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* Correspondence:
Rafail Kushak, PhD., Dr. Sci.
Pediatric Gastroenterology' & Nutrition
Massachusetts General Hospital
55 Fruit Street, VBK 107
Boston, MA 02114-2698
Phone: (617) 726-7451
Fax: (617) 724-2710
E-mail: Kushak.Rafail@mgh.harvard.edu
Click here for another research article on Blue Green Algae.

Reprinted with permission from the Journal of the American Nutraceutical Association.

Favorable Effects of Blue-Green Algae Aphanizomenonflos-aquae on Rat Plasma Lipids

Rafail I. Kushak, PhD,1* Christian Drapeau, MS,2 Elizabeth M. Van Cott,1
Hariand H. Winteri

'Combined Program in Pediatric Gastroenterology and Nutrition and Division of Laboratory Medicine
Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts
2Cell Tech, Kiamath Falls, Oregon

ABSTRACT
Background: Polyunsaturated fatty acids (PUFAs) are essential for human health. There are indications that the lipid fraction of blue-green algae Aphanizomenon flos-aquae contains about 50% PUFA and may be a good dietary source of PUFA. The purpose of this study was to investigate the effect of diets supplemented with algae on blood plasma lipids.

Methods: Rats were fed with four different semisynthetic diets: 1) standard, with 5% soybean oil; 2) PUFA-free with 5% coconut oil; 3) PUFA-free with 10% algae; 4) PUFA-free with 15% algae. After 32 days the levels of plasma fatty acids, triglycerides, and cholesterol were studied.

Results: Rats fed the PUFA-free diet demonstrated an absence of linolenic acid (LNA) in plasma; however, supplementation with algae resulted in the same level of LNA as controls, increased levels of eicosapentaenoic acid and docosahexaenoic acid, and a decreased level of arachidonic acid. Dietary supplementation with 10% and 15% algae decreased the plasma cholesterol to 54% and 25% of the control level, respectively (p<0.0005). Plasma triglyceride levels decreased significantly (p<0.005) after diet supplementation with 15% algae.

Conclusion: Algae Aphanizomenonfios-aquae is a good source of PUFA and because of potential hypocholesterolemic properties should be a valuable nutritional resource.


INTRODUCTION
Previous research identified the important role of dietary polyunsaturated fatty acids (PUFA) in human health. A deficiency in n-3 PUFA has been linked to immunosuppression,1 arthritis,2 cardiovascular diseases,3-6 mental7,8 and dermatological9 problems. Human and animal models containing n-3 PUFAs have anti-inflammatory activity2,10,11 that may be mediated by decreasing the arachidonic acid level and thereby suppressing the production of specific cytokines.12 Furthermore, n-3 fatty acids have been shown to decrease certain cancer risks,13,14 prevent platelet aggregation,6,15 and to lower blood cholesterol, possibly by stimulating its excretion into bile.3,16

The North American diet is believed to be deficient in PUFA, especially in n-3 fatty acids.17 Dietary supplementation with fish oil rich in n-3 eicosapentaenoic (EPA) and docosahexaenoic acids (DHA) has been recommended as a potential treatment for hypercholesterolemia.15,18 Much empirical evidence over the past decade suggests that Aphanizomenon flos-aquae (Aph. flos-aquae), a blue-green alga growing naturally in Upper Klamath Lake, Oregon, may be a good dietary source of PUFA. Nearly 50% of the lipid content of dried Aph. flos-aquae (5% to 9% of total dry weight) is composed of PUFA, mostly n-3 0:-linolenic acid.

In our experiments using rats as the animal model, Aph. flos-aquae not only served a source of dietary PUFA but also significantly lowered blood cholesterol and triglyceride levels.

METHODS
Animals: Thirty-two adult male Sprague-Dawley rats were randomly distributed into 4 groups. Animals were placed into individual wire cages, and maintained at 220 C with a 12-hour light-dark cycle. Food and water were supplied ad libitum. For 32 days the animals were fed with the following semipurified test diets based on the American Institute of Nutrition (AIN-76) standard:


Standard diet containing 5% soybean oil (SBO)

2. PUFA-deficient diet containing 5% coconut oil (PUFA-D)

3. PUFA-deficient diet containing 10% algae (AiglO)

4. PUFA-deficient diet containing 15% algae (Algl5)

The algal material used in this study was supplied by Cell

Tech (Klamath Falls, Oregon) and contained 6.3% lipids.

