Summer 2005 Volume 8, Issue 1

NCCContentsTherapies:Statins, Muscle Damage andCoenzyme Q10 . . . . . . . . . . .1

Supplements:A Literature review on Policosanol:An Alternative for ReducingHypercholesterolemia . . . . . . .3

Garlic Supplementation and Its Impact on Lowering the Risk of Cardiovascular andOther Diseases . . . . . . . . . .12

Functional Foods:Tea—Drink and Thrive . . . . . .9

Of Interest to Members:Thanks To Our Sponsors . . . .11

Editorial Staff . . . . . . . . . . . . .18

Key Contacts . . . . . . . . . . . . .20Four Easy Ways to Update yourAddress & Contact Informationwith ADA . . . . . . . . . . . . . . . .18

Meet Me in St. Louie . . . . . . .19

Chair’s Corner . . . . . . .2

Editor’s Notes . . . . . . .16

NEXT ISSUE• Winter 2005Editor’s Deadline, Nov. 1• Spring 2005Editor’s Deadline, Feb. 1

A Diete t ic Pract ice Group of the Amer ican Diete t ic Associa t ion

cont. on page 7Summer 2005 Volume 8, Issue 1

Page

1

Nutrition InComplementary Care

THERAPIES:Statins, Muscle Damageand Coenzyme Q10Gale Maleskey, MS, RD

With some36 million peo-ple consideredas candidatesfor cholesterol-lowering statindrugs, nutrition professionals are like-ly to have a number of clients takingone or another of these drugs. Clientsmay ask about a potential side effectof statins that has been in the popularpress recently—muscle pain, or amuch more serious condition, rhab-domyolysis, which involves muscle tis-sue breakdown and can be fatal.Anyone who does an Internet searchon the topic will find commercialwebsites recommending that statinusers take an over-the-counter nutri-tional supplement, CoenzymeQ10(CoQ10), to reduce the risk of muscledamage. While the argument for thisuse of CoQ10 is intriguing, the con-sensus among traditional health careprofessionals seems to be that it is pre-mature to support the widespread useof CoQ10 at this time.1

Complementary care practitioners, onthe other hand, are likely to recom-mend it as safe and effective, if costly.This summary will help nutrition pro-fessionals to have an informed discus-

sion with statin-taking clients regard-ing the use of CoQ10.

The connection between statindrugs and CoQ10

Statin drugs inhibit 3-hydroxy-3-methylglutaryl coenzyme A reductase,an enzyme in the mevalonate metabol-ic pathway. This pathway is commonto both cholesterol biosynthesis andthe synthesis of Coenzyme Q10 (alsocalled ubiquinone). 2 It is in this meta-bolic pathway that an important regu-latory step in CoQ10 synthesisoccurs—the formation of the iso-prenoid side-chain from acetyl-CoA.It is well documented that statin drugscan lower serum CoQ10 levels.3

However, it is less clear that lowerserum levels correspond to lowerCoQ10 levels within muscle cells.Statin-induced myopathy may haveseveral causes, with CoQ10 deficiencybeing just one of those causes.4

CoQ10 acts as an electron carrierin the mitochondrial respiratorychain, where it serves to transportelectrons from complex I (NADH-quinone oxidoreductase) and complexII (succinate-ubiquinone oxidoreduc-tase) to complex III (ubiquinol:cytochrome c oxidoreductase). CoQ10also serves to transfer electrons liberat-ed from the beta-oxidation of fattyacids to complex III to the mitochon-drial respiratory chain. This transfer ofelectrons produces energy-generating

Winter 2005 Volume 7, Issue 3Page

3cont. on page 4

Summer 2005 Volume 8, Issue 1Page

2

Chair’s Corner:SSuussaann AAlllleenn RRDD,, CCCCNN

SUPPLEMENTS: A Literature Review onPolicosanol: An Alternative for

Reducing Hyprcholesterolemia

Katherine Stephens-Bogard MS RD CDE

For the past year, I’ve been waiting in the wings ofNCC leadership gathering ideas. Now, together withNCC’s Executive Committee, and our committedmembers who chose to come along for what promisesto be a most exciting ride - here we go – I hope youare all as excited about the future of NCC as I am!!

Let me first say a huge thanks to Rick Hall for anexcellent job as last year’s Chair. Secondly; pleaseshare in my welcome to newly elected board mem-bers: Doug Kalman, Mary Alice Gettings, NatalieLedesma; newly appointed board members: DebFord, Caren Baltasi, Bob Maloof and our not so new,new board members: Laura Lagano and Kathie Swift.Together with each their own advanced CAM knowl-edge and expertise, and leadership experience, beassured they will most efficiently and effectively rep-resent NCC’s members.

On behalf of the entire Board and membership, Iextend a heart-felt thank you to past advisors andboard members whose terms are now expired. Eachhelped make NCC the amazing DPG that it is andtheir tremendous commitment is evident in theircountless hours of very productive work.

My mission as Chair is to get the word out; growmembership by leaps and bounds and set NCC apartas THE premier DPG! After all, it doesn’t have to beyour specialty of practice but what RD isn’t gettingasked questions about CAM therapies? Membershipin NCC can potentially cross over all other DPGsand I don’t think it’s wrong to have a ìsky’s the limitîgoal list that gets us to this level.

To be certain though, we’ll have quite a task in get-ting this job done and we’ll need all the funding andexpertise we can get! NCC needs you – each andevery one of you. If you have ANY potential contactsfor funding/sponsoring, please submit them to KathieSwift. Every little bit will count!

What’s more, now more than ever, NCC needs thecommitment of our members for whatever time theycan spare. I encourage you to let me know where youwish to become involved. What better satisfaction canyou derive than knowing you had a personal hand inNCC’s success!

In the new and changing face of our profession,dare I say, NCC’s success directly contributes to thesuccess of the profession at large. CAM is here to stay.

Heart disease is the lead-ing cause of death in theUnited States. A major con-tributor to cardiac morbidityand mortality is arterioscle-rosis - consequent to dyslipi-demia – notable by elevatedlow density lipoprotein(LDL), triglyceride (TG),and depressed high densitylipoprotein (HDL).1 With60,000 miles of vessels in the human body suscepti-ble to injury, inflammation, and subsequent plaqueformation, is it any wonder that the healthcare com-munity at large and the pharmaceutical industry inspecific are interested in attenuating arteriosclerosis?

The 2001 National Cholesterol Education ProgramAdult Treatment Panel III (NCEP ATP III) recom-mends total cholesterol (TC) < 200 mg/dl and LDL< 130 mg/dl without coronary heart disease (CHD)risk equivalent. For those with CHD risk equivalent,an LDL of < 100 mg/dl is recommended and forthose with major CHD risk < 70 mg/dl. For menand women respectively, HDL should be > 45 mg/dland > 55 mg/dl. In both sexes, TG should be < 150mg/dl. To facilitate attainment of optimal serumlipid levels, the panel recommends therapeuticlifestyle (TLC) interventions of diet and exercise forthree months. Failure of TLC to achieve target serumlipid levels warrants pharmacological intervention.Characteristically, the initial drugs of choice are the5-hydroxy–3-methylglutaryl-coenzme-A (HMG CoA)reductase inhibitors - ìstatins.î 2 Research has shownthat statins typically lower LDL by 18% to 55% andTG by seven percent to 30% while concomitantlyraising HDL by five percent to 15%.2,3 These areimpressive and important statistics because for every

one percent reduction in total and LDL cholesterollevels there is a two percent reduction in CHD.1 Yet,for many the side effects of statins - myositis, myalgia,and hepatoxicity - preclude utilization.4,5 For theseindividuals and/or for those who prefer a more natu-ral approach, policosanol appears to be a viable alter-native. This article therefore will investigate the bio-chemistry and metabolism; indications and con-traindications; dosage; and efficacy of policosanol.

Biochemistry and Metabolism

Policosanol is a mixture of aliphatic alcohols derivedfrom variety of plant sources: sugarcane, wheat germoil, and beeswax.6-8 Specifically, policosanol is a mix-ture of 24-34 carbon alcohols comprised primarily ofoctosanol (28-c), but also tetracosanol (24-c), hexa-cosanol (26-c), heptacosanol (27-c), nonacosanol (29-c), triacosanol (30-c), dotriacontanol (32-c), andtetratriacontanol. The specific percentage of eachvaries depending on the source.6 Despite similar bio-chemical motieties, policosanol derived from sugar-cane is the most potent and thus most effective.5-8

By simultaneously inhibiting hepatic cholesterolsynthesis and lipid peroxidation while increasing thedegradation of LDL, policosanol favorably altersserum lipid levels. Reduction in LDL is 21% to 29%with a corresponding eight to 15% elevation inHDL.6-9

Clinical Efficacy

Policosanol’s favorable effects on dyslipidemia areseen in those with type II hypercholesterolemia,including the elderly, post menopausal women, andthose with comorbid atherosclerotic risk factors (Type2 Diabetes Mellitus (DM), hypertension (HTN), andangina).7-17

The preponderance of data on the efficacy of poli-cosanol is published by Castano et al. Their clinicaltrials and subsequent reports have included short andlong term studies, randomized placebo controlled tri-als, and comparative studies versus statins, fibrates,and other pharmacological agents.

As published in Drugs and Aging, Castano et al.compared 10 mg policosanol to 10 mg atorvastatin ina head-to-head single blind-randomized control trial.Though atorvastatin reduced LDL by 29% versus23.1% for policosanol, both reductions were nonethe-less statistically and clinically significant. Additionally,both substances reduced the LDL-HDL ratio (26.2%

We know it, ADA knows it and the public knows it.Now let’s get to the business of making it happenright! With a working knowledge of CAM, I believeRDs can finally and confidently call themselves ìTHEnutrition expertsî.

I encourage any of you with any questions to con-tact me directly. Also, in the future feel free to bringideas/issues on any topic to the Board’s attentiondirectly via a voting member or to me. I have anopen door policy; my direct line is (800) 917-3688.I’m looking forward to a lot of phone calls!!!

To the future!

The views expressed in this newsletter are those of the authors and donot necessarily reflect the policies and/or official positions of the AmericanDietetic Association.

We invite you to submit articles, news and comments. Contact us forauthor guidelines.

