiding philosophy is a food-based ap-ach. For individuals who do nott fish, other options may be pur-ed, such as designer foods high inse fatty acids, foods fortified withse fatty acids, or even supple-nts (189). The RDs expertise iso needed to translate recommenda-ns for fatty acids to the appropriateergy intake to achieve a healthfultary pattern.onsumers lack knowledge on howuse the Nutrition Facts labels, orredient lists to determine fattyd contents, RDs must also beare that individuals vary in theirponse to dietary fat and must bele to recommend appropriate di-ry fat changes when necessary. Myts Translator, a calculator thatnslates fat/fatty acid recommenda-ns into daily limits, is available from

AHA at www.myfatstranslator.. Implicit in this is the need too monitor adherence to food-basedtary recommendations.s RDs stay abreast of current di-ry recommendations, it is impor-t that they effectively respond toics where there is not yet scientificreement, as is the case with n-6FA. Consequently, RDs will beled upon to provide guidance in ar-s where the science is still emerg-. As always, the evolution of theence-base brings clarity and formsbasis for ongoing revisions in di-ry recommendations and conse-ent dietary patterns.

erences. American Diabetes Association. Nutritionrecommendations and interventions for di-abetes. A position statement of the Ameri-can Diabetes Association. Diabetes Care.2007;30:S48-S65.

. De Backer G, Ambrosioni E, Borch-JohnsenK, Brotons C, Cifkova R, Dallongeville J,Ebrahim S, Faergeman O, Graham I, Man-cia G, Manger Cats V, Orth-Gomer K, PerkJ, Pyorala K, Rodicio JL, Sans S, Sansoy V,Sechtem U, Silber S, Thomsen T, Wood D;Third Joint Task Force of European andOther Societies on Cardiovascular DiseasePrevention in Clinical Practice. Europeanguidelines on cardiovascular disease pre-vention in clinical practice. Third JointTask Force of European and Other Societ-ies on Cardiovascular Disease Preventionin Clinical Practice. Eur Heart J. 2003;24:1601-1610.

. Priori SG, Aliot E, Blomstrom-Lundqvist C,Bossaert L, Breithardt G, Brugada P,

Camm JA, Cappato R, Cobbe SM, Di Mario 15C, Maron BJ, McKenna WJ, Pedersen AK,Ravens U, Schwartz PJ, Trusz-Gluza M,Vardas P, Wellens HJ, Zipes DP; EuropeanSociety of Cardiology. Update of the guide-lines on sudden cardiac death of the Euro-pean Society of Cardiology. Eur Heart J.2003;24:13-15.

. Van de Werf F, Ardissino D, Betriu A, Cok-kinos DV, Falk E, Fox KA, Julian D,Lengyel M, Neumann FJ, Ruzyllo W, Thy-gesen C, Underwood SR, Vahanian A, Ver-heugt FW, Wijns W. Task Force on theManagement of Acute Myocardial Infarc-tion of the European Society of Cardiology.Management of acute myocardial infarctionin patients presenting with ST-segment el-evation. The Task Force on the Manage-ment of Acute Myocardial Infarction of theEuropean Society of Cardiology. EurHeart J. 2003;24:28-66.

. Lichtenstein AH, Appel LJ, Brands M, Car-nethon M, Daniels S, Franch HA, FranklinB, Kris-Etherton P, Harris WS, Howard B,Karanja N, Lefevre M, Rudel L, Sacks F,Van Horn L, Winston M, Wylie-Rosett J.American Heart Association NutritionCommittee, Diet and Lifestyle Recommen-dations Revision 2006: A Scientific State-ment from the American Heart AssociationNutrition Committee. Circulation. 2006;114:82-96.

. Kris-Etherton PM, Harris W, Appel LJ.AHA Scientific Statement: Fish consump-tion, fish oil, omega-3 fatty acids and car-diovascular disease. Circulation. 2002;106:2747-2757.

. National Cholesterol Education Program.Third Report of the National CholesterolEducation Program (NCEP) Expert Panelon Detection, Evaluation, and Treatment ofHigh Blood Cholesterol in Adults (AdultTreatment Panel III) final report. NationalHeart, Lung and Blood Institute, NationalInstitutes of Health. September 2002. NIHPublication No. 02-5215.

. National Cholesterol Education Program(NCEP) Expert Panel on Detection, Evalu-ation, and Treatment of High Blood Choles-terol in Adults (Adult Treatment Panel III)final report. Circulation. 2002;106:3143-3421.

. US Department of Health and Human Ser-vices, US Department of Agriculture. Di-etary Guidelines for Americans 2005.Available at: http://www.healthierus.gov/dietaryguidelines/. Accessed July 10, 2007.

. UK Scientific Advisory Committee on Nu-trition. Advice on fish consumption: Bene-fits and risks. April 2004. Available at:http://www.sacn.gov.uk/pdfs/fics_sacn_advise_fish.pdf. Accessed July 10, 2007.

. FAO/WHO Technical Report No. 916. Diet,Nutrition and the Prevention of ChronicDiseases. Geneva, Switzerland: WorldHealth Organization; 2003.

. Institute of Medicine. Dietary Reference In-takes for Energy, Carbohydrate, Fiber, Fat,Fatty acids, Cholesterol, Protein and AminoAcids. Washington, DC: National Acade-mies Press; 2002.

. Hotamisligil GS. Inflammation and meta-bolic disorders. Nature. 2006;444:860-867.

. American Dietetic Association. Hyperlipid-emia Evidence Analysis Library. Availableat: http://ebg/adaevidencelibrary.com/template.cfm?templatebibliography&key224. Ac-cessed October 15, 2005.. Dietitians of Canada. Practice-Based Evi-

September 2007 Journal ofdence in Nutrition. Available at: http://www.dieteticsatwork.com/pen. Accessed Janu-ary 14, 2007.

. US Department of Agriculture. NutrientData Lab. Available at: http://www.nal.usda.gov/fnic/foodcomp/search/. AccessedJanuary 14, 2007.

