20
Fall 2005 Volume 8, Issue 2 NCC Contents CPE: Modulating Chronic Pain: The Role of Nutrition and Botanicals . . . . . . . . . . . . .21 Supplements: New Dietary Supplements for the Management of Chronic Pain . .29 Of Interest to Members: Thanks To Our Sponsors . . . .39 Editorial Staff . . . . . . . . . . . . .38 Going to FNCE? . . . . . . . . .39 Chair’s Corner . . . . . .22 Editor’s Notes . . . . . . .22 NEXT ISSUE • Winter 2006 Editor’s Deadline, Nov. 1 • Spring 2006 Editor’s Deadline, Feb. 1 • Summer 2006 Editor’s Deadline, Apr. 15 A Dietetic Practice Group of the American Dietetic A s s o c i a t i o n cont. on page 23 Fall 2005 Volume 8, Issue 2 Page 21 Nutrition In Complementary Care F rustratingly difficult to treat, chronic pain is not uncom- mon. The Chronic Pain Association estimates that 50 million Americans live with, or more aptly endure, chronic pain daily. 1 Management of chronic pain generally falls into five domains: mechanical, pharmacological, cognitive/behavioral, nutritional, and complementary/alter- native therapies. Mechanical therapies include physical therapy, massage, exer- cise, hydrotherapy, and biofeedback. Pharmacological treatments are pre- scriptive and over-the-counter (OTC) preparations. The cognitive/behavioral domain includes mind-body therapies and counseling. Nutritional recommen- dations involve diet modifications and dietary supplements. Complementary/ alternative therapies include the use of herbs and botanicals. As the biochemi- cal understanding of pain and inflam- mation has been further elucidated, the use of dietary modifications and herbal supplementation as pain modifiers has been explored. CPE: Modulating Chronic Pain: The Role of Nutrition and Botanicals Sheila Sedig, MS RD The Inflammatory Process To understand how diet and botani- cals may influence the inflammatory process and accompanying pain response, it is first necessary to review that process and the biochemical ele- ments involved. Acute inflammation caused by injury or infection is a nor- mal physiological response that allows for healing and the ultimate return of normal tissue function. When inflam- mation is chronic, however, it can lead to chronic pain. Many factors con- tribute to this process. The broad process of pain perception begins with nociceptors (pain receptors) that send messages of mechanical, ther- mal, electrical, or chemical irritation via the afferent nerves to the central nerv- ous system, then the brain. Once such a message reaches the brain, it is inter- preted based on the physical pain stim- ulus and also on psychological aspects. These psychological elements encom- pass cultural and personal attitudes regarding pain, the individual’s prior experience of pain, and previous pain expression. 2 Psychological aspects of pain perception can be altered by mind- body therapies. The brain’s interpreta- tion of the pain is then sent via efferent nerves back to the nociceptors, causing a reaction to the pain - increased or decreased sensitivity to the pain stimu- lus and release of chemical modulators that affect perception of pain as well as tissue response to pain, primarily via the inflammatory cascade. It is this part of the process that is affected by medica- tions, diet, and botanical constituents. When a pain stimulus arrives at the nociceptor site, surrounding cells begin

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Page 1: Nutrition In Complementary Care NCC Fall 2005 Volume 8... · Fall 2005 Volume 8, Issue 2 Page 21 Nutrition In Complementary Care Frustratingly difficult to treat, chronic pain is

Fall 2005 Volume 8, Issue 2

NCCContents

CPE: Modulating Chronic

Pain: The Role of Nutrition and

Botanicals . . . . . . . . . . . . .21

Supplements:New Dietary Supplements for the

Management of Chronic Pain . .29

Of Interest to Members:Thanks To Our Sponsors . . . .39

Editorial Staff . . . . . . . . . . . . .38

Going to FNCE? . . . . . . . . .39

Chair’s Corner . . . . . .22

Editor’s Notes . . . . . . .22

NEXT ISSUE• Winter 2006Editor’s Deadline, Nov. 1• Spring 2006Editor’s Deadline, Feb. 1• Summer 2006Editor’s Deadline, Apr. 15

A Diete t ic Prac t ice Group o f the Amer ican Diete t ic A s s o c i a t i o n

cont. on page 23Fall 2005 Volume 8, Issue 2

Page

21

Nutrition InComplementary Care

Frustratinglydifficult totreat, chronic

pain is not uncom-mon. The ChronicPain Associationestimates that 50

million Americans live with, or moreaptly endure, chronic pain daily.1

Management of chronic pain generallyfalls into five domains: mechanical,pharmacological, cognitive/behavioral,nutritional, and complementary/alter-native therapies. Mechanical therapiesinclude physical therapy, massage, exer-cise, hydrotherapy, and biofeedback.Pharmacological treatments are pre-scriptive and over-the-counter (OTC)preparations. The cognitive/behavioraldomain includes mind-body therapiesand counseling. Nutritional recommen-dations involve diet modifications anddietary supplements. Complementary/alternative therapies include the use ofherbs and botanicals. As the biochemi-cal understanding of pain and inflam-mation has been further elucidated, theuse of dietary modifications and herbalsupplementation as pain modifiers hasbeen explored.

CPE: ModulatingChronic Pa i n :The Role of Nutrition and BotanicalsSheila Sedig, MS RD

The Inflammatory Process

To understand how diet and botani-cals may influence the inflammatoryprocess and accompanying painresponse, it is first necessary to reviewthat process and the biochemical ele-ments involved. Acute inflammationcaused by injury or infection is a nor-mal physiological response that allowsfor healing and the ultimate return ofnormal tissue function. When inflam-mation is chronic, however, it can leadto chronic pain. Many factors con-tribute to this process.

The broad process of pain perceptionbegins with nociceptors (pain receptors)that send messages of mechanical, ther-mal, electrical, or chemical irritation viathe afferent nerves to the central nerv-ous system, then the brain. Once such amessage reaches the brain, it is inter-preted based on the physical pain stim-ulus and also on psychological aspects.These psychological elements encom-pass cultural and personal attitudesregarding pain, the individual’s priorexperience of pain, and previous painexpression.2 Psychological aspects ofpain perception can be altered by mind-body therapies. The brain’s interpreta-tion of the pain is then sent via efferentnerves back to the nociceptors, causinga reaction to the pain - increased ordecreased sensitivity to the pain stimu-lus and release of chemical modulatorsthat affect perception of pain as well astissue response to pain, primarily via theinflammatory cascade. It is this part ofthe process that is affected by medica-tions, diet, and botanical constituents.

When a pain stimulus arrives at thenociceptor site, surrounding cells begin

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Fall 2005 Volume 8, Issue 2Page

22

C h a i r ’s Corner:Susan Allen RD, CCN

E d i t o r ’s Notes:Sarah Harding Laidlaw, MS RD MPA

It is September so it must be time for FNCE! Anotheryear has passed by quickly and the NCC leadership, likethe other DPG group’s leadership, is putting finishingtouches on plans for exciting events and presentations atthis year’s meeting in St. Louis. We hope to see many ofyou there and ask that you stop by, say hello, and if youare so inclined, volunteer for one of the many opportu-nities that NCC has to offer. Don’t miss us at the DPGShowcase and Product Marketplace and plan to attendthe informational breakfast Sunday morning at 7AMand the reception that evening. For more informationon the breakfast, reception, and NCC sponsored pre-sentations, see page 36.

As newsletter editor I am always interested in whatyou, our members, want to know more about. In addi-

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

NCC EDITORIAL STAFFEditor

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, WebmasterEML Coordinator

Gretchen Forsell, MPH RD

I don’t know about your part of the world, but herein Chicago we’re having our first taste of fall. After along hot summer, it’s very refreshing to have a breath ofcrisp, cool air. Though it won’t be long before naturestarts it’s slow shut down for the winter, it is also a timefor new beginnings: the start of school, sports seasons,perhaps even a new fall wardrobe!

This is also the time of year NCC plans for it’s newbeginning – the slate of officers for the 06-07 year. Nowis the time to get involved! Leadership can be reward-ing, especially when you know you’re contributing tomaking a difference for the future of the dietitian’s rolein CAM. It’s through likeminded leadership that we cancontinue the momentum we’ve begun. Who will joinus???

Currently NCC is searching for a treasurer. If youhave direct financial experience – great, however, pleaseknow that this position requires more ability to learnand become involved than it does as a financial wizard.Specific training and mentorship from ADA and ourcurrent treasurer will be available and as a board mem-ber, you will also have involvement in all NCC activi-ties. If you are interested in running for treasurer orother available positions, please contact NatalieLedesma, our Nominating Committee Chair or medirectly for more details.

Speaking of new beginnings, NCC leadership is com-mitted to the needs of its members. Shortly afterFNCE, a random sampling of our members will receivea survey. It is very important that we have 100%

involvement in this survey. With the information ofwho our members are and what they need most fromtheir membership, we can ensure that NCC effectivelymeets members’ needs and continues on its path ofgrowth and expansion. The information will help usattract sponsorship dollars that are critical to fund pro-gramming necessary to continue to position NCC as aleading DPG of ADA.

As we go to print, many of us are looking forward toattending this year’s FNCE in St Louis. NCC is veryexcited to have such a presence this year and we hopeall attending will be able to take full advantage of allNCC has to offer.