Send change-of-address notification to the American DieteticAssociation, 120 South Riverside Plaza, Ste. 2000, Chicago, IL 60606-6995.

Copyright © 2005 Nutrition in Complementary Care, a Dietetic PracticeGroup of the American Dietetic Association. All material appearing in thisnewsletter is covered by copyright law and may be photocopied or other-wise reproduced for noncommercial scientific or educational purposesonly, provided the source is acknowledged. For all other purposes, the writ-ten consent of the editor is required.

Annual Subscription Rates (in U.S. dollars, payable in U.S. funds)Individuals who are ineligible for ADA membership . . . . . . . . . . . . . . . . . . . . . . . . . . . .$35/yearBack issues . . . . . . . . . . . . . . . . . . . . . . . . . $10 each, 4 for $35For international orders, add $5 shipping and handling per annual subscription and foreach back issue order of 1–4 issues. For orders of 5 or more back issues, shipping is $6.50and $1.50 for each additional issue. Make checks payable to NCC DPG#18 and mail to theTreasurer. See back cover for address. ISSN 1524-5209

NNCCCC EEDDIITTOORRIIAALL SSTTAAFFFFEditor

Sarah Harding Laidlaw, MS RDCopy Editor

Rebecca Schauer, RDPublications Chair

Laura W. Lagano, MS RDEditors

Christian Calaguas, MPH RDKaren Lyon, RD

Sheryl Murphy, RDDanielle Torisky, PhD RD

CPE EditorKatherine Stephens-Bogard, RD

Web SiteSusan Moyers, PhD MPH LD/N, Web Editor

Cory Gransee, WebmasterKaren Higgins, MS RD, Heads Up!

Kathie Swift, MS RD, ResourcesEML Coordinator

Gretchen Forsell, MPH RD

Summer 2005 Volume 8, Issue 1Page

4 Summer 2005 Volume 8, Issue 1Page

5

cont. from page 4cont. from page 3

cont. on page 5

A Literature Review on Policosanol: An Alternative for Reducing Hypocholesteremia

atorvastatin versus 25.5% policosanol) and TG levels.Interestingly, only policosanol significantly increasedHDL by 5.3%. Furthermore, policosanol was bettertolerated both biochemically and clinically comparedto atorvastatin. Nine subjects in the atorvastatincohort reported adverse events including gastritis,myalgia, and myositis, compared to none in the poli-cosanol treated cohort. Within the atorvastatingroup, but not the policosanol group, there was amild but significant increase in creatine phosphoki-nase (CPK) and creatinine. In contrast, the poli-cosanol group but not the atorvastatin group hadreduced alanine transaminase (ALT), glucose, andCPK levels. Thus, though the overall reduction inLDL was greater with atorvastatin compared to poli-cosanol, it was not without cost.10

Earlier trials comparing policosanol to lovastatin,pravastatin, and simvastatin elicited similar findings.13,

15-17 In the lovastatin comparison trial, Costano et al.demonstrated equivocal LDL reductions with 20 mglovastatin versus 10 mg policosanol. In the poli-cosanol treated cohort, HDL increased 17% overbaseline, whereas the lovastatin treated group realizeda reduction in HDL. Another plus for policosanolwas the absence of hepatoxicity - lovastatin increasedserum transaminases (ALT and aspartate aminotrans-ferase (AST)) and CPK - policosanol, however, didnot.13

Benitez et al. reported virtually the same data intheir head-to-head trial of policosanol and pravas-tatin. The eight-week randomized trial of 10 mg eachpravastatin and policosanol yielded a greater LDLreduction 26% versus 21% for policosanol andpravastatin respectively. HDL elevations in the poli-cosanol cohort were double that seen in the pravas-tatin treated cohort. ALT and AST levels were signifi-cantly increased in the statin drug treated cohort, butnot in the policosanol cohort.16

The comparative trial conducted by Illnait et al. ofpolicosanol and simvastatin yielded equivocal LDLreductions, while policosanol but not simvastatinresulted in a significant increase in HDL. The preva-lence of hepatoxicity and muscle tissue breakdownwas absent in the policosanol cohort, but apparent inthe simvastatin group.17

Aside from these studies, Costano et al and others

have published numerous reports discussing the mer-its of policosanol in healthy and diseased (Type 2DM, nephrotic syndrome, and those with atheroscle-rotic risk factors) populations.18-20 As in the studiespreviously detailed, the participants were initiallyplaced on a lipid lowering diet, and then randomizedto receive policosanol (5-20 mg q HS) or placebo. Ineach of the trials, the lipoprotein fractions andparameters (T-chol, LDL, HDL, TG, and LDL-HDLratio) improved statistically, significantly, and clinical-ly in a dose dependent manner; and without hepatox-icity as measured by CPK, ALT, and AST. If thatwere not impressive enough, other markers for risk ofCHD (platelet aggregation, intimal thickness, andangina) also improved without troublesome sideeffects.18-21, 23-24

Indications and Contraindications

As described in the studies reviewed, policosanolappears to be safe for individuals with type II hyperc-holesterolemia who have not adequately responded todietary intervention; furthermore, no clinical or bio-chemical adverse reactions were noted in the elderly(60-80 year olds), postmenopausal women, or thosewith concomitant atherosclerotic morbidity includingType 2 DM.9-23 Despite its exemplary safety in theaforementioned populations, policosanol is con-traindicated during pregnancy and lactation or inchildren/adolescents.6

Due to its synergistic effect, caution is warranted inthose individuals on concurrent anti-platelet/anti-coagulant therapies (CoumadinÆ, PlavixÆ, andaspirin).6, 24 Policosanol has not been directly studiedrelative to its interaction with other pharmacologicalagents, and thus safety or lack thereof is not immedi-ately available. However, concurrent use of poli-cosanol with calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors, beta blockers,anti-depressants, oral hypoglycemic agents, diuretics,and thyroid hormones occurred without adverseeffects reported.9-24 Additionally, in an animal model,policosanol did not interact with pharmacologicalsubstrates metabolized via the cytochrome P450 sys-tem.25

Clinical efficacy is noted with a dose as low as fivemilligrams daily. The magnitude of improvementincreases with the dose. Dosages greater than 40 mgdaily have not been studied.26 Policosanol manufac-tured from sugarcane is the preferred substrate as ithas been extensively studied.6-9

Take-Home Message

In this era of evidence based medicine, it is reason-able to recommend policosanol to individuals whohave not achieved target lipid levels with TLC - dietand exercise intervention. The data suggests that poli-cosanol is better tolerated biochemically and subjec-tively than the statin drugs, and thus may be worthyof consideration as a first line pharmacotherapueticregime. Minimally, policosanol is a viable alternativeto statins in those individuals who can not toleratethe HMG CoA reductase inhibitors.

Katherine Stephens-Bogard MS RD CDE, is a dia-betes educator/exercise physiologist, in southwesternPennsylvania. She is CPE coordinator for the NCCnewsletter. Contact Katherine at: or 725-250-6298(phone) or 724-250-6263 (fax).References:1. American Heart Association. Available at: http://www.ameri-canheart.org. Accessed 5/30/05.2. National Cholesterol Education Program. Executive Summaryof the Third Report of the National Cholesterol EducationProgram (NCEP) Expert Panel on Detection, Evaluation, andTreatment of High Blood Ccholesterol in Adults (AdultTreatment Panel III): US Dept of Health and Human Services;2001. NIH publication 01-3305.3. National Cholesterol Education Program. Third Report of theExpert Panel on the Detection, Evaluation and Treatment ofHigh Blood Cholesterol in Adults (Adult Treatment Panel III).Available at:http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3upd04.htm. Accessed 6/1/05.4. Pasternak RD, Smith RC, Gundy SM, et al.ACC/AHA/NLBI clinical advisory on the use and safety ofstatins. J Am Coll Cardiol. 2002:40:567-572.5. Thompson PD, Clarkson P, Karas RH. Statin-associatedmyopathy. JAMA. 2003;289:1681-1690.6. Natural Medicines Comprehensive Database. Available at:http://www.naturaldatabase.com. Accessed 5/3/05.7. Janikula, N. Policosanol: A new treatment for cardiovasculardisease. Alter Med Review. 2002;7:203-217.8. Gouni-Berthold I, Berthold HK. Policosanol: Clinical phar-macology and therapeutic significance of a new lipid-loweringagent. Am Heart J. 2002;2:356-365.9. Castano G, Fernandez L, Mas R, et al. Comparison of theefficacy, safety and tolerability of original policosanol versusother mixtures of higher aliphatic primary alcohols in patients