. Health Canada. Canadian Nutrient File.Available at: http://www.hc-sc.gc.ca/fn-an/nutrition/fiche-nutri-data/index_e.html. Ac-cessed January 14, 2007.

. KIM (Keep It Managed) Software Programfor omega-3 and omega-6 fatty acid contentof foods. Available at: http://efaeducation.nih.gov/sig/kim1.html. Accessed January14, 2007.

. Health Canada. Available at: http://www.hc-sc.gc.ca/fn-an/index_e.html. AccessedJanuary 14, 2007.

. US Department of Agriculture, US Depart-ment of Health and Human Services. 2005Dietary Guidelines Advisory CommitteeReport. Available at: http://www.health.gov/dietaryguidelines/dga2005/report/. Ac-cessed October 15, 2005.

. National Heart Foundation of Australia. Areview of the relationship between dietaryfat and cardiovascular disease. Aust J NutrDiet. 1999;56:S5-S22.

. Nesheim MC, Yackine AL. Seafood Choic-es: Balancing Benefits and Risks. Washing-ton, DC: National Academies Press; 2007.Available at http://www.nap.edu/execsumm_pdf/11762.pdf. Accessed January 14, 2007.

. Obarzanek E, Sacks FM, Vollmer WM,Bray GA, Miller ER 3rd, Lin PH, KaranjaNM, Most-Windhauser MM, Moore TJ,Swain JF, Bales CW, Proschan MA, DASHResearch Group. Effects on blood lipids of ablood pressure-lowering diet: The DietaryApproaches to Stop Hypertension (DASH)Trial. Am J Clin Nutr. 2001;74:80-89.

. Jenkins DJ, Kendall CW, Marchie A,Faulkner DA, Wong JMW, de Souza R,Emam A, Parker TL, Vidgen E, LapsleyKG, Trautwein EA, Josse RG, Leiter LA,Connelly PW. Effects of a dietary portfolioof cholesterol-lowering foods vs lovastatinon serum lipids and C-reactive protein.JAMA. 2003;290:502-510.

. Gardner CD, Coulston A, Chatterjee L,Rigby A, Spiller G, Farquhar JW. The effectof a plant-based diet on plasma lipids inhypercholesterolemic adults: A randomizedtrial. Ann Int Med. 2005;142:725-733.

. Appel LJ, Sacks FM, Carey VJ, ObarzanekE, Swain JF, Miller ER 3rd, Conlin PR,Erlinger TP, Rosner BA, Laranjo NM,Charleston J, McCarron P, Bishop LM;OmniHeart Collaborative Research Group.Effects of protein, monounsaturated fat,and carbohydrate intake on blood pressureand serum lipids: Results of the Omni-Heart randomized trial. JAMA. 2005;294:2455-2464.

. Hu FB, Stampfer MJ, Manson JE, Rimm E,Colditz GA, Rosner BA, Hennekens CH,Willett WC. Dietary fat intake and the riskof coronary heart disease in women.N EnglJ Med. 1997;337:1491-1499.

. Pischon T, Hankinson SE, Hotamisligil GS,Rifai N, Willett WC, Rimm EB. Habitualdietary intake of n-3 and n-6 fatty acids inrelation to inflammatory markers amongUS men and women. Circulation. 2003;108:155-160.

. Tanasescu M, Cho E, Manson JE, Hu FB.

Dietary fat and cholesterol and the risk of


30

31

32

33

34

35

36

37

38

39

40

41

42

43

44

45

46

47

48

49

50

51

52

53

54

55

56

57

58

59

60

61

62

63

64

65

66

67

68

69

70

71

72

73

74

75

76

ADA REPORTS

160cardiovascular disease among women withtype 2 diabetes. Am J Clin Nutr. 2004;79:999-1005.

. Salmeron J, Hu FB, Manson JE, StampferMJ, Colditz GA, Rimm EB, Willett WC.Dietary fat intake and risk of type 2 diabe-tes in women. Am J Clin Nutr. 2001;73:1019-1026.

. Sacks FM, Katan M. Randomized clinicaltrials on the effects of dietary fat and car-bohydrate on plasma lipoproteins and car-diovascular disease. Am J Med 2002;113(suppl 9B):13S-24S.

. European Commission. Nutrition and dietfor healthy lifestyles in Europe: Scienceand policy implications. Eurodiet CoreReport. 2001. Available at: http://ec.europa.eu/health/ph_determinants/life_style/nutrition/report01_en.pdf. AccessedJuly 10, 2007.

. Hamazaki T, Okuyama H. The Japan Soci-ety for Lipid Nutrition recommends to re-duce the intake of linoleic acid. A reviewand critique of the scientific evidence.World Rev Nutr Diet. 2003;92:109-132.

. International Society for the Study of FattyAcids and Lipids. Adequate Intakes. Avail-able at: http://www.issfal.org.uk/adequate-intakes.html. Accessed July 10, 2007.

. Reaven PD, Grasse BJ, Tribble DL. Ef-fects of linoleate-enriched and oleate-en-riched diets in combination with alpha-tocopherol on the susceptibility of LDLand LDL subfractions to oxidative modi-fication in humans. Arterioscler Thromb.1994;14:557-566.

. Calder PC. Polyunsaturated fatty acids andinflammation. Prostaglandins Leukot Es-sent Fatty Acids. 2006;75:197-202.

. Akabas SR, Deckelbaum RJ. Summary of aworkshop on n-3 fatty acids: Current statusof recommendations and future directions.Am J Clin Nutr. 2006;83(suppl):1536S-1538S.

. Harris WS, Assad B, Poston C. Tissueomega-6/omega-3 fatty acid ratio and riskfor coronary heart disease. Am J Cardiol2006;98(4A):19i-26i.

. Ernst ND, Sempos CT, Briefel RR, ClarkMB. Consistency between US dietary fatintake and serum total cholesterol concen-trations: The National Health and Nutri-tion Examination Surveys. Am J Clin Nutr.1997;66:965S-972S.