Remember, my e-mail box is always open - I’d love tohear from anyone at any time about any topic. Let’s allcontinue to support the success of this fine group!

cont. on page 23

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Fall 2005 Volume 8, Issue 2Page

23cont. on page 24

to react to this pain signal by initiating the inflammato-ry cascade. Tissue damage from free radicals, histamines,or an acidic pH can also trigger this cascade. In brief,small blood vessels in the area become dilated, simulta-neously increasing blood flow to, and slowing flow inthe area. Endothelial cells in the region become swollen;small plasma proteins, primarily fibrinogen, leak intothe area; and various immune cells, mainly T-lympho-cytes and macrophages, are attracted to this space.Immune cells then begin to secrete cytokines, signalingchemicals that activate, coordinate, and regulate cellgrowth, tissue repair, immunity, and inflammation.Examples of cytokines include tumor necrosis factor(TNF), the interleukins (IL), and the interferons (IFN).Cytokines signal surrounding cells to produce thecyclooxygenase (COX) and 5-lipooxygenase (5-lipox)classes of enzymes. These enzymes then metabolize fatin the surrounding cells’ membranes to formeicosanoids – prostaglandins, leukotrienes, and throm-

boxanes. Some eicosanoids are pro-inflammatory, esca-lating the whole inflammatory cascade and continuingthe process, while other eicosanoids are anti-inflamma-tory, inhibiting the process. Inhibition of cytokine andeicosanoid production has become the mainstay ofpharmacotherapy in chronic pain including the ill-fatedcyclooxygenase (COX) inhibitors, rofecoxib and cele-coxib, and the non-steroidal anti-inflammatory drugs(NSAIDS). Ultimately, the purpose of this cascade is fortissue to respond to pain, heal any damage, fight offinfection, then stop the inflammatory cycle and returnto normal function. When inflammation is chronic andthis process is not halted, the inflammation continues,creating chronic pain. According to current research,this contributes to arthritis, atherosclerosis, diabetes,colitis, and many other prevalent chronic illnesses.3

How do diet constituents and botanicals modulatethis cascade? Diagram 1 illustrates the biochemical path-way of eicosanoid production indicating where thesenutritional and herbal compounds play a role.4 Dietaryfactors that most influence this process include fats:essential polyunsaturated omega-6 and omega-3 fattyacids, trans fatty acids, and omega-9 fatty acids. Herbalcompounds that most affect the cascade are those thatpromote or inhibit the eicosanoid production pathways.

Mind-body treatments also impact this process. Theirimpact occurs directly in the brain, because this cascadeoccurs with real physical pain and with imagined painor stress. When the brain registers psychological painmessages are sent via efferent nerves to various tissueswhich initiate the inflammatory cascade.5 Cognitive/behavioral therapies help to decrease these stress mes-sages. While these therapies will not be the focus of thisarticle, nutrition professionals treating individuals withchronic pain should be aware of their efficacy.

The Role of Diet in the Inflammatory Process

Omega-3, Omega-6, Trans Fatty Acids, and OilsBecause eicosanoid production originates in the fatty

acids found in the membranes of cells in the affectedarea, the specific fatty acids present in these cellsbecomes important. The predominant omega-6 fattyacids (n-6 FA) present in the diet tend to promoteinflammation, while omega-3 fatty acids (n-3 FA) workto inhibit inflammation (diagram 1). Our ancestral dietshad an n-6:n-3 ratio of approximately 1:1.6 but mayhave been as high as 3:1.7 This ratio allows the inflam-matory cascade to proceed beneficially – damage isrepaired and the tissue is returned to normal, healthyfunctioning. If this ratio is in favor of n-6 FA, however,the pro-inflammatory pathway dominates. The balanceof the n-3 FA anti-inflammatory response is inadequate.Enzyme availability for the conversion of fatty acids toeicosanoids also impacts the process. The fatty acidcomposition of cell membranes is directly influencedover time by the dietary fatty acid composition ingested.

cont. from page 21

Modulating Chronic Pain:The Role of Nutrition and Botanicals

tion I am always looking for those of you who are aspir-ing or established authors to provide articles of interestfor the newsletter. Among the topics that we would liketo include are updates from members on what you aredoing to integrate complementary nutrition into yourpractice; functional foods – new or updated informa-tion; therapies such as yoga, meditation, and acupunc-ture; nutragenomics; and functional approaches tonutrition therapy, just to name a few. Any and all ideasand volunteers to help write, recruit authors or to editare welcome. Please email me at [email protected] with your ideas or to volunteer. Better yet,introduce yourself at FNCE so we both can put a faceand voice with a name.

If you have not checked out the NCC Web site atrecently, or at all, I encourage you to do so. It is updat-ed on a regular basis by the Web Editor, Susan Moyers,PhD. MPH/LDN and Webmaster Corey Gransee. Onthere you will find up to date and cutting edge infor-mation on complementary nutrition as well as links tothe NCC leadership, current events, and the awesomeresource and member benefit – Natural MedicinesComprehensive Database.

Until next issue…. Or you meet me in St. Louis –Sarah.

E d i t o r ’s Notes – cont. from page 22

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cont. from page 23

cont. on page 26

Modulating Chronic Pain:The Role of Nutrition and Botanicals

The fatty acid ratio in the typical Western diet isreportedly about 16:1.8. Omega-6 FA are found prima-rily in beef, pork, chicken, whole milk dairy products,egg yolks, vegetable and seed oils, and packaged conven-ience foods – all staples of the American diet. Omega-3FA rich foods include cold water fatty fish (salmon,mackerel, halibut, tuna), flaxseed and flaxseed oil,canola oil, walnuts, and purslane, a green leafy veg-etable. These are not as common in a Western diet.9

Some researchers call the typical Western diet a pro-inflammatory diet.3

The ratio of n-6:n-3 has been the subject of severalstudies. Simopoulos’ synopsis of these is interesting. Aratio of 4:1 decreased total mortality by 70% in the sec-ondary prevention of cardiovascular disease. Rectal cellproliferation was reduced in patients with colorectalcancer when dietary n6:n-3 ratio was 2.5:1, but a 4:1ratio had no effect when the absolute amount of n-3remained constant. There is a breast cancer protectiveeffect in women who have a low dietary n-6:n-3 ratio. Aratio of 2-3:1 in patients with rheumatoid arthritis sup-pressed inflammation. A ratio of 5:1 was beneficial inasthmatics, but a ratio of 10:1 increased respiratory dis-tress. Thus, the optimal ratio of n-6:n-3 appears to bedisease-specific.10

Supplementation with fish oils high in n-3 FA hasalso been studied in inflammatory disease states, notablyheart disease and arthritis.11,12 Studies have shown thatfish oil supplements improve clinical markers for heartdisease by reducing triglycerides and by decreasingblood pressure, arrhyhmias, thrombosis, atheroscleroticplaques and risk of sudden death.13 In arthritis, studieshave shown decreases in joint stiffness and pain rating,delay in onset of fatigue, and improvement in overallmobility.14 The mechanism of action is related to thedose of n-3 FA, specifically eicosapentaenoic acid (EPA)and docahexaenoic acid (DHA) involved in theeicosanoid series 3 pathway. A high intake of EPA andDHA has been shown to lower several biomarkers ofinflammation: C-reactive protein (CRP), interleukin-6(IL-6), soluble tumor-necrosis factor (TNF), E-selectin,soluble intracellular adhesion molecule (SICAM-1), andsolube vascular adhesion molecule (SVCAM-1).15 CRPis a small protein synthesized by the liver and present insmall concentrations, but increases dramatically inresponse to acute inflammation. CRP production isstimulated by interleukin-1. Interleukin-6 and TNF arepro-inflammatory cytokines. E-selectin, SICAM-1, andSVCAM-1 are adhesion molecules produced byendothelial cells after cytokine activation, which medi-ate further inflammatory response.

Excessive intake of trans-fatty acids (TFA), abundantin the convenience, processed foods of the Americandiet, has also been shown to increase two markers of

inflammation: IL-6 and CRP.16,17 TFA block fattyacid metabolism by inhibiting the delta-6-desaturaseenzyme (diagram 1).18,19 It is well-established that thesefats contribute to heart disease.20,21

Olive oil, a monounsaturated fat, has been promotedas heart healthy. It does contain omega-9 fatty acids (n-9 FA) which are involved in the inflammatory cascadeand the production of eicosanoids (diagram 1). Omega-9 FA may enhance anti-inflammatory prostaglandinproduction by promoting the eicosanoid series 1 and 3pathways from n-6 and n-3 FA respectively. Other n-9FA sources include olives, avocados, pecans, almonds,peanuts, cashews, sesame oil, pistachio nuts, andmacadamia nuts.22

It appears, however, that canola oil may be better thanolive oil for cardiovascular protection. The Lyon DietHeart Study showed a reduction in cardiovascularevents when substituting n-3-rich canola oil for oliveoil.23 Vogel, et al also reported a post-prandial reductionin brachial artery flow–mediated vasodilation after con-sumption of an olive oil-containing meal, but not in ann-3 enhanced canola oil-containing meal.24 This vesselconstriction could lead to inflammatory sequelae.

Antioxidants and Flavonoids

It is well established that antioxidants, including vita-mins and phytonutrients, play a role in reducing freeradical damage to tissue, preventing initiation of theinflammatory cascade. Vitamin C and carotenoids,found in fruits and vegetables, have proven antioxidantability. An article in 1993 by Ames, Shigenaga, andHagen supported the recommendation of encouragingAmericans to eat at least five servings of fruits and veg-etables per day because of this antioxidant activity.25

Ames, Gold, and Willett confirm the antioxidant prop-erties of vitamin C and carotenoids, particularly in rela-tion to protecting DNA from oxidative damage. Theyalso report that one of folate’s roles is maintaining DNAstability and that fiber decreases the risk of coloncancer.26 Folate and fiber are constituents of fruits andvegetables. Meydani reinforces that n-3 and n-9 FA, aswell as vitamin E and other antioxidants found in fruits,vegetables, and nuts, play a role in reducing the expres-sion of cytokines, thus inhibiting the inflammatory cas-cade.27 Studies with apples reveal they contain strongantioxidant phytochemicals: catechin, quercetin, phlo-ridzin, and chlorogenic acid. These agents can lowerserum cholesterol, inhibit lipid oxidation, and decreasecancer cell proliferation.28 In an excellent review,Donaldson lists not only the antioxidant qualities offruits and vegetables, but also the protective vitamins,

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cont. from page 24 Modulating Chronic Pain:The Role of Nutrition and Botanicals

O M E G A - 6 O M E G A - 3Sources: Safflower,sunflower, sesameand corn oils

Primary Source:Flaxseed OilLinoleic Acid (LA)

Gamma-LinoleicAcid (GLA)

Sources: Eveningprimrose oil, blackcurrant oil, borageoil

Source: Blackcurrant oil

Alpha-LinoleicAcid (ALA)

SteardonicAcid (SDA)

Dihomo-gamma-linoleic Acid (DGLA)

Converted bycyclooxygenase-2 enzyme

(cox-2 enzyme)

Eicosanoid Series 1:anti-inflammatory

ArachidonicAcid

Sources: animalfats (meat anddairy)

DHA (ImportantBrain EFA)

EicosapentaenoicAcid (EPA)

Sources: Fish oil(coldwater fish,including sardines,salmon and mackerel)

Eicosanoid Series 3:Decreases pain

Anti-inflammatoryVasodilates

Decreases blood clottingDecreases platelet stickiness

Decreases blood pressure

Eicosanoid Series 2:Promotes pain

Promotes inflammationVasoconstricts

Increases blood clottingIncreases platelet stickiness

Increases blood pressure

Thromboxanes(inflammatory)

Leukotrienes(inflammatory)

Inhibited byBoswellia Complex,

Cramplex, garlic,onions, ginger,

flavanoid-rich herbs

Inhibited byaspirin, Boswellia

Complex, Cramplex,Saligesic, ginger,

garlic, onions,feverfew

Inhibited bysteriods, licorice,

feverfew

D I AGRAM 1. METABOLISM OF ESSENTIAL FATTY AC I D S

Converted byDelta-6-desaturase enzyme.