with type II hypercholesterolemia. Int J Clin Pharmacol Res.2002;22:55-66.10. Castano G, Mas R, Fernandez L, et al. Comparison of theefficacy and tolerability of policosanol with atorvastatin in elder-ly patients with type II hypercholesterolemia. Drugs Aging.2003:20:153-163.11. Castano G, Mas R, Fernandez JC, et al. Effects of poli-cosanol in older patients with type II hypercholesterolemia andhigh coronary risk. J Geron A Biol Sci Med Sci. 2001;56:M186-192.12. Castano G, Mas R, Fernandez L, et al. Effects of policosanolon postmenopausal women with type II hypercholesterolemia.Gynecol Endocrinol. 2000;14:187-195.13. Crespo N, Illnait J, Mas R, et al. Comparative study of theefficacy and tolerability of policosanol and lovastatin in patientswith hypercholesterolemia and non-insulin dependent diabetesmellitus. Int J Clin Pharmacol Res. 1999; 19:117-127.14. Mas R, Castano G, Illnait J, et al. Effects of policosanol inpatients with type II hypercholesterolemia and additional coro-nary risk factors. Clin Pharmacol Ther. 1999;64:439-447.15. Castano G, Mas R, Fernandez L, et al. Effects of policosanoland pravastatin on lipid profile, platelet aggregation andendothelemia in older hypercholesterolemic patients. Int J ClinPharmacolRes. 1999;19:105-116.16. Benitez M, Romero C, Mas R, et al. A comparative studyof policosanol versus pravastatin in patients with type II hyperc-holesterolemia. Curr Ther Res. 1997;58:859-867.17. Illnait J, CastanoG, Mas R et al. A comparative study on theefficacy and tolerability of policosanol and simvastatin for treat-ing type 11 hypercholesterolemia. Abstract from the 4thInternational Conference on Preventive Cardiology, June 29-July3, l997; Can J Cardiol. 1997;13:342B.18. Castano G, Mas R, Fernande JC, et al. Effects of policosanolon older patients with hypertension and type II hypercholes-terolemia. Drugs RD. 2002;3:159-172.19. Mirkin A, Mas R, Martinto M, et al. Efficacy and tolerabili-ty of policosanol in hypercholesterolemic postmenopausalwomen. Int J Clin Pharmacol Res. 2001;21:31-41.20. Batista J, Stusser R, Sacz F, et al. Effect of policosanol onhyperlipidemia and coronary heart disease in middle-agedpatients: a 14 month pilot study. Int J Clin Pharmacol Ther.1996;34:134-137.21. Castano G, Mas FR, Fernandez L, et al. A long-term studyof policosanol in the treatment of intermittent claudication.Angiogology. 2001:52:115-125.22. Valdes S, Arruzazabala ML, Fernandez L, et al. Effect ofpolicosanol on platelet aggregation in healthy volunteers. Int JClin Pharmacol Res. 1996;16:67-72.23. Menendez R, Mas R, Amor AM, et al. Effects of policosanoltreatment on the susceptibility of low density lipoprotein (LDL)isolated from healthy volunteers to oxidative modification invitro. Br J Clin Pharmacol. 2000;50:255-262.24. Arruzazabala ML, Valdex S, Mas R, et al. Comparative studyof policosanol, aspirin, and the combination therapy poli-cosanol-aspirin on platelet aggregation in healthy volunteers.Pharmacol Res. 1997;36:293-297.25. Mesa A. del R, Mas R, Noa M, et al. Toxicity of policosanolin Beagle dogs: one year study. Toxicol Lett. 73:131-139.26. Castano G, Mas R, Fernandez L, et al. Effects of poli-cosanol 20 versus policosanol 40 mg/day in the treatment ofpatients with type II hypercholesterolemia: a 6-month doubleblind study. Int J Clin Pharmacol Res. 2001;21:43-57.

A Literature Review on Policosanol: An Alternative for Reducing Hypocholesteremia

Summer 2005 Volume 8, Issue 1Page

7

cont. from page 1

Summer 2005 Volume 8, Issue 1Page

6

Therapies: Statins, Muscle Damage and CoenzymeQ10

ATP via oxidative phosphorylation. Even a smalldecrease in CoQ10 concentration may depress ATPproduction and cause organ dysfunction. Anothermajor role of CoQ10 is its antioxidant function inprotecting the cell from free-radical induced oxida-tion. Inside cells, CoQ10 can prevent damage tointracellular membranes of mitochondria and otherorganelles. CoQ10 also helps to reduce the oxidationof LDL, which has been implicated as an importantevent in progression of atherosclerosis. And CoQ10regenerates vitamin E, an important lipid-solubleantioxidant.3

How does depletion of CoQ10 contribute to mus-cle pain?

Little is known regarding how statins produce mus-cle injury, but one theory posits that a reduction inCoQ10 synthesis leads to a shift toward anaerobicmetabolism (with elevated lactate to pyruvate ratio)and mitochondrial dysfunction that can cause muscleweakness and pain, and ultimately, lead to muscle cellbreakdown.2 In animals, statin-induced ubiquinonedepletion has been found to cause decreased ATPproduction, increased injury after ischemia/reperfu-sion, increased mortality in cardiomyopathy, andskeletal muscle injury and dysfunction.4

Mitochondrial dysfunction has recently been demon-strated by muscle biopsy in statin users with musclecomplaints. These individuals did not have an eleva-tion in serum levels of creatine kinase (CK), the tradi-tional measure for muscle tissue breakdown, leadingresearchers to suggest that this test is not adequate fordiagnosing statin-related myopathy.5 CoQ10 supple-mentation helps to reduce this pain, it is thought,because it improves mitochondrial efficiency byrestoring normal transport of electrons in the respira-tory chain. This leads to more end product, ATP, andalso provides cellular protection against oxidativestress by reducing the number of free radicals generat-ed during the energy-producing process.1

Incidence of statin-related muscle complaints

There is a wide range of muscle complaints/condi-tions associated with statin use. A 2002 AmericanCollege of Cardiology/American HeartAssociation/National Heart, Lung and BloodInstitute clinical advisory on the use and safety of

statins defined 4 syndromes: statin myopathy (anymuscle complaint related to these drugs); myalgia(muscle complaints without serum creatine kinase(CK) elevations); myosititis (muscle symptoms withCK elevations); and, rhabdomyolysis (markedly ele-vated CK levels, usually > 10 times the upper limit ofnormal. (Normal CK level is 17-149 units/L.)1 Themost serious form of muscle damage, rhabdomyolysis,is considered rare.6 Fatal rhabdomyolysis has beenreported to occur at an incidence of less than 1 permillion statin prescriptions dispensed, with the excep-tion of cerisvastin (Baycol) which was associated withan incidence of more than 3 deaths per 1 million pre-scriptions dispensed, leading to its withdrawal fromthe market in 2001.6 In addition, the Food and DrugAdministration issued an alert on March 2, 2005,that rhabdomyolysis (serious muscle damage) hadbeen reported in patients taking rosuvastatin (market-ed as Crestor) as well as other statin drugs.7

The incidence of severe myopathy is low, perhaps 1in 1000 patients.8 Few data are available regardingfrequency of less serious events such as muscle weak-ness and pain, but literature suggests it is a fairlycommon complaint. An incidence of about 1-5 % ofpatients has been suggested.2

Symptoms and predisposing factors

There is a wide range of symptoms associated withstatin use, from fatigue, pain, and muscle weakness tosevere, life-threatening rhabdomyolysis.8 Predisposingfactors for severe myopathy include higher dosage,concurrent use of a fibrate drug or high-dose niacin,hypothyroidism, carnitine deficiency, advanced age,relatively low body weight, female sex, use of multiplemedications (clarithromycin, erythromycin,cyclosporine, protease inhibitors, ketoconazole, andothers) multi-system disease, acute illness or majorsurgery.8, 9 The combination of strenuous exerciseand statin use has also been associated with anincreased risk of skeletal muscle injury.9

Evidence to support the use of CoQ10 for statin-induced muscle damage

A recent study presented at the American College ofCardiology 54th Annual Scientific Session in March,

cont. from page 6Therapies: Statins, Muscle Damage and CoenzymeQ10

cont. on page 8

2005, by the study’s investigator, Patricia Kelly, D.O.reported that 18 of 21 patients with significantmyopathy who were taking statin therapy had a sig-nificant decrease in myopathic pain after 30 days sup-plementation with 100 mg/day of CoQ10 (p<.001)compared to a group of patients taking vitamin E.The CoQ10 had no effect on creatine kinase levels. Italso had no effect on blood lipid levels, and was welltolerated.10

Another recent study, by Australian researchers,found that patients who received 300 mg/day CoQ10for an average of two weeks before cardiac surgeryhad improved mitochondrial function (p= .012) andin vitro contractility of myocardial tissue (p=.001)compared to those who did not receive CoQ10.11

A literature search of MEDLINE found two clinicaltrials and three published case reports in whichCoQ10 was used to prevent or treat statin-associatedmyopathy. In one of these studies, 56 cancer patientstreated with at least 30 mg/kg a day of lovastatin alsoreceived 240 mg of oral CoQ10 in four daily divideddoses. The investigators reported that CoQ10 did notdecrease the frequency of musculoskeletal toxicity butdid significantly reduce its severity.12 In the otherstudy, 16 cancer patients were administered 35 mg/kgof lovastatin daily, along with 240 mg of oral CoQ10,for seven consecutive days. Treatment was repeatedevery four weeks. The authors found elevated serumCK levels in two patients with mild myalgia. Theyreported that this toxicity was almost completelyreversed with CoQ10 supplementation. However, itwas not reported if additional CoQ10 was given tothese two patients or if the original protocol achievedthat result.13

In one case study, a woman with rhabdomyolysisand liver toxicity recovered after discontinuation ofthree drugs, itraconazole, lovastatin, and niacin, andthe addition of 210 mg of CoQ10 daily.14 In anoth-er case study, a man developed myopathy shortly afterstarting 20 mg daily of lovastatin. The drug was dis-continued but muscle soreness and elevated CK levelspersisted for six months. CoQ10 was then started at30 mg daily, and a few days later the man was able toresume regular exercise without muscle cramps and

fatigue.15 In a third case, a woman with rhabdomyoly-sis, ophthalmoplegia (paralysis of the eye muscles),and mitochondrial encephalomyopathy with lacticacidosis (MELAS) and stroke-like episodes recoveredafter withdrawal of simvastatin and three monthstreatment with 250 mg of CoQ10 daily.16

What dosages/forms are recommended?

Generally, health care providers who support theuse of CoQ10 recommend a dose of 50 to 200mg/day. Some practitioners contend that a blood levelof 2.5 microgram/ml or higher is needed for optimaleffect, but this level apparently is difficult to reach.(Normal blood levels of CoQ10 are about 1.0 micro-grams/ml with deficiency in the range of 0.6 micro-grams/ml.)4 Langsjoen reported that long term obser-vations on 424 cardiac patients, treated with 75 to600 mg of CoQ10 per day for up to eight yearsfound no adverse effects or drug interactions.4

Finnish researchers found that a single dose of 30 mgof CoQ10 had only a marginal elevating effect onplasma levels in non-coQ10-deficient individuals,while a daily dose of 200 mg resulted in a 6.1-foldincrease in plasma levels.17 In 2002, a citizen petitionto the Food and Drug Administration requested thatlabels on statin drugs include a black-box warningstating that all statin users should be advised to take100-200 mg per day of supplemental CoQ10 toreduce the risk of myocardial and liver dysfunctionand myopathies.9 In March, 2005, the FDA issued adecision stating that the warning was not warrantedbased on current scientific evidence.