. Franz MJ, Bantle JP, Beebe CA, BrunzellJD, Chiasson JL, Garg A, Holzmeister LA,Hoogwerf B, Mayer-Davis E, MooradianAD, Purnell JQ, Wheeler M, American Di-abetes Association. Nutrition principlesand recommendations in diabetes. DiabetesCare. 2004;27(suppl 1):S36-S46.

. Gardner CD, Kraemer HC. Monounsatu-rated versus polyunsaturated dietary fatand serum lipids. A meta-analysis. Arterio-scler Thromb Vasc Biol. 1995;15:1917-1927.

. Ferrucci L, Cherubini A, Bandinelli S, Bar-tali B, Corsi A, Lauretani F, Martin A, An-dres-Lacueva C, Senin U, Guralnik JM. Re-lationship of plasma polyunsaturated fattyacids to circulating inflammatory markers.J Clin Endocrinol Metab. 2006;91:439-446.

. Food and Drug Administration, US Envi-ronmental Protection Agency. What youneed to know about mercury in fish andshellfish. EPA-823-R-04-005. March 2004.

Available at: http://www.cfsan.fda.gov/

8 September 2007 Volume 107 Number 9dms/admehg3.html. Accessed July 10,2005.

. Health Canada. Advisory. Information onmercury levels in fish. Available at: http://www.hc-sc.gc.ca/ahc-asc/media/advisories-avis/2002/2002_41_e.html. Accessed Janu-ary 14, 2007.

. Mozaffarian D, Rimm EB. Fish intake, con-taminants, and human health. Evaluatingthe risks and benefits. JAMA. 2006;296:1885-1899.

. Raiten DJ, Talbot JM, Waters JH. Life Sci-ences Research Office Report. Executivesummary of the report: Assessment of nu-trient requirements for infant formulas.Available at: http://www.nutritioninmedicine.com/PDF/Handouts/TermInfantHandout.pdf. Accessed July 10, 2007.

. Willerson JT, Ridker PM. Inflammation asa cardiovascular risk factor. Circulation.2004;109:II2-II10.

. Posner BM, Cobb JL, Belanger AJ, CupplesLA, DAgostino RB, Stokes J 3rd. Dietarylipid predictors of coronary heart disease inmen. The Framingham Study. Arch InternMed. 1991;151:1181-1187.

. Keys A. Coronary heart disease in sevencountries. Circulation. 1970;41:I1-I211.

. Schaefer EJ. Lipoproteins, nutrition, andheart disease. Am J Clin Nutr. 2002;75:191-212.

. Keys A, Anderson JT, Grande F. Serumcholesterol response to changes in the diet.IV. Particular saturated fatty acids in thediet. Metabolism. 1965;14:776-787.

. Hegsted DM, McGandy RB, Myers ML,Stare EJ. Quantitative effects of dietary faton serum cholesterol in man. Am J ClinNutr. 1965;17:281-295.

. Mensink RP, Katan MB. Effect of dietaryfatty acids on serum lipids and lipopro-teins. A meta-analysis of 27 trials. Arterio-scler Thromb. 1992;12:911-919.

. Mensink RP, Zock PL, Kester AD, KatanMB. Effects of dietary fatty acids and car-bohydrates on the ratio of serum total toHDL cholesterol and on serum lipids andapolipoproteins: A meta-analysis of 60 con-trolled trials. Am J Clin Nutr. 2003;77:1146-1155.

. Criqui MH, Golomb BA. Epidemiologic as-pects of lipid abnormalities. Am J Med.1998;105:48S-57S.

. Castelli WP, Anderson K, Wilson PW, LevyD. Lipids and risk of coronary heart dis-ease. The Framingham Study. Ann Epide-miol. 1992;2:23-28.

. Kris-Etherton PM, Yu S. Individual fattyacid effects on plasma lipids and lipopro-teins: Human studies. Am J Clin Nutr1997;65(suppl 5):1628S-1644S.

. Kris-Etherton PM. AHA Science Advisory:Monounsaturated fatty acids and risk ofcardiovascular disease. Circulation. 1999;100:1253-1258.

. Garg A. High-monounsaturated-fat dietsfor patients with diabetes mellitus: A meta-analysis. Am J Clin Nutr 1998;67(suppl):577S-582S.

. Nkondjock A, Shatenstein B, MaisonneuveP, Ghadirian P. Assessment of risk associ-ated with specific fatty acids and colorectalcancer among French-Canadians in Mon-treal: A case-control study. Int J Epidemiol.2003;32:200-209.

. Kushi L, Giovannucci E. Dietary fat andcancer. Am J Med. 2002;113(suppl 9):63S-

70S.. Lipworth L, Martinez ME, Angell J, HsiehCC, Trichopoulos D. Olive oil and humancancer: An assessment of the evidence. PrevMed. 1997;26:181-190.

. Saadatian-Elahi M, Norat T, Goudable J,Riboli E. Biomarkers of dietary fatty acidintake and the risk of breast cancer: Ameta-analysis. Int J Cancer. 2004;111:584-591.

. Lada AT, Rudel LL. Dietary monounsatu-rated versus polyunsaturated fatty acids:Which is really better for protection fromcoronary heart disease? Curr Opin Lipidol.2003;14:41-46.

. Baylin A, Kabagambe EK, Ascherio A,Spiegelman D, Campos H. High 18:2 trans-fatty acids in adipose tissue are associatedwith increased risk of nonfatal acute myo-cardial infarction in Costa Rican adults. JNutr. 2003;133:1186-1191.

. Lemaitre RN, King IB, Raghunathan TE,Pearce RM, Weinmann S, Knopp RH, Co-pass MK, Cobb LA, Siscovick DS. Cellmembrane trans-fatty acids and the risk ofprimary cardiac arrest. Circulation. 2002;105:697-701.

. Pietinen P, Ascherio A, Korhonen P, Hart-man AM, Willett WC, Albanes D, VirtamoJ. Intake of fatty acids and risk of coronaryheart disease in a cohort of Finnish men.The Alpha-Tocopherol, Beta-Carotene Can-cer Prevention Study. Am J Epidemiol.1997;145:876-887.