Requires Be, Mg, Zn.Inhibited by trans-fats, alcohol.

Converted by Delta-5-desaturase enzyme.Requires Vit. C, niacin, Zn.Enhanced by Omega-9’s.

PREFERREDPATHWAY

NOTE: Eicosanoids are also called Prostaglandins.

©Reprinted by permission - 8/2005www/drjlang.comCopyright by Dr. Janet Lang, DC

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Fall 2005 Volume 8, Issue 2Page

26

Modulating Chronic Pain:The Role of Nutrition and Botanicals of the proteoglycan matrix and the shock-absorbing gly-

cosaminoglycans (GAG), long unbranched polysaccha-rides. High doses of glucosamine have mild anti-inflam-matory effects by decreasing cytokine stimulated synthe-sis of COX-2 enzymes.38

Chondroitin sulfate is also a GAG and is derived fromshark and cow cartilage. Chondroitin acts as the founda-tion of the proteoglycan matrix in joint cartilage.39

Chondroitin protects cartilage from damage in threeways. It interferes with leukocyte elastase, an enzymethat promotes the production of pro-inflammatorycytokines from white blood cells. Chondroitin decreasesthe migration of white blood cells (WBC) into the pro-teoglycan matrix. When activated these WBC releasesignaling chemicals which promote further inflamma-tion. It also increases the production of proteoglycansand hyaluronic acid, another shock-absorbing GAG.40

Glucosamine and chondroitin are often used in com-bination for arthritis relief, however, there is a lack ofevidence that this combination is any better than eithercompound used alone. Because more investigation ofthese dietary supplements is warranted, the NationalCenter for Complementary and Alternative Medicine(NCCAM) is currently conducting the GAIT(Glucosamine/Chondroitin Arthritis Intervention Trial)study. This multicenter study will compare glucosaminealone, chondroitin alone, glucosamine and chondroitintogether, celecoxib (a COX-2 inhibiting NSAID), andplacebo. Results from this trial are expected to be pub-lished later this year.41

Recommended dosing of glucoasmine is 500 mg threetimes/day and for chondroitin it is 400 mg threetimes/day.37 Combination tablets commonly contain500 mg glucosamine and 400 mg chondroitin and thedosing recommends three or more tablets per day. Thereare combination tablets on the market with higher levelsof each substance with the same ratio.

There is some concern about glucosamine causing ele-vated blood sugar, but in studies this has not beenshown to negatively impact glycosylated hemoglobinlevels. Some preliminary evidence shows that chon-droitin may increase the risk of prostate cancer, so untilfurther studies are conducted men who have or are atrisk for prostate cancer should not use chondroitin.There is also some concern that because chondroitin issometimes made from bovine cartilage, there is a risk forbovine spongiform encephalopathy, mad cow disease. Todate there have been no reported cases of BSE in thosetaking chondroitin.42

The Role of Botanicals in the Inflammatory Process

minerals, phytochemicals and fiber constituents of thesefoods. He concludes with an outline for an anticancerdiet, part of which recommends 10 servings of vegeta-bles per day (including cruciferous and allium vegeta-bles) and four or more servings of fruits a day.29

More recently flavonoids, which include flavones andisoflavones (the latter are polyphenol plant chemicalswith a structure similar to mammalian estrogen), havereceived attention. These food components are found inabundance in soy products, highly pigmented fruits,and teas. The isoflavones genistein and daidzein, foundin soybeans, are active antioxidants.30 Flavonoids havebeen shown to have the following effects: anti-inflam-matory;31 eicosanoid synthesis inhibition and protectionof collagen;32 and the reduction of capillary permeabilityand fragility,33 which impacts the inflammatory cascadeat its inception, reducing the influx of the variouschemicals and cells that are involved in escalating theinflammatory response. Flavones have also been shownto inhibit the formation of free radicals from oxidationin an injured area, particularly by regulating nitric oxideproduction. When released from activated macrophages,nitric oxide can destroy tumor cells, intracellular bacte-ria, and parasites. In high concentrations, however, itcan destroy healthy endothelial tissue and contribute toinflammation.34 In a small study with dogs, monkeys,and humans, Folts showed this nitric oxide regulationfrom flavonoids in grape products and also revealed theanti-platelet aggregation role of these chemicals.35 Artsand Hollman report that the polyphenol subclasses,flavones, catechins, and lignans, exert beneficial effectsin cardiovascular disease and lung cancer.36 To furtherelucidate the exact mechanisms of these protectiveagents they recommend prospective studies using thesedifferent polyphenol subclasses.

Although animal products contain some antioxidants,the vast majority of antioxidants and flavonoids arefound in fruits, vegetables, nuts, and soybean products.The American Dietetic Association, the American HeartAssociation, the American Cancer Society, and severalother agencies have urged Americans to increase theirintake of fruits and vegetables. The American HeartAssociation also recommends increasing n-3 FA intake.Table 1: Dietary Recommendations to DecreaseInflammation summarizes a few recommendationsnutrition professionals can provide to clients.

Dietary Supplements: Glucosamine andChondroitin

Glucosamine sulfate belongs to the family of cartilageproteoglycans and is isolated from oyster and crabshells.37 Proteoglycans are protein-carbohydrate mole-cules which have many physiological functions. It hasbeen shown in joint cartilage to stimulate the synthesis

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cont. from page 6

cont. on page 28

Many botanicals have been used to reduce inflamma-tion and ease pain, several of which are included in dia-gram 1. Information on a few of the most commonlyused herbals for chronic inflammation follows. Some ofthe information for each product is taken from theNatural Medicines Comprehensive Database (NMCD),thus is not referenced each time. Many of these botani-cals are also used for other conditions, but only theiranti-inflammatory actions are discussed here.

Evening Primrose Oil, Black Currant Oil, and Borage Oil

These oils are sources of gamma linolenic acid (GLA).An omega-6 FA, GLA is a precursor to the anti-inflam-matory eicosanoid series 1 pathway and preferentiallyreduces IL-1-beta, a pro-inflammatory cytokine. GLA isconverted to dihomo-gamma-linolenic acid (DGLA), aprecursor to the potent anti-inflammatory prostaglandinE1 (diagram 1).43,44,45 Borage oil also provides steardonicacid (SDA), which is converted to EPA by delta-5-desaturase, competitively inhibiting arachidonic acid(AA) production and thus decreasing formation of theinflammatory leukotrienes via the eicosanoid series 2pathway (diagram 1).46 Barham, et al showed that usingEPA and GLA supplementation in combination

decreased the synthesis of pro-inflammatory AAmetabolites via delta-5-desaturase competitive inhibi-tion.47

Dosing: 540 mg to 2.8 g daily for evening primrose(Oenothera biennis) oil; best when used in combinationwith fish oils and vitamin E. There is no standarddosage for black currant (Ribes nigrum) oil. 1.1 to 1.4 gdaily up to 24 weeks has been used for borage (Boragoofficinalis) oil.

Licorice

Licorice (Glycyrrhiza glabra) inhibits the conversion ofDGLA to AA, ultimately decreasing the synthesis ofprostaglandins E and F2 alpha. These are pro-inflam-matory prostaglandins particularly active in gastrictissue and can contribute to ulcer formation.48,49

Dosing: There is no standard dosing for anti-inflam-matory effects, and it is usually used as the degly-dyrrhizinized (DGL) extract.

Feverfew

A small plant with feathery leaves, feverfew(Tanacetum parthenium) has been used for its therapeu-tic effects for generations. Like licorice, feverfew inhibitsthe production of AA from DGLA, preventing pro-inflammatory prostaglandin synthesis.50,51 Parthenolide,an active ingredient of feverfew, selectively inhibitsCOX-252 and chrysanthenyl acetate, an essential oil offeverfew that inhibits prostaglandin synthesis and mayhave analgesic affects.53

Dosing: There is no standard dosing given for anti-inflammatory effects, but 50 to100 mg of feverfewextract standardized to 0.2% to 0.35% parthenolide/dayhas been used for migraine relief. No topical dosing isgiven.

Garlic

There is a plethora of research about garlic (). Garlicis used as an antihypertensive, anti-cholesterolemic,antiviral agent, anticancer agent, GI protectant, andan aid in several other maladies. To maintain brevity inthe current discussion, garlic biochemically inhibits theproduction of pro-inflammatory thromboxanes andleukotrienes from AA. It is an antioxidant as well asanti-inflammatory agent. It is proposed that allicin isthe active ingredient in garlic.54,55

Dosing: There is no standard dosing for garlic, butthe more an individual consumes the more adverseaffects they may experience such as breath odor or GIdistress.

Turmeric

Turmeric is a spice from the root of the plant

TABLE 1. Di e t a ry Ways to De c rease In f l a m m a t i o n

Practical ways to change the fatty acid profile of the diet:• Gradually decrease the amount of beef, pork, and poultryand increase the amount of cold water fish over time. Forexample: replace chicken or ground beef with broiledsalmon or mackerel; replace a chicken salad sandwich witha tuna salad sandwich.• Use canola or olive oil in place of other vegetable oils forsalad dressings and in cooking.• Add ground flaxseed, walnuts, or pumpkin seeds to sal-ads, soups or cooked vegetables.• Use omega-3 fortified eggs.