Feed was provided by Purina Test Diets (Richmond, Indiana).

After the feeding trial, the animals were fasted overnight and euthanised by carbon dioxide inhalation. Plasma was collected by heart puncture in a tube containing 100 µl 0.5 M EDTA (pH 8.0), centrifuged at 3000 g for 15 minutes, and stored at -80ºC.

Lipid Analysis: Blood fatty acid analysis was performed using a direct transesterification method19 as modified by Mosers.20 In brief, 250 µl of plasma was vortexed with I ml methanol:methylene chloride (3:1). 50 nmol of 17:0 free fatty acid (internal standard) in 50 µl of hexane was added to this mixture. Under continuous vortexing 200 µl of acetyl chloride was added and the mixture was incubated in the oven at 75ºC for one hour. After cooling for 15 mm at room temperature, 4 ml of 7% potassium carbonate was added, vortexed, and then 2 ml of hexane was added. The mixture was vortexed for 60 sec and then centrifuged at 1750 g for 10 mm at 40C. The hexane layer was removed, 2 ml of acetonitrile was added and the mixture was centrifuged at 1120 g for S mm at 4ºC The hexane layer was removed, dried under nitrogen to a final volume of approximately 100 µl, and 1 µ1 of the sample was used for analysis. Fatty acid identification was performed on a Hewlett-Packard 5890 series II model gas chromatograph-mass spectrometer GC-MC with a Hewlett-Packard 5971 mass spectrometer (Hewlett-Packard, Wilmington Delaware). Soybean and coconut oils were methylated by acid methanolysis before fatty acid analysis. The algae material was soaked in methanol, extracted, and then methylated by acid methanolysis prior to fatty acid analysis.
Plasma triglycerides and cholesterol were measured on the automated clinical chemistry analyzer Roche BHO/H917 using corresponding Boehringer Mannheim kits.

Statistics: Statistical difference between groups was determined using unpaired student's t-test. Difference in fatty acid profiles was evaluated using repeated measures analysis and contrast tests.2 For all analyses, differences of p<0.05 were considered statistically significant.

RESULTS
Dietary Fatty Acids: Fatty acid composition of Aph. fios-aquac, soybean oil, and coconut oil used in this study is represented in Table 1. The composition of soybean and coconut oil in the present study is close to that found in the literature.22 Soybean oil is rich in linoleic acid (LA, 1 8:2n-6; 44.4% of total lipids) and contains a substantial amount of ot-linolenic acid (LNA, 18:3n-3; 8%). Aph. flos-aquae is richer in LNA (22.3%) and contains less LA (7.4%) than soybean oil. Aph.fios-aquae has also small amount (0.65%) of arachidonic acid (AA, 20:4n-6) and traces (0.08%) of EPA (20:5n-3). Coconut oil is free of both n-3 and n-6 fatty acids.

Fatty acid composition of the various diets is represented in Table 2. SBO and PUFA-D diets had a total of 5% lipids provided by soybean and coconut oils. Because of a slightly higher amount of lipids in algae (6.29%) than expected (5%), Alg10 and Alg15 diets contained correspondingly 5.13% and 5.20% of lipids. Ratios of PUFA to saturated fatty acids (SFA) and n-6 to n-3 varied considerably between the diets. 

Calculations showed that Aph. fLos-aquae contains 1.40% LNA and 0.46% LA of total algal dry weight. Diets containing 10% and 15% of algae (corresponds to 0.63% and 0.94% of algal lipids) provided a total dietary intake of 0.14% LNA and 0.047% LA for the Alg10 diet, and 0.21% LNA and 0.07% LA for the Alg15 diet (Table 2). Therefore, amounts of n-3 and n-6 PUFA in algae-supplemented diets were significantly lower than in the positive SBO control diet. The SBO diet contained 2.9 times more LNA and 44 times more LA than the Alg10 diet, and 1.9 times more LNA and 32 times more LA than the ALg15 diet. Furthermore, the n-6/n-3 ratio varied significantly between the algal (0.36) and the SBO (5.55) diets.
Because of the high SFA content in coconut oil, algae-supplemented diets contained more SFA than the SBO diet (Table 2). Alg10 and Alg 15 diets contained four times more SFA than the SBO diet. Therefore, the PUFAISFA ratio was significantly lower in the AlglO (0.05) and Alg15 (0.07) diets compared to the SBO (2.62) diet. The main SFAs in the Alg10 and Alg15 diets were lauric acid (12:0, ~1.84% of total diet), myristic acid (14:0, ~1.06%), and palmitic acid (16:0, ~1.08%).