Some practitioners recommend an initial loadingdose of 300 mg. with a meal that contains at leastone tablespoon of fat, such as peanut butter or oliveoil, followed by 200 mg/day in divided doses for oneweek, then 100 mg/day thereafter, taken with a mealthat contains some fat. Individuals who take CoQ10because of myopathy should also be urged to discusstheir symptoms with their physician, as there are clin-ical guidelines for reducing the risk of serious compli-cations.21

CoQ10 is normally fat-soluble, and some, but notall, research suggests that a fat-soluble form ofCoQ10 is absorbed better than CoQ10 in granular orpowder form.18-20 Fat-soluble forms generally come in

soft-gel caps, which are most often recommended.Several products also contain vitamin E. To increaseabsorption, the supplement should be taken with ameal that contains fat, and, if taking more than 100mg/day, in divided doses that contain no more than100 mg per dose. A specific CoQ10 formulation,UbiQGel (Tishcon Corporation, Westbury, NY) hasreceived orphan drug status from the FDA for thetreatment of mitochondrial cytopathies.9

Safety issues?

Langsjoen reported that CoQ10 has no adverseimpact on the cholesterol-lowering or anti-inflamma-tory properties of statin drugs.4 The National CancerInstitute (NCI) has stated that no serious toxicityassociated with the use of CoQ10 has been reported.22 The NCI reports that liver enzyme (transaminas-es) elevation has been detected in patients takingdoses of 300 mg/day for extended periods of time,but no liver toxicity has been reported. Researchers inone cardiovascular study reported a small number ofcases of rash, nausea, and upper abdominal pain.Other reported effects have included dizziness,insomnia, sensitivity to light, irritability, headache,heartburn and fatigue. CoQ10 can increase the con-tractility of the heart in patients with high bloodpressure. It can reduce the body’s response to theanticoagulant drug warfarin, and it can decreaseinsulin requirements in people with diabetes.22

Take Home Message

Given CoQ10’s good safety profile and its possiblebenefits, it seems appropriate and safe to recommendthis supplement to statin-users. Persons taking war-farin should inform their physician and have pro-thrombin times checked regularly. CoQ10 is availablein tablet or capsule form. Based on bioavailabilitystudies, the best preparations appear to be soft-gelatincapsules that contain CoQ10 in an oil base, emulsi-fied or soluble form and stick with a reputable prod-uct line. Recommended dosing appears to be a mini-mum of 100 mg/day or 200 mg/day in split doseswith meals.

Gale Maleskey, MS, RD, has been writing abouthealth and nutrition for more than 20 years. She main-tains a private practice in Pennsylvania’s Lehigh Valleyarea. Contact Gale at: maleskey@fast.net.

References 1.Pasternak RC, Smith RC, Grundy SM, et al.ACC/AHA/NHLBI clinical advisory on the use and safety ofstatins. J Am Coll Cardiol. 2002; 40:567-572.2.Thompson PD, Clarkson P, Karas RH. Statin-associatedmyopathy. JAMA. 2003; 289:1681-1690.3.Hargreaves IP. Ubiquinone: cholesterol’s reclusive cousin. AnnClin Biochem. 2003; 40: 207-218. 4.Langsjoen PH, Langsjoen AM. The clinical use of HMG CoA-reductase inhibitors and the associated depletion of coenzymeQ10. A review of animal and human publications. BioFactors.2003; 18:101-111. 5.Phillips PS, Haas RH, Bannykh S. Statin-associated myopathywith normal creatine kinase levels. Ann Intern Med, 2002; 137:581-585.6.Nawarskas JJ. HMG-CoA reductase inhibitors and CoenzymeQ10. Cardiol Rev. 2005; 13:76-79.7.FDA Alert for Health Care Professionals. Available at .Accessed 3/15/058.Can statins cause chronic low-grade myopathy? (Editorial) AnnIntern Med. 2002; 137:617-618. 9.Koumis T, Nathan JP, Rosenberg JM. Strategies for the preven-tion and treatment of stain-induced myopathy: is there a role forubiquinone supplementation? Am J Health Syst Pharm. 2004; 61:515-519. 10.Kelley P. Coenzyme Q10 improves myopathic pain in statin-treated patients. [Abstract] J Am Coll Cardiol. 2005;45:3A. 11.Rosenfeldt F, Marasco S, Lyon W, et al. Coenzyme Q10 ther-apy before cardiac surgery improves mitochondrial function andin vitro contractility of myocardial tissue. J Thorac CardiovascSurg. 2005; 129:25-32.12.Thibault A, Samid D, Tompkins AC, et al. Phase I study oflovastatin, an inhibitor of the mevalonate pathway, in patientswith cancer. Clin Cancer Res. 1996: 2:483-91.13. Kim WS, Kim MM, Choi HJ, et al. Phase II study of high-dose lovastatin in patients with advanced gastric adenocarcino-ma. Invest New Drugs. 2001: 19:81-83. 14.Lees RS, Lees Am. Rhabdomyolysis from the coadministra-tion of lovastatin and the antifungal agent itraconazole. N Engl JMed. 1995:333:664-884. Letter. 15.Walravens PA, Greene C, Frerman FE. Lovastatin, isoprenes,and myopathy. Lancet. 1989: 2:1097-1098. Letter.16.Chariot P, Abadia R, Agnus D, et al. Simvastatin-inducedrhabdomyolysis following by a MELAS syndrome. Am J Med.1993; 94:109-110. 17. Kaikkonen J, Tuomainen TP, Nyyssonen K, Salonen JT.Coenzyme Q10: absorption, antioxidant properties, determi-nants, and plasma levels. Free Radic Res. 2002; 36:389-397. 18.30. Weiss M, Mortensen SA, Rassig MR, et al. Bioavailabilityof four oral coenzyme Q10 formulations in healthy volunteers.Molec Aspects Med. 1994;15:273–80.19.Kaikkonen J, Nyyssonen K, Porkkala-Sarataho E, et al. Effectof oral coenzyme Q10 on the oxidation resistance of humanVLDL + LDL fraction: absorption and antioxidative propertiesof oil and granule-based preparations. Free Radic Biol Med.1997;22:1195–202.20.Chopra RK, Goldman R, Sinatra ST, Bhagavan HN. Relativebioavailability of coenzyme Q10 formulations in human subjects.Int J Vitam Nutr Res. 1998;68:109–13.21.Dr Michael T. Murray online, Coenzyme Q10 athttp://www.fda.gov/bbs/topics/news/2005/NEW01159.html.Accessed 3/28/05.22.National Cancer Institute, CoenzymeQ10: Adverse effects.Available at http://www.nci.gov/cancertopics/pdg/cam/coenzymeQ10/HealthProfessional/page. Accessed 3/21/05.

Summer 2005 Volume 8, Issue 1Page

9Summer 2005 Volume 8, Issue 1Page

8

cont. from page 5Therapies: Statins, Muscle Damage andCoenzymeQ10

cont. on page 10

FUNC TIONALFOODS: Tea – Drink and Thrive Anita Kobuszewski, MS, RD

Ah! Tea...it quenches yourthirst on a sizzling summerday and is as cozy and satisfy-ing as a warm pair of socks inthe winter. Tea has been servedas a beverage for centuries- yetit remains one of the world’smost popular drinks, secondonly to water. Tea is both inex-

pensive and one of the simplest beverages to prepare.One pound of tea will yield about 200 cups, com-pared to a pound of coffee, which yields about 40cups.

Tea naturally contains ingredients that will help thebody fight disease by protecting healthy cells and tis-sues against damage. Researchers continue to examinethe role tea plays in fighting cancer and heart disease.Tea may help reduce the risk of some forms of cancerand help reduce blood cholesterol levels.

Tea is a Species of the Evergreen Shrub, You Say?

How many kinds of tea are there? One. The nameof the plant from which all teas are produced isCamellia sinensis, a species of the evergreen shrub.The three main categories of tea are derived fromhow each one is processed. Names of the subcate-gories are then labeled according to where the tea wasgrown geographically. The three categories of teainclude black, green and oolong. There are over 3000different varieties of teas. Note that the fermentationprocess referred to takes place by the action ofenzymes naturally occurring in the tea leaves.

• Black tea is most popular in the United States,Great Britain, Europe and India. It is fermented byexposing the newly harvested leaves to air in a dampplace. This natural chemical process is what producesits deep red-brown color and unique rich flavor. The

term “Orange Pekoe” refers to the specific leaf sizeof any black variety of tea and is not a variety oftea itself. Some varieties of black tea include:Assam, Ceylon, Darjeeling, Earl Grey, EnglishBreakfast, Keemun, and Souchong.

• Green tea is popular in Japan, China andbecoming more and more a favorite in the UnitedStates. It is dried without fermenting. Green tea isnaturally processed by quick steaming or heatingof the raw tea leaves. Jasmine and chrysanthemumteas are a blend of the dry flowers combined witheither green or black tea. Some other green teavarieties, whose names are derived from wherethey are grown include: Sencha, Gunpowder, andJasmine.

• Oolong tea is semi-fermented and is a combi-nation of both green and black tea. It has a green-ish-brown color. The taste of good quality oolongtea is peachy and mellow. Some varieties include:Formosa, Oolong Orange Blossom, OrchidOolong and Ti Kuan Yin Iron Goddess tea.1, 2, 3

Herbal Tisanes

Noteworthy is the topic of herbals or moreappropriated termed, tisanes. Tisanes don’t comefrom the Camellia sinensis plant and aren’t reallyteas. Tisanes are a collection of plant leaves, herbs,spices, roots, flowers and flavorings steeped in hotwater to make an infusion. Some varieties oftisanes include: Chamomile, Lemon Rose andPeppermint. This article refers to teas fromCamellia sinensis only.1, 3

The Drink For Good Health

Having been around for at least 5,000 years, teawas first identified by Chinese scholars for itsmedicinal attributes. Today, scientists continue tolook at the potential role tea has in the preventionof heart disease and cancer. The results of currentresearch is positive, exciting and has made tea evenmore popular.

Tea, like fruits, vegetables, nuts and seeds con-tain various types of phytochemicals. In Greek theword ‘phyto’ means plant. Some phytochemicalsfunction as antioxidants. Antioxidants protect cellsfrom the effects of oxidation and free radicals inthe body. Antioxidants have been credited aspotentially offering protection from diseases and

conditions ranging from some cancers to aging.