. Kromhout D, Menotti A, Bloemberg B, Ara-vanis C, Blackburn H, Buzina R, DontasAS, Fidanza F, Giampaoli S, Jansen A,Karvonen M, Katan M, Nissinen A,Nedeljkovic S, Pekkanen J, Pekkarinen M,Punsar S, Rasanen L, Simic B, Toshima H.Dietary saturated and trans fatty acids andcholesterol and 25-year mortality from cor-onary heart disease: The Seven CountriesStudy. Prev Med. 1995;24:308-315.

. Ascherio A, Hennekens CH, Buring JE,Master C, Stampfer MJ, Willett WC.Trans-fatty acids intake and risk of myo-cardial infarction. Circulation. 1994;89:94-101.

. Sun Q, Ma J, Campos H, Hankinson SE,Manson JE, Stampfer MJ, Rexrode KM,Willett WC, Hu FB. A prospective study oftrans fatty acids in erythrocytes and risk ofcoronary heart disease. Circulation. 2007;115:1858-1865.

. Mozaffarian D, Rimm EB, King IB, LawlerRL, McDonald GB, Levy WC. Trans fattyacids and systemic inflammation in heartfailure. Am J Clin Nutr. 2004;80:1521-1525.

. Gatto LM, Sullivan DR, Samman S. Post-prandial effects of dietary trans fatty acidson apolipoprotein(a) and cholesteryl estertransfer. Am J Clin Nutr. 2003;77:1119-1124.

. Mauger JF, Lichtenstein AH, Ausman LM,Jalbert SM, Jauhiainen M, Ehnholm C,Lamarche B. Effect of different forms ofdietary hydrogenated fats on LDL particlesize. Am J Clin Nutr. 2003;78:370-375.

. Mozaffarian D. Trans fatty acidsEffectson systemic inflammation and endothelialfunction. Atheroscler Suppl. 2006;7:29-32.

. Mozaffarian D, Katan MB, Ascherio A,Stampfer MJ, Willett WC. Trans fatty acidsand cardiovascular disease. N Engl J Med.2006;354:1601-1613.

. Bakker EC, Hys AJA, Kester ADM, Vles

JSH, Dubas JS, Blanco CE, Hornstra G.

77

78

79

80

81

82

83

84

85

86

87

88

89

90

91

92

93

94

95

96

97

98

99

100

101

102

103

104

105

106

107

108

109

110

111

112

113

114

115

116

117

118

119

120

ADA REPORTSLong-chain polyunsaturated fatty acids atbirth and cognitive function at 7 y of age.Eur J Clin Nutr. 2003;57:89-95.

. Bakker N, Vant Veer P, Zock PL. Adiposefatty acids and cancers of the breast, pros-tate and colon: An ecological study.EURAMIC Study Group. Int J Cancer.1997;72:587-591.

. Kohlmeier L, Simonsen N, Vant Veer P,Strain JJ, Martin-Moreno JM, Margolin B,Huttunen JK, Fernandez-Crehuet NavajasJ, Martin BC, Thamm M, Kardinaal AF,Kok FJ. Adipose tissue trans fatty acidsand breast cancer in the European Commu-nity Multicenter Study on Antioxidants,Myocardial Infarction, and Breast Cancer.Cancer Epidemiol Biomarkers Prev. 1997;6:705-710.

. Ip C, Marshall JR. Trans fatty acids andcancer. Nutr Rev. 1996;54:138-145.

. Hu FB, van Dam RM, Liu S. Diet and riskof type II diabetes: The role of types of fatand carbohydrate. Diabetologia. 2001;44:805-817.

. Rainer L, Heiss CJ. Conjugated linoleicacid: Health implications and effects onbody composition. J Am Diet Assoc. 2004;104:963-968.

. Moloney F, Yeow TP, Mullen A, Nolan JJ,Roche HM. Conjugated linoleic acid supple-mentation, insulin sensitivity, and lipopro-tein metabolism in patients with type 2diabetes mellitus. Am J Clin Nutr. 2004;80:887-895.

. Riserus U, Basu S, Jovinge S, FredriksonGN, Arnlov J, Vessby B. Supplementationwith conjugated linoleic acid causes isomer-dependent oxidative stress and elevated C-reactive protein: A potential link to fattyacid-induced insulin resistance. Circula-tion. 2002;106:1925-1929.

. Riserus U, Vessby B, Arnlov J, Basu S.Effects of cis-9,trans-11 conjugated linoleicacid supplementation on insulin sensitiv-ity, lipid peroxidation, and proinflamma-tory markers in obese men. Am J ClinNutr. 2004;80:279-283.

. Masters N, McGuire MA, Beerman KA,Dasgupta N, McGuire MK. Maternal sup-plementation with CLA decreases milk fatin humans. Lipids. 2002;37:133-138.

. Ritzenthaler KL, McGuire MK, McGuireMA, Shultz TD, Koepp AE, Luedecke LO,Hanson TW, Dasgupta N, Chow BP. Con-sumption of conjugated linoleic acid (CLA)-enriched cheese does not alter milk fat orimmunity in lactating women. J Nutr.2005;135:422-430.

. Goyens PLL, Spilker ME, Zock PL, Katan,MB, Mensink RP. Conversion of -linolenicacid in humans is influenced by the abso-lute amounts of -linolenic acid and linoleicacid in the diet and not by their ratio. Am JClin Nutr. 2006;84:44-53.

. Eckel RH, Borra S, Lichtenstein AH, Yin-Piazza SY. Understanding the Complexityof Trans Fatty Acid Reduction in the Amer-ican Diet. American Heart AssociationTrans Fat Conference 2006. Report of theTrans Fat Conference Planning Group. Cir-culation. 2007;115:2220-2235.

. Harris WS, Poston WC, Haddock CK. Tis-sue n-3 and n-6 fatty acids and risk forcoronary heart disease events. Arthroscle-rosis. 2007;193:1-10.

. Dayton S, Pearce ML, Hashimoto S, DixonWJ, Tomiyasu U. A controlled clinical trial

of a diet high in unsaturated fat in prevent-ing complications of atherosclerosis. Circu-lation. 1969;40(suppl II):1-63.