Plasma Fatty Acids: Figure 1 shows a full rat plasma fatty acids profile. Plasma palmitate levels increased with palmitate dietary intake (r=0.60), reaching the highest level in the Alg15 group (p<0.0l). Plasma LA increased with dietary LA intake (r=0.67), being highest in the SBO group (p<0.001), which correlates with the high amount of LA in this diet. In rats fed coconut oil deficient in LA, the plasma LA level was 36% (p<0.0005) of the SBO control level. When the PUFA-D diet was supplemented with Aph. flos-aquae, plasma LA level was restored to 71% (ALg10) and 67% (ALg15) of the SBO level, in spite of the fact that algae-supplemented diets contained less than 3% of the amount of LA present in the control SBO diet.

FIGURE 1. Plasma fatty acids profiles in animals fed different diets (mean±iSEM).
In PUFA-D animals diet supplementation with algae increased plasma oleic acid and LA levels but decreased AA level.

Because of the high SFA content in coconut oil, algae-supplemented diets contained more SFA than the SBO diet (Table 2). Alg 10 and Alg 15 diets contained four times more SFA than the SBO diet. Therefore, the PUFAISFA ratio was significantly lower in the Alg10 (0.05) and Alg15 (0.07) diets compared to the SBO (2.62) diet. The main SFAs in the Alg1O and Alg15 diets were lauric acid (12:0, 1.84% of total diet), myristic acid (14:0, 1.06%), and palmitic acid (16:0, 1.08%).

FIGURE 2. Specific PUFA profile in rats plasma (mean±SEM).
Rats fed PUFA-D diet demonstrated an absence of LNA in plasma; however, animals fed Alg10 and Alg15 diets had the same level of LNA as controls, and increased EPA and DHA levels.

Plasma Fatty Acids: Figure 1 shows a full rat plasma fatty acids profile. Plasma palmitate levels increased with palmitate dietary intake (r=0.60), reaching the highest level in the Alg15 group (p<0.0l). Plasma LA increased with dietary LA intake (r=0.67), being highest in the SBO group (p<0.001), which correlates with the high amount of LA in this diet. In rats fed coconut oil deficient in LA, the plasma LA level was 36% (p<0.0005) of the SBO control level. When the PUFA-D diet was supplemented with Aph. flos-aquae, plasma LA level was restored to 71% (Alg10) and 67% (AIg15) of the SBO level, in spite of the fact that algae-supplemented diets contained less than 3% of the amount of LA present in the control SBO diet.

Plasma arachidonic acid (AA, 20:4n-6) also decreased with increasing AA dietary intake (r=-0.88) and was highest in the plasma of the SBO group (p<0.00 1). However, the plasma AA level correlated positively with the dietary level of the AA precursor LA (r=0.64), which was the highest in the SBO diet. Rats fed the PUFA-D diet, which contains no LA, had a plasma AA level significantly lower than controls fed the SBO diet (p<0.0l). However, supplementing the PUFA-D diet with Aph. flos-aquae further decreased plasma AA levels in a dose-dependent manner, in spite of the low LA and AA content in Alg10 and Alg15 diets.

In order to better appreciate the variation in plasma PUFA levels, Figure 2 shows the plasma lipid profile for some PUFAs on a different scale than Figure 1. Rats fed the PUFA-D diet had no plasma LNA, which is consistent with the absence of LNA in coconut oil. However, algae supplementation of the PUFA-D diet restored plasma LNA to the SBO (control) level, in spite of the fact that the algal diets contained only 35% (Alg10) and 52% (Alg15) of the LNA present in the SBO diet.

Feeding rats the PUFA-D diet increased plasma dihomo-y-linolenic acid (DGLA, 20:3n-6) 5 times above the SBO control level (p< 0.05). Algae supplementation of PUFA-D diet decreased plasma DGLA level in a dose-dependent manner. Levels found in the algae-treated animals were still higher than SBO controls, though this difference was not statistically significant (p<0.09).