Tea, fruits, vegetables, nuts and seeds containflavonoids. Flavonoids are a type of phytochemical.They have been shown to have an antioxidant effectthat prevents damage to cells by free radicals. Thesenaturally occurring free radicals can eventually con-tribute to heart disease and cancer. The antioxidantsin tea may help to keep cells and tissues healthy andcontribute to good cardiovascular health while alsoslowing down the aging process. The group of antiox-idants known as theaflavins, are thought to be effec-tive in preventing cardiovascular diseases by produc-ing mild reductions in serum low-density lipoproteins(LDL) and to restore blood vessel dilation to nearnormal levels in persons with heart disease.4

Polyphenols powerful antioxidants are naturallyoccurring chemical components of tea. Someresearchers have determined that drinking tea maydecrease one’s chances of getting cavities. Polyphenolshelp to suppress the growth of cavity-causing bacteriain dental plaque and reduce acid production. Dentalplaque causes gum disease, a leading cause of toothloss in adults. The polyphenols found in green teashave been determined by some researchers to be aninhibitor of some types of cancer and various otherdiseases. In fact, dry, brewed tea has been said toexceed the antioxidant activity of more than 22 fruitsand vegetables and the benefits range from reducingthe risk of oral, digestive, lung, and colon rectal can-cers to stroke.5-7

Research continues to be done on the prizes won bytea consumption and its drawbacks. Additional scien-tific studies on the role of the antioxidants in teamust be done to make conclusions regarding its con-tributions to health. Of one consequence is the possi-bility of a drug-food interaction when green teas areconsumed with certain medications.5-7

Tea Made Right

For a good cup of traditional tea follow these direc-tions:

1. One teaspoon of loose tea or one single serve teabag will make a bright flavored, clear 6-oz cup of tea.

2. Rinse the teapot with hot water to warm up thepot. Always use china, stainless steel or glass. Other

metals may give off a flavor.

3. Bring the cold, fresh water to a boil, 212 degreesFahrenheit. Water that has been kept warm for aperiod of time will make flat-tasting tea.

4. Place the tea bag or the loose tea leaves in thepot and pour the water directly over the leaves.

5. Allow the tea to steep (let stand to extract flavorsand colors) 3 to 5 minutes.

6. Serve immediately. Tea doesn’t hold well.8

Tea and Caffeine

Tea naturally contains about one-half the amountof caffeine per cup as a comparable cup of coffee.What’s a safe amount of caffeine to intake on a dailybasis? Most healthy adults can consume about two tothree cups of medium brewed coffee or 200 to 300milligrams per day. Translated into tea-terms that isequivalent to about five cups of medium brewed tea.The longer the tea steeps, the higher caffeine contentin the tea.

If caffeine makes you agitated, gives you insomnia,causes abdominal discomfort or if you have a heartcondition where caffeine has been contraindicated thedecaffeinated variety may be your best selection. Theycan taste just as hearty without the buzz.9

Caffeine may have some adverse cardiac effectsincluding possible increase in homocysteine levels dueto high concentrations of polyphenols and may havean increasing or lowering effect on blood sugar.Caffeine is a central nervous system stimulant andmay have an adverse effect on blood pressure in casu-al, but not habitual users due to one’s ability tobecome accustomed to regular caffeine inake.4

Interactions

Use of caffeine-containing (regular) tea can increaseboth adverse and therapeutic effects of certain drugsand herbal preparations. Consuming large amounts oftea has been shown to increase urinary calcium andmagnesium excretion. Black tea may reduce theabsorption of iron from supplements and has beenshown to reduce the absorption of non-heme iron

from food. In most people, this is not clinically sig-nificant but consuming black tea with meals maylessen the adverse effect. When taken with milk, milkhas been shown to bind with antioxidants in blacktea thus reducing their favorable effects.4

Although caffeine has been reported to haveantiplatelet effects thereby reducing the ability ofblood platelets to clot, the interaction has not beenshown in humans. Tea, particularly the caffeinatedtype, may interfere or interact with numerous pre-scription medications.4

Take Home Message

Tea has been known to be a healthy and enjoyablebeverage for centuries. As more and more research isconducted, it is likely that we will see more and morefavorable information about its benefits. Just as withany natural substance, there are people who seek touse it for self medication and may think that if someis good, more is better. Tea can provide that extraedge when we want to be mentally alert. For healthbenefits, one to four cups of tea per day have beenshown to be beneficial for cardiovascular diseasereduction.4 It is prudent to advise patients who con-sume large amounts of tea to read any drug insertsand to ask their nutrition professional, physician orpharmacist about any potential adverse effects.Switching to decaffeinated beverages may be all thatis necessary for patients who enjoy their tea andwould like its health benefits, but must also take pre-scription medications.

Anita Kobuszewski, MS, RD is a food coach, author,television and radio personality and educator and a fac-ulty member at Merritt College of Oakland, CA.Contact Anita at: anita@AnitaBeHealthy.com or 510-865-3834 fax.References:1. Wolke RL. Kitchen Science Explained: What Einstein Told HisCook. 2002. New York, NY: W W Norton & Co.2.The Oolong Tea. Available at:http://www.oolongtea.org/e/index.html. Accessed 6/24/05 3. Tea Association of the United States of America. Available at:http://www.teausa.com/general/teasym/400c.cfm. Accessed6/24/05. 4. Natural Medicines Comprehensive Database; Black Tea.Available at: http://www.naturaldatabase.com. Accessed6/24/05.

Summer 2005 Volume 8, Issue 1Page

10 Summer 2005 Volume 8, Issue 1Page

11

cont. on page 13

cont. from page 9Functional Foods: Tea – Drink and Thrive

cont. from page 10Functional Foods: Tea – Drink and Thrive

5. Fox Chase Cancer Center. Available at:http://www.fccc.edu/publications/nutrition. Accessed 6/24/05.6. Science Daily. Available at:http://www.sciencedaily.com/releases/2001/05/010523072047.htm. Accessed 6/24/05. 7. University of Arizona, College of Agriculture and LifeSciences. Available at:http://ag.arizona.edu/nsc/new/news/news1-99.htm. Accessed6/24/05. 8. Gisslen W. Coffee and Tea. In: Professional Cooking. 1983.New York, NY: John Wiley & Sons, Inc.9. Dyuff, RL. The American Dietetic Association’s Complete Foodand Nutrition Guide. 2nd ed. 2002 Hoboken, NJ: John Wiley &Sons, Inc..

Thank You to Our Sponsors!Without you, much of what we are able to do

would not be possible.

DIAMONDPharmavite/ Nature Made

PLATINUMCentrum

Celestial SeasoningsNutrition 21

GOLD

Nutrilite Division of Access Business Group

Metagenics

Vitamin Nutrition Information Service (VNIS)

SILVER

Almond Board of California

National Starch & Chemical Co.

BRONZE

OatVantage

Pioneer Nutritionals

Solgar

FRIENDS OF NCC

American Botanical Council

Canyon Ranch

Wild Oats Natural Marketplace

Summer 2005 Volume 8, Issue 1Page

13Summer 2005 Volume 8, Issue 1Page

12

cont. from page 12 Supplements: Garllic Supplementation and its Impact onLowering the Risk of Cardiovascular and Other Diseases

SUPPLEMENTSGarlic Supplementation, and itsImpact on Lowering the Risk ofCardiovascular and OtherDiseasesGretchen K. Vannice, MS, RD

Among the botanical andnutritional supplements cur-rently being researched andused for lowering the risk ofdisease, garlic (Alliumsativum) is one of the mostextensively studied. Nearly2000 scientific studies haveinvestigated its health bene-fits, including its effects on

cardiovascular health; its anti-microbial, anti-fungal,anti-protozoal, and antioxidant activities; and itsimpact on the immune system andchemoprevention.1

Garlic and Cardiovascular Disease Prevention

Research studies, both animal and human, haveshown garlic to be effective at lowering cholesterol.1,2

Two meta-analyses of randomized human clinical tri-als conducted in the early 1990s reported a signifi-cant cholesterol-lowering effect of garlicsupplements.3,4 In trials with a one to three monthduration, supplemental garlic resulted in an averagereduction in serum total cholesterol (TC) of 9%to12% while triglycerides decreased 8% to 27% witha mean decrease of 13%.3 In five randomized place-bo-controlled studies of hypercholesterolemics(>200mg/dl), subjects in the garlic-supplementationgroup consistently showed a significantly greaterdecrease in TC.2 In 40 studies that investigated theeffect of various garlic preparations on the total cho-lesterol of 43 groups of patients and volunteers, themean decrease in serum cholesterol was 10.6% (treat-ments lasted three weeks to several months).1

Even more interesting results were found in a ran-domized double-blind placebo-controlled trial over48 months (n = 280) using high-resolution ultra-

sound to measure arterial plaque. While the placebogroup’s arteriosclerotic plaque increased an average of15.6%, the plaque of those in the treatment groupwho received 900mg/day of garlic actually decreasedan average of 2.6%.5 The authors hypothesized thatgarlic’s demonstrated ability to inhibit platelet aggre-gation was responsible for the dramatic reduction.6

Another suggested mechanism of action for garlic’slipid-lowering effects comes from an in vivo animalstudy, in which authors suggested that garlic exerts itsanti-atherogenic effects through inhibition of smoothmuscle cell phenotypic change and proliferation.7 Inthis study, a garlic-enriched diet fed to rabbitsreduced the surface area of the thoracic aorta, coveredby fatty streaks, by 64% and significantly reducedaortic arch (the bend in the second section of theaorta.) cholesterol. It also significantly inhibited(~50%) the development of thickened, lipid filledlesions in preformed neointimas (inner coating of thevessel) in the right carotid artery.7 Garlic’s ability toattenuate age-related increases in aortic stiffness wasalso shown in a human cross-sectional observationalstudy (n = 101).8