. Turpeinen O, Karvonen MJ, PekkarinenM, Miettinen M, Elosuo R, Paavilainen E.Dietary prevention of coronary heart dis-ease: The Finnish Mental Hospital Study.Int J Epidemiol. 1979;8:99-118.

. Leren P. The Oslo-Diet Heart Study: Eleven-year report. Circulation. 1970;42:935-942.

. Xiao C, Giacca A, Carpentier A, Lewis GF.Differential effects of monounsaturated,polyunsaturated and saturated fat ingestionon glucose-stimulated insulin secretion, sen-sitivity and clearance in overweight andobese, non-diabetic humans. Diabetologia.2006;49:1371-1379.

. Trevisan M, Krogh V, Freudenheim J,Blake A, Muti P, Panico S, Farinaro E,Mancini M, Menotti A, Ricci G. Consump-tion of olive oil, butter, and vegetable oilsand coronary heart disease risk factors.The Research Group ATS-RF2 of the Ital-ian National Research Council. JAMA.1990;263:688-692.

. Canadian Diabetes Association ClinicalPractice Guidelines Expert Committee.Clinical practice guidelines for the preven-tion and management of diabetes in Can-ada. Can J Diabetes 2003;27(suppl 2):S1-S163. Available at: http://www.diabetes.ca/cpg2003/downloads/cpgcomplete.pdf. Ac-cessed July 10, 2007.

. Zock PL, Katan MB. Linoleic acid intakeand cancer risk: A review and meta-analy-sis. Am J Clin Nutr. 1998;68:142-153.

. Shoda R, Matsueda K, Yamato S, UmedaN. Epidemiologic analysis of Crohn diseasein Japan: Increased dietary intake of n-6polyunsaturated fatty acids and animalprotein relates to the increased incidence ofCrohn disease in Japan. Am J Clin Nutr.1996;63:741-745.

. Sturdevant RA, Pearce ML, Dayton S. In-creased prevalence of cholelithiasis in meningesting a serum-cholesterol-loweringdiet. N Engl J Med. 1973;288:24-27.

. Pearce ML, Dayton S. Incidence of cancerin men on a diet high in polyunsaturatedfat. Lancet. 1971;1:464-467.

. Tsai CJ, Leitzmann MF, Willett WC, Gio-vannucci EL. The effect of long-term intakeof cis unsaturated fats on the risk for gall-stone disease in men: A prospective cohortstudy. Ann Intern Med. 2004;141:514-522.

. Lands WE. Primary prevention in cardio-vascular disease: Moving out of the shad-ows of the truth about death. Nutr MetabCardiovasc Dis. 2003;13:154-164.

. Calder PC, Grimble RF. Polyunsaturatedfatty acids, inflammation and immunity.Eur J Clin Nutr 2002;56(suppl):S14-S19.

. Tsimikas S, Reaven PD. The role of dietaryfatty acids in lipoprotein oxidation and ath-erosclerosis. Curr Opin Lipidol. 1998;9:301-307.

. Simopoulos AP. Evolutionary aspects ofdiet and essential fatty acids. World RevNutr Diet. 2001;88:18-27.

. Simopoulos AP. Essential fatty acids inhealth and chronic disease. Am J ClinNutr. 1999;70(suppl 3):560S-569S.

. Salem N Jr, Wegher B, Mena P, Uauy R.Arachidonic and docosahexaenoic acids arebiosynthesized from their 18-carbon pre-cursors in human infants. Proc Natl AcadSci U S A. 1996;93:49-54.

. Pawlosky RJ, Hibbeln JR, Lin Y, Goodson

S, Riggs P, Sebring N, Brown GL, Salem N

September 2007 Journal ofJr. Effects of beef- and fish-based diets onthe kinetics of n-3 fatty acid metabolism inhuman subjects. Am J Clin Nutr. 2003;77:565-572.

. Hussein N, Ah-Sing E, Wilkinson P, LeachC, Griffin BA, Millward DJ. Long-chainconversion of [13C]linoleic acid and alpha-linolenic acid in response to markedchanges in their dietary intake in men. JLipid Res. 2005;46:269-280.

. Goyens PL, SpilkerME, Zock PL, KatanMB,Mensink RP. Compartmental modeling toquantify alpha-linolenic acid conversion afterlonger term intake of multiple tracer boluses.J Lipid Res. 2005;46:1474-1483.

. Agency of Healthcare Research and Qual-ity. Effects of omega-3 fatty acids on car-diovascular risk factors and intermediatemarkers of cardiovascular disease. 2004.Available at: http://www.ahrq.gov/clinic/epcsums/o3cardrisksum.htm. Accessed Oc-tober 15, 2005.

. Djousse L, Pankow JS, Eckfeldt JH, Fol-som AR, Hopkins PN, Province MA, HongY, Ellison RC. Relation between dietarylinolenic acid and coronary artery diseasein the National Heart, Lung, and BloodInstitute Family Heart Study. Am J ClinNutr. 2001;74:612-619.

. Hu FB, Stampfer MJ, Manson JE, RimmEB, Wolk A, Colditz GA, Hennekens CH,Willett WC. Dietary intake of alpha-lino-lenic acid and fatal ischemic heart diseaseamong women. Am J Clin Nutr. 1999;69:890-897.

. Dolecek TA. Epidemiological evidence ofrelationships between dietary poly-unsat-urated fatty acids and mortality in theMultiple Risk Factor Intervention Trial.Proc Soc Exp Biol Med. 1992;200:177-182.

. Albert CM, Oh K, Whang W, Manson JE,Chae CU, Stampfer MJ, Willett WC, HuFB. Dietary alpha-linolenic acid intake andrisk of sudden cardiac death and coronaryheart disease. Circulation. 2005;112:3232-3238.

. de Lorgeril M, Salen P, Martin JL, Mon-jaud I, Delaye J, Mamelle N. Mediterra-nean diet, traditional risk factors and therate of cardiovascular complications aftermyocardial infarction: Final report of theLyon Diet Heart Study. Circulation. 1999;99:779-785.