Practical ways to increase fruits and vegetables in thediet:• Make fresh fruit and vegetables visible in the home; theyare more likely to be eaten if they are seen.• Add frozen or fresh cut vegetables to soups, salads, orpasta dishes.• Add berries to muffins, waffles, or pancakes. Add otherfresh or frozen fruits to cereals or yogurt.• Buy, wash, cut up, and place fruits and vegetables inindividual containers to use easily and quickly during busytimes.• Take dried fruit in the car, to the office, and visibly leaveon the counter to snack on during the day.

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Dosing: Extracts with 120 mg to 240 mg of thesalacin component have shown efficacy, but the higherend dose is recommended to achieve results.63 It alsoappears that one must use white willow for at least oneweek before some pain relief is experienced.

Indian FrankincenseIndian frankincense (Boswellia serrata) extract has

been used for its anti-inflammatory, anti-arthritic, andanalgesic effects. The resin of the plant containsboswellic acids that inhibit the synthesis of the 5-lipoxenzymes and the formation of leukotrienes. These acidsmay also decrease GAG degradation and cartilage dam-age, which may explain their anti-arthritic qualities.64

Kimmatkar, Thawani, Hingorani, and Khiyani used theextract in 30 patients in a double-blind, cross-over,washout study for eight weeks and found that allpatients receiving the herbal therapy reported decreasedknee pain and swelling and increased knee flexion andwalking distance.65

Dosing: 333 mg three times/day is standard dosingfor osteoarthritis and 3600 mg/day for rheumatoidarthritis.

Devil’s Claw

An African plant, the root of Devil’s claw(Harpagophytum procumbens) contains several activeingredients, one of which is harpagoside. This chemicalappears to have anti-inflammatory effects by inhibitingthe inflammatory pathways of both COX-2 and lipoxy-genase. It may also inhibit nitric oxide synthase, anenzyme that produces the free radical nitric oxide.66

While Devil’s claw has been used for centuries, there issome controversy regarding the quality of the researchdone with this compound (see dosing below).

Dosing: Chrubasik, Conradt, and Black recommendthat more thorough research on Devil’s claw is needed,but they do state studies using at least 50 mg ofharpagoside/day do seem to show effectiveness withpain relief.67

Bromelain

Bromelain (Ananas comosus), a crude extract from thestem and fruit of pineapple, contains various proteinasesthat have anti-edematous, anti-inflammatory,antithrombotic, and fibrinolytic activities.68 By decreas-ing immune cell migration to injured areas and decreas-ing activation of leukocytes already present in aninjured area, bromelain inhibits the inflammatory cas-cade, primarily decreasing prostaglandin E2 and throm-boxane A2. It also decreases plasma fibrinogen levels,

Curcuma longa, a member of the ginger family. Its com-ponent curcumin has several actions in the inflammato-ry cascade. It inhibits COX-1, COX-2, and lipooxyge-nase enzymes, thus decreasing formation of the inflam-matory prostaglandins - leukotrienes and thromboxane.Curcumin also inhibits the damaging action of nitricoxide and several enzymes: phospholipase, collagenase,elastase, and hyaluronidase. Curcumin inhibits the for-mation of monocyte chemoattractant protein-1 (MCP-1), interferon-inducible protein, tumor necrosis factor(TNF), and interleukin-12 (IL-12); all involved ininflammation or free radical damage which then pro-motes inflammation.56,57

Dosing: Curcumin has been found to be safe forhumans at doses from 1125 to 2500 mg curcumin/dayand as high as 8000 mg/day, this for three months.57

GingerGinger (Zingiber officinale) has been used in rheuma-

toid arthritis (RA) and osteoarthritis (OA), providingsome relief of pain. Using a standardized and highlyconcentrated extract of two different ginger species(Alpinia galangal and Zingiber officinale), Altman andMarcussen found a statistically significant decrease inthe symptoms of OA in a group of 247 patients.58 Theactual data from this study are interesting: subjectively,the percentage of responders with a reduction in kneepain was 63% in the ginger group versus 50% for con-trols (p=0.048) over the 6-week course of the study.When using a 100 mm visual analog scale to determinepain, it was found that subjects had a reduction in kneepain when standing (24.5 mm versus 16.4 mm;p=0.005) and a reduction in knee pain after walking 50feet (15.1 mm versus 8.7 mm; p=0.016). There was alsoa decreased use of rescue medication in the ginger groupversus the control group during the study. It is pre-sumed that the anti-inflammatory effect of gingercomes from its inhibition of the COX and 5-lipoxenzymes and decreased production of the cytokinesTNF-alpha, prostaglandin-E2 and thromboxaneB2.59,60,61

Dosing: A standard dosing of ginger extract for OA is170 mg three times per day or 255 mg two times perday.

White Willow

White willow (Salix alba) comes from the bark of theSalix tree species and contains flavonoids and salicin,which is metabolized to salicylate upon absorption.Flavonoids are discussed above. Salicylates, like aspirin,decrease the production of pro-inflammatoryprostaglandins, thus inhibiting inflammation. Whitewillow bark has been found to be particularly helpful inthose with low back pain.62

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SUPPLEMENTS: New Dietary Supplements forManagement of Chronic Pain Wendy Van Ausdal, BS, Stacey J. Bell, DSc, RD,Greg T. Grochoski, BS

All of us, rich or poor, young or old, have onething in common: we experience pain. Pain isthe signal that the body uses to notify the brain

that something is wrong. In its less serious form, paintells us that we need to rest and recover. At higher, morepersistent levels, pain prompts us to take medicine orsee a doctor.

There are two categories of pain: acute and chronic.Acute pain can appear as the result of disease, inflam-

mation, or injury, and its onset isusually sudden. Acute pain generallyends when the original cause of thepain is treated and healing occurs.Chronic pain, on the other hand,tends to come on more gradually. Itpersists over a longer period of time,and is often resistant to medicaltreatments. Studies report that 12%1

to 58%2 of the population now expe-riences chronic pain. Factors such assex, age, professional status, and envi-ronment (ie: rural or urban) mayaccount for this wide range.

Pharmaceutical Treatment Optionsfor Chronic Pain

There are a number of ways thatchronic pain sufferers can manage and

lessen—even eradicate, in somecases—their discomfort. While popu-lar natural treatments—from relax-ation therapy to exercise, herbs toacupuncture—can certainly be bene-ficial, the most common method ofconventional pain relief is analgesicadministration (Table 1). Analgesicsare a class of medications that include

both over-the-counter (OTC) drugs and prescriptionmedicines. One recent pain survey conducted at a veter-an’s hospital studied 300 randomly chosen patient

charts and found that 75% of the chronic pain patients(ages 30 to 90) were prescribed at least one analgesicand most (61%) received two or more.3 Of the anal-gesics prescribed, 67% were NSAIDs (non-steroidalanti-inflammatory drugs), 44% were opioids (strongprescription painkillers), and 29% were acetaminophen(a drug that reduces pain and fever but not inflamma-tion).

NSAIDs can be very useful for treating mild to mod-erate pain and for reducing inflammation; however,they can also have a number of potentially problematicside effects. NSAIDs can irritate the lining of the stom-ach and gastrointestinal tract, leading to digestive upset,peptic ulcers, and bleeding in the digestive tract.Bleeding in areas other than the GI tract is also com-mon because this class of drugs reduces platelet aggre-gation.4 In addition, using NSAIDs can increase therisk of cardiovascular (CVD) events. It was for this rea-son that two popular prescription NSAIDs (the COX-2inhibitors rofecoxib and valdecoxib) were recently with-drawn from sale. All NSAID labels must now highlightthe potential for increased risk of CVD events.5

Opioids are potent prescription drugs that are chemi-cally related to morphine and have many side effects,most notably that they slow the gastrointestinal tractand they are addictive. Over time, an individual’s opi-oid use often increases because the body adapts to thedrug and thus responds less well to it—a conditioncalled tolerance. People who take opioids over longperiods of time usually become dependent on them.4

Acetaminophen also treats pain, though it has noanti-inflammatory actions. Although the exact site andmechanism of action are not clearly defined, acetamin-ophen appears to produce analgesia by raising the painthreshold, predominantly through a central rather thanperipheral mechanism. It does not affect blood clottingand has almost no adverse effect on the stomach. Highdoses of acetaminophen drugs, however, can lead toirreversible liver damage.4

Due to the risks of known—as well as potentiallyunknown—side effects of conventional drugs, peoplesuffering from chronic pain are always searching fornew, safer treatments. Many patients turn to dietarysupplements. The purpose of this article is to reviewtwo dietary supplements for pain relief—krill oil andplant-based B-ring flavonoids and flavans (BRFF).

Krill Oil

There are nearly a hundred species of krill, smallshrimplike crustaceans that populate the oceans of theworld. One useful form of krill oil is derived fromAntarctic krill (Euphausia superba). This species feedson nutrient-rich phytoplankton, which probably

Wendy Van Ausdale

Stacey J. Bell

Greg T. Grochoski, BS

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accounts for the krill oil’s potent antioxidants, includingvitamin A, vitamin E, and astaxanthin. Researchersspecifically studied krill oil for pain relief because it isalso rich in eicosapentaenoic acid (EPA) and docosa-hexaenoic acid (DHA), both long-chain omega-3polyunsaturated fatty acids (PUFAs). The two double-blind, prospective studies discussed below support a rolefor krill oil in pain relief for premenstrual syndromeand osteoarthritis.

Premenstrual Syndrome (PMS)

Seventy women diagnosed with PMS were randomlyassigned to receive two grams daily of krill oil or equiva-lent doses of fish oil during the first month of the study,and then the same doses cyclically (8 days prior to andday one and two of menstruation) during the secondand third months. At baseline and on days 45 and 90,the scores of a self-assessment questionnaire for PMS,which is based on the diagnostic criteria for premen-strual syndrome of the American College ofObstetricians and Gynecologists, were assessed, as wasthe frequency of analgesic use for menstrual pain.