EPA was absent in the plasma of rats fed the PUFA-D diet. However, when the diet was supplemented with 10% and 15% algae, plasma EPA increased 6 times (p<0.005) and 1.7 times (p>0.l) above the SBO control level, respectively. The DHA (22:6n-3) concentration in the plasma of rats fed the PUFA-D diet was 35% lower than in controls, although this difference did not reach statistical significance. Supplementation with 10% algae increased the plasma DHA level by a factor of 2 (p<0.05), but supplementation with 15% algae did not affect the plasma DHA level. The effect of algae on EPA and DHA levels in rat blood plasma may not be dose-dependent.

Thus, supplementation of the PUFA-D diet with algae normalizes fatty acid levels in plasma of PUFA-deficient animals and makes their PUFA profile similar to controls.

FIGURE 3. Lipid levels and PUFA/SFA ratio in rats fed different diets (MeaniSEM). * P~0.0l. PUFA-D diet supplemented with algae decreased triglycerides and cholesterol levels in rat blood plasma.

Plasma Triglycerides and Cholesterol: Algae affected not only free fatty acids but also other lipids in the blood. The PUFA-D diet did not significantly decrease plasma triglyceride levels relative to SBO controls (Figure 3). However, supplementation of the PUFA-D diet with 15% algae decreased plasma triglycerides to 24% of the SBO control level (p<0.005). The PUFA-D diet supplemented with 10% algae did not affect significantly the plasma triglyceride levels. Levels of triglycerides in blood plasma positively correlated with PUFAISFA ratio (r=0.87).

Cholesterol concentration in plasma was very sensitive to diet supplementation with algae (Figure 3). Rats fed the PUFA-D diet had a lower cholesterol level (p <0.05) than the SBO controls. The PUFA-D diet supplemented with algae caused a further dose-dependent decrease in the plasma cholesterol level. Supplementation with 10% and 15% algae decreased the plasma cholesterol level to 54% and 25% of the SBO control level (p <0.0005), respectively. Cholesterol and triglyceride levels were positively correlated (r =0.91).

Cholesterol levels also positively correlated to plasma PUFAISFA ratio (r=0.8 1) and to plasma stearic acid (r-0.86). On the other hand, blood cholesterol was strongly negatively correlated with plasma myristic acid (r = -0.99). From a dietary standpoint, blood cholesterol was related only to dietary palmitic acid (r = -0.95).


DISCUSSION
The results reported here demonstrate that, in the rat model, Aph. flos-aquae appears to be a good source of PUFA. Calculations showed a good correlation between dietary and serum levels of LA. However, the correlation between dietary and serum LNA was poor. Rats fed the PUFA-deficient diet supplemented with Aph. flos-aquae had blood levels of LNA comparable to levels found in rats fed a soybean oil diet containing nearly three times the amount of LNA. This suggests a higher bioavailability of LNA in Aph. flos-aquae compared to soybean oil. Furthermore, in spite of the fact that blood levels of LNA were similar in rats fed SBO and algae-supplemented diets, there were significantly higher blood levels of EPA in the rats fed the Aph. flos-aquae diet. It has been previously suggested that increased dietary SFA increased the rate of conversion of LNA to EPA, whereas increased dietary n-6 PUFA decreased this conversion by 40~50%.23 This dual effect could explain the fact that rats fed algae-supplement ed diets, which contained significantly more SFA, had higher blood levels of EPA than rats fed the SBO diet, which contained significantly more LA.

When the two main plasma n-6 PUFA (LA and AA) were analysed as a profile, there was a very good positive correlation between LA dietary intake and the total level of n-6 PUFA. However, the n-6 PUFA profiles in rat plasma were different between the various groups. Supplementing diets with algae led to a dose-dependent decrease in plasma AA and concomitant accumulation of of LA. This could be due to Aph. flos-aquae's content of phycocyanin. Phycocyanin, the blue pigment in blue-green algae, was recently shown to have significant anti-inflammatory properties24,25 which seemed to be mediated by an inhibition of AA metabolism.26 The presence of phycocyanin in the algae supplemented diets may have inhibited AA synthesis and consequently promoted the accumulation of LA.