. Mozaffarian D, Ascherio A, Hu FB,Stampfer MJ, Willett WC, Siscovick DS,Rimm EB. Interplay between differentpolyunsaturated fatty acids and risk of cor-onary heart disease in men. Circulation.2005;111:157-164.

. Brouwer IA, Katan MB, Zock PL. Dietaryalpha-linolenic acid is associated with re-duced risk of fatal coronary heart disease,but increased prostate cancer risk: A meta-analysis. J Nutr. 2004;134:919-922.

. Koralek DO, Peters U, Andriole G, RedingD, Kirsh V, Subar A, Schatzking A, HayesR, Leitzmann MF. A prospective study ofdietary alpha-linolenic acid and the risk ofprostate cancer (United States). CancerCauses Control. 2006;17:783-791.

. de Lorgeril M, Salen P. -linolenic acid,coronary heart disease, and prostate can-cer. J Nutr. 2004;134:3385.

. Christensen JH, Riahi S, Schmidt EB, Mol-gaard H, Kirstein Pedersen A, Heath F,Cosedis Nielsen J, Toft E. n-3 Fatty acidsand ventricular arrhythmias in patients

with ischaemic heart disease and implant-


121

122

123

124

125

126

127

128

129

130

131

132

133

134

135

136

137

138

139

140

141

142

143

144

145

146

147

148

149

150

152

153

154

155

156

157

158

159

160

161

162

163

164

165

166

167

ADA REPORTS

161able cardioverter defibrillators. Europace.2005;7:338-344.

. Schrepf R, Limmert T, Claus Weber P,Theisen K, Sellmayer A. Immediate effectsof n-3 fatty acid infusion on the induction ofsustained ventricular tachycardia. Lancet.2004;363:1441-1442.

. Brouwer IA, Heeringa J, Geleijnse JM,Zock PL, Witteman JC. Intake of very long-chain n-3 fatty acids from fish and inci-dence of atrial fibrillation. The RotterdamStudy. Am Heart J. 2006;151:857-862.

. Mozaffarian D, Lemaitre RN, Kuller LH,Burke GL, Tracy RP, Siscovick DS; Cardio-vascular Health Study. Cardiac benefits offish consumption may depend on the typeof fish meal consumed: The CardiovascularHealth Study. Circulation. 2003;107:1372-1377.

. Hu FB, Bronner L, Willett WC, StampferMJ, Rexrode KM, Albert CM, Hunter D,Manson JE. Fish and omega-3 fatty acidintake and risk of coronary heart disease inwomen. JAMA. 2002;287:1815-1821.

. Siscovick DS, Raghunathan T, King I,Weinmann S, Bovbjerg VE, Kushi L, CobbLA, Copass MK, Psaty BM, Lemaitre R,Retzlaff B, Knopp RH. Dietary intake oflong-chain n-3 polyunsaturated fatty acidsand the risk of primary cardiac arrest.Am J Clin Nutr 2000;71(suppl):208S-212S.

. Albert CM, Hennekens CH, ODonnell CJ,Ajani UA, Carey VJ, Willett WC, RuskinJN, Manson JE. Fish consumption and riskof sudden cardiac death. JAMA. 1998;279:23-28.

. Dolecek TA, Granditis G. Dietary polyunsat-urated fatty acids and mortality in the Mul-tiple Risk Factor Intervention Trial (MR-FIT). World Rev Nutr Diet. 1991;66:205-216.

. He K, Song Y, Daviglus ML, Liu K, VanHorn L, Dyer AR, Greenland P. Accumu-lated evidence on fish consumption and cor-onary heart disease mortality: A meta-analysis of cohort studies. Circulation.2004;109:2705-2711.

. He K, Song Y, Daviglus ML, Liu K, VanHorn L, Dyer AR, Goldbourt U, GreenlandP. Fish consumption and incidence ofstroke: A meta-analysis of cohort studies.Stroke. 2004;35:1538-1542.

. Wang C, Harris WS, Chung M, Lichten-stein AH, Balk EM, Kupelnick B, JordanHS, Lau J. n-3 fatty acids from fish or fish-oil supplements, but not -linolenic acid,benefit cardiovascular disease outcomes inprimary- and secondary-prevention stud-ies: A systematic review. Am J Clin Nutr.2006;84:5-17.

. de Deckere EA. Possible beneficial effect offish and fish n-3 polyunsaturated fatty ac-ids in breast and colorectal cancer. Eur JCancer Prev. 1999;8:213-221.

. Nkondjock A, Shatenstein B, MaisonneuveP, Ghadirian P. Specific fatty acids andhuman colorectal cancer: An overview.Cancer Detect Prev. 2003;27:55-66.

. Calviello G, Di Nicuolo F, Gragnoli S, Pic-cioni E, Serini S, Maggiano N, Tringali G,Navarra P, Ranelletti FO, Palozza P. n-3PUFAs reduce VEGF expression in humancolon cancer cells modulating the COX-2/PGE2 induced ERK-1 and -2 and HIF-1al-pha induction pathway. Carcinogenesis.2004;25:2303-2310.

. MacLean CH, Newberry SJ, Mojica WA,Khanna P, Issa AM, Suttorp MJ, Lim YW,

Traina SB, Hilton L, Garland R, Morton 151

0 September 2007 Volume 107 Number 9SC. Effects of omega-3 fatty acids on cancerrisk: A systematic review. JAMA. 2006;295:403-415.

. SanGiovanni JP, Chew EY. The role ofomega-3 long-chain polyunsaturated fattyacids in health and disease of the retina.Prog Retin Eye Res. 2005;24:87-138.

. Peet M, Stokes C. Omega-3 fatty acids inthe treatment of psychiatric disorders.Drugs. 2005;65:1051-1059.

. Hibbeln JR, Nieminen LR, Blasbalg TL,Riggs JA, Lands WE. Healthy intakes ofn-3 and n-6 fatty acids: Estimations consid-ering worldwide diversity. Am J Clin Nutr.2006;83(suppl):1483S-1493S.