The oxidative modification of low-density lipopro-tein (LDL) is considered an important mechanism inthe development of atherosclerosis.9 Oxidized LDLpromotes vascular dysfunction and contributes toatherogenesis “by exerting direct cytotoxicity towardendothelial cells, by increasing chemotactic propertiesfor monocytes (movement of the monocytes torespond to chemicals), by transforming macrophagesto foam cells via scavenger receptors, and by enhanc-ing the proliferation of various cell types (e.g.,endothelial cells, monocytes, and smooth musclecells).” In vitro research has demonstrated that garlicsuppresses LDL oxidation by reducing the formationof thiobarbituric acid reactive substances (TBARS);TBARS is a biological response indicating the oxida-tion of LDL cholesterol.10 Small-scale human studieshave suggested that garlic supplementation increasesthe resistance of plasma LDL to oxidation.11,12 Thepotential antiatheroscleotic effect was seen in a studywhere 10 healthy volunteers were given 600 mg/dayof garlic powder for two weeks in a placebo-con-trolled, randomized, double-blind crossover trial.Serum lipid and lipoprotein levels were not lowered

in this short time period, however, the ex vivo suscep-tibility of apolipoprotein B-containing lipoproteins tooxidation was significantly decreased (-34%).11 A 10-month study compared the effects of aged garlicextract (AGE) with placebo on the lipid profiles ofmoderately hypercholesterolemic men. In a subgroupof the study population, researchers specifically exam-ined platelet function and lipoproteins’ susceptibilityto oxidation. A trend toward decreased susceptibilityof lipoproteins to oxidation was observed duringAGE administration compared with the placebo peri-od.12

In placebo-controlled trials of a dried garlic powderon hypertension, three studies showed a significantreduction in systolic blood pressure and four showeda reduction in diastolic blood pressure.13 Overall,from the average of all seven trials, the garlic groupshowed a significant reduction in blood pressurecompared to the placebo groups.iIn a promising,small open-label pilot study, a garlic preparation con-taining 1.3% allicin was evaluated in patients withsevere hypertension (diastolic blood pressure >115mm Hg). Sitting blood pressure fell significantly fivehours after the dose, with a significant decrease indiastolic blood pressure (p < 0.05) five to14 hoursafter the dose.14

Garlic also increases fibrinolytic activity andinhibits platelet aggregation, in part because of thepresence of ajoenes, allyl methyl trisulfide, vinyldithi-ins, and other sulfur compounds produced by thebreakdown of allicin.15 Both regular-use and singledoses of garlic have been shown to inhibit plateletaggregation.16,17

Allicin (allyl 2-propenethiosulfinate or diallyl thio-sulfinate) is thought to be the principal bioactivecompound of garlic. When garlic is chopped orcrushed, the enzyme alliinase is activated and it inturn acts on the allin present in garlic to produceallicin. Recent investigations examining clinical trialsthat failed to replicate the earlier success of garlic onlowering serum lipid levels have pointed to the needfor careful preparation, testing, and storage of garlicto ensure adequate levels of active allicin are availableto release in vivo. While study methodology has been

cited as a possibility for inconsistent results in sometrials, more substantial evidence points to the incon-sistency in preparations with trials using fresh garlic;garlic powder; garlic extract (both fresh and aged); aswell as tablets of compressed garlic powder. It hasbeen suggested that consistent lipid-lowering isdependent on standardization of garlic supplements.18

In addition, alliinase is acid-sensitive. A recent dou-ble-blind, randomized, placebo-controlled study of46 participants evaluated the hypocholesterolemiceffect of an enteric-coated garlic supplement, stan-dardized for allicin-releasing potential in 46 mild tomoderate hypercholesterolemic subjects. The 12-weekstudy administered 880mg/day of enteric-coated gar-lic tablets standardized to provide a total of 9.6 mg(1.09%) allicin per day, or a matching placebo tablet.The garlic group (n=22) had a significant reductionin total cholesterol and LDL while the placebo group(n=24) had a non-significant increase in total choles-terol and LDL cholesterol. HDL-cholesterol was sig-nificantly increased in the placebo group compared tothe garlic group, while no significant difference intriglycerides or LDL/HDL ratio was observedbetween groups.19 AGE supplementation has beenshown to be effective in lowering plasma concentra-tion of total cholesterol by 7% and LDL cholesterolby 10%, in hypercholesterolemic men, comparedwith subjects consuming a placebo. Supplementationof AGE in animal diets similarly reduced plasma con-centrations of total cholesterol and triacylglycerol by15% and 30%, respectively. These and additional invitro studies have suggested that the cholesterol-low-ering action of garlic might be attributed in part todepressed cholesterol synthesis in the liver.20

Antimicrobial Qualities of Garlic

Garlic has also been investigated as a treatment forits anti-microbial effectiveness.21 An in vitro study ofgarlic extract on human cytomegalovirus showed thatgarlic had a dose-dependent inhibitory effect; thestrongest anti-viral effect was demonstrated when gar-lic was applied continuously.22 A second in vitro studyof the antimicrobial activity of spices showed garlic ashighly effective in killing Staphylococcus epidermidisand Salmonella typhi (93%) and yeasts were totallyeradicated in one hour by garlic extract.23

cont. on page 13

cont. on page 54

Summer 2005 Volume 8, Issue 1Page

14 Summer 2005 Volume 8, Issue 1Page

15cont. on page 16

The University of Arizona is offering NCC membersa great opportunity for learning! “Nutrition & Cardiovascular

Health” - a 16.5 CPEU online course offered by the Program inIntegrative Medicine. Sign up online at:

www.integrativemedicine.arizona.edu and receive a 10% discount.To obtain the discount use the code: NCC1

MEMBER BENEFIT

Additionally, in a randomized clinical trial (n = 210)comparing two weeks of supplementation withallicin, beta-carotene, or ascorbic acid for the treat-ment of Helicobacter pylori (H. pylori), only theallicin proved effective.24 H. pylori is the bacteriumresponsible for serious gastric diseases, such as ulcersand cancer. In vitro research has also shown garlicalone can be effective at inhibiting the growth of H.pylori, as well as in synergistic combination with thedrug omeprazole.25 Another in vitro experimentshows that allicin has a strongly antimicrobial effect,inhibiting Entamoeba histolytica, an intestinal para-site.26

Garlic and Cancer Prevention

Garlic is known to have anti-tumor properties andis reported to enhance immune function by stimulat-ing lymphocytes and macrophages to destroy cancercells.27,28 A prospective study of 42,000 Iowa womenaged 55-69 revealed that garlic consumption wasinversely associated with cancer risk. For example,women with the highest consumption of garlic had a50% reduction in risk of colon cancer compared towomen who did not consume garlic.29 An in vitrostudy of human leukemia cells also showed thatajoene will inhibit proliferation and induce apoptosisof human leukaemia CD34-negative cells and has

been shown to induce 30% apoptosis in myeloblastsfrom a chronic myeloid leukaemia patient in blasticcrisis. Acute myeloid leukaemia (AML) is a heteroge-neous malignant disease in which disease progressionat the level of CD34-positive cells has a major impacton resistance to chemotherapy and relapse.30 A reviewof the protective role of nutrients against bladder can-cer recommended garlic as having great promise inchemoprevention.31 Additionally, animal studyshowed that supplementation with garlic effectivelyprevented oral precancer in rats.The authors suggest-ed that garlic does so by improving the activation ofNK cells, the function of T-lymphocytes, and thelevel of interleukin-2.32

Another study suggested that S-allylcysteine, anoth-er component of garlic, exerts its chemopreventiveeffects by modulating lipid peroxidation and enhanc-ing antioxidant activities in the target organ, as wellas in the liver and circulation.33 Other studies havesimilarly suggested that the chemopreventive activityof garlic is due to the presence of these organosulfurcompounds, and it has also been observed that it is apotent free-radical scavenger, with S-allylcysteine(SAC) and S-allymercapto-L-cysteine as the compo-nents with the highest radical-scavenging activity.34

In addition, garlic has been investigated for itsimpact on the immune system. An in vitro studydemonstrated that the garlic derivative alliin exertedimmuno-modulatory effects on certain functions ofthe peripheral blood cells.35 And finally, in a random-ized placebo-controlled trial of 146 volunteers, thegroup taking garlic supplements were less likely tohave colds and recover faster if they did, than theplacebo group.36

Adverse Reactions and Interactions

The consumption of raw garlic can produce adverseeffects, such as bad breath, body odor, and gastroin-testinal discomfort; these effects are mostly dose-relat-ed.37,38 It can also cause blood platelet dysfuction,including an increased risk of bleeding and prolongedbleeding time.38

Consuming large amounts of garlic, or taking garlic

supplements concomitantly with supplements knownto have anticoagulant/antiplatelet potential, mayincrease the risk of bleeding. Those that containangelica, clove, ginger, ginkgo, red clover, turmeric,vitamin E, or willow, are a few examples. In addition,individuals taking anticoagulant/antiplatelet drugssuch as heparin or warfarin should avoid excessiveamounts of fresh garlic, or garlic supplements, due toan increased risk of abnormal bleeding. Another riskis increased platelet inhibition by non-steroidal anti-inflammatory drugs and indomethacin.38

Take Home Message

For persons looking to try natural and traditionalmethods for managing cholesterol levels, severalforms of garlic may be effective. For example, takingonce daily a medium garlic clove (approximately 4gm of garlic), crushed and allowed to stand for 10minutes to stabilize its active compounds, as a supple-ment or used raw in food. Garlic extract powder con-taining 1.3% allin in doses of 200-400 mg threetimes daily has been used effectively in clinical trialsfor hyperlipidemia and hypertension. Aged garlicextract with a typical alliin content of 0.03% inamounts up to 7.2 grams has also been used in clini-cal trials.38

Incorporating fresh, raw garlic into one’s daily dietis generally a good health practice. The plethora ofgarlic research completed in the last two decades ispromising, and provides good rationale for includinggarlic in the diet, especially in those at risk for cardio-vascular disease. It’s important to read supplementlabels, because commercially prepared garlic prepara-tions vary significantly in the way they are prepared.They are available in capsule, liquid, and enteric coat-ed tablets. Just as with herbal supplements, there ispotential for herb-drug interactions. Any person tak-ing garlic for therapeutic purposes should informtheir health care provider.