This study suggests that Aph. flos-aquae has significant hypocholesterolemic properties when compared to soybean oil. Many studies have demonstrated the hypocholesterolemic properties of n-3 PUFAsI627,25 and the negative correlation between PUFAISFA ratios and blood cholesterol levels.29.3() In this study, cholesterol levels were positively correlated with the PUFAISFA ratio. The main SFAs present in the diet of the algae-treated groups were lauric, myristic, and palmitic acids, which have all demonstrated to promote hypercholesterolemia to some degree.31-33 This suggests that the hypocholesterolemic effect of Aph.fios-aquae is likely to be mediated by factors other than its fatty acid content. Specifically Aph. flos-aquae contains a significant amount of chlorophyll (1-2% dry weight) which has been shown to stimulate liver function and increase bile secretion.34 A synthetic derivative of chlorophyll has been shown to reduce blood cholesterol.35 Therefore, it is possible that Aph. fiosaquae chlorophyll is responsible for the increased liver function and secretion of cholesterol into bile. Spirulina, another blue-green algae, has also been shown to affect cholesterol metabolism by increasing HDL levels.36 According to other sources 37 the hypocholesterolemic effect of blue-green algae (Nostoc commune) is related to their fibers.

In conclusion, this study demonstrated that Aph. flos-aquac is a good source of PUFAs with strong hypocholesterolemic properties. Aph. flos-aquae's ability to increase serum levels of LNA, EPA, DHA, and to lower the level of AA in rats makes it a good candidate for future nutritional research in humans.

ACKNOWLEDGMENT
We are indebted to Dr. David J. Schaeffer, for assistance in statistical analysis and to Dr. M. Laposata for the critical review of the manuscript. We are also grateful for the grant provided by Cell Tech and the grant from the Clinical Nutrition Reseach Center at the Massachusetts General Hospital (P30 DK4056 I).


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The Journal of the American Nutraceutical Association

Co-Editors
Christopher M. Foley, MD - Dr. Foley brings over 20 years of private practice as an internist to his position as director of Integrative Health at HealthEast Care System in St. Paul, Minnesota. Dr. Foley serves on the teaching faculty at the University of Minnesota, School of Pharrnacy.

Allen M. Kratz, PharmD - Dr. Kratz is a former faculty member at the Philadelphia College of Pharmacy and Science. He was the first pharmacist appointed to the editorial board of The Merck Manual (12th. edition). He is the co-author of a chapter on Alternative Health Care in REMINGTON: The Science and Practice of Pharmacy (19th. edition). Dr. Kratz is the ft)under of HVS Laboratories and resides in Naples, Florida.

Editorial Board
Jerome B. Block, MD - Professor of Medicine, UCLA School of Medicine. Former chief, Division of Medical Oncology, Department of
Medicine, Harbor-UCLA Medical Center, Torrance, California.

Derrick DeSilva, MD - President, American Nutraceutical Association and practicing physician (internal medicine) in Edison, New Jersey. He has lectured in medicine, both nationally and internationally, and hosts a nationally syndicated radio talk show~Ask the Doctor that focuses on nutraceuticals and integrative medicine.

Jeanette Dunn, EdD, RN, CNS - Former Associate Dean of Nursing, University of Tennessee. She is co-director of the Foundation for Care Management based in Kirkland, Washington.

Clare M. Hasler, PhD - Executive director of the Functional Foods for Health Program, University of Illinois. She is also an assistant professor of nutrition, Department of Food Science and Human Nutrition, University of Illinois at Urbana-Champaign.

Mark J.S. Miller, PhD - Research professor and director of pediatric laborataries, Department of Pediatrics, Albany Medical College, Albany, New York.

Arthur J. Roberts, MD - Former director of the Jersey Shore Heart Institute, Neptune, New Jersey. His teaching and research appointments held have included: clinical professor of surgery, Temple University; associate professor and director, Adult Cardiac Surgery, University of Florida; professor and chairman, Department of Cardiothoracic Surgery, Boston University Medical Center.

Anthony J. Silvagni, DO, PharinD, MSc, FACOFP - Dean, College of Osteopathic Medicine, Nova Southeastern University, Ft. Lauderdale, Florida. Former faculty member, Philadelphia College of Pharmacy and Science.

Jack 0. Taylor, MS, DC, DACBN - Maintains a private practice in Rolling Meadow, Illinois. He is a oonsultant to hospitals and clinics internationally. He has served on the advisory board of the committee on diet and nutrition of the National Institutes of Health, Oftice of Alternative Medicine.

C. Wayne Weart, PharmD, BCPS, FASHP - Professor and chair, Department of Pharmacy Practice, and associate professor, Department of Family Medicine, Medical University of South Carolina, Charleston, South Carolina.

Bruce Woolley, PharmD - Professor, pharmacology and nutrition, Brigham Young University. Editor of the Utah Pharmaceutical Association Therapeutics Letter.