. Schaefer EJ, Bongard V, Beiser AS,Lamon-Fava S, Robins SJ, Au R, TuckerKL, Kyle DJ, Wilson PW, Wolf PA. Plasmaphosphatidylcholine docosahexaenoic acidcontent and risk of dementia and Alzhei-mer disease: The Framingham HeartStudy. Arch Neurol. 2006;63:1545-1550.

. van Gelder BM, Tijhuis M, Kalmijn S,Kromhout D. Fish consumption, n-3 fattyacids, and subsequent 5-y cognitive declinein elderly men: The Zutphen Elderly Study.Am J Clin Nutr. 2007;85:1142-1147.

. Beydoun MA, Kaufman JS, Satia JA, Ro-samond W, Folsom AR. Plasma n-3 fattyacids and the risk of cognitive decline inolder adults: The Atherosclerosis Risk inCommunities Study. Am J Clin Nutr. 2007;85:1103-1111.

. Innis SM, Palaty J, Vaghri Z, Lockitch G.Increased levels of mercury associated withhigh fish intakes among children from Van-couver, Canada. J Pediatr 2006;148:759-763.

. Innis SM. Polyunsaturated fatty acids inhuman milk: An essential role in infantdevelopment. Adv Exp Med Biol. 2004;554:27-43.

. Innis SM. Essential fatty acids in growthand development. Prog Lipid Res. 1991;30:39-103.

. Farquharson J, Cockburn F, Patrick WA,Jamieson EC, Logan RW. Effect of diet onthe fatty acid composition of the majorphospholipids of infant cerebral cortex.Arch Dis Child. 1995;72:198-203.

. Makrides M, Neumann MA, Byard RW,Simmer K, Gibson RA. Fatty acid composi-tion of brain, retina, and erythrocytes inbreast- and formula-fed infants. Am J ClinNutr. 1994;60:189-194.

. Elias SL, Innis SM. Newborn infantplasma trans, conjugated linoleic, n-6 andn-3 fatty acids are related to maternalplasma fatty acids, length of gestation andbirth weight and length. Am J Clin Nutr.2001;73:807-814.

. Koletzko B, Braun M. Arachidonic acid andearly human growth, is there a relation?Ann Nutr Metab. 1991;35:128-131.

. Innis SM. Trans fatty acid intakes duringpregnancy and early childhood. AthersoclerSuppl. 2006;7:17-20.

. Chen ZY, Pelletier G, Hollywood R, Rat-nayake WM. Trans fatty acid isomers inCanadian human milk. Lipids. 1995;30:15-21.

. Innis SM, King J. Trans fatty acids in hu-man milk are inversely associated withconcentrations of essential all-cis n-6 andn-3 fatty acids and determine trans, butnot n-6 and n-3, fatty acids in plasma lipidsof breast-fed infants. Am J Clin Nutr. 1999;70:383-390.. Mosley EE, Wright AL, McGuire MK,McGuire MA. Trans fatty acids in milkproduced by women in the United States.Am J Clin Nutr. 2005;82:1292-1297.

. Friesen R, Innis SM. Trans fatty acids inhuman milk in Canada declined with theintroduction of trans fat food labeling. JNutr. 2006;136:2558-2561.

. Carnielli VP, Wattimena DJ, Luijendijk IH,Boerlage A, Degenhart HJ, Sauer PJ. Thevery low birth weight premature infant iscapable of synthesizing arachidonic and do-cosahexaenoic acids from linoleic and linole-nic acids. Pediatr Res. 1996;40:169-174.

. Uauy R, Mena P, Wegher B, Nieto S, SalemN Jr. Long chain polyunsaturated fattyacid formation in neonates, effect of gesta-tional age and intrauterine growth. PediatrRes. 2000;47:127-135.

. Williams CM, Burdge GC. Long-chain n-3PUFA: Plant v marine sources. Proc NutrSoc. 2006;65:42-50.

. Ponder DL, Innis SM, Benson JD, SiegmanJS. Ponder DL, Innis SM, Benson JD, Sieg-man JS. Docosahexaenoic acid status ofterm infants fed breast milk or infant for-mula containing soy oil or corn oil. PediatrRes. 1992;32:683-688.

. Innis SM. Essential fatty acid transfer andfetal development. Placenta. 2005;26:S70-S75.

. Helland IB, Saugstad OD, Smith L, SaaremK, Soluoll R, Ganes T, Drevon CA. Similareffects on infants of n-3 and n-6 fatty acidssupplementation to pregnant and lactatingwomen. Pediatrics. 2001;108:E82-E92.

. Innis SM, Gilley J, Werker J. Are human-milk long-chain polyunsaturated fatty ac-ids related to visual and neural develop-ment in breast-fed infants? J Pediatr. 2001;139:532-538.

. Innis SM. Perinatal biochemistry andphysiology of long chain polyunsaturatedfatty acids. J Pediatr. 2003;143:S1-S8.

. Ceruku SR, Montegomery-Downs HE, Far-kas SL, Thoman EB, Lammi-Keefe CJ.Higher maternal plasma docosahexaenoicacid during pregnancy is associated withmore mature neonatal sleep-state pattern-ing. Am J Clin Nutr. 2002;76:608-613.

. Jorgensen MH, Hernell O, Hughes E,Michaelsen KF. Is there a relation betweendocosahexaenoic acid concentration inmothers milk and visual acuity develop-ment in term infants. J Pediatr Gastroen-terl Nutr. 2001;32:293-296.

. Hibbeln JR, Davis JM, Steer C, Emmett P,Rogers I, Williams C, Golding J. Maternalseafood consumption in pregnancy andneurodevelopmental outcomes in childhood(ALSPAC study): An observational cohortstudy. Lancet. 2007;369:578-585.

. Innis SM. Dietary (n-3) fatty acids andbrain development. J Nutr. 2007;137:855-859.

. Ghys A, Bakker E, Hornstra G, van denHount M. Red blood cell and plasma phos-pholipid arachidonic and docosahexaenoicacid at birth and cognitive development at4 years of age. Early Human Dev. 2002;69:83-90.