Gretchen Vannice, MS, RD has worked in health edu-cation, complementary medicine, dietary supplementresearch and has developwd evidence-based educationprograms for health practitioners. She is currentlyResearch Coordinator for Nordic Naturals, where shefacilitates human clinical trials using Nordic Natural

fish oil products. Contact Gretchen at: gvannice@jps.net.References 1. Blumenthal M, ed. Herbal Medicine: Expanded CommissionE Monographs. Newton, MA: Integrative MedicineCommunications, 2000:139-148. 2. Prasad K, Mantha SV, Kalra J, et al. Prevention of hypercho-lesterolemic atherosclerosis by garlic, an antioxidant. JCardiovasc Pharmaol Ther 1997;2:309-320.3.Warshafsky S, Kamer RM, Sivak SL. Effect of garlic on totalserum cholesterol: A meta-analysis. Ann Intern Med1993;199:599-605.4. Silagy C, Neil A. Garlic as a lipid-lowering agent: A meta-analysis. J R Coll Physicians Lond. 1994;28:39-45.5. Koscielny J, Klussendorf D, Latza R, et al. The anti-athero-sclerotic effect of Allium sativum. Atherosclerosis. 1999;144:237-249.6. Cf. Ackermann RT, Mulrow CD, Ramirez G, et al. Garlicshows promise for improving some cardiovascular risk factors.Arch Intern Med. 2001;161:813-824. 7. Campbell JH, Efendy JL, Smith NJ, et al. Molecular basis bywhich garlic suppresses atherosclerosis. J Nutr. 2001;131:1006S-1009S. 8. Breithaupt-Grogler K, Ling M, Boudoulas H, et al. Protectiveeffect of chronic garlic intake on elastic properties of aorta in theelderly. Circulation. 1997;96:2649-2655.9. Keaney JF. Atherosclerosis: From lesion formation to plaqueactivation and endothelial dysfunction. Mol Asp Med.2000;21:99-166.10. Lau BH. Suppression of LDL oxidation by garlic. J Nutr.2001;131:985S-988S.11. Phelps S, Harris S. Garlic supplementation and lipoproteinoxidation susceptibility. Lipids. 1993;28:475-477.12. Steiner M, Lin RS. Changes in platelet function and suscep-tibility of lipoproteins to oxidation associated with administra-tion of aged garlic extract. J Cardiovasc Phamacol. 1998;31:904-908. 13. Silagy CA, Neil HA. A meta-analysis of the effect of garlicon blood pressure. J Hyperten. 1994;12:463-468.14. McMahon FG, Vargas R. Can garlic lower blood pressure? Apilot study. Pharmacotherapy. 1993;13:406-407.15. Bordia A, Joshi HK, Sanadhya YK, et al. Effect of the essen-tial oil of garlic on serum fibrinolytic activity in patients withCAD. Atherosclerosis. 1977;28:155-159.16. Kiesewetter H, Jung F, Pindur G, et al. Effect of garlic onthrombocyte aggregation, microcirculation, and other risk fac-tors. Int J Clin Pharmacol Ther Toxicol. 1991;29:151-155.17. Bouillin DJ. Garlic as a platelet inhibitor. Lancet.1981;1:776-777.18. Lawson LD, Wang ZJ, Papdimitriou D. Allicin release undersimulated gastrointestinal conditions from garlic powder tabletsemployed in clinical trials on serum cholesterol. Planta Med.2001;57:13-18. 19. Kannar D, Wattanapenpaiboon N, Savige GS, et al.Hypocholesterolemic effect of an enteric-coated garlic supple-ment. J Am Coll Nutr. 2001;20:225-231.20. Yeh Y-Y, Liu L. Cholesterol-lowering effect of garlic extractsand organosulfur coupounds: Human and animal studies. JNutr. 2001;131:989S-993S. 21. Salman H, Bergman M, Bessler H. Effect of a garlic deriva-

cont. from page 14 Supplements: Garllic Supplementation and its Impact onLowering the Risk of Cardiovascular and Other Diseases

cont. from page 13Supplements: Garllic Supplementation and its Impact onLowering the Risk of Cardiovascular and Other Diseases

cont. on page 15

cont. from page 15

Summer 2005 Volume 8, Issue 1Page

16 Summer 2005 Volume 8, Issue 1Page

17

tive (alliin) on peripheral blood cell immune responses. Int JImmunopharm. 1999; 21:589-597.22. Nai-lan G, Dao-Pei L, Woods GL, et al. Demonstration ofthe anti-viral activity of garlic extract against humancytomegalovirus in vitro. Chin Med J. 1993;106:93-96.23. Arora DS, Kaur J. Antimicrobial activity of spices. Int JAntimicrob Agents. 1999;12:257-262.24. Kockar C, Ozturk M, Bavbek N. Helicobacter pylori eradi-cation with beta-carotene, ascorbic acid, and allicin. ActaMedica. 2001;44:97-100. 25. Jonkers D, van den Broek E, van Dooren I, et al.Antibacterial effect of garlic and omeprazole on Helicobacterpylori. J Antimicrob Chemother. 1999;43:837-839. 26. Ankri S, Miron T, Rabinkov A, et al. Allicin from garlicstrongly inhibits cysteine proteinases and cytopathic effects ofEntamoeba histolytica. Antimicrob Agents & Chemother.1997;41:2286-2288. 27. Craig WJ. Health-promoting properties of common herbs.J Am Clin Nutr. 1999;70:491S-499S. 28. Thomson M, Ali M. Garlic (Allium sativum): A review of itspotential use as an anti-cancer agent. Curr Cancer Drug Targets.2003;3:67-81.29. Steinmetz KA, Kushi LH, Bostick RM, et al. Vegetable,fruit, and colon cancer in the Iowa women’s health study. Am JEpidemiol. 1994;139:1-15.30. Ahmed N, Laverick L, Sammons J, et al. Ajoene, a garlic-derived natural compound, enhances chemotherapy-inducedapoptosis in human myeloid leukemia CD34-positive resistantcells. Anticancer Res. 2001;21:3519-3523.31. Kamat AM, Lamm DL. Chemoprevention of bladder can-cer. Urol Clin North Am. 2002;29:157-168.32. Tang Z, Sheng Z, Liu S, et al. [The preventing function ofgarlic on experimental oral precancer and its effect n naturalkiller cells, T-lymphocytes and interleukin-2.] [Chinese.] HunanI Ko Ta Hsueh Hsueh Pao. 1997;22:246-248.33. Balasenthil S, Ramachandran CR, Nagini S. S-allylcysteine,a garlic constituent, inhibits 7,12-dimethylbenz[a]anthracene-induced hamster buccal pouch carcinogenesis. Nutr Cancer.2001;40:165-172.34. Sundaresan S, Subramanian P. S-allylcysteine inhibits circu-latory lipid peroxidation and promotes antioxidants in N-nitrosodiethylamine-induced carcinogenesis. Pol J Pharmacol.2003;55:37-42.35. Salman H, Bergman M, Bessler H, et al. Effect of a garlicderivative (alliin) on peripheral blood cell immune responses. IntJ Immunopharmacol.1999;21:589-597.35. Josling P. Preventing the common cold with a garlic supple-ment: A double-blind, placebo-controlled survey. Adv Ther.2001;18:189-193.36.Banerjee SK, Maulik SK. Effect of garlic on cardiovasculardisorders: a review. Nutr J. 2002 1:4. Available at:http://www.nutritionj.com/content/1/1/4. Accessed 8/1/03.37.Garlic (Allium satavium). Available at: http://www.natural-database.com/(zd5iln45jenbpv45lcugien3)/nd/Search.aspx?li=1&st=2&cs=&s=ND&pt=100&sh=0&id=300. Accessed 6/26/05.

Supplements: Garllic Supplementation and its Impact onLowering the Risk of Cardiovascular and Other Diseases

Editor’s Notes:SSaarraahh HHaarrddiinngg LLaaiiddllaaww,, MMSS RRDD MMPPAA

The new ADA year is upon us and with a newExecutive Committee and many exciting plans; NCCwill continue to move forward in promoting ourmembers as experts in Complementary Nutrition.This issue is an excellent resource for those of youwho work with clients with cardiovascular disease.With so much controversy surrounding the use ofstatin drugs to lower lipids, people are constantlylooking for alternatives. This issue offers informationon some of those alternatives as well as an excellentdiscussion on the role of Co Q 10 as an adjunct tostatin therapy.

As always, I welcome suggestions for topics andarticles from authors-experienced and not so experi-enced. If you would like to join the newsletter teamor write an article for an upcoming newsletter, do nothesitate to contact me. For author guidelines, pleasego to the NCC Web site:www.ComplementaryNutrition.org.

The annual Food and Nutrition Conference andExhibition in St Louis, MO is quickly approaching.On page 19 you will find a listing of presentationssponsored by NCC and others of potential interest tomembers. As you can see, the offerings for those incomplementary care appear to be growing exponen-tially. We certainly hope that you will be able to bethere this year and to join us in learning more cuttingedge complementary care information that can beapplied in practice every day.

For questions, comments, or to submit an articlecontact me at peaknut@cascadeaccess.com or 702-346-7968. I hope to hear from many of you.

NNUUTTRRIITTIIOONN IINN CCOOMMPPLLEEMMEENNTTAARRYY

Web site: www.ComplementaryNutrition.org

Member ElectronicMail List:Contact Gretchen Forsellto get connected(gisanRD@aol.com)

Summer 2005 Volume 8, Issue 1Page

18 Summer 2005 Volume 8, Issue 1Page

19

Four easy ways toupdate your addressand contact informa-tion with ADA

The American Dietetic Association (ADA) wants tomake it as easy as possible for you to keep youraddress, e-mail, and telephone information current.ADA offers four convenient methods for you to sub-mit this information: the Web, phone, fax or e-mail.Here is a step-by-step guide for you to change yourADA membership information so we can keep youabreast of all the current benefits and services and lat-est happenings in the field of dietetics.

Perhaps the easiest way to update your ADA mem-bership information is through the online businesscenter. Go to the ADA Web site at HYPERLINK“http://www.eatright.org” www.eatright.org and typeyour ADA membership number in the Member LogOn box, located at the right of the Web page. Next,click on Profile at the upper right. Enter your ADAnumber and your Web-only password as requested.

Your profile page will display, showing your currentADA contact information. To edit any of this infor-mation, including your e-mail address, click on theUpdate Contact Information button at the top left.You will now see a screen that enables you to makeany needed changes and add new information. Makeall changes and then click the Accept button locatedat the bottom of the page.

Your revised profile will appear. Review the infor-mation and click the Accept button again for the sys-tem to incorporate your changes. A new screen withdemographic questions now displays. Providing theanswers to these questions helps ADA develop newprograms and member services. After answering thequestions, click Accept. Your information will beupdated within 24 hours. It’s that easy!

It takes a slightly different process to change youraffiliate (state) association. From your Profile screen,click the ADA Member Payment button at the topleft. Use the pull-down menu to choose your affiliate.