Editorial Review Panel

Wayne Agnew, MD - Full associate and president, Arlington Women's Clinic, Arlin('ton, Texas.

Victoria Arcadi, DC. DLCCP - Maintains a private practice in California and is a faculty member of the post graduate department at the Cleveland Chiropractic College in Los Angeles, California.

Marilyn Barrett, PhD - Founder and President, Pharmacognosy Consulting Services, Redwood, California.

Paul A. Berns, MD - Faculty member, University of Southern California Medical School, Los Angeles and Hebrew University, Jernsalem, Israel. Medical Director of the Pain Rehabilitation Center at Cedars-Sinai Towers, Los Angeles.

Russell Blaylock, MD - Board certified neurosurgeon. Clinical assistant professor, University of Mississippi Medical Center, Jackson, Mississippi.

Deborah Burkhart, RN, CCP - Director of Optimal Health Center; Santa Rosa, California.

Shanaz M. Tejani-Butt, PhD - Associate professor of pharmacology/toxicology, Philadelphia College of Pharmacy, University of the Sciences in Philadelphia.

Lisa R. Colodny, PharmD, BCNSP - Clinical Coordinator, Broward General Medical Center, Ft. Lauderdale, Florida.

Sylvia Crawley, MD - Former professor of medicine (cardiology), Emory University.

Mitchell J. Ghen, DO -Clinical associate professor, Nova Southeastern College of Osteopathic Medicine, Fort Lauderdale, Florida.

Joel Dennis Feinstein, MD - Assistant clinical professor of medicine, University of California at Los Angeles.

S. David Garshowitz, BSc Phm, EACA - President of San Total Health Pharmacy and York Downs Pharmacy, Ontario, Canada.

Jerry Hendricks, PhD - Professor, Department of Food Sciences, Oregon State University, Corvalis, Oregon.

Glen Hyland, MD - Board-certified radiation oncologist in Bismarck, North Dakota and clinical associate professor, University of North Dakota School of Medicine, Bismark, North Dakota.

Gitte S. Jensen, PhD - Assistant professor, faculty of medicine, McGill University, Montreal, Canada.

Richard L. Kingston, PharmD, CSPI - Vice president and senior clinical toxicologist, Prosar International Poison Center., St. Paul, Minnesota, assistant professor pharmacy, College of Pharmacy, University of Minnesota.

Jack J. Kleid, MD - Associate clinical professor of medicine and cardiology, University of California San Diego, School of Medicine.

Morris Maizels, MD - Dept. of Family Practice, Kaiser Perinanente, Woodland Hills, California. Coordinator of Kaiser-Permanente
National Headache Consortium.

Ronald Nickel, PhD - Associate professor of pharmacy practice and director of continuing education, College of Pharmacy, Medical University of South Carolina, Charleston, South Carolina.

Mary O'Brien, MD - Associate professor of medicine, University of North Carolina, director of geriatric services - Coastal AHEC.

David Perlmutter, MD - Board-certified neurologist with an integrative medical practice in Naples, Florida.

Norbert A. Pilewski, RPh, PhD - Associate professor of pharmacognosy, Duquesne University, School of Pharmacy. Pittsburgh, Pennsylvania.

Douglas J. Pisano, RPh, PhD - Associate professor of pharmacy administration. Massachusetts College of Pharmacy and Allied Sciences, Boston, Massachusetts.

June Riedlinger, RPh, PharmD - Associate professor of clinical pharmacy at Massachusetts College of Pharmacy and Allied Health Sciences, Boston., Massachusetts.

Steven Rosenblatt, MD,PhD, LAc - Founder and Pasi President, California Acupuncture College and cofounder and clinical director, UCLA Acupuncture Clinic, Los Angeles, California.

Manuel Sandoval, PhD - Assistant professor at Albany Medical University, Albany, New York.

Andrew L. Rubman, ND - Associate professor of clinical medicine, College of Naturopathic Medicine, University of Bridgeport, Bridgeport, Connecticut.

David Tatro, PharmD - Drug information consultant, San Francisco, California. Editor, Drug hitero('rion Fa('ts.

Randy Tobler, MD - Board-certified obstetrician and gynecologist, assistant professor in clinical OB-GYN. Washington University School of Medicine, St. Louis, Missouri.

Eugene R. Zampieron, ND, AHG - Founding board member and professor of Botanical Medicine and Ethnobotany, University of Brideport College of Naturopathic Medicine, Bridgeport, Connecticut.

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