Both krill oil and fish oil significantly (p<0.001)decreased abdominal pain on days 45 and 90. Krill oil,but not fish oil, also significantly improved two otherindices of pain: joint pain and breast tenderness

(p<0.001). In addition, krill oil significantly improvedphysical score measurements (swelling, bloating, andweight gain) and psychological score measurements(stress, irritability, depression, and feeling overwhelmed)at both 45 (p<0.001) and 90 (p<0.001) days. The onlyother significant improvements in the fish oil groupwere reduced weight gain on days 45 (p<0.04) and 90(p<0.01) and swelling on day 90 (p<0.001).

Although both these marine oils decreased the use ofanalgesics, krill oil was significantly more effective thanfish oil (p<0.03), resulting in a 50% reduction inibuprofen and acetaminophen use by day 90. In thisstudy, krill oil appeared to reduce pain related to men-strual cramps within 45 days and improve other PMSsymptoms, such as swelling, bloating, stress, and depres-sion.6

Krill Oil for PMS Pain: Mechanism of Action

Pain associated with PMS was reduced due to the pro-duction of less potent prostaglandins (PGs) and throm-boxanes (TXs) as well as a reduction in muscle contrac-tions. Diets high in omega-6 fatty acids and low inomega-3s decrease endometrial blood flow which hasbeen associated with pain (i e: abnormal cramping).Compared to those with no pain, women with painfulmenstrual cramps have higher circulating levels of themetabolites PGE2 and PGF2a, which are derived fromarachidonic acid (AA), an omega-6 fatty acid. In con-trast, eicosanoids derived from omega-3 fatty acids likekrill oil (e.g. PGE3) reduce the contraction of smoothmuscle, including the uterine muscle, and produce lesspain. Most NSAIDs also decrease the AA metabolitesand also result in decreased pain.7 At this point the exactreason for krill oil’s efficacy at reducing pain isunknown, however through more research this shouldbe determined.

Osteoarthritis

Ninety subjects diagnosed with cardiovascular disease,rheumatoid arthritis, or osteoarthritis, as well asincreased levels of C-reactive protein (CRP), a marker ofinflammation, were randomly assigned to receive aplacebo or 300 mg of krill oil per day for 30 days. Atbaseline and on follow-up visits on day 7, 14, and 30,blood was drawn for serum CRP analysis, and patientscompleted the Western Ontario and McMaster(WOMAC) University Osteoarthritis Index question-naire. Krill oil significantly lowered CRP compared toplacebo (krill oil: 2.49 mg/dl at baseline and 1.75 mg/dl

Table 1. Common Analgesic Non-Steroidal Anti-Inflammatory Drugsand Opioids.*

NSAIDs Opioids

Aspirin Morphine

Ibuprofen Codeine

Naproxen Fentanyl

Celecoxib Meperidine

Rofecoxib Methadone

Valdecoxib Propoxyphene

Diclofenac Levorphanol

Indomethacin Hydromorphone

Ketoprofen Oxycodone

Mefenamic acid Oxymorphone

Piroxicam Pentazocine

*Adapted from: Pain (Chapter 78).The Merck Manual of MedicalInformation—Second Home Edition,Online Version. Available at:http://www.merck.com/mmhe/sec06/ch078/ch078d.html. Accessed 6/16/05.

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studies confirmed COX-2 inhibition and anti-inflam-matory action. The following scientific study supportsthe efficacy of BRFF.

Osteoarthritis

In a double-blind study, 52 patients (ages 40 to 75)with mild to moderate osteoarthritis were given a place-bo or the BRFF extract (125 mg) twice daily for 90days. Patients underwent clinical and biochemical evalu-ations and completed the WOMAC UniversityOsteoarthritis Index for assessment of pain, stiffness,and functional impairment at baseline and on days 30,60, and 90. BRFF significantly decreased WOMACpain scores compared to baseline at day 30 (3.17 and2.65; p=0.058) and at day 90 (3.17 and 2.67; p=0.045).There was no reduction in pain with the placebo. BRFFsignificantly improved scores for stiffness (30 days:p=0.004; 60 days: p=0.002; 90 days: p=0.003) andfunctional impairment (30 days: p=0.006; 60 days:p=0.016; 90 days: p=0.018), while the placebo did not.This study supported a role for BRFF in reducing painassociated with osteoarthritis.13 Another study has beenplanned and is due to begin in late 2005.

BRFF for Joint Pain: Mechanism of Action

Traditional NSAIDs work by inhibiting both COX-1and COX-2 enzymes, resulting in a reduction of bothbeneficial and pain-inducing forms of PGs and TXs.COX-1 inhibition causing a reduction of beneficialeicosanoids, which are linked to the production of PGsregulating normal physiological function, is thought tobe related to many of the reported side effects associatedwith NSAIDs, such as gastric erosion. Newer NSAIDforms (e g: rofecoxib, valdecoxib, and celecoxib) weredesigned to inhibit, in a highly selective manner, onlythe COX-2 enzyme, and are thus sometimes referred toas COX-2 selective NSAIDs. Therefore, fewer NSAID-associated side effects occur with COX-2 selectiveNSAIDs, which do not inhibit the COX-1 enzyme. Useof the COX-2 selective NSAIDs rofecoxib and valdecox-ib, however, produced an increased risk of CVD andhave been banned from sale by the Food and DrugAdministration.5 Some scientists have theorized that thelack of COX-1 inhibition by COX-2 selective NSAIDsmay be responsible for the increase in CVD risks. Theyeven recommend that using highly COX-2 selectiveNSAIDs without the use of COX-1 inhibitors should beavoided.14

BRFF plant extract inhibits both COX-1 and COX-2enzymes. But unlike COX-2 selective NSAIDs, it is nota highly selective COX-2 inhibitor. In addition, BRFF

at day 14 versus placebo: 2.87 mg/dl at baseline and3.79 mg/dl at day 14; p=0.004). The WOMAC pain(p=0.003), stiffness (p=0.056), and functional impair-ment (p=0.021) scores were also significantly improvedby day 14 in those subjects taking krill oil, but notthose in the placebo group. The use of acetaminophenwas reduced by 31% with krill oil compared to a reduc-tion of only 6% in the placebo group (p=0.012).8

Krill Oil for Osteoarthritis Pain: Mechanism of Action

Omega-3–rich krill oil modulates the function ofeicosanoids by competing with omega-6 fatty acids. Theeicosanoids (PGs, TXs) regulate vascular constriction,platelet aggregation, and inflammation.9 Potent forms ofPGs and TXs are produced from AA, an omega-6 fattyacid, when it is liberated from cellular membranes andconverted by enzymes called cyclooxygenase-1 (COX-1)and cyclooxygenase-2 (COX-2).10 For example PGE2,an immunosuppressive prostaglandin, is responsible forgenerating pain at the site of inflammation.11

The same COX enzymes, however, also preferentiallyproduce less potent forms of PGs and TXs when theomega-3 fatty acid EPA is liberated from cellular mem-branes. Diets rich in long-chain omega-3 PUFAs, forinstance, result in the production of more PGE3 thanTX5 than diets devoid or low in omega-3 fatty acids.The incorporation of omega-3 and omega-6 fatty acidsinto cellular membranes is competitive. So whenomega-3 fatty acids are sufficiently supplied in the diet,EPA preferentially replaces the omega-6 fatty acid AA incell membranes,12 thereby reducing pain and inflamma-tion.10

B-Ring Flavonoids and Flavans

Pain management has also been demonstrated by anewly developed, patent-pending, proprietary plantextract containing free B-ring flavonoids and flavans(BRFF). It is standardized to baicalin and catechin,which are derived from two herbs long used in tradi-tional Chinese medicine – Chinese skullcap (Scutellariabaicalensis) and black catechu (Acacia catechu) from thebark of the acacia tree. Chinese skullcap has been usedto treat inflammatory-related disorders in China andJapan for centuries. Historically, black catechu andmore than 1000 other species of its genus have beenutilized as astringents to treat gastrointestinal disorders,diarrhea, and indigestion and to stop bleeding. Chineseskullcap and black catechu were two of only a feworganic plant extracts to show inhibition of COX-2after initial screening. Subsequent in vitro and animal

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References:1. Smith BH, Elliott AM, Chambers WA, et al. The impact of

chronic pain in the community. Fam Pract. 2001;18:292-299.

2. Hoffman PK, Meier BP, Council JR. A comparison ofchronic pain between an urban and rural population. JCommunity Health Nurs. 2002;19:213-224.

inhibits 5-lipoxygenase (5-LOX), an enzyme that canproduce leukotrienes, biological compounds involved ininflammation. This combination of enzyme inhibitionprovided by BRFF appears to avoid the safety problemsencountered by NSAIDs and COX-2 selective NSAIDs.No gastrointestinal ulcerations were observed in micro-histological slides of the stomach of either mice or rats,suggesting that the dual inhibition of COX and 5-LOXallows for greater gastrointestinal tolerance.15 During the90-day human study, no CVD risk factors worsened(e.g. blood pressure, pulse rate, and plasma thrombintime levels). Long-term safety of BRFF has yet to beconfirmed.

Take Home Message

The management of chronic pain is difficult becausemost drugs eventually lose their effectiveness or pro-duce side effects. New effective products without sideeffects are welcomed. Although many pain-fightingmedications (OTC and prescription) exist, many indi-viduals seek safe, natural alternatives. To d a y, krill oil iso f f e red in products from several different companiesand BRFF has been available to the United States pub-lic since 2003. Krill oil and BRFF extracts have beens h own to reduce chronic pain both effectively ands a f e l y.

Wendy Van Ausdal, BS, is Science Information Specialistwith IdeaSphere Inc. She is the corresponding author forthis article. She maintains the research library and writesresearch support summaries for products in development.Contact Wendy at 801-492-7398, Fax: 801-763-0789 [email protected].

Stacey J. Bell, DSc, RD, is Research Scientist withIdeaSphere Inc. She has been a registered dietitian andresearch scientist for 30 years. Contact Stacey at 616-340-1612 or [email protected]

Greg T. Grochoski, BS, is Chief Science Officer ofIdeaSphere Inc. He spent 40 years at Alticor (formerlyAmway) retiring in 2002 as its Senior Vice President andChief Innovations Officer. Contact Greg at 616-464-5000or [email protected].