Scroll down to the bottom (past the DPG listing) andclick on PAY BY CREDIT CARD button. There isNO payment required. You will then see a new screenshowing your new affiliate. Click Submit. All of yourchanges will be made within 24 hours.

If you prefer, you can e-mail address or contactinformation changes to HYPERLINK “mailto:mem-brshp@eatright.org” membrshp@eatright.org. Or youcan fax changes to us at 312/899-4812. You may alsocall the Member Service Center at 800/877-1600,ext. 5000 between 8 a.m. and 5 p.m. Central time,Monday through Friday.

ADA wants to ensure that you receive all of thebenefits, services and communications that yourmembership provides. So, no matter which methodyou choose to notify ADA of changes to your contactinformation, please do this as quickly as possible soyou don’t miss out!

MEET ME IN ST. LOUIE, LOUIEActivities of Interest to NCCMembers – FNCE 2005

October 23Anthocyanins and Flavonoids: Cancer PreventionPotential? - CPE Level: 3

Define and identify the nutrients and the foods thatare best sources of anthocyanins and flavonoids.Suggest potential health benefits and outline thepotential mechanisms of action. Susan Bowerman MS,RD; Kim Stote PhD, MPH, RD, Christine Sardo,MPH, RD

Genomics and Nutrition: Intersection 101 -CPE Level: 3

Verbalize the basic genetic concepts important for thetranslation of nutrition and genomics information tothe public. Envision the impact research advancesmay have on clinical practice. Ruth DeBusk PhD, RD;Colleen Fogarty MS, RD

October 24Dietary Supplement Use in the USA: Who’s UsingWhat and Why - CPE Level: 2

Obtain and use current data on the prevalence of andmotivations for dietary supplement use in the UnitedStates. Apply innovative methods for assessing totaldietary intake (including dietary supplements) indietetic practice. Mary Frances Picciano PhD; JohannaDwyer DSc, RD; Joanne Holden MS

NCC SPONSORED PRESENTATION:

Nutritional Neuroscience: Having a PositiveImpact on ADHD and Autism - CPE Level: 3

Identify specific genetic polymorphisms and resultantmetabolic disorders related in children with ADD,ADHD and other Autism Spectrum Disorders.Recommend appropriate interventions based onnutritional deficiencies or malregulations that resultfrom biochemical/physiologic defects. Jeff BradstreetMD; Victoria Kobliner MS, RD

Integrative Nutrition Philosophy: Implication inWomen’s Health CPE Level: 1

Identify the scientific evidence of inflammatory

response as it relates to the arachidonic and eicos-apaentonic pathways and design nutrition recommen-dations to optimize health outcomes. Understandhow diet may modulate various functions in the bodyand may lend to beneficial or detrimental roles inwomen’s health. Thomas Incledon MS, RD; JosephineConnolly Schoonen MS, RD

Phytochemicals to the Rescue in Cellular Warfare -CPE Level: 2

Gain knowledge on mechanisms of action of healthpromoting phytochemicals in the prevention of can-cer and cardiovascular disease. Explain the complexi-ties relating fruit and vegetable intake to cancer risk. Diane Birt PhD; Winston Craig PhD, MPH, RD

Beyond Calcium: Isoflavones, Vitamin D andOmega-3 PUFA Hold Keys to Bone Health -CPE Level: 3

Outline the new recommendations on vitamin D.Describe the health benefits that omega-3 polyunsat-urated fatty acids may provide for the strength ofbones. Robert Heaney MD; Ruth Carey RD; KennethSetchell PhD

October 25NCC SPONSORED PRESENTATION:

Teas: Traditional Beverages or Functional Foods? -CPE Level: 3

Characterize the pattern of beverage consumptionand associated nutrient intakes in the United States.Define and identify the principal phytochemicalcomponents of various teas and tisanes (herb teas).Cynthia Thomson PhD, RD, FADA; Jeffrey BlumbergPhD, FACN

Dietary Supplements and Ergogenic Aids: LessonsFrom a Sports Nutritionist - CPE Level: 2

Describe several popular nutritional ergogenic aidsused by athletes. Discuss the athletic enhancementevidence and claims associated with the aids. Be pre-pared to communicate usage or avoidance messageswith athletes, patients and clients. Carrie Peterson MS,RD

Epigenetics: Cutting-Edge Science in Maternal andFetal Nutrition - CPE Level: 3

Discuss recent research in maternal nutrition regard-ing the roles that high-quality protein, omega-3 fattyacids, choline, zinc, iron and other emerging nutri-ents play in ensuring proper fetal and early post-nataldevelopment and in the lifelong health of the off-spring. Miriam Erick MS, RD; Christina WilliamsPhD

Set Your Sites on Success.FNCE 2005 is the national opportunity to build and

s t rengthen your Professional Development Portfolio and

career path. Take advantage of over 20 hours of CPE.

Spend time discovering products and solutions at the Expo.

Enjoy networking with your colleagues in newly renovated

downtown St. Louis.

Register now atwww.eatright.org/fnce

AmericanDieteticAssociation

EXPLORE. EDUCATION

DISCOVER. NETWORKING

ADVANCE. SOLUTIONS

NCC 2004-2005 LEADERSHIP CONTACT

INFORMATION

EEXXEECCUUTTIIVVEE CCOOMMMMIITTTTEEEE

Susan Allen-Evenson RD, CCNChair 7771 Lake St Ste 3WRiver Forest, IL 60305Office: 800-917-3688Home: 708-366-8947Cell: 630-853-8891

Rick Hall, MS RD Immediate Past Chair 3618 West Summit Walk DriveAnthem, AZ 85068voice: 602-284-4607

Douglas S. Kalman MS RD, FACNChair-Elect Miami Research Associates6280 Sunset Drive #600Miami, Fl 33143Work: 305-666-2368Fax: 305-669-8966dkalman@miamiresearch.com

Gretchen Forsell, MPH, RD, LD Treasurer 2002 Highland DrNorfolk, NE 68701daytime: 402-644-7256fax: 402-644-7254Alt email:

Mary Alice Gettings, MS, RD, LDN,CDESecretary 205 Opal DriveCranberry Twp., PA 16066Work: 724-774-3003Home: 724-742-9638Fax: 724-774-0971

Deborah S. Ford MS RD, CCNEducation Chair5 Warren RoadVan Wert, OH 45891-2548Home: 419-238-3321Work: 419-238-3020

Caren Baltasi, LD, CCNLiaison Chair 3326 N Sacramento AveChicago, IL 60618Phone: 773-407-4687Caren133@hotmail.com

Laura W. Lagano, MS RDPublications Chair 931 Bloomfield StHoboken, NJ 07030Phone: 201-963-4945Cell: 201-988-8086Fax: 201-963-5764Lwlagano@optonline.net

Natalie Lagomarcino Ledesma MS RD Nominating Chair Cancer Resource CenterUCSF Comprehensive Cancer Center1600 Divisadero St, B101San Francisco, CA 94143-1725Home: 415-642-4919Cell: 415-505-5086Fax: 415-885-3701

Robert M. Maloof, MA RD, CCNMember Services Chair Therapeutic Lifestyle Center220 Lyon St. NW Suite 800Grand Rapids, MI 49503Work: 616-224-0548Fax: 616-776-6478

ADA STAFF LIAISON

Aiysha Johnson, MA American Dietetic Association120 Riverside Plaza, Suite 2000Chicago, IL 60606-6995voice: 800-877-1600 ext. 4778direct: 312-899-4778fax: 312-899-4812AJohnson@eatright.org

PROFESSIONAL ISSUES DELEGATE

Helen W. Lane, PhD RD Mail Code ADJohnson Space CenterHouston, TX 77058Phone: 281-483-7165Fax: 281-483-3379

OTHER LEADERS

Rita Kashi Batheja, MS RD CDNReimbursement/Legislative ChairMembership Committee Chair825 Van Buren StBaldwin Harbor, NY 11510daytime/eve: 516-868-0605krbat1@juno.com

Ruth DeBusk, PhD, RDTechnical Resource Advisor

Mahan Center2625 Mitcham DriveTallahassee, FL 32308-5404Daytime: 850-877-5865fax: 850-877-7936

Rebecca Ephraim RD, CCNStrategic Planning AdvisorPhone: 773-588-8185

Gretchen Forsell, MPH, RD, LD Electronic Mail List Coordinator 2002 Highland DrNorfolk, NE 68701Daytime: 402-644-7256Fax: 402-644-7254?

June GnassNominating Committee Chair-Elect1900 Sycamore LaneDurham, CA 95938-9744Home: 530-891-8523Work: 530-891-9357Fax: 530-891-9357

Annie Griffin, RD, LDCPE Committee Chair13611 Ferlace Ct NWPickerington, OH 43147Phone: 740-927-0773ahsugriffin@hsu.com

Kathie Swift, MS RD, LDNExternal Fundraising Committee Chair 235 Champlain DrPlattsburgh, NY 12901Phone/Fax: 518-563-9421

7/14/05

Mona Treadwell, MS, RDNominating Committee Member 13890 Ivy St.Thornton, CO 80602-9159Home: 303-426-0831

Sarah Harding Laidlaw, MS, RD, MPA1045 Raptor CircleMesquite, NV 89027

PRSRT STDUS POSTAGE PAIDGrand Junction, CO

PERMIT 229

Work: 303-726-7528

Susan Pitman, MA, RDOperations AdvisorWashington, DC 20016-2046Voice: 202-273-1220Fax: 202-273-1220

NCC STAFF

Katherine L. Bernard, MS RD CDNAdministrative Assistant90 Panamoka TrailRidge, NY 11961voice: 631-929-3834fax: 631-209-1569

Cory Gransee?Webmaster7653 E. Camino St?Mesa, AZ 85207phone: 480-213-0801corygransee@cox.net

Sarah Harding Laidlaw, MS RD MPANewsletter Editor1045 Raptor CircleMesquite, NV 89027Voice: 702-346-7968fax: 702-346-9031

Susan Moyers, PhD, MPH, LD/NWeb editor 1605 Send WayLutz, Fl 33549Voice: 813-948-9040Fax: 813-948-0010

Rebecca Schauer, RD, LDCopy Editor2916 42nd Ave SouthMinneapolis, MN 55406Ph/fax: 612-722-6080Work: 612-626-9445