. Helland IB, Smith L, Saarem K, SaugstadOD, Drevon CA. Maternal supplementa-tion with very-long-chain n-3 fatty acidsduring pregnancy and lactation augmentschildrens IQ at 4 years of age. Pediatrics.2003;111:e39-e44.

. Cohen JT, Bellinger DC, ConnorWE, Shay-

witz BA. A quantitative analysis of prena-

168

169

170

171

172

173

174

175

176

177

178

179

180

181

182

183

184

185

186

187

188

189

A Delegates Leadership Team on April1 December 31, 2011. ADA authorizesre t/support paper, in its entirety, pro-v quests to use portions of the positionm ers at 800/877-1600, ext 4835, orp

D, RD (Penn State University, Uni-v DN (University of British Columbia,V

, PhD, RD (Ohio University, Athens,O th Israel Deaconess Medical Center,B ractice Dietetic Practice Group (De-b n management specialist, self-em-p unn, MA, RD (Keene State College,K (The Center for Genetics, Nutritiona

Bruce E. McDonald, PhD, FCIFST(U , Canada); Catherine J. Field, PhD,R AB, Canada); Frances Johnson, RD(P , British Columbia, Canada); RhonaH Waterloo, Waterloo, ON, Canada).

orkgroup: Sonja Connor, MS, RD(c ; Norman Salem Jr, PhD (contenta

ADA REPORTStal intake of n-3 polyunsaturated fattyacids and cognitive development. Am JPrev Med. 2005;29:366-374.

. Lauritzen L, Jorgensen MH, Mikkelsen TB,Skovgaard M, Straarup EM, Olsen SF, HoyCE,Michaelsen KF.Maternal fish oil supple-mentation in lactation: Effect on visual acu-ity and n-3 fatty acid content of infant eryth-rocytes. Lipids. 2004;39:195-206.

. Lauritzen L, Jorgensen MH, Olsen SF,Straarup EM, Michaelsen KF. Maternalfish oil supplementation in lactation: Effecton developmental outcome in breast-fed in-fants. Reprod Nutr Dev. 2005;45:535-547.

. Jensen CL, Voigt RG, Prager TC, Zou YL,Fraley JK, Rozelle JC, Turcich MR,Llorente AM, Anderson RE, Heird WC. Ef-fect of maternal docosahexaenoic acid in-take on visual function and neurodevelop-ment in breast-fed infants. Am J Clin Nutr.2005;82:125-132.

. Dunstan JA, Mori TA, Barden A, Beilin LJ,Holt PG, Calder PC, Taylor AL, PrescottSL. Effects of n-3 polyunsaturated fattyacid supplementation in pregnancy on ma-ternal and fetal erythrocyte fatty acid com-position. Eur J Clin Nutr. 2004;58:429-437.

. Carlson SE, Werkman SH, Peeples JM,Cooke RJ, Tolley EA. Arachidonic acid sta-tus correlates with first year growth in pre-term infants. Proc Natl Acad Sci U S A.1993;90:1073-1077.

. Carlson SE, Cooke RJ, Werkman SH,Tolley EA. First year growth of preterminfants fed standard compared to marine-oil n-3 supplemented formula. Lipids.1996;27:901-907.

. Carlson SE,Werkman, SH, Tolley EA. Effectof long-chain n-3 fatty acid supplementationon visual acuity and growth of preterm in-fants with and without bronchopulmonarydysplasia. Am J Clin Nutr. 1996;63:687-697.

. Ryan AS, Montalto MB, Groh-Wargo S, Mi-mouni F, Sentipal-Walerius J, Doyle J,Siegman JS, Thomas AJ. Effect of DHA-containing formula on growth of preterminfants to 59 weeks postmenstrual age.Am J Human Biol. 1999;11:457-467.

. Olsen SF, Sorensen JD, Secher NJ, Hede-gaard M, Henriksen TB, Hansen H, GrantA. Randomized controlled trial of effect offish oil supplementation on pregnancy du-ration. Lancet. 1992;339:1003-1007.

. Olsen SF, Secher NJ. Low consumption ofseafood in early pregnancy as a risk forpreterm delivery; prospective cohort study.BMJ. 2002;324:447-456.

. Bulstra-Ramakers MT, Huisjes HJ, VisserGH. The effects of 3g eicosapentaenoic aciddaily on recurrence of intrauterine growthretardation and pregnancy induced hyper-tension. Br J Obstet Gynaecol. 1995;102:123-126.

. Malcolm CA, McCulloch DL, MontgomeryC, Shepherd A, Weaver LT. Maternal doco-sahexaenoic acid supplementation duringpregnancy and visual evoked potential de-velopment in term infants: A double blind,prospective, randomised trial. Arch DisChild Fetal Neonatal Ed. 2003;88:F383-F390.

. Olsen SF, Secher NJ, Taber A, Weber T,Walker JJ, Gluud C. Randomized clinicaltrials of fish oil supplementation in highrisk pregnancy. BJOG. 2000;107:382-395.

. Onwude JL, Lilford RJ, Hjartardottir H,Staines A, Tuffnell D. A randomised double

blind placebo controlled trial of fish oil inhigh risk pregnancy. Br J Obstet Gynaecol.1995;102:95-100.

. Birch EE, Castaneda YS, Wheaton DH,Birch DG, Uauy RD, Hoffman DR. Visualmaturation of term infants fed long-chainpolyunsaturated fatty acid-supplementedor control formula for 12 mo. Am J ClinNutr. 2005;81:871-879.

. Hoffman DR, Birch EE, Castenda YS,Fawcett SL, Wheaton DH, Birch DG, UauyDR. Visual function in breast-fed term in-fants weaned to formula with or withoutlong-chain polyunsaturates at 4 to 6months: A randomized clinical trial. J Pe-diatr. 2003;142:669-677.

. Heird WC, Lapillonne A. The role o

Documents

Position of the American Dietetic Association and Dietitians of Canada: Dietary Fatty Acids