3. Clark JD. Chronic pain prevalence and analgesic prescrib-ing in a general medical population. J Pain Symptom Manage.2002;23:131-137.

4. Pain (Chapter 78). The Merck Manual of MedicalInformation—Second Home Edition, Online Version. Availableat: http://www.merck.com/mmhe/sec06/ch078/ch078d.html.Accessed 6/16/05.

5. U.S. Food and Drug Administration. Center for DrugEvaluation and Research. Available at:http://www.fda.gov/cder/drug/infopage/COX2/default.htm.Accessed 9/1/05.

6. Sampalis F, Bunea R, Pelland MF, et al. Evaluation of theeffects of Neptune Krill Oil on the management of premenstru-al syndrome and dysmenorrhea. Altern Med Rev. 2003;8:171-179.

7. Sales KJ, Jabbour HN. Cyclooxygenase enzymes andprostaglandins in pathology of the endometrium. Reproduction.2003;126:559-567.

8. Deutsch L. Evaluation of the effects of Neptune krill oil onchronic inflammation and arthritic disease. Submitted to theJournal of the American College of Nutrition. April 2005, accept-ance pending..

9. Simopoulos AP. Essential fatty acids in health and chronicdisease. Am J Clin Nutr. 1999;70:560S-569S.

10. Galperin C, German BJ, Gershwin ME. Nutrition andDiet in Rheumatic Diseases. In: Shils ME, Olson JA, Shike M,et al. eds. Modern Nutrition in Health and Disease. 9th ed.Philadelphia, PA: Lippincott Williams & Wilkins, 1998:1339-1351.

11. Warner TD, Mitchell JA. Cyclooxygenases: new forms,new inhibitors, and lessons from the clinic. FASEB J.2004;18:790-804.

12. Spector AA. Lipid Metabolism: Essential Fatty Acids. In:Biochemical and Physiological Aspects of Human Nutrition.Philadelphia, PA: Saunders, 2000;365-383.

13. Sampalis JS, Aurelian C, Remer Z. A randomized, dou-ble-blind, placebo-controlled trial of a novel dual COX/LOXinhibitor on WOMAC scores in patients suffering fromosteoarthritis. Submitted to J Rheumatol, 2005, acceptancepending.

14. Davies NM, Jamali F. COX-2 selective inhibitors cardiactoxicity: getting to the heart of the matter. J Pharm PharmaceutSci. 2004;7:332-336.

15. Silva S, Jia Q, Mesches MH, et al. Safety evaluation of anaturally derived, dual cyclooxygenase and lipoxygenaseinhibitor. Submitted to Food Chem Toxicol. 2005, acceptancepending.

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fatty acids. This can effectively blunt the pro-inflamma-tory side of the cascade in cells with a high n-6:n-3 FAratio in their membranes.

Dosing: standard dosing is based on that typicallyconsumed in Asian countries, about three cups/day;however, one to ten cups/day has been reported.

Any new oral compound can potentially cause adversereactions so recommendations for the use of botanicalsshould be in conjunction with a review of medication,medical, and allergy history. These botanicals are gener-ally safe when used in standard doses, but should not berecommended for pregnant or lactating women, as safe-ty testing during these states is inadequate. In general,these botanicals should be monitored in those on anti-coagulant or antiplatelet medications.

Mind-Body Therapies

Although this article addresses diet and herbal thera-pies that may be used to suppress inflammation andchronic pain, it must be mentioned that mind-bodytherapies have proven useful as well. As mentioned inthe inflammatory process section, the inflammatory cas-cade can occur with real, physical pain as well as withimagined pain or stress. Thus modalities that addressthe psychological component of pain can be effective.These include aromatherapy massage;79 imagery, medita-tion, and cognitive-behavioral therapy;80 and therapeutictouch.81,82 Nutrition professionals should provide notonly recommendations for orally consumed products,but also as many options for treatment as possible to aperson enduring chronic pain. Referring clients withchronic pain to appropriate mind-body therapy practi-tioners is warranted.

Take Home Message

As research continues to reveal the fascinating bio-chemical basis for pain and inflammation, nutritionprofessionals can convert this scientific knowledge intopractical advice for those suffering from chronic pain bymaking recommendations about dietary manipulationsand botanical compounds that positively impact thebody’s response to pain and inflammation. Helpingclients modify the omega-6:omega-3 fatty acid profile oftheir diets, decreasing trans fatty acid intake, andincreasing antioxidant and flavonoid ingestion may helpclients restore some balance in their cellular response toinflammation. Reviewing with them the possible bene-fits of various dietary supplements and botanicals andrecommending mind-body therapies that may enhancefunction should be a part of what nutrition profession-als offer. With a basic understanding of these biochemi-cal pathways and markers, new advances in the efficacy

thus interfering with the normal process of inflamma-tion.69 Further, bromelain appears to modulate immunefunction, aiding the body in destroying tumor cells,removing burn debris, and healing wounds.70

Dosing: 200 to 400 mg daily for 30 days hasbeen used for acute knee pain. Two tablets of a combi-nation of rutin (100 mg), trypsin (48 mg), and brome-lain (90 mg) three times daily has been used for OA.Magnesium activates bromelain, while zinc supplementsand potato and soybean protein can inhibit bromelainactivity. Those with pineapple allergies may also havebromelain allergy.

Chili Peppers

Chili peppers of the capsicum species contain cap-saicin. Capsaicin binds to nociceptors in the skin andcauses release of substance P, a sensory neurotransmitterthat mediates pain. Capsaicin first increases sensitivityin the area to which it is applied causing an itching,burning, or pricking feeling. However, after repeatedtopical application, desensitization and pain relief occur.This is thought to be due to the depletion of substanceP over time.71 Capsaicin has been used topically for lowback pain72 and diabetic neuropathy pain.73

Dosing: Topical creams that contain 0.025% to0.075% capsaicin concentrations have been used inresearch. These creams do take some time for full anal-gesic effect to occur, so clients must use them consis-tently 3 to 4 times a day for several days to obtain thedesensitization that leads to pain relief. These creamsshould never be used on open wounds.

Green Tea

Green tea is not fermented, which distinguishes itfrom black (fermented) or oolong (partially fermented)tea. Like garlic, there are numerous studies involvinggreen tea, but for purposes of this discussion, theimportant active chemicals are the flavonoids. Thesepolyphenols act in ways similar to other compoundscontaining these constituents.

The flavonoids in green tea are primarily catechins.These chemicals have several actions. First, they inhibitthe COX-1 enzyme system,74 but they may also inhibitthe 5-lipox enzyme system and the production of pro-inflammatory leukotriene-B4.75 Second, they inhibit IL-1 beta induced COX-2 activity and the enzyme respon-sible for nitric oxide production.76 Third, they may alsoprotect joint cartilage by decreasing the proteoglycanand collagen damage that occurs from oxidative andmechanical injury.77 There is also some evidence thatgreen tea flavonoids might inhibit lipoprotein oxida-tion,78 thus decreasing the availability of cell membrane

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Consumption of (n-3) fatty acids is related to plasma biomarkersof inflammation and endothelial activation in women. J Nutr.2004;134:1806-1811.

16. Baer DJ, Judd JT, Clevidence BA, et.al. Dietary fatty acidsaffect plasma markers of inflammation in healthy men fed con-trolled diets: a randomized crossover study. Am J Clin Nutr.2004;79:969-973.

17. Mozaffarian D, Pischon TT, Hankinson SE, et.al. Dietaryintake of trans fatty acids and systemic inflammation in women.Am J Clin Nutr. 2004;79:606-612.

18. Larque E, Garcia-Ruiz P, Perez-Llamas F, et.al. Dietarytrans fatty acids alter the compositions of microsomes and mito-chondria and the activities of microsome delta-6-fatty aciddesaturase and glucose-6-phosphatase in livers of pregnant rats. JNutr. 2003;133:2526-2531.

19. Boovens J, Louwrens CC, Katzeff IE. The role of unnatu-ral dietary trans and cis unsaturated fatty acids in the epidemiol-ogy of coronary artery disease. Med Hypotheses. 1988;25:175-182.

20. Ascherio A, Katan MB, Zock PL, et.al. Trans fatty acidsand coronary heart disease. N Engl J Med. 1999;340:1994-1998.

21. Khan F, Elherik K, Bolton-Smith C, Barr R, Hill A,Murrie I, Belch JJ. The effects of dietary fatty acid supplementa-tion on endothelial function and vascular tone in healthy sub-jects. Cardiovasc Res. 2003;59:955-962.

22. Rotella P. Healthy fats – essential fatty acids. Available at:http://goodfats.pamrotella.com. Accessed 8/5/05.

23. de Lorgeril M, Salen P, Martin JL, et.al. Mediterraneandiet, traditional risk factors, and the rate of cardiovascular com-plications after myocardial infarction: final report of the LyonDiet Heart Study. Circulation. 1999;99:779-785.

24. Vogel RA, Corretti MC, Plotnick GD. The postprandialeffect of components of the Mediterranean diet on endothelialfunction. J Am Coll Cardiol. 2000;36:1455-1460.

25. Ames BN, Shigenaga MK, Hagen TM. Oxidants, antioxi-dants, and the degenerative diseases. Proc Natl Acad Sci USA.1993;90:7915-7922.

26. Ames BN, Gold LS, Willett WC. The causes and preven-tion of cancer. Proc Natl Acad Sci USA. 1995;92:5258-5265.

27. Meydani M. Soluble Adhesion molecules: surrogate mark-ers of cardiovascular disease? Nutr Rev. 2003;61:63-68.

28. Boyer J, Liu RH. Apple phytochemicals and their healthbenefits. Nutr J. 2004;3:5

29. Donaldson MS. Nutrition and cancer: a review of the evi-dence for a cancer diet. Nutr J. 2004;3:19.

30. Tall JM, Raja SN. Dietary constituents as novel therapiesfor pain. Clin J Pain. 2004;20:19-26.

31. Machiex JJ, Fleurier A, Billot J. Fruit phenolics. BocaRaton, FL:CRC Press; 1990.

References:1. The Chronic Pain Association. Available at:

http://www.theacpa.org. Accessed 8/4/05.

2. McCaffrey R, Frock TL, Garguilo H. Understanding chronicpain and the mind-body connection. Holistic Nursing Practice.Nov/Dec 2003;281-287.

3. Seaman DR. The diet-induced proinflammatory state: acause of chronic pain and other degenerative diseases? JManipulative Physiol Ther. 2002;25:168-179.

4. Lang J. The new balancing female hormones. LangIntegrated Health Seminars presented at Toledo, OH. 2004.

5. Pawlak L. Fat cells and inflammation: heart disease,Alzheimer’s, and diabetes. Institute for Natural Resources confer-ence presented at Tucson, AZ. 2005.

6. Simopoulos A. Omega-3 fatty acids in health and diseaseand in growth and development. Am J Clin Nutr. 1991;54:438-463.

7. Cordain L, Boyd-Eaton S, Sebastian A, et. al. Origins andevoluation of the Western diet: health implications for the 21stcentury. Am J Clin Nutr. 2005;81:341-354.

8. Rakel, DP, Rindfleisch A. Inflammation: nutritional, botan-ical, and mind-body influences. South Med J. 2005;98:303-310.

9. Eliopoulos C. Controlling inflammatory conditions withdiet. Available at: http://www.nadona.org. Accessed 8/4/2005.

10. Simopoulos A. The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomed Pharmacother.2002;56:365-379.

11. Lichtenstein AH, Trans fatty acids, plasma lipid levels, andrisk of developing cardiovascular disease: a statement for health-care professionals from the American Heart Association.Circulation. 1997;95:2588-2590.

12. Berbert AA, Kondo CR, Almendra CL, Matsuo T, Dichi I.Supplementation of fish oil and olive oil in patients withrheumatoid arthritis. Nutrition. 2005;21:131-136.

13. Harris WS, Appel LJ. New guidelines focus on fish, fishoil, omega-3 fatty acids. American Heart Association Statement.2002. Available at: http://www.americanheart.org. Accessed8/5/05.

14. Pattison DJ, Harrison RA, Symmns DPM. The role ofdiet in susceptibility to rheumatoid arthritis: a systematic review.J Rheum. 2004;31:1310-1319.

15. Lopez-Garcia E, Schulze M, Manson JE, et. al.

of diet and botanicals for managing chronic pain can beincorporated into the nutrition professional’s practice.

Sheila Sedig, MS, RD is a clinical dietitian and educa-tor at the Southern Arizona VA Health Care System inTucson, Arizona. Contact Sheila [email protected] or 520-629-4659.

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cont. from page 34 Modulating Chronic Pain:The Role of Nutrition and Botanicals32. Bucci L. Nutrition applied to injury rehabilitation and

sports medicine. Boca Raton, FL:CRC Press; 1995.

33. Combs G. The vitamins: fundamental aspects in nutritionand health. New York, NY: Academic Press; 1992.

34. Krol W, Czuba ZP, Threadgill MD, Cunningham BDM,Pietsz G. Inhibition of nitric oxide (NO) production in murinemacrophages by flavones. Biochem Pharm. 1995;50:1031-1035.

35. Folts JD. Potential health benefits from the flavonoids ingrape products in vascular disease. Adv Exp Med Biol.2002;505:95-111.

36. Arts JC, Hollman PC. Polyphenols and disease risk in epi-demiologic studies. Am J Clin Nutr. 2005;81:317S-325S.

37. Morelli V, Naquin C, Weaver V. Alternative therapies fortraditional disease states: osteoarthritis. Am Fam Physician.2003;67:339-344.

38. Alvarez-Soria MA, Largo R, Diez-Ortego E, et al.Glucosamine inhibits IL-1ß-induced NF-kappa B activation inhuman osteoarthritic chondrocytes. American College ofRheumatology Meeting;2002. Abstract 118.

39. Pipitone VR. Chondroprotection with chondroitin sul-fate. Drugs Exp Clin Res. 1991;17:3-7.

40. Mazieres B, Combe B, Phan Van A, et.al. Chondroitinsulfate in osteoarthritis of the knee: a prospective, double blind,placebo controlled multicenter clinical study. J Rheumatol.2001;28:173-181.

41. Questions and Answers: Available at: NIHGlucosamine/chondroitin arthritis intervention trial (GAIT).http://nccam.nih.gov/news. Accessed 8/1/2005.

42. Natural Medicines Comprehensive Database. Monograph.Available at: http://www.complementarymedicine.org. Accessed7/28/05.

43. Wu D, Meydani M, Leka LS, et.al. Effect of dietary sup-plementation with black currant seed oil on the immuneresponse of healthy elderly subjects. Am J Clin Nutr.1999;70(4):536-543.

44. Hornych A, Oravec S, Girault F, et.al. The effect ofgamma-linolenic acid on plasma and membrane lipids and renalprostaglandin synthesis in older subjects. Bratisl Lek Listy.2002;103:101-107.

45. Furse RK, Rossetti, RG, Seiler CM, et.al. Oral administra-tion of gammalinolenic acid, an unsaturated fatty acid with anti-inflammatory properties, modulates interleukin-1beta produc-tion by human monocytes. J Clin Immunol. 2002;22:83-91.

46. Ziboh VA, Naguwa S, Van K, et.al. Suppression ofleukotriene B4 generation by ex-vivo neutrophils isolated fromasthma patients on dietary supplementation with gammali-nolenic acid-containing borage oil: possible implication in asth-ma. Clin Dev Immunol. 2004;11:13-21.

47. Barham JB, Edens MB, Fonteh AN, et.al. Addition ofeicosapentaenoic acid to gamma-linolenic acid-supplementeddiets prevents serum arachidonic acid accumulationin humans. J

Nutr. 2000;130:1925-1931.

48. Turpie AG, Runcie J, Thomson TJ. Clinical trial of degly-cyrrhizinized liquorice in gastric ulcer. Gut. 1969;10:299-302.

49. Tewari SN, Wilson AK. Deglycyrrhizinated liquorice induodenal ulcer. Practitioner. 1973;210:820-823.

50. Collier HO, Butt NM, McDonald-Gibson WJ, et.al.Extract of feverfew inhibits prostaglandin biosynthesis. Lancet.1980;2:922-923.

51. Makheja AN, Bailey JM. The active principle in feverfew.Lancet. 1981;2:1054.

52. Hwang D, Fischer NH, Jang BC, et.al. Inhibition of theexpression of inducible cyclooxygenase and proinflammatorycytokines by sesquiterpene lactones in macrophages correlateswith the inhibition of MAP kinases. Biochem Biophys ResCommun. 1996;226:810-818.

53. Pugh WJ, Sambo K. Prostaglandin synthetase inhibitorsin feverfew. J Pharm Pharmacol. 1988;40:743-745.

54. Agarwal KC. Therapeutic actions of garlic constituents.Med Res Rev. 1996;16:111-124.

55. Dillon, SA, Lowe GM, Billington D, et.al. Dietary sup-plementation with aged garlic extract reduces plasma and urineconcentrations of 8-isoprostaglandin F2-alpha in smoking andnonsmoking men and women. J Nutr. 2002;132:168-171.

56. Ramsewak RS, DeWitt DL, Nair MG. Cytotoxicity,antioxidant and anti-inflammatory activities of curcumins I-IIIfrom Curcuma longa. Phytomedicine. 2000;7:303-308.

57. Chainani-Wu N. Safety and anti-inflammatory activity ofcurcumin: a component of turmeric (Curcuma longa). J AlternComplement Med. 2003;9:161-168.

58. Altman RD, Marcussen KC. Effects of a ginger extract onknee pain in patients with osteoarthritis. Arthritis Rheum.2001;44:2461-2462. Comment.

59. Srivastava KC, Mustafa T. Ginger (Zingiber officinale)and rheumatic disorders. Medical Hypotheses. 1989;29:25-28.

60. Thomson M, AlQattan KK, Al-Sawan SM, et.al. The useof ginger (Zingiber officinale Rosc.) as a potential anti-inflam-matory and antithrombotic agent. Prostaglandins Leukot EssentialFatty Acids. 2002;67:475-478.

61. Frondoza CG, Sohrabi A, Polotsky A, et.al. An in vitroscreening assay for inhibitors of proinflammatory mediators inherbal extracts using human synoviocyte cultures. In Vitro CellDev Biol Anim. 2004;40:95-101.

62. Chrubasik S, Eisenberg E, Balan E, et.al. Treatment of lowback pain exacerbations with white willow bark extract: a ran-domized double-blind study. Am J Med. 2000;109:9-14.

63. Chrubasik S, Kunzel O, Model A, et.al. Treatment of lowback pain with a herbal or synthetic anti-rheumatic: a random-ized controlled study. Willow bark extract for low back pain.Rheum. 2001;40:1388-1393.

64. Gupta I, Parihar A, Malhotra P, et.al. Effects of gum resin

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NUTRITION IN COMPLEMENTARY

Web site: www.ComplementaryNutrition.orgMember ElectronicMail List:Contact Gretchen Forsellto get connected([email protected])

Going to FNCEOctober 22-24, 2005?Mark your Calendar

for these NCC activ i t i e s

Membership Appreciation & Awards Breakfast,Sunday, October 23, 7am-8:30am, Renaissance Grand,Majestic D, Breakfast with Douglas A. Balentine, PhD.Flavinoids: Food & Beverage Sources and NewResearch Perspectives about their Unique HealthBenefits Re c o g n i zed by academics and goernment agenciesas a global expert on tea chemisry and the health benefitsof teas and dietary flavanoids, Dr. Balentine is curre n t l yleader of the Health and Wellness Technology Group andthe Un i l e ver Health Institute. Sp o n s o red by Li p t o n .

NCC Member Networking Reception, Sunday,October 23, 6:30pm-8:30pm, Renaissance Grand,Crystal Ballroom. Join your NCC colleagues for anevening of light hors d’oeuvres and live jazz. Be sure tointroduce yourself to your execxutive commitee andbecome involved in the fastest growing DPG. In partner-ship with Dietitians in Business & CommunicationsDPG. Sponsored by Prothera, Kyowa-Hakko, andPharmavite.

NCC Yoga at FNCE Begin and end your busy day dur-ing FNCE with a relaxing and invigorating yoga session.Register at the ADA Foundation booth in the ExhibitionHall or on site at the Renaissance Grand, Portland BentonRoom. Space is available on a first-served basis. A $10contribution to the ADA Foundation is suggested.

NCC SPONSORED PRESENTATIONS:

October 24 – Nutritional Neuroscience: Having aPositive Impact on ADHD and Autism Jeff Bradstreet,MD and Victoria Kobliner, MS, RD Identify specificgenetic polymorphisms and resultant metabolic disordersrelated in children with ADD, ADHD, and AutismSpectrum Disorders. Recommend appropriate interven-tions based on nutritional deficiencies or malregulationsthat result from biochemical/psychological defects.

October 25 – Teas: Traditional Beverages orFunctional Foods? Cynthia Thomson PhD, RD, FADAand Jeffrey Blumberg PhD, FACN Characterize the pat-tern of beverage consumption and associated nutrientintakes in the United States. Define and identify the prin-ciple phytochemical components of various teas andtisanes (herb teas). Suggest a role to reduce the risk forcancer and cardiovascular disease by explaining theresearch approaches.

Thank You to Our Sponsors!

Without you, much of what we are able to do

would not be possible.

DIAMONDLipton

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C o n g ratulations to the follow i n g

NCC Award Wi n n e r s

For Excellence in Service AwardRosalyn Franta Kulik, MS, RD

For Excellence in Practice AwardDave Grotto, RD, LDN

Thank you from all of us for yourcountless hours and dedication to making NCC

the exemplary DPG that it is today.

CPE Questions:1. True/False: Individual pain perception is influ-

enced by physiological and psychological factors.

2. Which eicosanoid series is anti-inflammatory?

A. Series 2 and Series 3 B. Series 1

C. Series 1 and Series 2 D. Series 1 and Series 3

3. Which dietary oil is an excellent source of alpha-linolenic acid?

A. Olive oil B. Corn oil C. Black currant oil

D. Flaxseed oil E. Fish oil

4. Which pathway describes the pain signalingprocess?

A. Pain stimuliefferent nervesbrainafferentnervesnociceptor

Modulating Chronic Pa i n :The Role of Nutrition and

B o t a n i c a l s

Modulating Chronic Pain:The Role of Nutrition and Botanicals

of Boswellia serrata in patients with chronic colitis. Planta Med.2001;67:391-395.

65. Kimmatkar N, Thawani V, Hingorani L, et.al. Efficacyand tolerability of Boswellia serata extract in treatment ofosteoarthritis of knee – a randomized double blind placebo con-trolled trial. Phytomedicine. 2003;10:3-7.

66. Wegener T, Niels-Peter L. Treatment of patients witharthrosis of hip or knee with an aqueous extract of Devil’s claw(Harpagophytum procumbens DC). Phytotherapy Res.2003;17:1165-1172.

67. Chrubasik S, Conradt C, Black A. The quality of clinicaltrials with Harpagophytum procumbens. Review. Phytomedicine.2003;10:613-623.

68. Cooreman WM, Scharpe S, Demeester J, et.al. Bromelain,biochemical and pharmacological properties. Pharma Acta Helv.1976;51:73-97.

69. Brien S, Lewith G, Walker A, et.al. Bromelain as a treat-ment for osteoarthritis: a review of clinical studies. Evid BasedComplement Alternat Med. 2004;1:251-257.

70. Maurer HR. Bromelain: biochemistry, pharmacology andmedical use. Cell Mol Life Sci. 2001;58:1234-1245.

71. Mason L, Moore RA, Derry S, et.al. Systematic review oftopical capsaicin for the treatment of chronic pain. Brit Med J.2004;328:991.

72. Frerick H, Keitel W, Kuhn U, et.al. Topical treatment ofchronic low back pain with a capsicum plaster. Pain.2003;106:59-64.

73. Tandan R, Lewis GA, Krusinski PB, et.al. Topical cap-saicin in painful diabetic neuropathy. Controlled study withlong-term follow-up. Diabetes Care. 1992;15:1434.

74. Mohseni H, Zaslau S, McFadden D, et.al. COX-2 inhibi-tion demonstrates potent anti-proliferative effects on bladdercancer in vitro. J Surg Res. 2004;119:138-142.

75. Choi JH, Chai YM, Joo GJ, et.al. Effects of green tea cat-echin on polymorphonuclear leukocyte 5’-lipoxygenase activity,leukotriene B4 synthesis, and renal damage in diabetic rats. AnnNutr Metab. 2004;48:151-155.

76. Ahmed S, Rahman A, Hasnain A, et.al. Green teapolyphenol epigallocatechin-3-gallate inhibits the IL-1 beta-induced activity and expression of cyclooxygenase-2 and nitricoxide synthase-2 in human chondrocytes. Free Radic Biol Med.2002;33:1097-1105.

77. Adcocks C, Collin P, Buttle DJ. Catechins from green tea(Camellia sinensis) inhibit bovine and human cartilage proteogly-can and type II collagen degradation in vitro. J Nutr.2002;132:341-346.

78. Ali M, Afzal M. A potent inhibitor of thrombin stimulat-ed platelet thromboxane formation from unprocessed tea.Prostaglandins Leukot Med. 1987;27:9-13.

79. Howarth A. Goodscents. Nursing Standard. 2005;19:20-21.

80. Astin JA. Mind-body therapies for the management ofpain. Clin J Pain. 2004;20:27-32.

81. Smith DW, Arnstein, P, Rosa KC, et.al. Effects of integrat-ing therapeutic touch into a cognitive behavioral pain treatmentprogram. Report of a pilot clinical trial. J Holist Nurs.2002;20:367-387.

82. Denison, B. Touch the pain away: new research on thera-peutic touch and persons with fibromyalgia syndrome. HolistNurs Pract. 2004;18:142-151.

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C P E Q u e s t i o n s Modulating Chronic Pain:The Role of Nutrition and Botanicals

B. Pain stimulinociceptorafferentnervesbrain efferentnervesnociceptorreaction to stimuli

C. Pain stimulinociceptorefferentnervesbrain afferentnervesnociceptorreaction to stimuli

5. Which foods are rich sources of omega-3 fattyacids?

A. Corn oil, pork loin, chicken breast, cheese

B. Apples, evening primrose oil, olive oil, garlic,onions

C. Halibut, salmon, walnuts, flaxseed

6. A common concern in using botanicals to attenu-ate the inflammatory cascade/response is the poten-tial interaction with OTC and prescriptive medica-tions. Which drug class poses the greatest concern:

A. Hormone replacement therapy

B. Anti-neoplastics

C. Anti-coagulants/anti-platelets

D. Anti-psychotics

7. Which botanical preparations facilitate modulationof pain?

A. Aspirin, NSAIDS, soybeans, fish

B. Apples, pineapples, soy products, glucosaminechondroitin

C. Licorice, feverfew, white willow, Indian frankin-cense

8. Other than dietary manipulation and the safe inte-gration of herbs/botanicals what other non-phar-macological interventions might a clinician suggest?

A. NSAIDS B. Acupuncture C. Aromatherapy

D. Massage E. Meditation F. Mediterranean diet

Questions 9 and 10 are based on the followingpatient scenario:

A working mother of 3 teenagers presents to your cliniccomplaining of chronic pain. She states that she has notime to cook; and even if she did it would be a waste oftime because her teenagers will not eat what she prepares.She tells you that her mornings are much too rushed to fixbreakfast and if she eats at all it is from the kiosk vendorin the building lobby or fast food. In taking her food his-tory her 24-hour recall includes the following: coffee withnon-dairy powdered creamer, whole grain bagel, grilled

PLEASE CIRCLE THE CORRECT ANSWERS:1. T F 2. A B C D 3. A B C D E 4. A B C D 5. A B C 6. A B C D 7. A B C 8. A B C D E F 9. T F 10. A B C

CPE Reporting Form • Fall 2005EXPIRATION DATE: 09/07Please Print or type

Name:

Address:

ADA Membership #:

Daytime phone:

Evening phone:

Email address:

NCC Member Yes No

This activity has been approved for two hours of CPE credit. You will benotified if hours are not approved.

Cost: $12 NCC Members $20 non NCC MembersMake checks payable to NCC-DPG #18

Mail to: Gretchen Forsell2002 Highland DriveNorfolk, NE 68701

For 2 Hours CPE Credit

chicken salad with cheese and ranch dressing, granola barfor a snack, and a fast food burger no bun and diet colafor dinner.

9. True/False: Her diet may be exacerbating thepain experience/response.

10. Which breakfast(s) will provide her with nutri-tional components to modulate pain while simultane-ously meeting her “need” to “grab-n-go”?

A. Single serve carton of milk, breakfast cereal bar

B. Blueberry pancakes topped with fresh blueber-ries and hot green tea?

C. Single serve carton of soymilk, apple, handful ofwalnuts.

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NCC 2005-2006 LEADERSHIPCONTACT INFORMATION

EXECUTIVE COMMITTEE

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

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Gretchen Forsell, MPH, RD, LD Treasurer 2004 - 20062002 Highland DrNorfolk, NE 68701daytime: 402-644-7256fax: 402-644-7254

Natalie Lagomarcino Ledesma MS RD Nominating Chair 2005 - 2006 Cancer Resource CenterUCSF Comprehensive Cancer Center1600 Divisadero St, B101San Francisco, CA 94143-1725Work: 415-885-7608Fax: 415-885-3701

Caren Baltasi, LD, CCNLiaison Chair Phone: 773-407-4687Deborah S. Ford MS RD, CCNEducation Chair

5 Warren RoadVan Wert, OH 45891-2548Home: 419-238-3321Work: 419-238-3020

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

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ADMINISTRATIVE ASSISTANTKatherine L. Bernard, MS RD CDN90 Panamoka TrailRidge, NY 11961Phone: 631-929-3834Fax: 631-209-1569

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